Term
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Definition
| The end to end joining of two distinct vessels. This is important because it provides collateral circulation if one of them is occluded. |
|
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Term
What are the layers surrounding the heart?
What is the anatomical position of the heart (direction of the apex? |
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Definition
Parietal pericardium (outer fibrous layer, inner serous layer), Visceral pericardium (epicardium).
The apex is 45 degrees anterior and 45 degrees to the left. |
|
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Term
| What is a Silhouette sign? |
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Definition
| It is a loss of normal borders between thoracic structures in a CXR. Eg: pneumonia obscuring the borders of the heart. |
|
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Term
| What is cardiac tamponade? |
|
Definition
| Compression of the heart due to a collection of fluid in the pericardial cavity. |
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Term
Describe the following features, including their location:
Auricle, Pectinate muscle, crista terminalis, fossa ovalis, and coronary sinus. |
|
Definition
Auricle - ear-like appandage coming off each of the atria
Pectinate muscle - the muscular inner surface of the atria
Crista terminalis - Crest dividing the pectinate muscle from the smooth posterior surface of the right atrium. Contains the SA node.
Fossa ovalis - remnant of the foramen ovale in the right atrium.
Coronary sinus - The site of the venous return of the coronary circulation. Empties into the right atrium. |
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Term
Describe the following features, including their location:
Conus arteriosus, trabeculae carnae, papillary muscles, and septomarginal trabeculae. |
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Definition
Conus arteriosus - smooth top of the RV chamber tapering to the pulmonary valve.
Trabeculae carnae - muscle lining the ventricles
Papillary muscles - specialized muscles in the ventricles stabilizing the valves via the chordae tendinae.
Septomarginal trabeculae - Includes the moderator band in the RV. connects the septum to the papillary muscles, providing a shortcut for the conduction system. |
|
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Term
| What is the aortic vestibule? |
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Definition
| The smooth upper part of the LV equivalent to the conus arteriosus of the RV. |
|
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Term
| Describe the path of the coronary arteries, listing each major branch. |
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Definition
| Left coronary artery divides into the Left Anterior Descending artery (LAD) which flows in the interventricular groove, and the left circumflex artery which flows in the atrioventricular groove. The right coronary artery flows further then divides into the marginal branch and continues on to the back. The posterior descending artery (PDA) can be supplied by the right coronary artery and/or the left circumflex depending on dominance. (right more common) |
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Term
| How is the blood supply of the interventricular septum determined? |
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Definition
| Anterior 2/3 supplied by the LCA. This includes the AV bundle and bundle branches. Posterior 1/3 including the AV node supplied by the posterior interventricular branch. |
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Term
| Describe the coronary venous system. |
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Definition
| Great cardiac vein (anterior), middle cardiac vein (posterior), and small cardiac veins (inferior). These lead to the cardiac sinus (where it all collects). Anterior cardiac veins (right atrium) drain into the atrium directly. |
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Term
| What is the vitelline vascular system? What comes is derived from it? |
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Definition
| It is the system to the yolk sac. The yolk sac is the blood producing organ for the early embryo. It becomes the intrahepatic inferior vena cava, hepatic veins, and the hepatic portal system. |
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Term
| What are the 3 sequential systems in venous development? What comes from each of them? |
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Definition
| 1. Cardinal: veins above the heart - brachiocephalic vein, superior vena cava, pelivc and leg veins. 2. Subcardinal: Segment of the inferior vena cava, Renal and gonadal veins. 3. Supracardinal: late-forming azygos system. |
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Term
| What is the sinus venosus? What does it become in the adult? |
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Definition
| It is where all veins in the embryo converge. Left horn becomes the coronary sinus. Right horn becomes the posterior smooth wall of the RA. |
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Term
| What is the bulbus cordis and what does it become in the adult? |
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Definition
