Term
| What is Compliance a property of? |
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Definition
| The wall of the artery (due to its composition). |
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Term
| What is the major controller of vascular resistance? |
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Definition
| The small muscular arterioles (their radius is regulated by smooth muscle contraction). |
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Term
| Finish this sentence: Cardiac output is a function of... |
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Definition
| HR, Preload, Afterload and Contractility |
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Term
| What determines the control of arterial pressure in the short term? |
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Definition
| Rate of blood into the arterial system compared to rate of blood out of the arterial system. |
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Term
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Definition
| Increased sodium excretion in the urine as a result of increased mean arterial pressure - with more sodium leaving via urine, the total body sodium is decreased, which leads to a decrease in extracellular fluid (ECF) volume, resulting in a lowering of mean arterial pressure; Pressure natriuresis can only occur if the kidneys are funcitoning properly |
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Term
| What are some ways in which problems with the kidneys can cause HTN? |
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Definition
1) Plaque proximal to the kidney or renal artery stenosis - means a higher arterial pressure is required to push blood past the narrowed area so that it can be filtered by the kidney;
2) Glomerular disease (ex: decreased permeability, thickening of the wall,etc.) - means that higher tubular pressures (and therefore higher arterial pressures) are required to process soduium;
3) Hormonal disturbances that affect sodium reabsorption - increased reabsorption due to hormonal imbalance can lead to increased total body sodium, which leads to increased ECF volume, which in turn leads to increased BP until the BP reaches a high enough level that the renal tubules are flooded with so much sodium that the amount excreted ends up being normal again |
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Term
| When and How does the Renin-Angiotensin System Function? |
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Definition
TO INCREASE BP - WHEN: When ECF volume/ arterial pressure/ sodium intake is low; HOW: increased renin leads to increased reabsorption of sodium, which then leads to increased ECF volume and a subsequent increase in arterial pressure;
TO DECREASE BP - WHEN: occrs when sodium intake is high; HOW: decreased renin leads to decreased sodium reabsorption, so more sodum is excreted in the urine, resulting in lower total body sodum, which results in lower ECF volume, which ultimately results in lower BP; NOTE - the renin-angiotensin system is not as good at decreasing BP as it is at increasing BP, so we also have the hormonal natriuretic compounds (Ex: Atrial natriuretic peptide - ANP) to help decrease BP |
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Term
| When is Atrial Natriuretic Peptide (ANP) released? |
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Definition
| When the atria are stretched - the atria are stretched by increased ECF, which is caused by increased total body sodium - in this way ANP is triggered to help decrease BP |
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Term
| How does Atrial Natriuretic Peptide (ANP) work? |
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Definition
| It is a vasodilator (especially in the kidney) - it opposes vasopressin, aldosterone and the Renin-Angiotensin system; By vasodilating renal vessels, more blood is filtered by the kidneys, leading to an increase in sodium excretion, and therefore a decrease in total body sodium, resulting in lower ECF volume and ultimately lowering arterial pressure |
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Term
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Definition
| Inhibits Na/K ATPase - increasing sodium excretion and increasing intracellular calcium concentrations, which causes an increase in contractility (a decrease in preload); There is an endogenous digitalis-like substance (a cardiac glycoside) that may be increased in people with HTN, it is excreted by the kidneys; Because of the increased intracellular calcium, you also see an increase in peripheral vascular resistance (which causes increased arterial pressure) |
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Term
| How can (psychological) Stress cause HTN? |
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Definition
| Stress activates the SNS; If the SNS is activated without physical activity there is widespread vasoconstriction which leads to an increase in mean arterial pressure |
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Term
|
Definition
| Wall Stress = (P* radius)/ (wall thickness *2) |
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Term
| What are the Consequences of Chronic HTN for the Heart Muscle? |
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Definition
| Contracting against increased pressures will, by way of LaPlace's Law, lead to increased wall thickness, but no change in the chamber size (radius); Increased wall thickness translates into increased stiffness of the walls (because the new muslce that is put down in hypertrophy is not normal cardiac muscle, it has a lower contractility); The greater the left ventricular hypertrophy, the more pressure is required to fill it (increased preload) which leads to increased left atrial pressure which backs up to cause increased pulmonary congestion, ultimately leading to congestive heart failure if allowed to persist |
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Term
| What are the Consequences of Chronic HTN for Arterial Smooth Muscle? |
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Definition
| Arterial smooth muscle will hypertrophy, leading to vascular remodelling; The hypertrophy causes increased peripheral resistance which leads to further increases in pressure (sometimes the pressure is so high that if it persists for a long time untreated and then you treat them, the new lower BP will not be enough to get blood thru the remodeled vessles to perfuse the organs and patients may experience orthostatic hypotension, CNS symptoms, etc.); In larger arteries, the hypertrophy occurs in an outward direction, in the small muscular arterioles (which are the largest determinant of peripheral vascular resistance) the hypertrophy is both outward AND inward. |
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Term
|
Definition
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Term
|
Definition
|
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Term
|
Definition
|
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Term
| Factors Contributing to Excitation |
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Definition
| Automaticity (inherent rate); Excitability (SNS, PNS, etc.); Conductivity |
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Term
| Factors Determining Cardiac Contraction |
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Definition
| Elasticity (allows stretch; Starling's law says that the greater the stretch, the more forceful the contraction); Inotropy (force of the contraction); Chronotropy (pulse) |
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Term
| What is Responsible for the Excitation-Contraction Coupling in the heart? |
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Definition
| The neuromuscular junciton |
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Term
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Definition
| Caused by Slow-leaking of Calcium; Phase 0 of the AV node has a lower slope than that of the SA node (and the slope of the Purkinje fibers is even lower than that of the AV node), so if the SA node doesn't fire by the time the AV node reaches its threshold (at the end of phase 0), the AV node fires (this is sort of a back up system to make sure that the heart will still beat); The various slopes of the phase 0 help to explain the fact that the rate for the Purkinjes is slower than that of the AV node, which is, in turn, slower than the rate of the SA node |
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Term
| Pulseless Electrical Activity (PEA) |
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Definition
| AKA Electromechanical Dissociation (an older term); Excitation is occuring, but it is not coupled up with contraction |
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Term
| In Which Direction will the Deflection of the EKG be in the Electricty is Coming Toward the Positive Electrode? |
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Definition
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Term
| In Which Direction will the Deflection be if the Electricity is going Away from the Positive Electrode? |
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Definition
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Term
| In Which Direction will the Deflection be if the Electricity is Going Perpendicular to the Positive Electrode? |
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Definition
| Flat/ No deflection OR a very small positive/ upward deflection |
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Term
| What are the 3 Categories of EKG Leads? |
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Definition
| 1) Bipolar Limb Leads (I,II, III); 2) Unipolar Limb Leads (AVR, AVL, AVF); 3) Unipolar Precordial Leads (V1,V2,V3, V4,V5,V6) |
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Term
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Definition
| White electrode negative; Black electrode positive |
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Term
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Definition
| White electrode negative; Red electrode positive |
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Term
|
Definition
| Black electrode negative; Red electrode positive |
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Term
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Definition
| Placed on Upper Right Chest; Part of leads I and II (negative in both cases) and Lead AVR (positive in that case) |
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Term
|
Definition
| Placed on Upper Left Chest; Positive as part of Leads I and AVL, Negative as part of Lead III |
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Term
|
Definition
| Place on Left Abdomen; Part of Leads II,III and AVF; Always Positive |
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Term
| Memory Trick to Remember Electrode Placement |
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Definition
| "White upper Right, Smoke (black) over Fire (red)" |
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Term
|
Definition
| Always the ground; Place it anywhere |
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Term
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Definition
| White electrode is positive; Negative electrode is computer generated at the center of the triangle created by the white, black and red electrodes |
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Term
|
Definition
| The black electrode is positive; Negative electrode is computer generated at the center of the triangle created by the white, black and red electrodes |
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Term
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Definition
| The Red electrode is positive; Negative electrode is computer generated at the center of the triangle created by the white, black and red electrodes |
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Term
| How many wires/ electrodes are needed to create the 6 Limb Leads (I,II,III,AVR, AVL, and AVF)? |
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Definition
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Term
| What are the First 2 things you Should Do when You Get an EKG? |
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Definition
1) Check the patient name;
2) Check Lead AVR - it should be deflected downward, if it's not the paitent either has a big problem (ex: situs inversus, dextrocardia, etc.), or the EKG electrodes/ wires are wrong |
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Term
| How Many wires/ electrodes are needed to create the 6 Precordial Leads? |
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Definition
| 6 (one for each lead since they're unipolar; all 6 electrodes are positive and the negative electrode is computer generated at about the AV node) |
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Term
| Where is the Positive Electrode for V1 placed? |
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Definition
| 4th Intercostal Space at the Right Sternal Border |
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Term
| Where is the Positive Electrode for V2 placed? |
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Definition
| 4th Intercostal Space at the Left Sternal Border |
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Term
| Where is the Positive Electrode for V3 Placed? |
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Definition
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Term
| Where is the Positive Electrode for V4 Placed? |
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Definition
| Between the 5th and 6th Intercostal Space in the Midclavicular Line |
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Term
| Where is the Positive Electrode for V5 Placed? |
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Definition
|
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Term
| Where is the Positive Electrode for V6 Placed? |
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Definition
| Between the 5th and 6th intercostal space (i.e. same level as V4) in the Midaxillary line |
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Term
| How Many Wires/ Electrodes do you Need to Create a 12 Lead EKG? |
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Definition
| 9 (3 for the 6 Limb Leads, and 6 for the 6 Precordial Leads) |
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Term
| Why are EKG Machines Defaulted to Lead II? |
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Definition
| Because the electrical current of the heart normally goes in a direction that is most similar to the direction of Lead II with red as the positive (exploring) electrode |
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Term
| Which Lead(s) "Show" the Right Ventricle? |
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Definition
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|
Term
| Which Lead(s) "Show" the Septum? |
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Definition
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Term
| Which Lead(s) "Show" the Anterior portion of the Left Ventricle? |
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Definition
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Term
| Which Lead(s) "Show" the Left Lateral Portion of the Left Ventricle? |
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Definition
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Term
| Which Lead(s) "Show" the Left Wall of the Left Ventricle (but not the very most lateral portion)? |
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Definition
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Term
| Which Lead(s) "Show" the Inferior Wall of the Left Ventricle? |
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Definition
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Term
| What Artery Supplies the Anterior Wall of the Heart? |
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Definition
| Left Anterior Descending Artery |
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Term
| What Artery Supplies the Inferior Wall of the Heart? |
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Definition
| The Right Coronary Artery |
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Term
| What Artery Supplies the Nodes/ Pacemakers of the Heart? |
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Definition
| The Nodal artery, which branches off of the Right Coronary Artery; If the nodal artery is occluded, you start losing supply to the nodes (SA is furthest out on the artery, so it goes first and heart rate will decrease as the AV node takes over pacing, when/ if the AV node is lost the Purkinje's will take over pacing and the HR will drop further still) |
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Term
| If the Axis is Normal, what should Leads I and AVF look like? |
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Definition
| Both should show positive/ upward deflections |
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Term
| If the Axis is Deviated Left, what should Leads I and AVF look like? |
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Definition
| Lead I will have an upward/ positive deflection, and Lead AVF will have a negative/ downward deflection |
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Term
| If the Axis is Deviated Right, what should Leads I and AVF look like? |
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Definition
| Lead I will have a negative/ downward deflection, and Lead AVF will have a positive/ upward deflection |
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Term
| If the Axis is in "No Man's Land"/ Indeterminate, what should Leads I and AVF look like? |
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Definition
| Both will have a negative/ downward deflection (in addition, Lead AVR will have a positive/ upward deflection) |
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Term
| What do you need to look at if you see a ST depression? |
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Definition
| The reciprocal lead (ex: the reciprocal of lead III is lead AVL because they're basically oriented in directly opposite directions) - you need to check because while an ST depression could be ischemia, it could also be indicative of a reciprocal ST elevation, which represents injury or pre-infarct and is a serious finding with clinical significance |
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Term
| What is the significance of ST depression in Lead V2? |
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Definition
| It could be an ischemic event in the septum, but it could also indicate ST elevation from the posterior wall of the heart showing up reciprocally; There are no EKG leads that show the posterior wall of the heart, but you can look for reciprocal changes in the leads to the anterior heart (mostly V2) |
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Term
| What tissue makes up the Intima? |
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Definition
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Term
| What tissue makes up the Media? |
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Definition
| The media is usually the thickest part of the vessel wall; It is made up of a mix of connective tissue and smooth muscle (the ratio depends on the size/ type of artery) |
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Term
| What tissue makes up the Adventitia? |
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Definition
| Connective tissue; This layer contains the vasa vasorum |
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Term
| What is the arrangement of the elastic and smooth muscle fibers of the aorta and why is the beneficial? |
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Definition
| They are arranged in a spiral fashion (as opposed to concentric/ stacked rings); This is beneficial because, in this way, they absorb the high pressures coming off of the heart, but when the elastic fibers recoil, they provide propulsion to the downstream location |
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Term
| What Changes does Radiation Therapy cause to vessels? |
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Definition
| It causes damage to the vessel walls, transudation of proteins, disruption of the endothelium with clotting and thrombus formation and a reduced lumen diameter. |
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Term
| What are Some examples of Endothelial Cell Activators, and what do they do? |
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Definition
| EXAMPLES - cytokines and bacterial toxins, hemodynamic stress and lipids (cholesterol is the #1 offender), glycosylation end products of Diabetes mellitus, Viruses, Complement Molecules, Hypoxia; These substances/ processes irritate endothelial cells via production of adhesion molecules, cytokines, vasoactive and coagulaiton molecules; Cytokines recruit cells which can clog the lumen of the vessel; Vasoactive and coagulation molecules can cause overgrowth of clots which may occlude the lumen or grow into the wall itself; The walls of vessels can get weakened by these processes |
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Term
| What is the Extracellular Matrix made of/ Where does it come from? |
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Definition
| It is made of protein fibrils (not cells) and contains no nuclei (since it has no cells); It is made up of cellular products from endothelial cells (laminin and fibronectin) and Smooth Muscle Cells (collagens, elastin, proteoglycans) |
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Term
| What are the Functions of Extracellular Matrix? |
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Definition
| Adds volume and support to vessels; However, sometimes the added volume can result in stenosis or focal displacement of the usual elastic fibers and smooth muscle cells so that there's a potential for wall weakness. |
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Term
| What are the Categories of Damage to the Extracellular Matrix? |
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Definition
1) Mechanical (ex:pressure sores, penetrating wounds, etc.)/ Physical (ex: irradiation);
2) Immunological/ Toxins (ex: endotoxins from bacteria, etc.);
3) Multifactorial (ex: atheroma formation in atherosclerosis) |
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Term
|
Definition
| Artery Sclerosis; Involves thickened vessel walls plus a loss of elasticity; Three Patterns/Types - Monckeberg's, Arteriolosclerosis, and Atherosclerosis |
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Term
|
Definition
| A type of arteriosclerosis; Seen in the elderly; Calcium deposition in the media and internal elastic membrane; Vessels are able to be seen on x-ray; No clinical effect |
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Term
| What happens to the intimal with aging? |
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Definition
| It thickens; this is normal |
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Term
|
Definition
| A type of arteriosclerosis; Arteriole sclerosis; An end product of HTN and Diabetes mellitus; Thickened intima and media |
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Term
| Epidemiology of Atherosclerosis |
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Definition
| The leading cause of death in the developed world; In the US - 11 million people have CAD, 1.5 million have MIs annually, 500,000 MI deaths annually cost $100 billion, 200,000 CVA deaths annually, 50 million people are candidates for lipid therapy |
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Term
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Definition
| Form in muscular arteries and elastic arteries, but not in arterioles; Contents - cells, lipids, neovascularization; Can eventually see calcium deposition; Macrophages (called in by endothelial/ tissue damage along with clot formation) ingest cholesterol and phagocytize it to become foam cells, the foam cells eventually break down and the cholesterol comes out again - this is part of the process of atheroma formation/ the mechanism of atherosclerosis |
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Term
| Initial Sites of Atherosclerosis |
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Definition
| The process starts out at bifurcations where pressure changes and turbulence are most prominent; The current theory of atherosclerosis pathogenesis is that it is an inflammatory process |
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Term
| Sites of Arteriosclerosis |
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Definition
| More in the abdominal aorta than in the thoracic aorta because the thoracic part is surrounded by the soft contents of the mediastinum, and the abdominal aorta is rubbing up against the lumbar spince |
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Term
| Lab Studies Recommended by the Mayo Clinic for Atherosclerosis Risk |
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Definition
| Lipid Profile (total cholesterol, LDL, HDL, Triglycerides); Fibrinogen (to see how the liver is producing clotting factors); C-Reactive Protein (an acute phase reactantl can be elevated in any inflammatory process); Homocysteine; CT scan of the heart to evaluate Calcium in the arteries |
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Term
| What is Homocysteine and what is its potential role in Atherosclerosis? |
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Definition
| Homocysteine binds to plasma proteins and generates peroxides which damages endothelium (a precursor to the type of atherosclerosis that involves fibrous plaques without lipid contents); Normally homocysteine is converted into the harmless cystathionine via the enzyme cystathionine beta-synthase which is B6 dependent, thus, patients who have low B6, B12 and folate levels will have elevated homocysteine levels and may then develop atherosclerosis |