| It is a swelling right before exit out of the developing heart. It becomes the conus arteriosus (RV) and the aortic vestibule (LV). These are the smooth outflow portions of both ventricles. |
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Term
| What is the truncus arteriosus? What does it become in the adult? |
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Definition
| It is the main outflow pathway from the developing heart. It becomes the pulmonary trunk and the aorta. |
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Term
| What is the first partition in the developing heart? Then what happens? How does the blood flow? |
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Definition
| The endocardial cushions fuse to separate blood flow into left and right sides. The septa begin to form. Blood flows in the right atrium, then it can go left atrium left ventricle right ventricle or just direct to the right ventricle and out through the bulbus cords. |
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Term
| Describe the developmental division of the atria. |
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Definition
| The septum primum is the first division. It grows until it obscures the foramen primum (just the hole between the atria). Then the foramen secundum forms higher up in the septum primum to allow for continued communication. The septum secundum then develops as a sort of flap covering the septum secundum. Its edge forms the foramen ovale, creating a unidirectional flutter valve. |
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Term
| Why doesn't the IV septum grow to join the endocardial cushion? What happens instead? |
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Definition
| If it joined the cushion, the left ventricle would have no exit. Instead a spiral septum forms in the truncus arteriosus dividing it into the pulmonary trunk and the aorta. This grows to fuse with the IV septum and cushions allowing for exit from both ventricles. |
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Term
| What is the ductus arteriosus and what does it become in the adult? The ductus venosus? |
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Definition
| The ductus arteriosus is a bypass connecting the pulmonary arteries to the aorta. It becomes the ligamentum arteriosum. The ductus venosus is a bypass around the liver feeding umbilical blood directly to the inferior vena cava. Becomes the ligamentum venosum. |
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Term
| Why do septal defect symptoms get worse with time? |
|
Definition
| Right after birth the systemic and pulmonary pressures are equal. As the baby grows the pressure difference increases leading to worsening symptoms. |
|
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Term
| What are the 4 defects associated with the Teratology of Fallot? |
|
Definition
A faulty spiral septum is the primary cause. This leads to:
1. Pulmonary stenosis. 2. IV septal defect. 3. Overriding aorta. 4. R. ventricular hypertrophy. |
|
|
Term
| What are the 3 spiral septum defects? |
|
Definition
| 1. Teratology of Fallot. 2. Persistent Truncus arteriosus. 3. Transposition of the great arteries. |
|
|
Term
| What is the Nernst Equation? |
|
Definition
|
|
Term
| Which ions are more concentrated outside the cell? Inside? Which are important for depolarization/repolarization? |
|
Definition
Outside: Sodium, Calcium. Both have + equilibrium potentials. Important for depolarization.
Inside: Potassium. Has a - equilibrium potential. Drives the potential of the cell due to the fact that it's the ion that has the highest permeability. Important for repolarization. |
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Term
| What 3 major types of signals open and close the channels involved in cardiac action potentials? |
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Definition
| 1. Voltage dependence 2. Time dependence 3. Ligand dependance |
|
|
Term
|
Definition
| Conductance is the inverse of resistance. E=IR, g=IE. |
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Term
| What is the equation for membrane potential using conductance (cord conductance eqn)? What does it mean? |
|
Definition
Vm = (gk/g total)*Ek +(gna/g total)*Ena
This means that membrane potential is determined by the equilibrium potentials of the ions weighted by their conductance. |
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Term
| Name and describe the 5 phases of the cardiac action potential. |
|
Definition
Phase 4: Resting. Determined by K permeability. Ik1 (inward rectifier)
Phase 0: Upstroke. Driven by Na channels. Ina, Ica
Phase 1: Notch. Due to Ito.
Phase 2: Plateau. Due to slow closing Ca channels, Ik1 blockage, and slow opening Ik.
Phase 3: Repolarization. Due to Ik1 & Ik fully activating and Ica fully inactivating.
Phase 4: Resting. Maintained by Ik1 |
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Term
Two ion channels have activation and inactivation gates. What what are they, and what are their names?
What do they have to do with refractory periods? |
|
Definition
Na: m - activation (fast. Closed at rest, opens w/voltage stimulation, Threshold at -70 mV), h - inactivation (open at rest, closes at higher voltages).
Ca (L type): d - activation (slow), f - inactivation (slow closing due to time dependency - leads to Phase 2 plateau)
Ca opens at a higher voltage so it can still be triggered when the h gate is closed. This is the relative refractory period.
If the voltage is so high the h gate and f gate are closed that's the absolute refractory period. |
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Term
| Describe some of the differences between the fast response action potential (Na) and the slow response AP (Ca). |
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Definition
| Fast: Faster activation and inactivation, Faster upstroke, faster conduction, higher safety margin, and shorter refractory period (approx. = AP duration, Slow longer than AP duration). |
|
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Term
| List and describe the different K currents. |
|
Definition
Ito: transient outward. Creates the notch seen in Phase 1.
Ik1: Inward rectification. Responsible for maintaining the resting potential. Is blocked at higher voltages allowing the Phase 2 plateau. Once the voltage drops sufficiently, it re-opens and aids in Phase 3 repolarization.
Ik: Delayed rectifier. Composed of ultra rapid (Ikur - only in the atria), rapid (Ikr), and slow (Iks) components. Net activation is slow, also contributing to the plateau.
Ligand gated Ik's: just know they exist. |
|
|
Term
| Current flow in the heart is decremental. What does this mean? |
|
Definition
| It means that the current flow decreases with distance. |
|
|
Term
| What are the electrically conducting channels in gap junctions called? |
|
Definition
| Connexins. Different types vary in their electrical properties (resistance). |
|
|
Term
| What does the space constant tell us? |
|
Definition
| The distance over which the voltage has decayed to 1/3 its original value. Space constant=root(Rm/Ri). The voltage travels farther if the membrane resistance is higher (acts as an insulator keeping charge in), and internal resistance is lower (travel through gab junctions is easy). |
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|
Term
| What does the time constant tell us? |
|
Definition
| The time it takes for the voltage to decline by 1/3. T=RC (resistance*capacitance) |
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|
Term
| What is the point of the time and space constant lecture? |
|
Definition
| We need an amplifier or the signal won't propagate. The action potential is that amplifier that allows the signal to propagate. High amplitude and low threshold of the action potential are also important for its propagation. |
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Term
| What are the only two areas in the heart where resting cells are depolarized to -60mV? |
|
Definition
| The SA node and AV node. This requires action potentials be activated by the slow acting mechanism (Ca channels) leading to the delay required for ventricle filling. It is due to their relative leakiness. The downside of this is a lower margin of safety - AV node is the most likely spot for the conduction system to fail. |
|
|
Term
| What is special about M cells? |
|
Definition
| They are vulnerable to changes in conditions. This can lead to big changes in their action potential duration. Epicardium and Endocardium each also have unique AP characteristics. |
|
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Term
| What is automaticity? Which cells have this property? |
|
Definition
It is the property of cells that undergo Phase 4 depolarization, and thus can self stimulate.
The SA node, Atrial cells, AV node, and purkinje fibers all have this property in decreasing amounts. |
|
|
Term
| What 2 mechanisms cause automaticity? |
|
Definition
| Pacemaking is caused by 1. Membrane voltage clock: increasing If (funny channels), and decreasing Ik. 2. Sarcolemmal Ca clock: Rhythmic release of Ca from sarcolemma. This is pumped out w/ a 1:3 Ca:Na exchanger leading to depolarization. |
|
|
Term
| Which imaging technique is best for view valves? Which is best for coronary arteries? |
|
Definition
|
|
Term
What do the different parts of the EKG represent?
Specifically: What occurs at the P wave? PR segment? QRS complex? ST segment? T wave? |
|
Definition
P wave - atrial depolarization
PR segment - AV firing
QRS complex - ventricular depolarization
ST segment - Plateau Phase
T wave - repolarization |
|
|
Term
| Why is the T wave positive? |
|
Definition
| I travels in the opposite direction of the depolarization (since the first cell to depolarize is the last to repolarize). Since it is a negative charge going away it looks the same as a positive coming toward: positive. |
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|
Term
| What is the definition of a Q wave? R wave? S wave? |
|
Definition
Q: The first deflection if it is negative.
R: Any upward deflection.