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Term
| What is Malignant Hypertension, and why is it so harmful? |
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Definition
| A BP of at least 200/120 mmHg; It causes fibrinoid extravasation and deposition - plasma proteins are forced into the vessel wall by the high pressures; eventually enough fibrinoid may get into the wall that it compresses the smooth muscle cells and kills them - in the long term, the vessel wall can burst and the patient can hemorrhage |
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Term
| What is the end Result of Hypertensive Vascular Disease |
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Definition
| Almost no lumen, hyaline sclerosis, and necrosis/ scarring of the downstream tissues causing resultant organ failure (ex: renal failure) |
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Term
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Definition
| A focal dilatation of a vessel wall; TRUE aneurysm - the dilatation has the same wall composition as the rest of the vessel; FALSE aneurysm - the wall in the area of the aneurysm is broken and blood goes out into the surrounding soft tissues, stagnants and forms lines of Zahn |
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Term
| What is the Number One Cause of Death in Aneurysm Patients? |
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Definition
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Term
|
Definition
1) Infective - direct extension (from the outside) or via circulation (arrising in the lumen), Labs: blood cultures; 2) Immune-Mediated - with immune complexes in the serum or in the vessel wall, Labs: ANCA, anti-EC, RF, ANA, Total Ig, IgM levels;
3) Other - irradiation, mechanical trauma, toxins, get a good history |
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Term
|
Definition
| An infected aneurysm (doesn't mean fungal necessarily) |
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Term
| What happens with Untreated Temporal Giant Cell Arteritis? |
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Definition
| It begins effecting blood vessels further down the body |
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Term
| Test for Giant Cell Arteritis |
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Definition
|
|
Term
| Morphology of Giant Cell Arteritis |
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Definition
| Thick vessel wall, tiny lumen, internal elastic membrane with lymphocytes, look for giant cells; There may be a focal necrotic zone on the tongue when the giant cell arteritis progresses downward, so check the patient's mouth |
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Term
| 4 Types of Giant Cell Arteritis Involving the Aorta |
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Definition
Type I - ascending aorta;
Type II - descending aorta;
Type III - both;
Type IV - pulmonary arteries |
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Term
|
Definition
| AKA Pulseless Disease; Usually occurs in patients less than 40 yo; SXS - difficulty breathing, no radial pulses, heaviness in the chest; Fibrotic vessel wall, virtually no lumen; Effects vessels coming off of the aorta |
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Term
|
Definition
| Thick vessel wall, narrow lumen; NO renal or pulmonary involvement; Rapid development of HTN; Significant lymphocytosis in the adventitia |
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Term
|
Definition
| AKA "mucocutaneous lymph node syndrome"; Coronary artery aneurysms; Arteritis (fibrosis) in renal and testicular vessels; Seen in kids |
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Term
| Leukocytoclastic Vasculitis |
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Definition
| AKA Acute Microscopic Polyangitis; Hemoptysis, hematuria, palpable nodules; Neutrophils and lymphocytes; No granulomata (unlike with Wegener's); Test for p-ANCA |
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Term
|
Definition
| SXS - severe epistaxis, hemoptysis, pleuritic pain, hematuria; c-ANCA; Granulomas in parenchyma adjacent to and extending into vessels |
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Term
|
Definition
| AKA Thromboangiitis obliterans; Affects mostly the radial and tibial arteries in men under 35; Hypersensitivity to tobacco and cold; Can affect adjacent veins and nerves; Biopsy shows intimal thickening and atrophy of the overlying skin; 25% of patients have a family history of the disease; Secondary Raynaud's (Raynaud's that overlaps another autoimmune disease) may occur and is a vasoconstriction that involves cold induced pain and a distinct color change |
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Term
| S/S of Tumors and Tumor-Like Conditions of Blood Vessels |
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Definition
| Colored (red or purple) area that is pulsatile on palpation |
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Term
|
Definition
| Females - 250g; Males - 350 g; Cardiomegaly - >400g |
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Term
| 5 Major Components of Cardiac Myocytes |
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Definition
| 1) Cell Membrane and tubules; 2) Sarcoplasmic reticulum (calcium reservoir); 3) Contractile proteins; 4) Mitochondria (10x the amt found in skeletal muscle); 5) Nucleus; You can damage all components except for the nucleus and regain myocyte function, as long as treatment is timely |
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Term
| 2 Types of Natriuretic Peptides |
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Definition
| A Type - from atrial myocardial cells; B Type - from ventricular myocardial cells |
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Term
|
Definition
| 80% of people are Right Coronary Dominant (right or left coronary dominance depends on whether the right or left coronary artery gives off blood supply to the posterior surface of the heart); Intercoronary anastamoses are used as necessary; The Subendocardium is at risk becuase it is furthest away from the coronary vessels |
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Term
| Normal Components of Heart Valves |
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Definition
| Endocardial surfaces, fibrosa (collagen core for strength), spongiosa (allows for stretching), and ventricularis (elastin, stretch recovery) |
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Term
|
Definition
| STENOSIS - chronic valve obstruction, filling defect; REGURGITATION - valve closure incompetence, emptying defect; Endpoint - mechanical dysfunction, increased myocardial workload |
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Term
|
Definition
| The #1 cyanotic disease of neonates; Involves - ventricular septal defect (VSD), overriding aorta, Right ventricle outflow obstruction, and right ventricle hypertrophy |
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Term
| What is considered a positive CK-MB level for an MI? |
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Definition
|
|
Term
| When might Troponin I be positive? |
|
Definition
|
|
Term
| Acute Myocardial Infarction (MI) Timeline |
|
Definition
| Time | Gross | Micro | | 0.5-4 H | None | Wavy fibers? | | 4-12 H | Mottling | Coag necrosis, RBCs | | 12-24 H | Dark | Necrosis, segmented neutrophils | | 24-72 H | Yellow Center | Increasing Segs, loss of nuclei and striations | | 3-7 D | Brown border, soft center | Nuclear dust, myocytes, disintegration, phagocytes | | 7-10 D | Max Softness | Marginal granulation tissue | | 10-14 D | Gray Depression | New vessels and collagen | | 2-8 Wk | Light Gray | More collagen, decreased cells | | >2 MO | White Scar | Dense CT |
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Term
| What can be a Potential Complication of Reperfusing Cardiac Muscle? |
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Definition
| When you break up the clot occluding a coronary vessel, the reprefused muscle is able to carry out one good contraction, so the heart contracts, but doesn't have enough ATP to release the contraction so the heart is stuck in contraction and the patient dies of cardiac arrest; At autopsy, the cardiac muscle demonstrates contraction bands (fibers that are still overlapped/ contracted) |
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Term
| What is one of the criteria for Sudden Cardiac Death? |
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Definition
| The patient must be dead within one hour of having an MI |
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Term
|
Definition
| Right-sided heart failure secondary to pulmonary disorders |
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|
Term
| What causes Acute Cor Pulmonale? |
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Definition
|
|
Term
| What causes Chronic Cor Pulmonale? |
|
Definition
| Emphysema, Pulmonary HTN, etc. |
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|
Term
| What are the Outcomes of Cor Pulmonale? |
|
Definition
| Pressure backs up into the portal system and the systemic circulation, patients may get minimal lung congestion |
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|
Term
| What are the effects of Cor Pulmonale on the Heart? |
|
Definition
| Myocardial dysfunction, dilatation, congestive failure, sudden death |
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|
Term
| What Conditions Predispose someone to Cor Pulmonale? |
|
Definition
| 1) Obstructive Pulmonary Diseases (Fibrotic Endstage) - COPD, interstitial fibrosis, CF, Bronchiectasis, pneumoconioses; 2) Vascular Diseases of the Pulmonary System (blood flow interruption) - Thromboembolism, HTN, arteritis, obstruction, mets; 3) Abnormal Chest Movement (Restrictive) - spine, obesity, neuromuscular disease; 4) Inducing Arterial Constriction (decreased oxygen saturation) - hypoxia, acidosis, altitude, airway obstruction |
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Term
| SXS and Prognosis of Aortic Valve Stenosis |
|
Definition
| Deposits preven cusp opening, leading to increased Left ventricular pressure; 50% of patients with Angina as a result of stenosis are dead in 5 years; 50% of patients with CHF as a result of the stenosis are dead in 2 years |
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|
Term
| SXS of Mitral Valve Stenosis |
|
Definition
| Nodules behind the leaflet on the annulus with normal function; At risk for regurgitation or stenosis, conduction abnormalities, or infection |
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|
Term
| What Component of the Extracellular Matrix does Marfan Syndrome affect? |
|
Definition
| Marfan's is caused by a mutation of the gene encoding for Fibrillin-1 |
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|
Term
| When Should Blood Cultures be Drawn in the Work-Up of a Patient with Suspected Infective Endocarditis? |
|
Definition
|
|
Term
|
Definition
| S/S - fever, flu-like sxs, murmur; DX - blood cultures, ECHO; Most Common Sites - Aortic and/ or Mitral valves; Vegetations - friable, can give rise to thromboemboli; Acute vs. Subacute? - need a good history; Big Red Flags - cardiac abnormality or surgery, IV drug abuse; 50% mortality rate; BUGS - 50% of cases are caused by strep, 10% by staph |
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|
Term
|
Definition
| DUE TO - hypercoaguable states, circulating tumor products; Vegetations are sterile (no organisms seen with special stains) and nondestructive; Patients with marantic vegetations are at risk for emboli to the brain and kindeys |
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|
Term
|
Definition
| DILATED - heavy, flabby heart - idopathic, molecular defects of the sarcomere, contractile (systolic) dysfunction results; HYPERTROPHIC - think idiopathic hypertrophic subaortic stenosis (of the septum, IHSS), Primarily a diastolic dysfunction (because heart muscle has hypertrophied into the chamber, so the chamber can't fill), obstruction |
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Term
| Idiopathic Dilated Cardiomyopathy |
|
Definition
| Systolic dysfunction with hypocontraction; Fiber hypertrophy, Increased subendocardial fibrosis; Etiologies - idiopathic, post-viral (ex: URI), ethanol toxicity, pregnancy, genetic (autosomal dominant, X-linked to dystrophin) |
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Term
| Hypertrophic Cardiomyopathy |
|
Definition
| Diastolic dysfunction without dilatation, extreme LVH, Decreased Left ventricle volume (decreased filling, decreased output, increased PV pressure); Left ventricle chamber distortion; Outflow obstruction in 25% of patients with this condition; Associated with over 100 gene mutations |
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Term
|
Definition
| Infiltrative (ex: space occupying lesions/masses) and Mechanical Insults - amyloid, sarcoid, irradiation, endocardial fibrosis; Other myocarditis causes - viral (coxsackie A & B, CMV, HIV), allergic reaction, systemic diseases (amyloidosis, sarcoidosis, etc.); Dx via serologic titers, biopsy |
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Term
| Fibroelastosis of Endocardium |
|
Definition
| Constrictive/ Restrictive cardiomyopathy |
|
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Term
| "Bread and Butter" Pericarditis |
|
Definition
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Term
|
Definition
| Assume malignancy in the area or a proteinaceous exudate with a gravity of > 3g/sec; 20-40% of RA patients can get pericarditis which may end up causing pericardial adhesions if allowed to progress |
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Term
|
Definition
| Clonal neoplasms (not necessarily malignant); 90% present with obstructive symptoms; Some recur post-operatively; Myxoid CT is the bulk of the volume of the myxoma |
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Term
| Heart Transplant Rejection |
|
Definition
| Angiopathy - since the heart is denervated, the patient can have MIs and not feel them (Silent MIs) or sudden death; With Rejection the there may be Significant myocardial patchy infiltrates; Immunosuppressive drugs used to prevent rejection may cause significant intimal fibrosis |
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Term
| What are the Determinants of Cardiac Output? |
|
Definition
| The flow demanded, which is determined by tissue metabolic demands and homeostatic requirements; If the flow demanded and the flow provided are equal, you have circulatory success (ideally you want them to be equal at a normal mean arterial pressure); If the flow provided is less than the flow demanded, you have circulatory failure |
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Term
| What are the Determinants of Cardiac Output? |
|
Definition
| Heart rate and stroke volume. |
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Term
| What are the 3 Components of Stroke Volume? |
|
Definition
| Preload, Afterload, and Contractility. |
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Term
|
Definition
| A fraction of stroke volume goes backward, so the amount going forward (output) decreases; Acute solution - increase SNS stimulation; Chronic Solution - increase extracellular fluid volume, increase stroke volume, and increase preload (since ECF increases, you get increased arterial and venous pressures, which may lead to edema/ pulmonary edema [poor gass exchange]) |
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Term
| How is the Hypertrophy of the heart that is caused by HTN different from the hypertrophy caused by Increased Preload? |
|
Definition
| With increased preload, the radius of the heart's chambers increase and the heart responds via the law of LaPlace by increasing wall thickness to balance things out, so you end up with hypertrophy in such a way that the ratio of radius:wall thickness is normal; With HTN (i.e. increased afterload), the pressure portion of the law of LaPlace has increased, so wall thickness increases to balance it out, however, in this situation, there is no increase in radius, so your ratio of radius: wall thickness is abnormal |
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Term
| When in the Heart Cycle would you hear a Murmur caused by Mitral Regurgitation? |
|
Definition
| Between S1 and S2 (systole) |
|
|
Term
| When During the Heart Cycle would you Hear a Murmur Caused by Aortic Regurgitation? |
|
Definition
| Between S2 and S1 (Diastole) |
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Term
| Arterial-Venous Malformations |
|
Definition
| A type of "high-output state" since there are more areas for the blood to flow than usual, the heart has to pump out more blood; A-V malformaitons cause decreased peripheral resistance, so BP falls and the body responds by increasing extracellular fluid volume |
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Term
| How Does the Body Respond to Mitral Valve Stenosis? |
|
Definition
| With mitral valve stenosis, the left ventricle filling is decreased, and the body tries to fix this low LVEDV (left-ventricular end diastolic volume) by increasing extracellular fluid volume to increase pressures in order to push past the stenotic valve; The problem is that pressures can get so high that blood backs up into the pulmonary vessels and you get pulmonary congestion due to the increased pulmonary vascular pressures |
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Term
| Role of Calcium and ATP in Myocardial Contraction |
|
Definition
| For a cardiac action potential, L-Type calcium channels in the myocardium open and calcium comes in. This calcium promotes calcium to be released from the sarcoplasmic reticulum (this is called calcium-induced calcium-release). In order for the contraction to stop, calcium needs to get taken back up into the sarcoplasmic reticulum. This occurs via the sarcoplasmic endoplasmic reticulum ATPase (SERCA). So, if ATP is in short supply, calcium reuptake qill be slower than normal - the ventricles won't relax as quickly as a result and therefore filling is delayed. (Lack of ATP can occur as a result of myocardial ischemia; The rate of relaxation is a lusotropic effect, so you would say that ischemia has a negative lusotropic effect). |
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Term
| SNS effects on Myocardial Calcium Use |
|
Definition
| SNS stimulation causes myocardium to let more calcium in, this calcium influx means that more calcium is released from the sarcoplasmic reticulum (and released faster) and that SERCA activity is increased, so calcium is also taken up faster; The end result is: Faster, stronger, shorter contractions with SNS stimulation |
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Term
| What Happens When Myocardial Oxygen Needs are Increased? |
|
Definition
| The myocardium is already really good at extracting oxygen from blood, so if myocardial oxygen needs increase, the myocardium can't just extract more oxygen from the blood (since it's close to max already), so coronary blood flow must be increased to meet the demand; If it can't, not enough oxygen and not enough ATP will be available for the myocardium, there won't be enough calcium available for a contraction (so systolic failure) and the lack of ATP means that the calcium that is there can't get taken up by SERCA to end the contraction that is able to occur (higher than normal calcium during diastole means that the heart can't relax and fill) |
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Term
|
Definition
| Digitalis increases contractility by inhibiting the sodium/ potassium ATPase, which causes an increase in intracellular sodium in myocardial cells. This sodium is exchanged for calcium, which facilitates the contraction. |
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Term
| Effects of Prolonged Stimulation of the Heart |
|
Definition
1) Decrease in the # of B1 receptors in the heart and phosphorylation of some of the remaining B1 receptors (which decreases their activity) - overall result is that you get a decreased responsiveness to catecholamines;
2) Increased membrane Gi proteins in the heart - so you get inhibition of adenylyl cylcase activity leading to a decrease in cAMP;
3) Increased expression of mRNA for the L-Type Calcium channel;
4) Increased phospholamban (an inhibitor of SERCA);
5) Re-expression of the fetal type of myosin - this myosin contracts more slowly and uses less oxygen than adult myosin (the heart is trying to preserve its energy);
6) Hypertrophy and apoptosis of heart muscle; Increased CT in the heart as well;
** Since the long-term effects of excessive catecholamine stimulation are so harmful, one treatment for impaired contractility is to block the B1 receptors (i.e. Beta blockers), even though stimulation of B1 receptors increases contractility; ACE Inhibitors and angiotensin II blockers work by the same logic |
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Term
|
Definition
| Represents atrial depolarization; With sinus rhythm, the P wave is upright in Lead II; the P wave may be inverted or absent |
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Term
|
Definition
| The first 'negative' deflection of the QRS complex; May be absent; May or may not be pathological |
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Term
|
Definition
| First 'upward' deflection of the QRS complex; ALWAYS positive; May be absent; Has amplitude if present |
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Term
|
Definition
| ALWAYS 'negative'; Follows R wave if present; May be absent; Has amplitude if present |
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Term
|
Definition
| Represents Repolarization; Normally upright/ positive; May indicate pathology; Always follows the QRS complex |
|
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Term
|
Definition
| Represents ventricular depolarization |
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Term
|
Definition
| Represents AV Conduction time |
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Term
|
Definition
| Represents ventricular depolarization and repolarization time; Can be altered/ prolonged by certain medications (ex: cipro) - refractoriness gets dispersed, and the patient becomes more susceptible to sudden cardiac death |
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Term
|
Definition
| If the rhythm is regular, you can get a rough estimate of rate by the number of large boxes between R waves. The peak of the first R wave is the "start" the next large box is 300, the following one is 150, etc. counting this way until you hit the next R wave. Count goes: 300bpm ,150,100, 75, 60, 50, etc. If the rhythm is irregular, you need to figure out the average beats per span of time - you can also measure the rate of the fastest area and the rate of the slowest area and report the rate as a range between those values (ex: HR is 60-90 bpm); If you suspect the rate is below 60, you look at a 6 second strip and count the number of beats within that time, then multiply this number by 10 to get the rate (ex: 3.5 beats in a 6 second strip, rate = 3.5 x10 = 35bpm) |
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Term
| Right Axis Deviation Boundaries |
|
Definition
| Greater than or equal to +105 degrees (these are Dr. Glasses values, other people define the boundaries of axis slightly differently) |
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Term
|
Definition
| -29 degrees to +105 degrees (these are Dr. Glasses values, other people define the boundaries of axis slightly differently) |
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Term
| Left Axis Deviation Boundaries |
|
Definition
| Greater than or Equal to -30 degrees |
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Term
| Indeterminate Axis Deviation Boundaries |
|
Definition
| Roughly between +180 and -90 degrees (these are Dr. Glasses values, other people define the boundaries of axis slightly differently); AKA "no man's land"; Called indeterminate because you can't determine if the axis got there by way of an extreme left or an extreme right axis |
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|
Term
| What is the axis if the EKG is Positive in Lead I and Positive in Lead II? |
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Definition
|
|
Term
| What is the Axis if the EKG is Positive in Lead I and Negative in Lead II? |
|
Definition
|
|
Term
| What is the Axis if the EKG is Negative in Lead I and Negative in Lead II? |
|
Definition
|
|
Term
| What is the Axis if the EKG is Negative in Lead I and Positive in Lead II? |
|
Definition
|
|
Term
| What does an Isoelectric Lead tell you About the Axis of the EKG? |
|
Definition
| If you have a lead that is isoelectric, then the axis will be perpendicular to that lead (ex: if Lead I is positive and Lead II is isoelectric, then the axis is perpendicular to Lead II and in the direction of a positive lead I - i.e the axis points to -30 degrees) |
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|
Term
| What Condition has a Right Axis Deviation as a criteria? |
|
Definition
| Right Ventricular Hypertophy |
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|
Term
| What is the Rhythm if there is a Constant R-R Interval, and P Waves that are Upright in Lead II? |
|
Definition
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|
Term
| Criteria of Normal Sinus Rhythm |
|
Definition
1) P wave of sinus origin (upright P in II and inverted P in AvR);
2) Constant P wave configuration in each lead (i.e. all P waves look the same);
3) Constant P-P interval (i.e. the rate is regular);
4) Normal P-R Interval (between 0.12 and 0.20 seconds);
5) Rate between 60 and 100 bpm |
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|
Term
| What is a Normal P-R Interval? |
|
Definition
|
|
Term
| 4 Variations of Sinus Rhythm |
|
Definition
1) Normal Sinus Rhythm;
2) Sinus Bradycardia;
3) Sinus Tachycardia;
4) Sinus Arrhythmia (this is just a variation of normal that represents a variation in sinus rhythm related to changes in breathing) |
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|
Term
| 4 General Types of Arrhythmias |
|
Definition
1) Supraventricular;
2) Ventricular;
3) Atrioventricular and Intraventricular Block;
4) Preexcitation Syndromes |
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|
Term
| What is the Rhythm if it is Regular with NO P Waves? |
|
Definition
| Junctional (note: the junction conducts slower than the SA node, so the rate would likely be in the 40-60 bpm range) |
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|
Term
|
Definition
| Sinus node is unable to produce a cardiac impulse, so you see no P wave, but hopefully another area of the heart will beat, initiating an "escape beat" (if the escape beat is juncitonal in origin, the QRS complex will be narrow; if it's ventricular in origin, the QRS complex will be wide); This is a medical emergency, and treatment is a pacemaker |
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|
Term
| What are the 5 Irregular Rhythms? |
|
Definition
1) Atrial or Ventricular Ectopy;
2) Atrial Fibrillation (AF);
3) Atrial Flutter (AFL);
4) Multifocal Atrial Tachycardia (MAT);
5) Mobitz I Second Degree AV Block (AKA Wenckebach) |
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|
Term
|
Definition
| Beats that arrise from some ectopic (non-SA, non-AV, etc.) site; Premature; When ectopic beats occur, the heart may or may not contract |
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|
Term
| What are the 5 Types of Atrial Dysrhythmias? |
|
Definition
1) Atrial Premature Depolarizations (APD);
2) Paroxysmal Atrial Tachycardia (PAT);
3) Atrial Fibrillation (AF);
4) Atrial Flutter (AFL);
5) Atrial Fib-Fluttler (AF-FL) - this is where you can't tell whether it's AF or AFL, so you call it a combination |
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|
Term
| Types of Ventricular Conductions seen with Atrial Premature Depolarizations (APDs) |
|
Definition
1) Normal Conduction - the premature depolarization of the atria transmits to a normal ventricular conduction/ normal QRS complex;
2) Abberent Conduction - the QRS complex is wide (it's not always easy to differentiate between ventricular premature depolarizations and APDs in this case);
3) Blocked Conduction - the atrial depolarization doesn't cause a ventricular conduction (perhaps becuase the ventricular system is still refractory), no QRS Complex is seen |
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|
Term
| Findings that Support Abberency of Ventricular Conduction with Atrial Premature Depolarizations (APDS) |
|
Definition
1) Ectopic P wave preceding the beat (P wave will look different from normal SA Node-generated P waves because it's being created by a different area);
2) Right Bundle Branch Block (RBBB) Pattern;
3) Identical vector in normal and premature complex;
4) Ashman's Phenomenon (the longer the ventricular cycle, the longer the refractory period following it and vice versa); Aberrancy occurs because part of the ventricular conduction system is refractory, but part of it is not so you get a ventricular conduction but it isn't normal |
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|
Term
|
Definition
| Regular; 1:1 Conduction (for every P wave, there's a QRS complex); Rate 150-250; Paroxysmal (PAT) and Non-Paroxysmal (NPAT) - PAT is much more common than NPAT (NPAT may be caused by digitalis toxicity) |
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|
Term
| Supraventricular Tachycardia (SVT) |
|
Definition
| A regular HR with narrow QRS complexes and P waves that are difficult to discern; DDx includes Paroxysmal Atrial Tachycardia (in reality, PAT is a type of SVT) |
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|
Term
| Wolff-Parkinson-White Syndrome |
|
Definition
| A pre-excitation syndrome caused by an abnormal conduction pathway (known as a Kent Bundle) through the Atria to the ventricles; The conduction through the heart doesn't follow its normal pathway, and conduciton through the bypass tract is faster than through the normal conduction system and you can get retrograde conduction of the impulse through the bypass tract as well; The heart rate can get so fast as to be life-threatening in some cases of WPW Syndrome |
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|
Term
| Diagnostic Criteria of Wolff-Parkinson-White Syndrome |
|
Definition
| Initial slurring onf the QRS Complex (called a delta wave, this is the most impotant finding for Dx of WPW Syndrome); Short P-R interval; Prolonged QRS interval; Secondary T wave change (not always present) |
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Term
|
Definition
| Irregularly irregular; Atrial Rate 400-600bpm; No consistent baseline atrial activity (undulating baseline); Ventricular Response: Controlled (60-100bpm), Rapid (>100bpm), Slow (<60bpm); No P waves |
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Term
|
Definition
| Atrial Rate of 250-350bpm; Atrial rate is a multiple of the ventricular rate (ex: 3 atrial beats per 1 ventricular beat would be a 3:1 flutter, If flutter is 1:1 the ventricular rate would have to be 250-350 bpm); Flutter (F) waves seen (downward atrial waves); Regular or variable AV response; Can "co-exist" with atrial fibrillations (called atrial fib-futter); "Flutter" waves can look like a SAW TOOTH pattern (not all flutter waves have that pattern though, so it's not a diagnostic criteria); NOTE - whenever you see a normal/ narrow QRS complex tachycardia at (almost exactly) 150bpm, it is atrial flutter until proven otherwise; If an AV block is present along with the atrial flutter, the atrial rate will be constant, but the ventricular response will vary since not all atrial beats will get through the conduction system to trigger the ventricular conducting system |
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|
Term
| Multifocal Atrial Tachycardia (MAT) |
|
Definition
| Irregularly irregular; Tachycardia; P waves seen clearly; Multiple P-wave Morphologies (you must see >2 morphologies to make the Dx); DDx - atrial fibrillations (treatment is different, so it's important to make the distinction); Note - the setting in which you would see MAT is one in which the patients tend to be very sick with some sort of respiratory problem, so MAT tends to be seen in the ICU |
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|
Term
| Benign Ventricular Dysrhythmias |
|
Definition
| Benign means they don't increase the risk of sudden cardiac death; Examples: VPDs in healthy individuals, VPDs that go away with exercise, Accelerated idioventricular rhythm (AIVR), Ventricular parasystole |
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|
Term
| Potentially Lethal Ventricular Dysrhythmias |
|
Definition
| VPDs (wide QRS complexs) that are multiform, R on T and/ or provoked by exercise; Ventricular tachycardia (sustained or non-sustained); Ventricular Fibrillation |
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Term
|
Definition
| Classic Criteria: QRS Duration >0.14 sec, Fusion beats (activity coming from the atria and the ventricles fuses, fusion beats are pathognomonic for V.tach), A-V Dissociation, Superior QRS Axis |
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|
Term
|
Definition
| Torsade is a variant of Ventricular Tachycardia caused by prolongation of the QT Interval; Treatment is to shorten the QT interval or override the pacing; This condition doesn't respond to typical antiarrhythmetic medications; Patients are pulseless during the run of Torsade |
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Term
|
Definition
| Defined by a prolonged PR interval (>0.2sec) |
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|
Term
| Mobitz I- 2nd Degree AV Block (Wenckebach) |
|
Definition
| Irregular Rhythm; P waves present; PR Interval prolongs gradually (P-P interval remains constant however); Dropped QRS Complex (ex: 3 p waves per 2 QRS complexes would be a 3:2 Wenckebach); "Grouped beating"; If the bloc is a 2:1 Wenckebach, there will be a "narrow" QRS Complex |
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|
Term
| Mobitz II 2nd Degree AV Block |
|
Definition
| Regular rhythm; 2 P waves per QRS complex; P-P interval constant; QRS Complex is usually wide (helps differentiate it from 2:1 Wenckebach); Infranodal block (i.e. the block is below the nodes, Mobitz II occurs lower in the conduction system than Mobitz I - risks are higher the lower in the conduction system you get block); Requires a pacemaker |
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Term
|
Definition
| Multiple P waves for each QRS; Slow ventricular rate (escape); AV dissociation - P waves "march through" QRS complexes, Possible capture beats (vs 3rd degree/ Complete heart block - AV dissociation) |
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|
Term
| Criteria for Right Bundle Branch Block (RBBB) |
|
Definition
| QRS interval is greater than or equal to 0.12sec (3 small boxes); RR' in leads V1 and (sometimes)V2; Prominant S waves in Leads I and V6 (normally, you don't see S waves there) |
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|
Term
| Criteria for Left Bundle Branch Block (LBBB) |
|
Definition
| QRS interval greater than or equal to 0.12 sec (3 small boxes); "QS" Pattern in V1 (negative/ downward deflection); RR' in leads I and V6 (looks like Devil's Tower in Wyoming) |
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|
Term
| Left Anterior Fascicular Block (LAFB) |
|
Definition
| One of the most common EKG abnormalities because the left anterior fascicle (LAF) is easy to damage; The LAF conducts left to right so it shifts the axis to the left when damaged; Criteria for LAFB - Marked Left axis deviation (-45 to -90 degrees), Narrow QRS Complex |
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|
Term
| Left Posterior Fascicular Block (LPFB) |
|
Definition
| The left posterior fascicle (LPF) is a large structure and it is therefore hard to damage it, so if you have a LPFB, you've had a significant MI/ trauma; LPF Conducts right to left so damage to the LPF shifts the axis to the right; Criteria for LPFB - Marked Right Axis Deviation (+105 to +180 degrees), Narrow QRS Complex |
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|
Term
|
Definition
| RBBB + LAFB (left axis) or RBBB + LPFB (Right Axis); Both would have a wide QRS Complex due to the RBBBs |
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|
Term
| Non-Specific Intraventricular Conduction Delay (NSIVCD) |
|
Definition
| Wide QRS, Neither LBBB or RBBB criteria met |
|
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Term
|
Definition
| RR' in V1, QRS L.T is 0.11 sec |
|
|
Term
| Incomplete Bundle Branch Blcok |
|
Definition
| QRS Duration is exactly 0.11 seconds |
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|
Term
| Left Atrial Abnormality on EKG |
|
Definition
| EKG shows P Mitrale (an old term) - wide and notched P waves (greater than 3mm) in Lead II; EKG also shows Inverted (negative) terminal component of P wave in Lead VI |
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|
Term
| Right Atrial Hypertrophy on EKG |
|
Definition
| EKG Shows P-pulmonale - Tall (3mm) P waves in Leads II and III; Don't trust the computer interpretation 100% because the computer will call it right Atrial Hypertrophy even if the P-waves are less than 3mm tall |
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|
Term
| Left Ventricular Hypertrophy on EKG |
|
Definition
VOLTAGE CRITERIA - S wave in V1 and R wave in V6 must add up to 35mm (look at the tallest R wave and the deepest S wave, NOTE - in people under 35, the voltage must be 50 mm to meet criteria), also look at the tallest R wave in lead AVL to see if it is more than 11mm (doesn't meet voltage criteria if this is the only finding though);
ST CRITERIA - ST changes in leads V5 and V6 (T wave inversion with or without ST depression);
To be called LVH based on EKG findings, the EKG must meet voltage criteria or voltage and ST criteria (can't just meet ST Criteria, this is because ST changes alone suggest ischemia - the voltage criteria help to explain the ST changes, but even still you can't completely rule out ischemia) |
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|
Term
| Right Ventricular Hypertrophy on EKG |
|
Definition
| Right Axis Deviation AND Tall or "relatively tall" R waves in Lead V1 (usually there are no R waves - or just a tiny blip - in lead V1, so any R wave at all is considered "tall") |
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|
Term
| Diagnostic Criteria of Biventricular Hypertrophy |
|
Definition
| LVH pattern in precordial leads and Right axis deviation in limb leads; Less reliable findings - Tall R wave greater than or equal to 26mm in V5 or V6 and tall (or relatively tall) R wave in V1, High voltage in V3 or V4 (RS complex greater than or equal to 40mm) with LVH or RVH pattern, P-pulmonale or P-congenitale in limb leads and LVH pattern in precordial leads |
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|
Term
| Myocardial Ischemia on EKG |
|
Definition
| T wave inversion (the T wave is usually symmetrical as well) that is often localized to a particular area of the heart (ex: inferior ischemia shows up in leads II, III and AVF) |
|
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Term
|
Definition
| ST Elevation Myocardial Infarction - these patients often go immediately for intervention (Catheterization, CABG, etc.) |
|
|
Term
|
Definition
| Non-ST Elevation Myocardial Infarction |
|
|
Term
|
Definition
|
|
Term
| Myocardial Infarction on EKG |
|
Definition
| Q Wave formation; Diagnostic Criteria for Abnormal/ Pathologic Q waves is a width of greater than or equal to 0.04 seconds and/or a depth of greater than or equal to 25% of R waves |
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|
Term
|
Definition
| Â | ST Segment | T Wave | | Recent or Acute | Elevated | Inverted | | AI or Recent | Isoelectric | Inverted | | AI or Old | Isoelectric | Upright | | | | | NOTE: AI = Age Indeterminate |
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|
Term
| MI Location based on EKG Findings |
|
Definition
| Location | Leads | | Anterioseptal | V1-3 | | Anterior | V1-6 | | Inferior | 2,3,AVF | | Lateral | 1,AVL, V5, V6 | | Posterior | V1 (and Inferior leads) |
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|
Term
| Diagnostic Criteria of Pericarditis |
|
Definition
| ACUTE PHASE - Diffuse ST segment elevation in practically all leads with no reciprocal ST depression, No abnormal Q waves (unless superimposed to MI); SUBACUTE or CHRONIC PHASE - Inverted T waves in practically all leads with isoelectric ST segment, No abnormal Q waves (unless superimposed to MI) |
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|
Term
| Various ECG Findings in Pulmonary Embolism and Infarction |
|
Definition
| Sinus tachycardia (#1 finding), Right axis deviation, RBBB, Inverted T waves in II, III and AVF; Inverted T waves in V1-3; S1-Q3-T3 Pattern (S waves in lead I, Q waves in lead III, T wave inversion in Lead III); Atrial Tachyarrhythmias; Posterior Axis deviation |
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|
Term
| ECG Findings in Hyperkalemia |
|
Definition
| MILD- Peaking T waves with narrow base (T waves at least 10 mm tall); ADVANCED - flattening P waves, first degree AV block, mild intraventricular blocks and failure of cardiac capture by artificial pacemaker; FAR ADVANCED - Absent P waves, advanced AV blocks, advanced intraventricular blocks, ventricular tachyarrhythmias, ventricular standstill and even death |
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|
Term
| ECG Findings In Hypokalemia |
|
Definition
| MILD - Prominant U waves (an extra wave after T and before the next P); ADVANCED - peaking P waves (pseudo P-pulmonale), AV conduction disturbances, failure of the cardiac capture by artificial pacemaker, predisposition to digitalis toxicity, various arrhythmias; NOTE - patients with hypokalemia are incredibly weak |
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|
Term
| ECG Findings in Calcium Imbalance |
|
Definition
Hypercalcemia - shortening of the QT interval due to shortening or absence of ST segment;
Hypocalcemia - prolongation ofthe QT interval due to lengthening of ST segment |
|
|
Term
|
Definition
| Chest X-ray; Echocardiography (ultrasound); Nuclear Cardiology; PET (not used much these days); CT/CTA; MRI; Coronary Angiography |
|
|
Term
| Cardiac Imaging with Chest X-Ray (CXR) |
|
Definition
| Not an optimal evaluation of cardiac anatomy; Can diagnose chamber enlargement, CHF, effusions, etc.; Certain congenital conditions have characteristic appearance |
|
|
Term
|
Definition
| Occurs when the rate of fluid accumulation in interstitium exceeds lymphatic clearance; Often seen in association with pulmonary effusion; Kerley B lines on CXR (edema in the interlobular septae, peripheral linear opacities); Prominent vasculature; "Cephalization of vasculature" (vessels normally taper as they travel peripherally, but in edema they are more prominent and actually can reach lung periphery and apices); Fluid may accumulate within fissures; Cardiomegaly |
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|
Term
|
Definition
| Congenital heart condition; Often diagnosed in utero; 4 Major Characteristics - Ventriculoseptal defect with left to right shut, Overriding aorta (spans right and left ventricles), Pulmonic stenosis, and RV hypertrophy; Surgical repair required (very complex); Classic CXR appearance - Boot Shaped heart (KNOW THIS - It's common on boards and will likely be on the cardio exam!); Another thing common on exams are "Tet Spells" - the kid will get blue and then squats down and they get better |
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Term
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Definition
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Term
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Definition
| Narrowing of the thoracic aorta at the level of the ligamentum arteriosum; Causes increased collateral flow through the internal mammary arteries (rib notching occurs from mechanical pressure in dialated collateral vessels); Aorta is visibly narrowed and appears as a "3" on CXR (Known as the "3 Sign"); Also causes post-stenotic dilatation (descending aortic aneurysm) |
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Term
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Definition
| Seen on CXR in patients with Aortic Coarctation (rib notching is also commonly seen on CXR of these patients) |
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Term
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Definition
| AKA Primary ciliary dyskinesia; Involves situs inversus (organs on the opposite side of the body), chronic sinusitis, infertility; Patients may experience hearing loss (due to problems with the hair cells in the ears); On CXR the heart will be on the wrong side of the heart (check to make sure that the film is displayed correctly!!), the gastic bubble will also be over on that side |
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Term
| Uses of Nuclear Cardiology |
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Definition
| Perfusion imaging is done very commonly - helps to identify infarct versus reversible ischemia (medical management vs revascularization) and is often followed by angiography (3 vessel disease requires CABG, not amenable to angioplasty and stenting); Radioactive tagged pharmaceutical (sestamibi) is injected and distributed to the myocardium, images are obtained at rest and with stress (stress can be exercise on a treadmill or pharmacologic - adenosine) |
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Term
| Interpretation of Nuclear Cardiology |
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Definition
| Activity (counts) are proportional to blood flow; Distribution of radiotracer should be relatively uniform, decreased activity (counts) indicates disruption of coronary blood flow; If activity is decreased at stress and rest this indicates infarction and non-viable mycardium (maximize medical therapy: beta blockers, statins, aspirin, etc.); If activity is decreased with stress and normal at rest, this indicates reversible ischemia (depending on vessel morphology at catheterization - angiogram - will require antioplasty/ stent vs. CABG); There are many variations of agents used and imaging protocols for these Cardiac Perfusion Studies |
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Term
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Definition
| TTE = Transthoracic Echo; TEE = Transesophageal Echo (more invasive, better visualization of the aortic root and ascending aorta - if this is abnormal a CT is obtained to confirm findings and rule out dissection or aneurysm); Largely used to evaluate valvular function and ejection fraction - stenosis, regurgitation, intracardiac thrombus (risk for stroke or limb ischemia), evaluate for ASD, VSD, PFO, effusion/ tamponade; Can be performed in the prenatal period in the OB's office |
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Term
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Definition
| Common femoral artery is accessed and a wire is advanced thru the needle into the abdominal aorta. The needle is then removed and a hollow catheter is then advanced over the wire. The wire and catheter are advanced to the aortic root and into the coronary arteries. ALWAYS advance the wire first and then the catheter to avoid dissection or vessel rupture. Iodinated contrast is injected and real time fluoroscopic images are obtained (multiple oblique projections). Evaluates for stenosis, occlusion, ejection fraction and chamber motion. As mentioned, if disease is seen in 3 vessels (Right coronary artery, left anterior descending, left circumflex) this requires a CABG (assuming the patient is a surgical candidate) |
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Term
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Definition
| Many places are performing cardiac CT to evaluate the coronary arteries - static exam (form, not function); NOT reimbursed by medicare or most insurance companies, and it is expensive ($2000-3000); Involves a very high dose of radiation to the chest (?increased risk of breast CA - not enough data yet); Technically difficult - you must "gate" the study (time it with the EKG cycle); HR must be <90 (give metoprolol or other beta blocker if not) and must have a regular rhythm (afib and other arrythmias precludes study); Can relatively accurately image coronary arteries and identify stenoses/ occlusions; Also used to detect coronary artery Calcium (indicator of atherosclerosis and potential stenosis) |
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Term
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Definition
| Excellent static and dynamic evaluation of the heart (you can tell form and function) - looks at/for ejection fraction, PDA, VSD, ASD, anomalies of coronary or pulmonary circulation, etc.; Evaluates - congenital heart diseas, aortic and pulmonary artery disease, pericardial disease, ventricular and valvular function, and cardiac masses; Cannot perform with pacemaker present; Involves no radiation but is a long, technically involved exam; Complicated physics dictate protocols for imaging |
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Term
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Definition
| Vascular imaging has progressed from invasive to non-invasive methods; Both arterial and venous imaging modalities exist; Excellent anatomic detail can be obtained; MRI, CT, Ultrasound, and angiography are the main methods of vascular imaging; Intervention can be planned and guided; A wide variety of pathologic conditions can be diagnosed - vasculitis, aneurysm/ pseudoaneurysm, arterial dissection, DVT, arterial stenosis/ occlusion, traumatic hemorrhage, etc. |
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Term
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Definition
| Invasive, radiation exposure; Iodinated contrast necessary for imaging (allergic reactions, potential renal damage); Vessel puncutred and wire introduced, then the needle is removed and a hollow catheter is advanced, next wire and catheter are advanced to the desired location (catheter always follows wire to prevent dissection or vascular rupture) and contrast is injected and images are obtained in real time |
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Term
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Definition
| CT scan with intravenous contrast (same risks as angiography - allergy, renal failure); Timed to catch contrast in target vessel (artery vs vein depending on clinical question); Radiation exposure; Excellent anatomic detail; Allows for imaging in multiple planes (acquire in axial, reformat in sagittal and coronal); Readily available, fast image acquisition; Less invasive than angiography (requires only peripheral IV - 22gauge or bigger) |
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Term
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Definition
| More technically difficult; Metallic implants/ pace makers contraindicated; Much longer examination (difficult with unstable patients); Gadolinium contrast safer than iodinated contrast (allergies exceedingly rare, there is some risk of nephrogenic systemic fibrosis - NSF - with GFRs <30); More susceptible to artifact and motion |
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Term
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Definition
| No radiation exposure; No contrast required; Best modality for evaluating for DVT; Other conditions - pseudoaneurysm s/p catheterization, AVF, transplant vasculature patency; Not as good anatomic detail as CTA or angiography; Readily available (portable exams possible); Much less expensive |
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Term
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Definition