S: Any downward deflection that is not the first deflection. |
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|
Term
| What is the difference between an interval and a segment on the EKG? |
|
Definition
Interval includes the length of a wave or waves.
Segment is between waves. |
|
|
Term
What is the PR interval?
The QRS interval?
The QT interval?
The ST segment? |
|
Definition
PR: (Start of P to start of Q) From initiation of atrial to initiation of ventricular activation
QRS: Total time of ventricular activation
QT: (Start of Q to end of T) Sum total of Action Potential (AP) duration in ventricle.
ST: The plateau phase (2). |
|
|
Term
What does Kirchoff's law tell us?
What is Einhoven's Equation?
Which leads are = out of I, II, and III? |
|
Definition
Kirchoff's Law: If you make recordings in a closed circuit you get 0.
II=I+III
Leg, Left are positive in that priority. |
|
|
Term
|
Definition
1. aVR
2. aVL
3. I
4. III
5. aVF
6. II
Note the boxes are at the + end of each lead. |
|
|
Term
How tall is each square on EKG paper?
How tall is 1 mV?
How much time is each square? |
|
Definition
| The large square is 5 mm tall, and 200 msec. long. 1 mV is 1 cm. |
|
|
Term
What is a normal HR?
How do you calculate a "rough estimate HR"?
How do you calculate a "precise" HR? |
|
Definition
60-100 BPM.
Count # of beats on page (10 sec.) multiply by 6. Also 300, 150, 100, 75, 60, 50.
1500/# of tiny boxes between beats. |
|
|
Term
What are the following standard intervals?
PR Interval?
QRS interval?
QTc interval? |
|
Definition
PR: 120-200 msec.
QRS: Up to 120 msec.
QTc: Female: up to 460 msec. Male: up to 450 msec. |
|
|
Term
| How do you calculate the corrected QT interval? |
|
Definition
QTc = QT/root(RR)
*RR is the interval between QRS complexes measured in sec. |
|
|
Term
How do you determine the axis quadrant?
More precisely?
How should the different axes (QRS, T, & P) relate? |
|
Definition
Look at I and aVF. Up means it must by going toward it, i.e. in that 180 degrees. Using both you can narrow it down to a single quadrant.
More precisely look for an isoelectric segment (aka most biphasic - neither up or down on net). Axis must be perpendicular to that lead.
All the axes should be approximately the same. |
|
|
Term
| What is the trick to know which lead is perpendicular to which? |
|
Definition
| Draw the star on the EKG paper. The lines connect perpendicular leads. |
|
|
Term
| What should happen progressively from V1 to V6? |
|
Definition
| There should be a progression from a predominantly downward to a predominantly upward QRS waveform. |
|
|
Term
| What should you draw on an EKG to evaluate it (a good trick)? |
|
Definition
| A curve from the P to the T ignoring QRS. If you can't or there's not a nice curve, you have a problem. |
|
|
Term
| What does ST elevation tell you? ST depression? |
|
Definition
ST elevation tells you there is transmural injury (whole wall affected). - STEMI
ST depression tells you it is just the endocardial tissue that's affected. Angina & NSTEMI
The elevation or lack thereof is due to the different geometry of the blockage. |
|
|
Term
| What can cause T wave inversion? |
|
Definition
Ischemia. First to depolarize may be the first to repolarize under these hypoxic conditions.
Note: The T wave is sensitive and can invert w/ hyperventilation, drinking cold water, etc. - look at your patient! |
|
|
Term
What is an abnormal Q wave a sign of?
What are the criteria for an abnormal Q wave? |
|
Definition
Infarction!
Duration >= 30 msec (about 1 small box) (20msec in V2&3)
Amplitude >= .1mV (1 small box)
Present in at least 2 contiguous leads (i.e. 2 inferior, 2 lateral, 2 anterior)
Note: Q wave in III is normal. |
|
|
Term
What are the 4 stages used to determine the age of the MI?