| Focal dilation of vessel; Contains all 3 vessel walls by definition (intima, media and adventitia intact); Can be due to atherosclerosis, HTN or both; Risk of rupture (hemorrhage, shock, death); Can be treated surgically or with endovascular techniques (metallic coils placed, occlude vessel, stops hemorrhage; Stents may also be used prior to rupture) |
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Term
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Definition
| Normal aortic size is <3cm; Aneurysm when > 3cm (as a rule of thumb, but if the rest of the aorta is, for example, 1.5 cm and it bumps out to 2.5 cm in a place, that's an aneurysm, even though it's <3cm); Treatment is mandated when >5cm (risk of rupture is >90% when it's this size, surgery is also indicated with rapid enlargement of the aneurysm, but "rapid" is subjective... some people suggest >1cm increase in 12 months); Symptoms of rupture: back pain, abdominal pain, hypotension; Important to diagnose and follow to ensure stability; Treatment includes surgery (much more morbid) or stent graft placement; With surgical repair, the aorta is clamped, cut and a graft is sewn in - there is a risk of anterior spinal artery occlusion (artery of ademkewitz - damage this and the patient will wake up paralyzed); Aneurysms are often found incidentally upon screening ultrasounds and work-up then requires CT with contrast for full evaluation |
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Term
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Definition
| Pertains to Aortic Aneurysms: 50% of ruptures don't make it to hospital; 50% of those arriving don't make it to OR; 50% of those patients don't leave the OP; 50% of those surviving to post-op don't make it home |
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Term
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Definition
| Can be seen in the setting of trauma or with HTN and thoracic aortic aneurysm; "Intimal flap" - defect in the intimal layer (blood can exit the true lumen of the artery and a channel is formed between the intima and the media); Seen with HTN, collagen vascular disease (Marfan's is classic); Stanford and Debakey classifications - Stanford is more widely used |
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Term
| Stanford Classification of Aortic Dissection |
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Definition
TYPE A - Ascending aortic involvement with or without descending involvement, emergent surgical repair required, can cause pericardial tamponade or dissect into coronary arteries and cause ischemia/ death, remember type A - Ascending (with or without the rest of the aorta);
TYPE B - Descending aortic involvement only, distal to the ligamentum arteriosum by definition, treatment is blood pressure control, if rapidly enlarging it may require surgery or stent graft (risk of rupture;
Either type may extend distally into the abdominal aorta, possibly all the way to the level of the iliac arteries (can occlude any branch including renals and mesenterics) |
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Term
| Debakey Classification of Aortic Dissection |
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Definition
TYPE I - ascending with or without descending (like Stanford Type A);
Type II - ascending dissection only;
Type III - desceding dissection only (Type three is like Stanford type B ... memory trick: the word "three" sounds like the letter "B") |
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Term
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Definition
| Arterial trauma can occur with both blunt and penetrating injuries; Frank rupture of a vessel is possible (disruption of all 3 layers); Can also disrupt just 1 or 2 layers - vessel becomes weak and dilates in a saccular fashion, called "false" aneurysm or pseudoaneurysm, very high risk of rupture (treatment needed), can often be coiled (metallic coild platinum wire is placed through the catheter), commonly seen after cardiac catheterization with low puncture (common femoral artery is target, pseudo with puncture of Superficial femoral artery), thrombin can also be injected with ultrasound in interventional radiology |
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Term
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Definition
| A type of arterial trauma; Commonly seen after arterial instrumentation; Abnormal connection between artery and vein; Risk of rupture due to arterial flow directly entering a thin walled vein; Treatment is surgical; Diagnosed with ultrasound |
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Term
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Definition
| Atherosclerotic disease is a major cause of morbidity and mortality in the US; Contributing factors include - smoking, elevated cholesterol, diabetes, genetic factors; Can affect any artery in the body - coronary, renal, peripheral arteries (supplying the limbs), aorta, etc. |
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Term
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Definition
| Occlusive atherosclerotic disease - ankle brachial index (ABI) is normally 1.0, anything less than 1.0 indicates narrowing in the peripheral arteries, 0.9- 0.5 indicates some degree of claudication, <0.5 indicates rest pain, and <0.3 indicates tissue gangrene/ ulcers; Treatment includes - surgical bypass (often required with complete occlusion) or endovascular repair (angioplasty, stent); The larger the vessel, the better the long term response to angioplasty (aspirin and plavix also used in conjunction for best long term results); Endovascular complication rate is 3-6% - hematoma at groin access site, pseudoaneurysm, AVF, vascular rupture/ occlusion |
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Term
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Definition
Renovascular HTN: renin-angiotensin-aldosterone axis (labile blood pressure, no response to multiple meds, abrupt onset with renal failure possible, 99% accounted for by atherosclerosis and fibromuscular dysplasia, Suspect in younger patients with HTN not responding to exercise and meds);
Fibromuscular dysplasia (FMD) - approximately 35% of cases of renal artery stenosis - medial layer hypertrophies, occurs in younger (30-50 yo) female patients, multiple areas of narrowing, beaded appearance, responds well to angioplasty alone (98% success);
Athersclerosis - causes 65% of cases of renal artery stenosis, usually seen in older and/or diabetic patients over 60 yo, affects a shorter, more proximal segment than FMD, angioplasty and stent are the treatment of choice |
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Term
| "Beads on a String" Appearance of the Renal Artery |
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Definition
| Seen with Fibromuscular Dysplasia (FMD) |
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Term
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Definition
| Older men with impotence, absent femoral pulses and buttock claudication with walking = Leriche Syndrome (aortoiliac occlusive disease) |
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Term
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Definition
| Pain and ischemia upon raising arms overhead |
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Term
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Definition
| Many different forms exist; Type can be suggested by location and size of vessel involved (small, medium or large - Takaysu is the most commonly seen form in large arteries); All types are characterized by irregular, multiple, scattered arterial stenoses; Follow up post treatment will often reveal a normal artery; Can cause thrombosis - stroke, limb ischemia, mesenteric ischemia, renal ischemia; Treatment is based on the type, and most require steroids |
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Term
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Definition
| Irregular narrowing of arteries |
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Term
| Deep Venous Thrombosis (DVT) |
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Definition
| Very common; Seen in a variety of patients, young and old; Increased risk with pregnancy, malignancy, smoking, oral contraceptive use, etc.; VIRCHOW'S TRIAD - stasis (commonly post-op), endothelial injury (ex diabetes, HTN, smoking), and hypercoagulability (ex: cancer, pregnancy, etc.); Risk of PE wiht migration of clot centrally; Deep Veins include SVC, IVC, innominate, subclavian, axillary, brachial, iliac, femoral and popliteal veins; Treatment is systemic anticoagulation |
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Term
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Definition
1) Stasis
2) Hypercoaguable state
3) Endothelial Injury |
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Term
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Definition
PE - if severe enough, this can cause death;
Phlegmasia cerulea dolens - arterial compromise from elevated venous pressures (think back pressures), emergent surgical thrombectomy or local TPA by interventional radiology;
SVC Syndrome - extrinsic compression of SVC causing thrombosis as a result of stasis (facial swelling = "plethora" a classic COMLEX question, angioplasty and stent can relieve symptoms but is often a palliative effeort due to underlying cause - lung CA, lymphoma, etc.);
Post Thrombotic Syndrome - Seen in 40-80% of patients with DVT, Pain, swelling, ulcers, thrombolysis is most effective in treating symptoms (TPA delivered directly onto the clot through venous catheter, imaging is done pre and post treatment) |
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Term
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Definition
| Gold standard for DVT diagnosis; Empty veins should compress with external pressure (such as from an ultrasound probe), but veins with clot in them will not compress |
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Term
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Definition
| A period of active contraction of the ventricles; A "pause" between the S1 and S2 heart sounds |
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Term
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Definition
| Sound made by the closure of the mitral and tricuspid valves, immediately after the atria empty into the ventricles |
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Term
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Definition
| Sound made by the closure of the aortic and pulmonic valves, immediately after the ventricles eject their stroke volume |
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Term
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Definition
| A period of passive ventricular filling; A "pause" between S2 and S1 |
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Term
| Auscultation of Aortic Stenosis |
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Definition
| Best heard at the 2nd Intercostal space (ICS) at the right upper sternal border; Heard just before S2 |
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Term
| Auscultation of Aortic Regurgitation |
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Definition
| Best Heard at the apex of the heart (5th intercostal spaces left midclavicular line); Heard between S2 and S1 |
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Term
| Auscultation of Mitral Stenosis |
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Definition
| Best heard at the apex; Heard during diastolic filling (just before S1) |
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Term
| Auscultation of Mitral Regurgitation |
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Definition
| Best heard at the apex; Heard between S1 and S2 |
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Term
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Definition
1) Systolic v. diastolic;
2) Duration;
3) Pitch (high, medium, low);
4) Quality (harsh, rumbling, blowing);
5) Intensity (crescendo, decrescendo, etc.);
6) Best heard location;
7) Areas of radiation (ex: axilla, carotids);
8) Grade;
9) Variation with respirations and/or change of position |
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Term
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Definition
1/6 - very faint, not always heard in all positions;
2/6 - quiet, but not difficult to hear;
3/6 - moderately loud;
4/6 - loud +/- thrills (where you can feel if on palpation);
5/6 - very loud +/- thrills, may be heard with stethoscope partly off the chest;
6/6 - may be heard with stethoscope completely off the chest +/- thrills |
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Term
| What would cause a murmur heard between S1 and S2? |
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Definition
| Aortic stenosis or mitral regurgitation; Listen to the carotids to differentiate (Aortic will radiate there, mitral won't); Also, think about where you're hearing the murmur the best (over which listening post) |
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Term
| What would cause a murmur heard between S2 and S1? |
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Definition
| Aortic regurgitation, or mitral stenosis |
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Term
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Definition
| Dilated (congestive), Hypertrophic, Restrictive |
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Term
| Congestive Heart Failure (Epidemiology and General Info) |
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Definition
| Affects 3 million people in the US; 400,000 new cases diagnosed each year; Medical therapy with - beta blocker, ace inhibitors or hydralazine/ nitrate may improve survival, however, currently the only potential "cure" is cardiac transplantation |
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Term
| Definition of Dilated (Congestive) Cardiomyopathy |
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Definition
| Cardiac enlargement and impaired systolic function of one or both ventricles |
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Term
| Etiology of Dilated (Congestive) Cardiomyopathy |
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Definition
| Acute myocarditis, Toxins, Idiopathic, Peripartum, Antrhacyclines, Multi-infarct, Viral (Coxsackie, HIV), Chagas (Worldwide this is the #1 identifiable cause, but not in the US), Rheumatic, EtOH |
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Term
| Epidemiology of Dilated (Congestive) Cardiomyopathy |
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Definition
| Incidence - 5-8/100,000; 3x more frequent in blacks and males; 75 types of specific diseases can produce this as a final common outcome; "idiopathic" is the most common cause; Poor prognosis - 50% mortality at 5 years; Familial linkage in 20% of patients |
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Term
| Clinical Manifestations of Dilated (Congestive) Cardiomyopathy |
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Definition
| Insidious - LV dilatation may be present many years before LV failure; Sub-acute after apparent recovery from systemic viral illness; Symptoms of failure - fatigue, weakness, chest pain (in 1/3 of patients), Dyspnea on exertion (DOE), orthopnea; Arrhythmias; Late symptoms - right heart failure (because the right heart is trying to pump through the high pressure in the lungs), edema, liver congestion |
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Term
| S/S of Dilated (Congestive) Cardiomyopathy |
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Definition
| JVD; S3 gallop; Mitral regurgitation (the valve is stretched by the cardiomyopathy); Hepatomegaly; Rales; Edema |
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Term
| Imaging of Dilated (Congestive) Cardiomyopathy |
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Definition
CXR - Cardiomegaly, Kerley B lines, Pleural effusions;
Echocardiogram - dilated, hypocontractile, multi-chamber enlargement, mitral regurgitation |
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Term
| EKG of Dilated (Congestive) Cardiomyopathy |
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Definition
| LA enlargement, Atrial fibrillation (atria are irritated by the stretch placed on them by the cardiomyopathy); LV enlargement; PVCs (just like the atria, the ventricles are irritated by the stretch); Q waves |
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Term
| Hemodynamicsof Dilated (Congestive) Cardiomyopathy |
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Definition
| Decreased stroke volume; Increased Left ventricular end diastolic pressure (LVEDP); LVEF; Increased pulmonary capillary wedge pressures (PCWP) |
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Term
| Therapy for Dilated (Congestive) Cardiomyopathy |
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Definition
| Vasodilators (decrease afterload); Diuretics; Inotropes (ex: digoxin, increases the force of contractions); Beta blockers; Nitrates; Anticoagulation; Surgery; CABG; Transplantation; Biventricular pacing (allows the heart to beat more effectively) |
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Term
| Management of Dilated (Congestive) Cardiomyopathy |
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Definition
PHYSICAL - cardiac rehab and exercise programs improve exercise tolerance and quality of life;
PHARMACOLOGIC - improved survival demonstrated with ace inhibitors (16-40%), hydralazine/ nitrates (20%), diuretics (no enhanced survival), digoxin (no enhanced survival), beta blockers (carvedilol, relieves sxs, improves ejection fraction and survival);
TRANSPLANTATION - >75% survival at 5 years |
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Term
| Apoptosis in Cardiomyopathy |
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Definition
Tightly regulated, energy-requiring process in which cell death follows a programmed sequence of events characterized by: loss of surface contact of the index cell to neighboring cells, cell shrinkage, condensation of chromatin into crescenteric caps at the nuclear periphery, eventually endonucleolytic digestion of nuclear DNA into characteristic multiples;
Transient pressure overload induces expression of proto-oncogenes - hypertrophy occurs due to activation of growth factors and cytokines; Growth factor persistence may activate apoptotic cascade; Cell death may be controlled by cysine proteases called CASPACES; Development of caspace inhibitors may be potential new therapies to prevent cardiomyopathy |
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Term
| What is the Normal Range for Ejection Fraction? |
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Definition
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Term
| Definition of Hypertrophic Cardiomyopathy |
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Definition
| Inappropriate myocardial hypertrophy often predominantly of the interventricular septum: Idiopathic hypertrophic subaortic stenosis (IHSS), Subaortic Stenosis, Hypertrophic obstructive cardiomyopathy (HOCM), Asymmetric septal hypertrophy (ASH) |
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Term
| Etiology of Hypertrophic Cardiomyopathy |
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Definition
| Familial, autosomal dominant; Sporadic; Metabolic (catecholamines, diabetes, thyroid); Frederick's Muscular Dystrophy |
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Term
| Physiologic Characteristics of Hypertrophic Cardiomyopathy |
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Definition
| Myocardial Hypertrophy out of proportion to hemodynamic load; Often obstruction to outflow due to hypertrophy of the left ventricular outflow tract (LVOT) and systolic anterior motion of the mitral valve; Diastolic dysfunction due to abnormal stiffness and resultant impaired ventricular filling; Genetically tansmitted in 50% of cases; Incidence is 0.02-0.2% of the population; Changes in genotypic expression of myocardial fibers leading to disorganized muscle bundles |
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Term
| Clinical Manifestations of Hypertrophic Cardiomyopathy |
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Definition
| A majority of patients are asymptomatic; Cardiac sudden death; CHF; Dyspnea (most common symptom); Syncope; Arrhythmia; Angina |
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Term
| Natural History of Hypertrophic Cardiomyopathy |
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Definition
Annual Mortality - 3%;
10-15% progress to dilated cardiomyopathy;
Most common abnormality in young adults who die suddenly |
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Term
| S/S of Hypertrophic Cardiomyopathy |
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Definition
| CHF; General, progressive dyspnea on exertion (DOE); Fatigue; Syncope; S3 or S4 heart sound; Increased murmur with valsalva |
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Term
| Echocardiography of Hypertrophic Cardiomyopathy |
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Definition
| Asymmetric septal versus diffuse hypertrophy; Systolic anterior motion (SAM) of mitral valve; Outflow tract gradient |
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Term
| Management of Hypertrophic Cardiomyopathy |
|
Definition
PHARMACOLOGIC - beta blockers (negative inotropic effect which makes the heart beat less forcefully, a mainstay of therapy), calcium blockers (verapamil), norpace, AV pacing;
EXERCISE - NO competitive, strenuous exercise;
Dual chamber pacing - reduces gradient by 50%, improves symptoms, long-term utility is not known;
Septal Myotomy/ Myectomy - long-term improvement, 3-5% operative mortality, non-surgical myectomy using ethanol;
Cardiac transplantation |
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Term
| Screening for Hypertrophic Cardiomyopathy |
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Definition
| Screen First degree relatives of patients with hypertrophic cardiomyopathy; Screen with - physical exam and history, ECG, Echocardiogram |
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Term
| Etiologies of Restrictive Cardiomyopathy |
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Definition
| Infiltrative diseases, MULTIPLE MYELOMA, Diabetes, Radiation, HYPEREOSINOPHILIC SYNDROME (Loeffler's), Amyloid, Sarcoid, Tumor, EMF, Hemocrhomatosis |
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Term
| S/S of Restrictive Cardiomyopathy |
|
Definition
| Biventricular failure, Right sided failure, Dyspnea on exertion (DOE), fatigue, Paroxysmal Nocturnal Dyspnea (PND), chest pain, Kussmaul's Sign (when the patients take a deep breath, the blood in the neck veins goes up - normally it should go down because when you inhale, the intrathoracic pressure decreases), S4, JVD, Atria are dilated because the ventricles don't relax in order to fill so the blood doesn't have an easy time getting out of the atria |
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Term
| EKG of Restrictive Cardiomyopathy |
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Definition
| LVH, Atrial arrhythmias, Atrial fibrillation |
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Term
| Hemodynamics of Restrictive Cardiomyopathy |
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Definition
| Decreased Stroke Volume, Ejection fraction is variable (and often normal), Decreased LV compliance, Square root sign, Decreased pulmonary capillary wedge pressure (PCWP) |
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Term
| Imaging of Restrictive Cardiomyopathy |
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Definition
CXR - Normal heart size, Pulmonary congestion;
ECHOCARDIOGRAPHY - myocardial speckling, increased a waves, Small or normal LV cavity |
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Term
| Therapy for Restrictive Cardiomyopathy |
|
Definition
| Beta blockers, Calcium channel blockers, Diuretics, Phlebotomy and Chelation therapy for patients with hemochromatosis as the cause of their restrictive cardiomyopathy |
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Term
| Constrictive Pericarditis |
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Definition
| Pericardial thickening/ fibrosis/ calcification causing impaired relaxation of the heart; Causes - post- CABG, TB, Radiation, tumor, idopathic |
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Term
| Findings with Constrictive Pericarditis |
|
Definition
S/S - Dyspnea on exertion (DOE), CP, Edema, Fatigue;
PE - JVD with Kussmaul's sign, Pulsus paradoxus, biventricular CHF;
CXR - LV enlargement, calcification, or normal;
Rx - diuretics, pericardial drainage, stripping |
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Term
| Definition of Infective Endocarditis |
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Definition
| Invasion of the endothelial lining of the heart by infective organisms producing inflammatory changes and an immune response |
|
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Term
| Definition of Subacute Bacterial Endocarditis |
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Definition
| A Systemic illness with and insidious course of weeks to months caused by organisms of low virulence (often indigenous flora) |
|
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Term
| Definition of Acute Bacterial Endocarditis |
|
Definition
| Acute illness with an abrupt onset of days to weeks with hectic course caused by highly virulent infectious organisms |
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Term
| Pulmonary Capillary Wedge Pressure (PCWP) |
|
Definition
Provides an indirect estimate of left atrial pressure (LAP); Measured by inserting balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a peripheral vein, then advancing the catheter into the right atrium, right ventricle, pulmonary artery, and then into a branch of the pulmonary artery.