What are their characteristics? |
|
Definition
1. Hyperacute - Tall, peaked T waves w/or w/out ST elevation. - minutes to hours (usually not recorded).
2. Acute - STEMI. ST segment elevated >= 1 small box. Q wave may start to appear. Minutes to days.
3. Evolving - T waves invert. ST slowly dropping to normal.
4. Old - Q wave persists indefinitely. ST usually goes to baseline. T wave inversion may or may not persist. |
|
|
Term
| How do you diagnose an NSTEMI? |
|
Definition
| ST depression, abnormal T wave. Or nothing. May need to be diagnosed w/ enzymes, and clinical presentation. |
|
|
Term
| Will a Q wave always appear in an MI? |
|
Definition
| No. There must be a substantial area of necrosis for the Q wave to appear. |
|
|
Term
| What are the criteria to diagnose an atrial abnormality (enlargement)? |
|
Definition
Lead II: R - amplitude >=2.5mm, L - Width >=3mm
OR
Lead V1: R - amplitude >=2.5mm, L - Area of negative component >= 1 mm^2 (1 small box). |
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|
Term
| What are the criteria for RVH? |
|
Definition
V1: R wave is larger than S wave
V6: S wave is larger than R wave
Right axis deviation
Usually a right atrial p wave abnormality will be present. |
|
|
Term
What are the criteria for LVH?
What is the strain pattern that often accompanies LVH? |
|
Definition
1. S wave in V1 + R wave in V5 or 6 >= 35mm
2. R in I + S in III >= 25mm
3. R in aVL >= 12mm
Note: Young people often have big volts. These criteria are only for people >35.
The strain pattern is ST depression and/or T inversion in inferior or lateral leads. |
|
|
Term
| What are some of the symptoms of bradycardia? |
|
Definition
Syncope, dizziness, poor exercise tolerance/fatigue, congestive heart failure.
Can be asymptomatic. |
|
|
Term
| What are the two mechanisms of sinus node dysfunction? |
|
Definition
1. Impulse formation
2. Impulse propagation |
|
|
Term
| What are the 4 disorders caused by problems with Sinus impulse formation? Describe them. |
|
Definition
1. Sinus bradycardia: Rate slower than 60 BPM
2. Chronotropic incompetence: Inadequate response to exercise.
3. Tachy-Brady Syndrome: Fast then slow beating. Afib, then SA node is stunned so it take a bit to come back.
4. Sinus arrest: just shuts down for a bit |
|
|
Term
| What is Sinoatrial exit block? |
|
Definition
| It causes sinus bradycardia. Occurs when the signal can't leave the SA node through the normal pathways, and must take the slower conducting heart muscle pathway. Either 1. The PP keeps getting shorter until one P fails to conduct (no signal - dropped beat). or 2. The PP is normal, and a beat drops the exact length of a PP interval. |
|
|
Term
|
Definition
| It can be due to a problem with the AV node itself, or due to the His-Purkinje system. |
|
|
Term
| What are the different types of AV block? Where do they originate? Describe them. |
|
Definition
1st degree: Originates in the AV node. PR prolongation due to slow conduction through AV node. No dropped beats.
2nd degree Mobitz Type 1 (Wenckebach): Originates in the AV node. Progresseily longer PR followed by a dropped beat.
2nd degree Mobitz Type II: Originates in the His-Purkinje system. Fixed PR delay with dropped beats.
3rd degree: Originates in the His-Purkinje system. Complete AV block. P and QRS are unrelated. |
|
|
Term
|
Definition
Transient loss of consciousness with loss of postural tone due to transient cerebral hypoperfusion.
Rapid onset, short duration, spontaneous complete recovery. |
|
|
Term
| What is the equation for blood pressure? Why is this important? |
|
Definition
BP = HR x SV x SVR
SV - Stroke volume
SVR - Systemic vascular resistance.
This equation explains syncope. |
|
|
Term
| What are the 3 main categories of syncope? Describe them. |
|
Definition
1. Reflex (neurally-mediated) syncope: aka Vasovagal syncope. Some stimulus leads to blood pooling. Sympathetic kicks in, but then parasympathetic over-reacts to counterbalance leading to low BP (HR + SVR affected).
2. Cardiovascular syncope: Due to Bradycardia (low HR), Tachycardia (low SV). or a structural defect preventing blood ejection (low SV).