NOTE: PCWP wasn't explained in any lecture, so this info was obtained from Wikipedia |
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Term
| Definition of Marantic Endocarditis (Libman- Sacks) |
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Definition
| Non-bacterial thrombotic endocarditis; Development of sterile thrombi on cardiac valves, often associated with systemic disease (eg mucinous secreting adenocarcinomas, lupus, uremia, etc.) |
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Term
| Defintion of Culture Negative Endocarditis |
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Definition
| Patients with infective endocarditis with persistently negative blood cultures: Fungal, Chlamydia, Q Fever |
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Term
| Locations of Infective Endocarditis |
|
Definition
| Valvular leaflets, Chordae Tendinae, Mitral and aortic rings, Ventricular endocardium, Great arteries (PDA, coarctation) - because they're areas of turbulent flow; Vegetations tend to grow on the low pressure side of the valves |
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Term
| Pathogenesis of Infective Endocarditis |
|
Definition
| Microscopic deposits of fibrin and platelets form on endocardial surfaces (due to trauma and/ or turbulent flow), these deposits are a nidus for infection; Bacterial colonization of "sterile vegetation" occurs during transient bacteremia which multiply beneath fibrin/ platelet clot (protected from phagocytosis); NOTE - Transient bacteremia is a normal occurrence in most individuals, susceptible individuals have - high level of agglutinating antibodies, leading to a large inoculum; Vegetations occur on low pressure side of high to low flow (mitral regurgitation - vegetations on the LA side, Aortic insufficiency(AKA Aortic Regurgitation) - LV side of valve, VSD - RV side of the septum); In cases of Acute bacterial endocarditis (such as that caused by staph aureus), 60% of patients had normal valves prior to illness |
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Term
| S/S of Acute Bacterial Endocarditis |
|
Definition
| Rapid onset with no prior S/S, Hectic Fevers, Rigors, Prostration, CHF, Embolic event |
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Term
| S/S of Subacute Bacterial Endocarditis |
|
Definition
| Insidious, intermittent fevers, manifestations of immunologic disease, arthralgias, myalgias, persistent back pain, flu-like symptoms, anorexia/ weight loss, splenomegaly; NOTE - these S/S look a lot like a viral illness, so be careful! |
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Term
|
Definition
| A clinical manifestation of Infective Endocarditis; Appear to be immune mediated; Vasculitic AG-AB complexes; True bacterial vegetative emboli; Petichiae; Splinter hemorrhage (immune complexes seen in nailbeds); Osler's Nodes - painful, tender, erythematous nodule in the skin of extremities often on the pulp of fingers; Janeway lesions - flat, non-tender red spots with irregular margins on the palms and soles; Clubbing |
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Term
|
Definition
| One of the peripheral stigmata associated with Infective Endocarditis; Immune complexes seen in nail beds |
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Term
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Definition
| One of the peripheral stigmata associated with Infective Endocarditis; Painful, tender, erythematous nodules in the skin of the extremities, often on the pulp of the fingers |
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Term
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Definition
| One of the peripheral stigmata associated with Infective Endocarditis; Flat, non-tender, red spots with irregular margins located on the palms or soles of the feet |
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Term
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Definition
| Seen in the retinas of patients with infective endocarditis; Oval hemorrhagic lesions with white centers; Thought to result from septic emboli |
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Term
| Cardiac Exam of A Patient with Infective Endocarditis |
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Definition
| Tachycardia (because of fever or valve problems); Systolic or diastolic murmur possibly changing in character; Evidence of CHF; ECG shows heart block |
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Term
| Diagnostic Laboratory Studies in Infective Endocarditis |
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Definition
| Normocytic Anemia, Leukocytosis, Elevated Sed Rate (a normal Sed rate almost rules out infective endocarditis), Immune pannel (50% of patients are RF positive which isn't diagnostic in and of itself, but is a good marker to monitor treatment effectiveness); Blood Cultures |
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Term
| Complications of Bacterial Endocarditis |
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Definition
| Death rate is variable depending on the organism (10-20% mortality); CHF is the usual case of death (Staph - 40% mortality, Yeast and Fungi - 75% mortality, Strep viridans - high cure rate); Valvular complications; Embolic - coronary, spleen, kidney, brain; Pericarditis secondary to MI or direct bacterial spread; Renal Artery occlusion; Mycotic Aneurysm (usually strep viridans) - embolic occlusion of arterial wall leading to a catastrophic bleed of the aorta or cerebral vessels; Septic and aseptic meningitis (CT before LP); Immune complex glomerulonephritis - renal insuffiency, hematuria |
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Term
| Microbiology of Infective Endocarditis in Native Valves |
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Definition
NON- IV Drug Users: Streptococcus viridans (50%), Staph aureus (20%), Enterococci (5%), Other Streptococci (5%), Staph epidermidis (3%);
IV Drug Users - Staph Aureus (57%), Streptococcus viridans (10%), Enterococci (8%), Staph epidermidis (3%), Other streptococci (2%) |
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Term
| Microbiology of Infective Endocarditis in Prosthetic Valves |
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Definition
EARLY - Staph epidermidis (33%), Other (20%), Gram neg (17%), Staph Aureus (15%), Streptococcus viridans (8%), Culture negative (5%), Enterococci (2%);
LATE - Streptococcus viridans (30%), Staph epidermidis (29%), Staph aureus (10%), Gram neg (10%), Others (10%), Enterococci (6%), Culture negative (5%) |
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Term
| #1 Bug Seen in Infective Endocarditis of Native Valves (NVE) in Non-IV Drug Abusers |
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Definition
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Term
| #1 Bug seen in Infective Endocarditis of Native Valves (NVE) in IV Drug Abusers |
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Definition
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Term
| #1 Bug seen in Early Infective Endocarditis of Prosthetic Valves (PVE) |
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Definition
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Term
| #1 Bug seen in Late Infective Endocarditis of Prosthetic Valves (PVE) |
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Definition
| A tie between Streptococcus viridans and Staph epidermidis |
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Term
| Prosthetic Valve Endocarditis (PVE) |
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Definition
IE of any part of a mechanical or biological valve substitute or on reconstructed native heart valves;
Serious complication; Death incidence is 30-70%; Early PVE - 37%, fulminant, staphylococcal origin; Late PVE - 67%, resembles subacute bacterial endocarditis; Echocardiography to find vegetations - TTE has a sensitivity of 20-30%, TEE has a sensitivity of 90-92%, and complications occur 68% of the time |
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Term
| Therapy/ Management of Infective Endocarditis |
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Definition
Ongoing assessment of change in clinical status - evidence of heart murmur, change in filling pressure, ECG change, evidence of peripheral emboli;
Antibiotic Therapy - based on the organism, often combination therapy for synergistic effect or to reduce drug toxicity from a single drug; Abx are given for 4-6 weeks;
There is rarely a medical cure for yeast/ fungal endocarditis - use amphotericin B for 1 week, then do surgery, then 6-8 more weeks of medical therapy |
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Term
| Indications for Surgery for Infective Endocarditis |
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Definition
Severe refractory CHF due to regurgitation;
Systemic Emboli (Recurrent, one episode with a large residual vegitation, or a large vegetation to start with);
Refractory Infection (lack of improvement or blood sterility in 1 week, or second relapse of infection);
Progressive intracardiac spread (ring abcess, AV block, Sinus of valsalva aneurysm rupture, subaortic aneurysm) |
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Term
| Recommended Prophylaxis for Endocarditis is Recommended in Patients With... |
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Definition
| Prosthetic cardiac valves; Previous bacterial endocarditis; Congenital malformations (cyanotic congenital heart disease, ventricular septal defect, patent ductus arteriosus, coarctation, bicuspid aortic valve); Rheumatic and acquired valvular dysfunction; Hypertrophic cardiomyopathy with obstruction; Mitral Valve Prolapse with Mitral regurgitation |
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Term
| When is Endocarditis Prophylaxis NOT Recommended? |
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Definition
In Patients With...
Isolated secundum atrial septal defect; Previous CABG; Mitral valve prolapse without mitral regurgitation; Physiologic, functional or innocent murmurs; Kawasaki disease without valvular dysfunciton; Prior rheumatic heart disease without valvular dysfunction; Cardiac pacemakers and implanted defibrillators; Surgical repair without residual beyond 6 months of secundum ASD, VSD or PDA |
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Term
| Cardiac Conditions for Which Prophylaxis with Dental Procedures is Recommended |
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Definition
| Prosthetic Valves; Previous Infectious Endocarditis; Heart transplant patients who develop valvulopathy; Congenital heart disease |
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Term
| Definition of Mitral Stenosis |
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Definition
| Resistance to flow through the mitral apparatus during diastolic filling, which also creates a gradient between the LA and the LV |
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Term
| Etiology of Mitral Stenosis |
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Definition
| Rheumatic valvulitis, Congenital stenosis, Myxoma (tumor), Vegetations, MAC (calcification) |
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Term
| Symptoms of Mitral Stenosis |
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Definition
| Dyspnea, Fatigue (due to poor forward flow), Palpitations, Hemoptysis (because blood has backed up into the lungs), CHF- Hepatic congestion, CVA, Pulmonary HTN, Hoarseness (because the atria are so large that they're compressing the recurrent laryngeal n.) |
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Term
| Signs/ Physical Exam of Mitral Stenosis |
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Definition
| Dilated or elevated JVD, Systolic pulsation of jugular vein, Opening snap, Diastolic rumble, MR murmur, Accentuated first heart sound |
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Term
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Definition
| Broad, notched P waves in leads II and V1 (becuase the atria are enlarged) with terminal negative forces; Atrial fibrillation; Right axis deviation |
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Term
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Definition
| LAE and prominence of pulmonary vasculature; Kerley B lines; Double density thru cardiac sillohuette (because the atria are so enlarged) |
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Term
| Echocardiography of Mitral Stenosis |
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Definition
| Gradient; Decreased ejection fraction slope; Increased pressure half time; Mitral Valve doming |
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Term
| Hemodynamics of Mitral Stenosis |
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Definition
| Nearly systemic pulmonary artery pressures (i.e. they're very high); Pulmonary capillary wedge pressure (PCWP)/ Left ventricular end diastiolic pressure (LVEDP) gradient (usually the two pressures are equal during diastole, a PCWP/ LVEDP gradient represents a pressure change between the atria and ventricle - increased in the atria during diastole); Normal area is 4-6 cm2 and Critical Mitral Stenosis is defined as <1cm2; Normal LV function |
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Term
| Medical Treatment of Mitral Stenosis |
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Definition
| No medical modality relieves the obstruction; Arrhythmia therapy; Anticoagulation (because these patients are predisposed to atrial fibrillations) |
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Term
| Indications for Surgical Treatment of Mitral Stenosis |
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Definition
| CHF Refractory to medications; Critical mitral stenosis (i.e. <1cm2); Surgery Types - Valvuloplasty; Commisurotomoy (surgical clearing of debris/ thickness of valve); Mitral Valve Replacement (gold standard) |
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Term
| Definition of Aortic Stenosis |
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Definition
| Obstruction to flow across the valve during LV systole, which creates a gradient between the LV and the aorta |
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Term
| Etiology of Aortic Stenosis |
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Definition
| Congenital; Rheumatic; Senile calcification (most common) |
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Term
| Symptoms of of Aortic Stenosis |
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Definition
| Chest pain (patients with this sxs have 50% mortality at 5 years); Syncope (50% mortality at 3-4 years); CHF (50% mortality at 1 year); The chest pain occurs because the muscle hypertrophies so much in trying to pump against the stenosis that it outgrows its blood supply |
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Term
| Signs/ Physical Exam of Aortic Stenosis |
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Definition
| Pulsus parvus (weak) et tardus (late); Crescendo- decrescendo murmur (the later in the cycle you hear the murmur, the more severe the stenosis); Palpable thrill; Ejection click; Delayed AV closure |
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Term
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Definition
| LVH; Conduciton delays; S wave in right precordial leads |
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Term
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Definition
| Normal heart size; Post stenotic aortic dilation |
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Term
| Echocardiography of Aortic Stenosis |
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Definition
| LVH; Calcified valve; Decreased opening; Increased velocity across valve |
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Term
| Hemodynamics of Aortic Stenosis |
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Definition
| >50% incidence of concomitant CAD; 2-3 cm2, critical is <0.8 cm2; Gradient across the valve |
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Term
| Medical Treatment of Aortic Stenosis |
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Definition
| Frequent follow up of LV size and gradient |
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Term
| Indications for Surgical Treatment of Aortic Stenosis |
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Definition
Critical aortic stenosis (<0.8cm2) +/- symptoms; Treatment Types - Mechanical valve (needs anti-coagulation, but lasts longer), Hetero/Homograft (no anti-coagulation needed, but deteriorates faster); Ross procedure (autograft, movement of the pulmonic valve to the aortic valve position and the placement of an artificial valve in the position of the pulmonic valve);
NOTE - Dr. Rosenblatt said this surgery has fallen out of favor, but Dr. Donnelly mentioned it as a treatment option (maybe just in kids????) |
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Term
| Definition of Aortic Regurgitation |
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Definition
| Blood flow "leaks" back across the closed aortic valve during diastole; Diastolic flow from the aorta to the left ventrical imposes volume overload on the LV |
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Term
| Etiology of Aortic Regurgitation |
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Definition
| Annular dilatation; Aortic Stenosis (senile/ congenital); Endocarditis; Dissection; VSD |
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Term
| Symptoms of Aortic Regurgitation |
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Definition
| Asymptomatic for many years; Fatigue; Circulatory (the heart has to enlarge to pump more blood so that the same amount ultimately goes forward as it did before the regurgitation began); CHF; Dyspnea; Edema; Chest pain |
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Term
| Signs/ Physical Exam of Aortic Regurgitation |
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Definition
| Cor bovinum; Prominant pulsation; Corrigan's Pulse; Durozier's sign (a double sound heard over the femoral artery when it is compressed distally); Quincke's Sign (pulsation of the capillary bed in the nail); Hill's Sign (a ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic severe AI); Demusset's Sign (Head bobbing and uvula pulsations due to the pressure/ in time with the Heart Rate); Aesthenic; Marfan's (prone to aortic dissections whcih can pull on the aortic valve); S3 gallop; Austin Flint murmur; High pitched diastolic blow |
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Term
| EKG of Aortic Regurgitation |
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Definition
| LV enlargement; LA enlargement |
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Term
| What is Another Name for Aortic Regurgitation? |
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Definition
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Term
| Imaging of Aortic Regurgitation |
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Definition
CXR - Cardiomegaly;
ECHOCARDIOGRAPHY - Dilated LV, dysmorphic AV, MV fluttering, Vegatations, large aorta |
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Term
| Hemodynamics of Aortic Regurgitation |
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Definition
| May have normal left ventricular ejection fraction (LVEF) until end stage |
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Term
| Medical Treatment of Aortic Regurgitation |
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Definition
| Preload (diuretics) and afterload therapy; Once CHF develops, 2 year survival is less than 50%; Frequent follow up for LV size and funciton |
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Term
| Surgical Treatment of Aortic Regurgitation |
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Definition
| Indicated with - Endocarditis failing medical therapy, Aortic Regurg due to dissection or to aortic dilatation > 55mm |
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Term
| Definition of Mitral Regurgitation |
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Definition
| Blood "leaks" across the mitral valve during diastole - contraction of the left ventricle ejects blood into the left atrium causing overload in both the LA and the LV |
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Term
| Signs/ Physical Exam of Mitral Regurgitation |
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Definition
| Dilated or elevated JVD; Systolic pulsation on jugular vein; Opening snap; Diastolic rumble; Mitral regurgitation murmur; Accentuated (he said diminished on a different slide??)first heart sound; High pitched holosystolic murmur; Displacement of apical impulse; Mitral Valve Prolapse click/ murmur |
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Term
| Etiology of of Mitral Regurgitation |
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Definition
| Mitral Valve Prolapse (MVP); Coronary artery disease (acute or chronic); Rheumatic |
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Term
| Symptoms of Mitral Regurgitation |
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Definition
| CHF; Fatigue; Paroxysmal nocturnal dyspnea (PND)/ Orthopnea; Emboli (increased LV); Edema |
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Term
| EKG of Mitral Regurgitation |
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Definition
| Atrial fibrillation; LV and LA enlargement; Q waves (indicative of previous infarcts); Mitral Valve Prolapse (-) T's inferior |
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Term
| CXR of Mitral Regurgitation |
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Definition
| Cardiomegaly; Double density of the LA (because it's so thick); Mitral annular calcification; Elevation of the left main bronchus (by the enlarged LA) |
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Term
| Echocardiography of Mitral Regurgitation |
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Definition
| Dilated LA; Abnormal valve; LV; WMA (posterior) |
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Term
| Hemodynamics of Mitral Regurgitation |
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Definition
| V waves; Increased pulmonary capillary wedge pressure (PCWP) and Pulmonary artery pressure (PAP); Decreased LV function; Decreased cardiac index |
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Term
| Medical Treatment of Mitral Regurgitation |
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Definition
| Preload and afterload therapy; Anticoagulation with atrial fibrillation; Treat ischemic heart disease |
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Term
| Surgical Treatment of Mitral Regurgitation |
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Definition
| Surgery indicated with - CHF refractory to medical therapy; Types of valves - mechanical, homo- or heterograft (tissue valves don't last very long in the mitral position); Annuloplasty; Mitral Valve repair |
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Term
| What are the Structural Exam Findings in Acute Coronary Syndrome? |
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Definition
| Somatic Dysfunction T1-6 (especially T2-3 on the left) with anterior infarction; Somatic dysfunction at C2 and cranial base with inferior infarction; NOTE - The osteopathic approach to acute coronary syndrome is NOT immediate OMT, the urgent structural issue is the intra-arterial thrombus, NOT the somatic dysfunction |
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Term
| Acute Treatment of Acute Coronary Syndrome |
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Definition
| Supplemental O2, Nitrates, Morphine, ASA (MONA: morphine, O2, nitrates, ASA); Thrombolytics, Re-vascularizae where necessary and possible; Ensure oxygen delivery to cardiac muscle |
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Term
| Continuing Treatment for Acute Coronary Syndrome Recovery and Prevention |
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Definition
| Comprehensive lifestyle modifications including stress management; Exercise is particularly important; OMT - Post-op, increase musculoskeletal efficiency (abnormal gait may increase cardiac work by up to 300%) |
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Term
| Epidemiology of Congenital Heart Disease |
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Definition
| Live born prevalence of 8/1000 live born infants in western countries; Live born prevalence is lower than the fetal prevalence; Prenatal incidence ranges from 0.5% to 39.5% (median about 7.9%), many of which are associated with gross chromosomal abnormalities; Up to 40% of spontaneous abourtion rate is associated with aneuploidy; Frequently encountered congenital malformation; Higher frequency with infants with chromosomal disorders, syndromes or associations (Trisomy 21,13, 18; Chromosome 22 deletion syndromes - DiGeorge or Velo-cardiac facial syndrome; VATER association, CHARGE association) |
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Term
| Congenital Heart Disease in Down Syndrome |
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Definition
| 50% of Down Syndrome patients have heart problems; 50% of those that do have a heart condition have an endocardial cushion defect |
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Term
| DiGeorge Syndrome/ Velocardiofascial Syndrome |
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Definition
| A 22q11 microdeletion; Involves contruncal cardiac defects (ex: transposition of the great vessels, Tetralogy of Fallot); Thymic Hypoplasia; Cleft lip/ palate leading to speech and feeding difficulties (lip and palate are affected because they're midline structures, and midline structures tend to be affected when hearts are affected); Low Calcium |
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Term
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Definition
| Elf-like face; Cocktail personality; Hypercalcemia/ Hypercalcuria; Supra Aortic/ Pulmonic Stenosis (whenever stenosis is seen just above either of these valves, screen for William Syndrome); Chromosome 7- Elastin Gene |
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Term
|
Definition
Major Features of CHARGE Syndrome (very common in CHARGE and relatively rare in other conditions):
1) Coloboma of the Eye - iris, retina, choroid, macula or disc, microphthalmos (missing eye) - causes vision loss;
2) Choanal atresia or stenosis (80-90%) - narrow (stenosis) or blocked (atresia), unilateral or bilateral, bony or membraneous;
3) Cranial Nerve Abnormality (50-60%) - Missing or decreased sense of smell, IX/X (70-90%) swallowing difficulties/ aspiration, VII (70%) unilateral or bilateral facial palsy;
4) Outer ear (40%) "snipped off" helix (outer fold), priminent antihelix (inner fold) which is discontinuous with tragus, triangular concha, decreased cartilage (flowwp), often stick out, usually asymmetric;
5) Middle ear (50%) malformed bones of the middle ear (ossicles), causing Conductive Hearing Loss;
6) Inner ear Malformed cochlea (Mondini defect) - small or absent semicircular canals, causing hearing loss and balance problems;
These patients often have congenital heart defects as well |
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Term
| Presentation of Congenital Heart Disease (General) |
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Definition
| Murmur, Arrhythmias, CHF, Cyanosis (common mixing lesion), palpitations, lightheadedness |
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Term
| Murmur in a Pediatric Patient |
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Definition
60% of newborns have a murmur;
BENIGN MURMURS - closing PDA, Peripheral pulmonary stenosis, Vibratory murmur; Stenotic Valve - aortic or pulmonary valve; RARE - L-to-R shunt, Valve regurgitation;
WATCHFUL WAITING IF - No cyanosis, normal 4 extremity BPs, Normal ECG and rhythm strip, no signs of CHF |
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Term
| Arrhythmia in a Pediatric Patient |
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Definition
Irregular Rhythm (Atrial Premature Beat or PVC) - Benign;
Slow Heart Rate - Less than 50-60 bpm is abnormal, exclude congenital heart disease (using L-TGA and AVCD) and maternal lupus (using Anti-Ro and La), Few neonates are paced in the neonatal period;
Fast Heart Rate (supraventricular tachycardia or ventricular tachycardia) - Frequent cause of hydrops, treated with adenosine or cardioversion, medical management and/or ablation |
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Term
| Age of Presentation of Pediatric Patients with Left to Right Shunting |
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Definition
| 4-8 weeks of age when peripheral vascular resistance falls |
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Term
| Age of Presentation of Pediatric Patients with Stenotic Valves |
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Definition
| Depends on the degree of stenosis (Eg: coarctation can present throughout life) |
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Term
| Age of Presentation of Pediatric Patients with Cyanotic Heart Disease |
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Definition
| Within the neonatal period |
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Term
| Management of Left to Right Shunts in Pediatric Patients |
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Definition
| Diuretics, Calories, Surgical/ catheterization repair |
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Term
| Management of Stenotic Valves/ Vessels in Pediatric Patients |
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Definition
Critical/ severe - need stabilization and urgent intervention, these patients are often cyanotic;
Mild to Moderate - elective intervention |
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Term
| Diagnosing Congenital Heart Diseases |
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Definition
Clinical Presentation raises suspicion;
Phyisical exam confirms that suspicion;
HYPEROXIA STUDY is used to confirm cyanotic heart disease (give the baby lots of oxygen, and then measure the PO2 - if it goes up to/ above 150, the problem is in the lungs, if not, the problem is in the heart);
An EKG and CXR can help make a diagnosis;
Imaging is everything;
Mainstay: echocardiography (especially transthoracic echo, reveals anatomy and hemodynamics);
Cardiac catheterization may be used for imaging, for viewing hemodynamics, and for intervention;
Newer diagnostic techniques include MRI, CT, and 3D echo |
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Term
| History Questions to Ask When Suspicious of Congenital Heart Disease |
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Definition
SYMPTOMS - Feeding (how much, how long, do they get short of breath), Respiratory rate, Sweating, Cyanosis, Syncope, Palpitations;
FAMILY HISTORY - Seizures (if the patient has had one, get an EKG becaue an arrhythmia may have made them anoxic and the anoxia may have been what caused the seizure), Congenital heart disease (especially in first degree relatives), Hypertrophic cardiomyopathy, Diabetes;
PAST MEDICAL HISTORY - Birth history, Failure to thrive, Recurrent chest infections, Asthma (if a person has wheezing for the first time, get a CXR because it could be the heart causing the problem), Seizures, Operations |
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Term
| Phyiscal Exam for Congenital Heart Disease in a Pediatric Patient |
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Definition
OBSERVATION - dysmorphic features, saturation monitor, oxygen, cyanosis, work of breathing, sweating, scars (thoracotomy, sternotomy), Chest deformities;
PALPATION - apex beat, thrills, heaves, pacemakers;
AUSCULTATION - Heart sounds (S1,S2, is S2 split? is the splitting fixed?, added sounds such as S3, S4 or an ejection click), Murmurs (Systolic - continuous with S1 or ejection type, Diastolic - early, mid or late, Continuous - extends from systole to diastole), Problems with the Right side of the heart are better heard on Inspiration, those on the Left side of the heart are better heard on Exhalation |
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Term
|
Definition
| Can be normal (as long as the split varies with inspiration/ exhalation) - the gap should be smaller with exhalation and wider with inhalation; If there is no change in the gap, then there is a communicaiton between the atria |
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Term
| Congenital Heart Disease Screening |
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Definition
| In Utero - 18 Week "anomaly" scan gives a 4 chamber view of the fetal heart and can show anomalies of cardiac position, single ventricle, and abnormalities of the atrio-ventricular valves; The limitations are that it is only 50-60% sensitive and cannot examine the entire heart |
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Term
| Uses of Cardiac Catheterization |
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Definition
| Angiography; Hemodynamic Studies (looking at pressures, saturation, infering flow); Interventions (balloon, stents, plugs, coils, discs) |
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|
Term
| If Resistance Increases, What Happens to Flow? |
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Definition
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|
Term
| What Determines Flow in Left to Right Shunts? |
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Definition
| Resistance (NOT pressure!!!) |
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Term
| Volume Overload in Left to Right Shunts |
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Definition
Volume loading - elevation in preload;
Chamber dilation - elevation in afterload;
Neurohumoral activation - elevation in HR;
Consequences - heart failure and pulmonary vascular disease;
Causes - ASD, VSD, Atrioventricular septal defect, PDA |
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Term
| Physiology of Left to Right Shunts |
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Definition
| The size of the shunt is determined by resistance to flow - If the shunt is small the resistance is across the defect, if the shunt is large the resistance is pulmonary vs systemic; Pulmonary artery pressure = pulmonary vascular resistance x shunt size |
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Term
| Clinical Manifestations of Left to Right Shunts |
|
Definition
Diaphoresis, pallor (abnormal autonomic tone, work);
Tachypnea (decreased pulmonary compliance);
Tachycardia;
Growth Failure (increased metabolic demands, poor intake) |
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Term
| Signs of Pediatric Heart Failure |
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Definition
| Increased work of breathing; Hepatomegaly (edema and elevated JVP are rare); Displaced apex, active precordium, gallop rhythm; Specific findings related to the lesion causing the heart failure |
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|
Term
| What is the Most Common Type of Atrial Septal Defect (ASD)? |
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Definition
| A Secundum ASD (which is a defect in septum primum) |
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|
Term
| When would you hear a more exaggerated splitting of S2 that doesn't vary with respiration? |
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Definition
| The splitting occurs when the right ventricle is overloaded or dilated, and the lack of variation with respiration is due to a communication between the right and left atria |
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|
Term
| What Causes the Murmurm Heard with an Atrial Septal Defect (ASD)? |
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Definition
| Turbulence of extra blood going through a normal-sized pulmonary valve |
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|
Term
| Embryology of an Atrial Septal Defect (ASD) |
|
Definition
| Failure of septation of the atrial septum |
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|
Term
| Physiology of an Atrial Septal Defect (ASD) |
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Definition
| Shunt at the atrial level which volume loads the right side of the heart; The degree of shunting is dependent on R>L ventricular compliance and pulmonary vascular resistance |
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|
Term
| Classification of an Atrial Septal Defect (ASD) |
|
Definition
Secundum ASD - defect in septum primum (fossa ovalis), this is the most common type of ASD;
Sinus venosus ASD - associated with anomalous venous drainage;
Primum ASD - endocardial cushion defect;
Coronary sinus ASD - rare |
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|
Term
| CXR of an Atrial Septal Defect (ASD) |
|
Definition
| Cardiomegaly, Pulmonary plethora, RV enlargement, Prominant Pulmonary artery |
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|
Term
| Clinical Manifestations of an Atrial Septal Defect (ASD) |
|
Definition
Clinical features are determined by the size of the shunt;
SYMPTOMS - dyspnea, poor activity tolerance, growth discrepancy, frequent chest infections;
SIGNS - Tachypnea (may be subtle), Active precordium, Widely split S2, diastolic rumble, Pulmonary flow murmur |
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|
Term
| Natural History of a Secundum ASD |
|
Definition
SMALL - <3mm defects will close on their own by 18 months of age, these "defects" probably represent a patent foramen ovale rather than a true cardiac malformation;
MODERATE - 3-5 or 5-8 mm, 80% of these defects will close on their own;
LARGE - these have little chance of closing spontaneously, surgical closure should typically be considered by mid-childhood |
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|
Term
| Management and Outcome of an Atrial Septal Defect (ASD) |
|
Definition
Whether to use a Conservative approach or Surgical Closure depends on: the type of atrial defect, the size of the shunt, +/- the size of the defect;
Significant defects don't close and shunt increases from childhood to adulthood;
Long-Term Sequelae - RV failure, Atrial dysrhythmias;
Secundum ASD - surgical closure or device occlusion;
Sinus venosus ASD - surgical closure with pulmonary vein baffle;
With closure, patients have an excellent long-term outcome |
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|
Term
| Murmur with a Small and Restrictive Ventricular Septal Defect (VSD) |
|
Definition
| The murmumr is from turbulence across the VSD; It is a plateau type murmur (the murmur doesn't span the entire space between S1 and S2 because the contraction of the heart squeezes the VSD shut, so you get an abrupt drop-off in the murmur) |
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|
Term
| Murmur with a Moderate VSD with Volume Load and RV HTN |
|
Definition
| The VSD stays open for the entire contraction, so the murmur spands most of S1 to S2 |
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|
Term
| Murmur with a Large VSD with Pulmonary HTN and Volume Load |
|
Definition
| The murmur is from turbulence as "extra" blood goes across the pulmonary valve (the blood doesn't create a murmur going across the VSD itself because the defect is so large) |
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Term
| Embryology of Ventricular Septal Defects (VSD) |
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Definition
| Defects of septation during development (downgrowth of ventricles) |
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Term
| Physiology of Ventricular Septal Defects (VSD) |
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Definition
| Volume loading on the right and left ventricle. Pressure load is dependent on the size of the defect |
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Term
| Classification of Ventricular Septal Defects (VSD) |
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Definition
| Based on Location of the defect in the ventricular septal wall: Membranous VSD, Muscular VSD, Inlet VSD (often endocardial cushion defect), Conoventricular VSD (includes malalignment of conal septum - ex: tetralogy of fallot or aortic outflow anomalies) |
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Term
| Outcomes of Ventricular Septal Defects (VSD) Based on Defect Size |
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Definition
70-80% --> Restrictive or small defect: most should become smaller or close spontaneously;
Infant with Moderate-Sized VSD: 40-50% will decrease in size (decrease shunt), normalization of elevated pulmonary artery pressures;
Large, non-restrictive VSD: defect and shunt remain large, pulmonary artery pressures high, clinical improvement implies something else, Pulmonary vascular disease |
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Term
| Factors Influencing Management of Ventricular Septal Defects (VSD) |
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Definition
| Type of VSD, Size of VSD, Age of the Child, Pulmonary Vascular Resistance level, Pressure Load, Volume Load |
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Term
| CXR of Ventricular Septal Defects (VSD) |
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Definition
| Increased pulmonary flow (large pulmonary vessels), Cardiomegaly |
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Term
| Treatment of Ventricular Septal Defects (VSD) |
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Definition
Symptoms or signs of significant shunt;
Medical therapy with digoxin, diuretics and ACE-Inhibitors;
Surgical Closure Indications - Persistent large shunt, CHF and growth failure, Pressure overload - persistant pulmonary artery HTN after 2 months of age (<1 year), Volume Overload - persistent cardiomegaly by echo or catheterization (later in life);
Technique - Patch closure using cardio-pulmonary bypass, or devise closure for muscular or membranous VSDs; Outcome following surgery is excellent; Surgery is often undertaken in infancy |
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Term
| Atrioventricular Septal Defect |
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Definition
AKA Atrioventricular canal defect or Endocardial cushion defect; 1/4 of all Down Syndrome patients have this;
Failure of septatio of the primitive heart tube at the junction of the atrium and the ventricle; Frequently associated with chromosomal abnormalities;
3 COMPONENTS - (1) Common AV Valve, (2) Atrial septal defect (primum), (3) Ventricular septal defect (inlet, muscular);
A "Complete" Atrioventricular Septal Defect involves all 3 components, a "Partial" Atrioventricular septal defect has 2 separate AV Valve orifices |
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Term
| Clinical Manifestations of Atrioventricular Septal Defect |
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Definition
| The Clinical S/S of the defect are that of the dominant lesion: If the dominant lesion is the atrial defect, the patient has S/S of an ASD, if the dominant lesion is the ventricular component the patient has S/S of a CSD, if the dominant lesion is the AV Valve regurgitation the patient will have "mitral" regurgitation |
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Term
| Conditions Associated with Atrioventricular Septal Defects |
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Definition
| Outflow tract obstruction (right or left), Unbalanced ventricle sizes |
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Term
| Atrioventricular Septal Defect Treatment and Outcomes |
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Definition
| Treatment is of the dominant portion of the lesion; Surgical repair includes patch closure and/ or separation of the AV valves and is typically done by one year of age or earlier; Outcome is good to excelled with primary one stage repair and long term status is based upon competence of the AV valves |
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Term
| Patent Ductus Arteriosus (PDA) |
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Definition
| A cause of left to right shunting; Communicaiton between the pulmonary artery and the aorta that is present during fetal development that fails to close after birth; NOTE - the recurrent laryngeal nerve runs around the PDA; Patients with a PDA will have a continuous (S1-S2-S1) murmur; PDAs account for 5-10% of congenital heart disease (excluding premies, since they often have a PDA due to immaturity, and not a true heart defect); Risks depend on shunt magnitude: Small, restrictive shunts - asymptomatic with a risk of endocardits, Moderate to large - heart failure, atrial "steal" (NEC in premies); Prostaglandins keep PDAs open, Indomethacin can help to close it medically by inhibiting prostaglandins |
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Term
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Definition
Endpoint of progressive PVOD (pulmonary vascular disease); Muscularization, thrombus, and obliteration of lung vessels; Increased vascular resistance, decreased shunt; Shunt Reversal - cyanosis, polycythemia; Paradoxical emboli, brain abscess; Pulmonary hemorrhage;
According to "Dr. Wiki" Eisenmenger's is a "process in which a left-to-right shunt caused by a VSD causes increased flow through the pulmonary vasculature, causing pulmonary HTN, which in turn, causes increased pressures in the right side of the heart and reversal of the shunt into a right-to-left shunt." |
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Term
| Sequelae of Longstanding Shunts |
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Definition
| Ventricular volume load; Pulmonary HTN; Pulmonary vascular disease; Eisenmenger's Syndrome |
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Term
| Pulmonary Vascular Disease (PVOD) |
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Definition
| Can be primary (rare) or secondary (a reactive process secondary to persistent, significant shunt lesions); More prevalent and early in Trisomy 21 |
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Term
| Medical Management of Pulmonary HTN/ Pulmonary Vascular Disease |
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Definition
| Assess reactive nature of pulmonary vascular resistance to oxygen and NO; Oxygen is a great vasodilator; Phlebotomy for sxs; Inhalation therapy (chronic inhaled NO (cGMP) and/or inhaled prostacyclin); Oral Therapy - Bosantin (an endothelin antagonist - endothelin is a vasoconstrictor), Sildenafil (Viagra) - a PDE inhibitor (cGMP); Intravenous therapy - IV prostacyclin |
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Term
| Types of Acquired Pediatric Heart Disease |
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Definition
Kawasaki Ds;
Myocarditis and dilated cardiomyopathy - occur in pediatrics, infrequent/ rare, cardiomyopathy may also have genetic causes including mitochondrial and metabolic disease;
Hypertrophic cardiomyopathy;
Ischemia |
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Term
| Kawasaki Disease (General) |
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Definition
Vasculitis;
Fever for > 5 days;
Diagnostic Criteria (must have 4 out of 5) - Oral mucosa changes, bilateral non-purulent conjunctivitis, truncal rash, peripheral extremities have edema, erythema and peeling, cervical lymphadenopathy > 1.5cm;
Lab Abnormalities - thrombocytosis, neutrophilia, anemia, ESR increase;
Non-Specific hydrops, uveitis, arthralgia, aseptic meningitis |
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Term
| Kawasaki Disease (Cardiac) |
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Definition
Myocarditis (rare);
Coronary Artery Disease - untreated up to 25% of patients develop complications, mild ectasia, small aneurysms, most resolve spontaneously, 1-2% develop giant coronary aneurysms stasis and stenosis, Reduced from 25% to <5% with current therapy but IVIG must be given within 7 days of onset of symptoms |
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Term
| Treatment of Kawasaki Disease |
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Definition
TREATMENT - to prevent cardiac sequelae (coronary artery aneurysms, etc.);
IVIG;
ASPIRIN - antiplatelet dose (persistent coronary dilatation, small aneurysms);
ANTICOAGULATION - (coumadin - giant aneurysms, low molecular weight heparin??);
Long Term - stenosis, bypass, antioplasty, possible risks for atherosclerosis |
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Term
| Pediatric Dilated Cardiomyopathy |
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Definition
Myocardial dysfunction leading to a dilation of ventricles; Dilated cardiomyopathy is the most common cause of CHF in humans; 15,000 new cases per year (kids + adults);
CAUSES - idiopathic, viral (coxsackie B, adenovirus), Autoimmune, Alcohol and drugs (anthracyclines, cocaine), pregnancy (1:10000), Ischemic heart disease, familial (30-40% of all cases, AD, AR, X-linked, Mitochondrial);
Dilated ventricles with impaired systolic function; Accounts for 50% of pediatric cases of cardiomyopathy; Incidence of 0.58/100,000 children; Infectious, mitochondrial, familial, metabolic (the heart needs carbs or fats to work so if you can't metabolize them or if you have a mitochondrial abnormality, you'll get a dilated cardiomyopathy), arrhythmic, toxic, inflammatory; Most are idiopathic; 1/2 to 1/3 are familial |
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Term
| Incidence of Dilated Cardiomyopathy in Children |
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Definition
| Incidence of 1.13 - 1.24 cases/ 100,000 children; Half of all cases by 1 year of age (an incidence that is 8-12 times as high as older ages); A second peak incidence occurs in adolescence; Higher incidences among black and hispanic children than among white children; Males > Females - 2 big causes are mutations in the dystrophin gene (in the case of Duchenne's and Becker's muscular dystrophies) and Tafazzin or G4.5 gene (in the case of Barth syndrome) and both of those genes are located on the X chromosome |
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Term
| Specific Forms of Dilated Cardiomyopathy in Children |
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Definition
Viral Myocarditis - Coxsackie B, Adenovirus, PCR (adeno - 40%, entero - 20%, HSV - 5%, CMV - 5%), Coxsackie protease cleaves dystrophin, IVIG therapy is frequently given;
Dystrophinopathies - Duchenne, Beckers (both are X-linked recessive);
Doxorubicin Cardiomyopathy - doxorubicin/ adriamycin is cardiotoxic, generates oxygen free radicals which affect the heart;
HIV - 25% of vertically transmitted children have systolic dysfunction;
Iron Overload Cardiomyopathy - Thalassemia |
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Term
| Hypertrophic Cardiomyopathy in Children |
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Definition
| Sarcomeric gene mutation; Autosomal Dominant; Echocardiographic diagnosis; 70% of mutations can be tested for; Secondary causes of hypertrophic cardiomyopathy must be considered (infant of diabetic mother, Abnormal aortic valve or aortic stenosis leading to left ventricular hypertrophy); Myocytes are disorganized (that's why these patients can get ventricular tachycardia or torsade de pointe) |
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Term
| Risk Factors for Sudden Death in Hypertrophic Cardiomyopathy |
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Definition
| Prior arrest; Family Hx of arrest; LVH of >30mm; Abnormal BP response to exercise; Spontaneous sustained Ventricular tachycardia; Non-sustained ventricular tachycardia on Holter monitor; Unexplained syncope |
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Term
| "Critical" Obstructive Cardiac Lesions in Neonates |
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Definition
| PDA provides systemic flow in cases of Aortic Stenosis and coarctation; PDA provides pulmonary flow in cases of pulmonary valve stenosis; Normally PDA closes by 1-2 days of life, but when it closes the patient with a critical obstruction will die since blood can't get where it needs to go without the PDA; Prostaglandins have revolutionized the care of cyanotic and obstructive heart lesions in neonates because they are used to keep the PDA open |
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Term
| Treatment of Aortic Stenosis in Children |
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Definition
Balloon Valvuloplasty - Indicated for: PSEG >50mmHg or myopathy, ST segment changes with exercise, age >20 years old, less than moderate aortic insufficiency;
Balloon Valvuloplast = controlled tear of fused commisures, curative for pulmonary valve but only palliative for the aortic and mitral valves, you have to balance relieving stenosis with creating regurgitation/ insufficiency; It is done by putting a pacing catheter into the right ventricle and then another catheter into the aorta (toward the left ventricle/ stenotic aortic valve), then pace the ventricle with the pacing catheter so that the heart doesn't beat for a few seconds while you inflate the balloon in the aortic valve space;
Can also treat Aortic Stenosis with Surgical Aortic Valve Replacement - indicated for aortic stenosis that is resistant to balloon angioplasty or for patients with a combination of aortic stenosis and aortic insufficiency (LV dysfunction, progressive LV dilatation, ST segment changes/ chest pain, PSEG > 50mmHg wiht significant aortic insufficiency/ regurgitation, significant ectopy seen on a Holter monitor) |
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Term
| Pros and Cons of Various Types of Replacement Valves |
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Definition
Mechanical Valves - good longevity, but requires life-long anticoagulaiton (there's a 1-2% risk of a hemorrhagic event per year), mechanical valves are more prone to perivalvar leaks;
Tissue Valves - Less durable, only last about 20 years, no long-term anticoagulation is needed, but you need to watch the valves for calcification (just as you would with any original valve), tissue valves are less prone to perivalvar leaks |
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Term
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Definition
| A procedure for aortic valve replacement; The pulmonic valve is moved to the aortic valve site (this autograft grows and can get re-innervated over time); A homograft is then put into the pulmonic valve position (replacement of this valve will need to occur in 15-20 years); This procedure is prone to autograft dilatation/ failure |
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Term
| Pulmonary Valve Disease in Children |
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Definition
| "Critical" means the baby is dependent on a PDA for survival; Typically presents early in life; Non-progressive (ie doesn't get any worse) except in the first 2 years of life; Can be cured by balloon valvuloplasty; May be prpesent as "membranous pulmonary valve disease" along with tricuspid valve and right ventricle hypoplasia; With pulmonary valve atresia, pressure in the right ventricle is 2-3x blood pressure; In Pulmonary valve disease, CXR appears largely normal except for a prominent pulmonary knob due to post-stenotic dilatation; Can be treated with valve surgery |
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Term
| Coarctation of the Aorta in Children |
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Definition
| May be associated wtih other levels of LV inflow or outflow obstruction; 70% of coarctation patients have a bicupsid aortic valve; "Infantile" type can have long-segment hypoplasia of the transverse arch of the aorta; Absent or diminished lower extremity pulses found on exam; Often present wiht systemic HTN that can persist after repair; Shows up as a "3 Sign" on CXR; Can be treated with stenting |
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Term
| Why would an infant with severe pulmonary valve stenosis and a large patent foramen ovale who just underwent a successful surgical balloon valvuloplasty with no residual obstruction be cyanotic? |
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Definition
| The valve is no longer stenotic, but the right ventricle is still stiff and creates a lot of resistance to flow so that the blood goes R to L from the RA in to the LA through the patent foramen ovale and the kid gets blue; Over time ther right ventricle will relax and the problem will reverse/ correct |
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Term
| When does "Blue" (Cyanosis) Happen? |
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Definition
| Blue happens when venous blood returns to the systemic circulation without passing through the lungs... ie in a Right to Left Shunt |
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Term
| If a child's lips are blue, what is the problem? |
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Definition
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Term
| What 1 Anomaly Explains All 4 Components of Tetralogy of Fallot? |
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Definition
| Anterior/ Superior deviatio nof the Conal Septum |
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Term
| What is seen on Angiography of a Patient with Tetralogy of Fallot? |
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Definition
| Upon injecting contrast into the right atrium, the aorta lights up (so you know there's a defect) |
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Term
| Why are Babies with Tetralogy of Fallot Cyanotic? |
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Definition
| Because some of the deoxygenated blood returning to the right side of the heart from the body sneaks around and out through the aorta withouth passing through the lungs first; The baby is NOT blue because there's not enough blood going to the lungs |
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Term
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Definition
| Occurs in patients with Tetralogy of Fallot when the subvalvar obstruction of the pulmonary tract closes down; Usually occurs in the morning with dehydration; Patients can break out of the tet spell by assuming the knee/ chest position (fills the right heart with blood); Need to give them: Oxygen, IV fluids, morphine, and phenylephrine (Increases systemic vascular restriction so the blood doesn't have as easy a time going out the aorta and may "choose" to go out the pulmonary artery instead). You also need to intubate/sedate/paralyze them and prepare to transfer them if they aren't able to break out of the tet spell |
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Term
| Surgical Repair of Tetralogy of Fallot |
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Definition
| "Leave the floor, Raise the roof"; Enlarges the pulmonary outflow tract in the anterior-posterior direction |
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Term
| "Egg on a String" Appearance of a Chest X-Ray |
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Definition
| Seen in Transposition of the great vessels |
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Term
| Transposition of the Great Vessels |
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Definition
| ~35% have VSDs; ~60% have subvalvar or valvar pulmonary stenosis (conal deviation); Many coronary artery patterns may be present; Saturation depends on the degree of mixing (ASD> VSD> PDA); A Balloon Atrial Septostomy may be performed to improve mixing (a baloon is used to open a communicaiton between the atria) until the patient can have an arterial switch operation - the balloon atrial septostomy is usually performed within the first day of life, and the switch operation within the first 3 days of life; An arterial switch operation restores the normal position of the great vessels and repairs any septal defects - switch surgery is currative |
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Term
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Definition
| A congenital heart condition in which the tricuspid valve is positioned abnormally low in the right side of the heart, resulting in an abnormally small right ventricle; Blood goes right to left via an ASD; Neonates are better while their PDAs are still open |
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Term
| "Snowman Sign" on Chest X-Ray |
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Definition
| Associated with Total Anomalous Pulmonary Venous Return in which pulmonary venous return enters the right atrium (there are several types of total anomalous pulmonary venous return including: below the diaphragm, supracardia, and intracardiac) |
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Term
| What are the Principal Mechanisms of Cardiac Arrhythmias? |
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Definition
| Altered automaticity, Triggered automaticity, Reentry, and Stimulation during a "vulnerable period"; Of these, Reentry is what medications for arrhythmias are targeting |
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Term
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Definition
| A property of certain cardiac cells to spontaneouls initiate an action potential; Automatic cells exhibit diastolic depolarization (during diastole the cells, principally the SA node, will depolarize); Under normal circumstances, the SA node is the dominant pacemaker, but the Purkinje fibers also exhibit automaticity; When automaticity is altered, the heart rate can change (ectopic pacemaker beats faster than the SA node overriding it, or the SA node slows for some reason, or a combination of the two) |
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Term
| Factors Increasing Automaticity |
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Definition
AUTONOMIC - increased sympathetic tone, increased catecholamines, decreased parasympathetics;
METABOLIC - increased carbon dioxide, decreased oxygen, increased acidity, increased temperature;
MECHANICAL - increased stretch;
DRUGS - digitalis;
ELECTROLYTES - decreased potassium, increased calcium;
Factors Decreasing Automaticity are exactly the opposite of those increasing automaticity; Drugs that decrease automaticity are antiarrhythmics and beta blockers |
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Term
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Definition
| A mechanism of cardiac arrhythmias; Involves automaticity arising in cells outside of the sinus node such as specialized atrial cells, the AV node, the Bundle of His and the Bundle Branches, and the Purkinje network |
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Term
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Definition
| One of the mechanisms of Cardiac arrhythmias (the least clinically important one); Automaticity arises from non-automatic cells (cells that are quiescent in the absence of an excitatory stimulus); When stimulated these non-automatic cells give rise to 2 or more action potetials or a long run of repetitive responses; For example - An implanted pacemaker fires and generates an inappropriate rhythm; Involves Afterdepolarization - the interruption of repolarization resulting in generation of an action potential; The role of triggered automaticity in the genesis of clinically observed dysrhythmias is unknown |
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Term
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Definition
The most common and clinically important mechanism of cardiac arrhythmias; Can occur in branched or parallel fibers; Begins in an area of a noncontiguous pathway (a split in the fibers created by ischemia), this noncontiguous pathway forms a loop and a block develops in one side of that loop. Opposite the block (in the other arm of the loop) is an area of slow conduction, which gives the blocked area time to repolarize so that it can be re-excited by the same impulse;
CAUSES Include - ischemia, valve disease, cardiac surgery, electrolyte imbalance;
Possible CLINICAL EFFECTS - depend on location, but include - premature atrial depolarization, supraventricular tachycardia, ventricular tachycardia, arrhythmia in preexcitation syndromes (ex: Wolff-Parkinson-White Syndrome);
NOTE - this is a difficult concept to explain in words, so looking at Dr. Glasses Slides (38-42 in the Cardiac Arrhytmia PPT) would be helpful |
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Term
| Stimulation During a "Vulnerable Period" |
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Definition
| Electrical activity that occurs when depolarization could happen (end of S and upslope of T) - the heart is vulnerable when it is repolarizing. The impulse will generate a "R-on-T" wave, which is dangerous and can lead to atrial or ventricular fibrillation |
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Term
| Supraventricular Dysrhythmias |
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Definition
| Common and clinically important; Includes - Atrial premature depolarizations, atrial tachycardia, atrial fibrillation, atrial flutter, and multifocal atrial tachycardia |
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Term
| Why are Atrial Premature Depolarizations (APDs) Clinically Important? |
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Definition
| Have an associated degree of morbidity, can occur quite frequently, and can be rather annoying to patients |
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Term
| Treatment of Atrial Premature Depolarizations (APDs) |
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Definition
| Withdraw Stimulants: nicotine, caffeine, EtOH, Emotional Stress, Inhalers, Pseudoephedrine; Can give medications such as low-dose beta blockers for a limited time |
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Term
| What are the Prinicipal Mechanisms of Atrial Tachycardia? |
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Definition
| Automaticity and Reentry; Recall that Non-Paroxysmal atrial tachycardia is associated with digitalis toxicity, and digitalis is known to increase automaticity |
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Term
| Treatment of Atrial Tachycardia |
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Definition
| Adenosine (can be uncomfortable as the patient converts back to a sinus rhythm); Beta blockade; Verapamil (less popular now that there's adenosine); Diving reflex/ Eyeball Pressure (works, but don't do it!); For Non-Paroxysmal Atrial Tachycardia (NPAT) - digitalis reversal/ withdrawal |
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Term
| Atrial Fibrillation (General) |
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Definition
| The most clinically important atrial dysrhythmia because AF has significant morbidity and mortality associated with it; Prevalence - 1.7% of women, 2.2% of men, and 2-4% of the populaiton over age 60; Most common underlying heart disease - Hypertensive heart disease, ischemic heart disease; Other Causes - cardiomyopathy, cardiac surgery, rheumatic heart disease, atrial septal defect, pulmonary embolism, thyrotoxicosis, CHF; Atrial fibrillation is the most common arrhythmia in patients over 60; Current thinking is that hte insertion site of the the pulmonary veins into the left atrium is the origination site of the atrial fibrillation due to an increase in automaticity |
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Term
| Types of Atrial Fibrillation |
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Definition
| Lone; Paroxysmal (sudden onset and end to the AF); Persistent (may still be able to reestablish a sinus rhythm in these patients); Permanent (can't reestablish a sinus rhythm) |
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Term
| Clinical Presentations of Atrial Fibrillation |
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Definition
| Asymptomatic, Incidental EKG finding, Palpitations/ irregular heart beat, rapid heart rate, acute or subacute myocardial ischemia, heart failure, pulmonary edema, hypotension, stroke (this is the chief morbidity of AF) |
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Term
| Treatment Considerations for Atrial Fibrillation |
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Definition
| Rhythm control; Antiarrhythmic agents (varying degrees of efficacy, none are great); DC Cardioversion (works well - ie the patient converts - but not everyone can maintain the sinus rhythm); AF ablation (pulmonary vein insertion site is ablated - has 60% efficacy on the first try); AV node ablation/ pacing (to prevent too slow heart rates); Drugs (including anticoagulation because of the risk of stroke |
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Term
| Considerations with Atrial Flutter |
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Definition
| Reentry, heart disease present; Can often be cured by low energy DC cardioversion (ie it takes less energy to convert these patients than to convert patients with atrial fibrillation); Drugs are needed for persistent cases of atrial flutter and rapid atrial pacing/ ablation is needed for recurrent cases |
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Term
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Definition
| Common; Includes - ventricular premature depolarizations (VPDs), Ventricular tachycardia, and ventricular fibrillation; Have Significant associated morbidity and mortality |
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Term
| Treatment Considerations for Ventricular Premature Depolarizations (VPDs) |
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Definition
| Treat the causes: Stimulants, medications (eg digitalis), Underlying heart disease(to help decide if the patient is at increased risk of sudden cardiac death, the best marker of risk is left ventricular ejection fraction (LVEF) which is an index of systolic ventricular function and is the best predictive/ prognostic factor in all of cardiology and can be assesed in many ways including echocardiography, and radionuclide studies) |
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Term
| Premature Ventricular Contractions (PVCs) |
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Definition
| 1 - occur in both normal and diseased hearts; 2 - incidence increases with age; 3 - may occur after excessive excitement, fatigue, heavy smoking or excessive tea, coffee or alcohol consumption; 4 - most persons with PVCs do not require treatment; 5 - frequent occurrence of multifocal PVCs usually indicates organic heart disease or digitalis intoxications |
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Term
| Clinical Considerations With Ventricular Tachycardia |
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Definition
| Are the monomorphic (uniform) or polymorphic (multiple forms); Is there QT Prolongation?; Is there evidence of Torsade de Pointes? (related to QT interval prolongation); Is the ventricular tachycardia sustained or nonsustained (where the vtach will stop and spontaneously convert to normal, or when the vtach lasts <30 seconds); Most patients that have ventricular tachycardia that is symptomatic have some sort of structural heart disease (ischemia heart disease, cardiomyopathy, mitral valve prolapse, valvular heart disease, etc.) |
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Term
| Classes of Ventricular Arrhythmias |
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Definition
Benign (30%) - Minimal risk of sudden cardiac death (SCD), Presents with palpitations and/or on routine exam, Has no serious hemodynamic consequences, Not associated with heart disease, Includes some PVCs and Nonsustained ventricular tachycardias (NSVTs);
Potentially Lethal (65%) - Modest to high risk of SCD, Presents with screening, No serious hemodynamic consequences, Heart disease present, Includes some PVCs and NSVTs;
Lethal (5%) - Highest risk of SCD, Presents with syncope or cardiac arrest, Has serious hemodynamic consequences, Heart disease is present, Includes some PVCs, NSVTs, Ventricular tachycardia and ventricular fibrillation |
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Term
| Goals of Antiarrhythmic Drug Therapy |
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Definition
| Prevent sudden cardiac death; Eliminate symptomatic sustained ventricular arrhythmias |
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Term
| Things to Consider with Antiarrhythmic Drugs |
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Definition
| Type of arrhyhmia; Response to previous therapy; Coexisting disease states (ex: lung disease that might make you want to use a drug that won't cause bronchoconstriction); Concomitant medications; LV function; Coexisting atrial arrhythmias |
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Term
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Definition
| The concept that through treatment we can cause worsening of the abnormal rhythm that we're trying to treat or that we can cause the development of a new arrhythmia; Usually occurs with drugs for ventricular dysrhythmias; For example, drugs may induce conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia, can also induce torsade de pointe by prolonging the QT interval |
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Term
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Definition
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Term
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Definition
| 900,000 hospitalizations(1995); Most frequent cause of hospitalization in the elderly; 5-10% of all hospital admissions |
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Term
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Definition
| Causes or contributes to about 250,000 deaths/ year; Up to 60-70% of patients die suddenly |
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Term
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Definition
| A pathophysiologic state in which an abnormality of myocardial function results in an inability of the ventricles to deliver adequate quantities of blood to metabolizing tissues at rest or during normal activty (i.e. the heart can't keep up with what the body is asking it to do); Can be chronic or acute; Hemodynamically characterized by an increase in left atrial pressure (LAP) and a decrease in cardiac output (CO) |
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Term
| Neurohumoral Changes in Heart Failure |
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Definition
| Increased sympathetic tone; Increased plasma catecholamines; Activation of the renin-angiotensin-aldosterone system (RAAS); Increased antidiuretic hormone (ADH, AKA vasopressin); Increased atrial natriuretic factor |
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Term
| Pathophysiologica Processes that Contribute to the Development of CHF |
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Definition
| Pressure overload; Volume overload; Loss of muscle; Decreased contractility; Restricted filling |
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Term
| Syndromes Causing Heart Failure |
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Definition
SYSTOLIC DYSFUNCTION - Reduced ability of the myocardial fibers to shorten (reduced ejection fractoin), can result in post-MI remodeling, Patients with decreased ejection fraction may be symptomatic or asymptomatic, Example - dilated cardiomyopathy;
DIASTOLIC DYSFUNCTION - impaired LV filling due to increased chamber stiffness or decreased relaxation (due to ischemic heart disease, MI, HTN, etc), Occurs more commonly in the elerly, May be responsible for up to 40% of CHF cases in adults, Ejection fraction is preserved, Example - hypertrophic cardiomyopathy;
Many patients have both a systolic and a diastolic dysfunction |
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Term
| A Rational Approach to the Patient with Heart Failure |
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Definition
| Determine etiology, assess severity, assess ventricular function (systolic, diastolic), Correct precipitating factors, Interventional correction where possible, Nonpharmacologic therapy, Exercise prescription, Pharmacologic therapy, Consider transplant |
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Term
|
Definition
| Dyspnea, Orthopnea, Edema, Fatigue, Weakness, Nocturia, Abdominal fullness |
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Term
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Definition
| Dyspnea, Tachycardia, Edema, Rales (sounds like cellophane crackling, can be wet or dry), S3 and S4 gallop sounds(S3 only occurs in patients with CHF, S4 can occur in patients with or without CHF), Elevated jugular venous pressure (internal jugular vein pressure - shine a light tangentially along the neck and measure with a ruler), Hepato-jugular reflux (press on the liver and see if the internal jugular veins get distended) |
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Term
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Definition
| Patients are at risk for CHF, but have no structural heart disease or symptoms of CHF; Includes Patients With - HTN, atherosclerosis, diabetes, obesity, metabolic syndrome, exposure to cardiotoxins (ex: CA drugs - adriamycin, MS drugs), and patients with a family history of cardiomyopathy |
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Term
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Definition
| Patients are at risk of CHF and have structural heart disease, but no signs or symptoms of CHF; Includes Patients With - previous MI, LV remodeling (LVH, Low ejection fraction), and Asymptomatic valvular disease |
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Term
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Definition
| A majority of patients being treated for CHF are in this category; Considered clinical CHF; Patients have structural heart disease and prior or current symptoms of CHF |
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Term
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Definition
| Refractory CHF requiring specialized interventions; Patients have marked symptoms at rest, require maximal medical therapy, and have recurrent hospitalizaitons |
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Term
| Functional Classification of CHF (According to NYHA) |
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Definition
CLASS I - symptom free; CLASS II - Symptoms of fatigue or dyspnea during ordinary activty; CLASS III - Symptoms of fatigue or dyspnea during any activity; CLASS IV - Symptoms of fatigue or dyspnea at rest;
NOTE - This is the classification system that is used more often (The ABCD classification isn't used as much) |
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Term
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Definition
| Improve clinical status/ quality of life by alleviating symptoms, Reduce risk of mortality and morbidity, Slow disease progression |
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Term
| What Produces Symptoms of CHF? |
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Definition
| Hemodynamic abnormalities - changes in cardiac function and peripheral hemodynamics |
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Term
| What Produces Progression of CHF? |
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Definition
| Neurohumoral abnormalities - activation of the renin-angiotensin system and sympathetic nervous system |
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Term
| Nonpharmacologic Treatment of CHF |
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Definition
Restriction of Sodium Intake - eliminate salt in cooking and at table, institute a low sodium diet;
Restriction of Physical Activity - reduce heavy labor, reduce periods of work, implement rest periods |
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Term
| Useful Oral Agents in CHF |
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Definition
| Diuretics; Inotropic Drugs (digitalis); Vasodilators (nitrates + hydralazine, and/or ACE Inhibitors such as captopril or enalapril) |
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Term
| Diuretic Therapy in Heart Failure |
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Definition
THIAZIDES - long acting, synergistic with loop diuretics, K+ and Mg++ depletion, ineffective in renal insufficiency;
LOOP DIURETICS - Short acting, NSAIDs may inhibit effects, may lead to electrolyte imbalance (which can cause arrhythmias);
METOLAZONE - synergistic with loop diuretics, effective even with GFR is low, beware of overdiuresis/ severe electrolyte imbalance, intermittent use is perferable;
POTASSIUM-SPARING AGENTS - weak diuretics, may be preferable to oral K+, extreme caution in renal failure, diabetes or with ACE Inhibitors, NSAIDs, and Beta-blockers |
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Term
| Effects of Digitalis Glycosides in Heart Failure |
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Definition
| Neurohumoral Effects - Increased baroreceptor sensitivity, decreased norepinephrine plasma concentrations, Withdrawal of elevated sympathetic nervous system tone, Decreased activation of Renin-Angiotensin-Aldosterone system |
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Term
| What did the ACTION-HF Consensus Recommend for the Management of CHF? |
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Definition
| "All patients with stable NYHA class II or III heart failure due to left ventricular systolic dysfunction should receive a beta blocker unless they have a contraindication to its use or have been shown to be unable to tolerate treatment with the drug; Beta blockers are generally used together with diuretics and ACE inhibitors" |
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Term
| Prognostic Indicators of Poor Outcome in CHF |
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Definition
| Decreased LV function, Presence of arrhythmias, Decreased hyponatremia, Increased plasma norepinephrine (not measured in clinical cardiology, but you can measure BNP and ANP), Exercise capacity, Age >70, Significant coronary artery disease (CAD) |
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Term
| Management Options in Intractable Heart Failure (ie CHF that is beyond drug therapy) |
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Definition
| Intra-aortic balloon counterpulsation, Heart transplant (best option if possible), Mechanical Support (external centrifugal pumps, implantable left ventricular assist devices) |
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Term
| Heart Transplantation Indications and Eligibility |
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Definition
INDICATIONS - unacceptable prognosis for 1 year survivial and/or unacceptable quality of life because of persistent cardiac symptoms that are unresponsive to medical and surgical options;
ELIGIBILITY - The patient must be free of any noncardiac condition that would shorten life expectancy or increase risk of death from rejection or from complications of immunosuppression, particularly infection |
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Term
| Contraindications to Heart Transplantation |
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Definition
| Age >55-65 years (age limit varies from program to program), Active infection, Active ulcer disease, Severe diabetes mellitus with end-organ damage, Severe peripheral vascular disease, Pulmonary function <60%, History of chronic bronchitis, Serum creatinine level >2mg/dL, Creatinine clearance <50mL/ min, Serum bilirubin level >2.5mg/dL, Transaminase levels >2x normal, Pulmonary artery systolic pressure >60mmHg, Mean transpulmonary gradient >15mmHg, High risk of life-threatening noncompliance (severe cognitive impairment, drug, tobacco or alcohol abuse, history of noncompliance with medication, diet regimen) |
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Term
| Indications for Implantable Cardioverter Defibrillation (ICD) |
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Definition
| Patients with ventricular arrhythmias (protection against death from ventricular tachycardia, protection against death from ventricular fibrillation) |
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Term
| What is High Blood Pressure? |
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Definition
| Blood pressure above which risk for vascular/ tissue damage increases |
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Term
| Atherosclerosis Risk Factors |
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Definition
| HTN, Obesity, Low HDL cholesterol, High homocysteine, Smoking, High LDL cholesterol, Glucose intolerance, Family History, Renal Insufficiency |
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Term
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Definition
Blood vessels - atherosclerosis;
Heart - left ventricular hypertrophy;
Brain - strokes, aneurysms;
Eyes - retinal ischemic changes |
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Term
| Essential vs. Secondary HTN |
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Definition
| Secondary HTN has an identifiable and reversible cause, it comprises 5% of hypertensive cases; Essential HTN has no identifiable or reversible cause, it comprises 95% of hypertensive cases |
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Term
| Pathophysiologic Causes of Essential HTN |
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Definition
| Heredity; Renal sodium retention (salt sensitivity); Renin-angiotensin-aldosterone axis; High cardiac output/ hyperkinetic circulation; Sympathetic overactivity/ stress; Born with too few nephrons; Increased intracellular calcium (causes constriction of the vascular smooth muscle, which increases peripheral vascular resistance); Vascular hypertrophy (increases peripheral vascular resistance); Imbalance of pressor/ depressor hormones; Associated diseases (diabetes, obesity); Environment (caffeine, potassium, magnesium, lead) |
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Term
| HTN in Special Populations |
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Definition
| African Americans have 2x the incidence of HTN compared to whites, and 4x the morbidity; African Americans have a lower # of nephrons, and tend to be more salt sensitive and have low renin; Diabetics - treatment goals are more aggressive; SYSTOLIC HTN OF THE ELDERLY - Systolic BP >160 with a normal diastolic, Caused by loss of vascular elasticity |
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Term
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Definition
| Historically, the goal was to get BP to <140/90, now this is being challenged (thinking is that this pressure is too high); Goal in Diabetics with Kidney Disease - 125/75 or as low as the patient will tolerate; Goal with Systolic HTN of the Eldery - Systolic <160, preferably <140 |
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Term
| Non-Pharmacologic Treatment of HTN |
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Definition
| Weight reduciton, Limit sodium intake, supplement potassium, calcium and magnesium, More dietary fiber, Less saturated fat, Stop Smoking, Limit Caffeine, Exercise, Relaxation techniques |
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Term
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Definition
Used in the 60s and 70s; Step 1 - diuretics (usu a thiazide), Step 2 - beta blockers (propranolol), Step 3 - direct vasodilator (hydralazine), Step 4 - ganglionic blocker (trimethaphan); If step 1 didn't control the HTN, step 2 was added, and so on;
Step therapy fell out of favor when new drugs became available in the 1980s, but it is now sort of making a comeback |
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Term
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Definition
| Diuretics, Centrally active alpha 2 agonists, Combined alpha and beta blockers, ACE Inhibitors, Direct Vasodilators, Natriuretic peptides, Beta blockers, Peripheral alpha 1 blockers, Calcium Channel blockers, Angiotensin II receptor blockers, Ganglionic blockers |
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Term
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Definition
HYDROCHLOROTHIAZIDE - cheap, effective (almost always works if you have normal renal function), few side effects, compliments the actions of other anti-hypertensives, Doesn't work so well in patients with renal insufficiency, they may need a loop diuretic;
KILL 2 BIRDS WITH 1 STONE.... Use the following in patients with HTN and Other Conditions, Such as....
ACE Inhibitors or Angiotensin II Receptor Blockers are good for diabetics or patients with CHF with low ejection fractions; Beta blockers are good for angina, systolic HTN of the elderly, or middle-aged white women; Peripheral alpha 1 blockers are good for men with enlarged prostates |
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Term
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Definition
An accelerated rise in BP high enough to cause end organ damage such as headache, papilledema, CHF (afterload is so high you just can't pump against it), Progressive renal failure; If there's NO end organ damage, it's just called "accelerated HTN";
ETIOLOGY - activation of the renin-angiotensin system (super high renin state), drives up BP and you get insudation of plasma proteins into the walls of the renal arterioles which damages them, causing fibrinoid necrosis of the renal arterioles. This generates ischemia, which leads to even higher renin levels, leading to a vicious cycle |
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Term
| Treatment of Malignant HTN |
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Definition
| Bring the BP down to 160/100 quickly, then normalize it over time. If you lower the BP too much before they've had time to equilabrate, they can have issues with ischemic strokes; USE - nitroprusside, fenoldapam (a dopamine 1 agonist that lowers BP by vasodilation), Labetalol, ACE inhibitors or Angiotensin II receptor blockers |
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Term
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Definition
1 - Estrogen;
2 - Sleep Apnea;
3 - Pheocrhomocytoma;
4 - Primary Hyperaldosteronism;
5 - Renal Artery Stenosis |
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Term
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Definition
Estrogen from birth control pills, or hormone replacement therapy;
Mechanism for causing HTN - mineralocorticoid effect;
Treatment of Estrogen-induced HTN - diuretics or just stop the drug |
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Term
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Definition
| If you stop breathing for long enough, you become hypoxemic and blood vessels at the base of the lungs shift blood up to the apices (where oxygen is) which increase pulmonary vascular resistance, this creates a high afterload for the right ventricle to work against and over a period of years you can get right ventricular failure; This right heart failure activates the renin-angiotensin-aldosterone system which leads to salt and water retention and vasoconstriction so that you get HTN; Sleep apnea is common in obese people; Patients will have a history of poor sleep, snoring, apneic periods, excessive daytime somnolence; Diagnosis of Sleep Apnea - history, polysomnography; Treatment of Sleep Apnea - nocturnal oxygen, diuretics, CPAP or BiPAP, ENT surgery, tracheostomy |
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Term
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Definition
Pheochromocytomas are RARE tumors that derive from chromaffin cells (which make catecholamines) - most put out norepinephrine, some put out epinephrine; Can be familial - Multiple Endocrine Neoplasia (MEN) II;
Clinical Presentation - Classic Triad of Headache, diaphoresis and palpitations; Patients often have pallor, nausea, tremor, and nervousness and 60% have permanent HTN; 50% of patients with pheochromocytoma have hypertensive crises - attacks last up to 1 hour (takes that long to metabolize the excess catecholamines) and may be triggered by drugs, anesthetics and surgery;
DIAGNOSIS is based on finding high levels of catecholamines or their metabolites in blood or urine and is made based on 24 hour urinary free catecholamines, metanephrines,and VMA, but you have to make sure the patient did the 24 hour urine collection correctly!; Plasma catecholamine levels aren't very reliable because people get nervous when they see needles and this makes their catecholamine levels go up (one solution is to put the needle in and let the patient relax in a dark room for a while before quietly/ calmly drawing the blood);
CLONIDINE SUPPRESSION TEST - done if the urine test comes back positive, Clonidine acts centrally to suppress catecholamines, so if the clonidine makes no difference in the level of catecholamines then the patient must have another source of catecholamine production (ie a pheochromocytoma); CT scan and MIBG (metaiodobenzylguanidine) scan are also useful (MIBG scan will light up in the location of the pheochromocytoma);
TREATMENT - Surgical removal, alpha blockers (Phentolamine), beta blockers;
PHEOCHROMOCYTOMAS are known as the 10% tumor: 90% are intra-abdominal (10% aren't) with most being in the adrenals, but some are found along the sympathetic chain ganglia or at the organ of Zuckercandl (where the sympathetic chain ganglia from each side meet), 10% are multifocal, and 10% are malignant |
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Term
| Primary Hyperaldosteronism and HTN |
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Definition
Primary Hyperaldosteronism is a high aldosterone, low renin state that is not repressible with salt loading; CAUSES - adrenal adenoma (most common), bilateral cortical nodular hyperplasia, adrenal carcinoma;
PRESENTATION - HTN, Spontaneous hypokalemia (ie low potassium for no reason such as diuretics), No edema (aldosterone escape), May have metabolic alkalosis;
DIAGNOSIS - HTN with hypokalemia for no apparent reason should trigger some red flags for this disease; Classic Work Up Includes: Check plasma renin activity, if it is low, do the following - (1) Salt load with IV saline or salt tabs and PO fluid, (2) Check plasma aldosterone after this - it should be low, if it's high it's a primary hypermineralocorticoid state, (2) CT scan of the adrenals (with thin slices) to find the locaiton of the tumor;
What Dr. Friedenberg Does: If the patient is NOT a surgical candidate he treats them with spironolactone and a diuretic (no sense subjecting them to the workup listed above if they're not going to be able to do anything about it surgically), if the patient IS a surgical candidate he checks a CT of the abdomen with thin slices thru the adrenals, if it's negative or shows bilateral disease he treats them medically, if it shows a unilateral adenoma he may check bilateral adrenal vein aldosterone levels to see if it lateralizes to the side with the lesion before proceeding to surgery;
TREATMENT - surgery works only for adenoma or CA, Medications: potassium sparing diuretics - spironolactone (start here, add the others if needed), tiramterene, amiloride |
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Term
| Renal Artery Stenosis(RAS) and HTN |
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Definition
Two Types of RAS - atherosclerotic (old people) and fibromuscular dysplasia (young people, women >men);
DIAGNOSIS - Ultrasound/ Doppler (Duplex scan) - very operator dependent, very time consuming, difficult to see the entire renal artery, difficult exam except in very thin patients (bowel gas interferes with imaging), usually not a helpful test; Magnetic Resonance Angiography (MRA) - expensive, claustrophobic, often can't do in patients with metallic implants, the IV contrast used (gadolinium) can cause a horrible condition known as nephrogenic systemic fibrosis in patients with renal insufficiency, very low false positive rate which makes it a great screening test, but it can overestimate the severity of the stenosis; CT angiography - non-invasive, good quality images, but utilizes a large iodinated contrast load; Angiography - invasive, has complications (radiocontrast toxicity, trauma at the puncture site, atheroembolization, vascular dissection), advantage is that you can do angioplasty/ stenting right away;
TREATMENT - Surgery: aortorenal bypass, splenorenal bypass (left kidney), hepatorenal bypass (right kidney); Percutaneous transluminal angioplasty; Stenting (ballooning alone is treatment of choice for FMD, you don't even need to stent it); Atherectomy; Medical Management;
INDICATIONS To Treat With Surgery or Interventional Radiology - Renal function so bad that without such treatment the patient will need dialysis, uncontrollable HTN, multiple episodes of "flash pulmonary edema" |
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Term
| When To Suspect Renal Artery Stenosis (RAS) |
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Definition
| Age of Onset: <25 think fibromuscular dysplasia (FMD), >50 think atherosclerosis; Patient is a Vasculopath (you hear bruits everywhere, they have a history of strokes, MIs, etc.); Sudden worsening of well controlled HTN; Malignant or accelerated HTN (since RAS can trigger these); Discrepancy in renal size on imaging study; Creatinine elevation with ACE Inhibitor or Angiotensin II receptor blocker; Hypokalemia with high renin and high aldosterone (a physiologic response to the kidney not getting enough blood) |
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