3. Syncope due to orthostatic hypotension: Due to failure to increase SVR (autonomic problem), or volume depletion. Affects those 40+. |
|
|
Term
| What do vessels develop from? |
|
Definition
|
|
Term
| What are the names of the different blood vessels? What are some of their characteristics? |
|
Definition
Large vein (Compliant due to semi-collapsed shape, have longitudinal bundles of smooth muscle) - Large/Elastic artery (fenestrated elastic lamellae)
Vein - Medium/Muscular artery (internal elastic membranes, scalloped intima)
Venule (target for histamine) - Arteriole (Controls most blood flow, has1-2 layers of smooth muscle)
Capillary: 1 RBC thick |
|
|
Term
| How much of blood volume is is the systemic arteries? The veins? Capillaries? |
|
Definition
Arteries 15%
Veins 60%
Capillaries 5%
Rest in heart and pulmonary |
|
|
Term
| What are the 3 layers in the walls of blood vessels? |
|
Definition
1. Tunica intima: Innermost layer. Endothelial cells, basement membrane, and collagenous tissue (inner elastic membrane).
2. Tunica media: Middle muscular layer. Mostly smooth muscle, with some reticular, collagen, and elastic fibers (all secreted by smooth muscle cells).
3. Tunica adventitia: Outer layer. Connective tissue with elastic fibers, collagen, and possibly smooth muscle. Blends into surrounding connective tissue. (This layer can be replaced w/ a serosa which has no fibrous layer) |
|
|
Term
|
Definition
| Those in the extremities. |
|
|
Term
|
Definition
| A shunt connecting arterioles to venules. Important for themoregulation. |
|
|
Term
|
Definition
| Endothelial support/stem cells (source of new endothelial cells and smooth muscle cells). |
|
|
Term
| What are the different types of capillaries? |
|
Definition
Continuous: Most common. Tight junctions, basement lamina.
Fenestrated: Endocrine organs, Kidney, GI, gall blader.
Discontinuous (sinusoidal): Liver, spleen, bone marrow. |
|
|
Term
|
Definition
| A glycoprotein scaffold on the surface of endothelial cells. Increases surface area. A substrate for whatever needs to get into the lumen. |
|
|
Term
|
Definition
| A fatty/fibrous buildup within the tunica intima of arteries. Monocytes and smooth muscle cells ingest LDL becoming foam cells, creating plaque. |
|
|
Term
| What happens if the tunica intima tears? |
|
Definition
| It can cause an aortic dissection. Blood gets between the middle and outer third of the tunica media. |
|
|
Term
| What are the 2 types of mechanisms of Tachyarrhythmias? What are the 3 mechanisms and which category do they fall into? |
|
Definition
1. Abrnomality in impulse formation.
Abnormal Automaticity: Pacemaker activity in non-SA cells. Increase slope of Phase 4 depolarization. Reduced threshold for Phase 0. Focal source.
Triggered Activity: Increased Calcium current leads to afterdepolarizations - can cause another AP. Focal source.
3. Abnormality in Impulse Propagation
Reentry: Creation of a circuit due to slow and fast conduction pathways. Heart just keeps firing. |
|
|
Term
What is Paroxysmal Supraventricular Tachycardia?
What are the 3 types? |
|
Definition
Also simply called SVT. Paroxysmal - Turns on and off. Regular, narrow QRS tachycardia.
1. AV nodal reentrant tachycardia (AVNRT): Circuit example.
2. AV reentrant tachycardia (AVRT): Accessory pathways are present. Delta wave in EKG. Eg: WPW
3. (Ectopic) Atrial tachycardia (AT): Something in the atria is triggering. Focal. |
|
|
Term
| What is atrial fibrillation? |
|
Definition
| It is a type of supraventricular tachyarrhythmias. It makes up 50% of all of them. Has an irregularly irregular ventricular rhythm, due to the atria firing like crazy. No discernible p waves. |
|
|
Term
|
Definition
| It comprises 10% of supraventricular tachyarrhythmias. Fires at a super fast rate, but it is regular. Often also have atrial fibrillation. Can be due to a circuit around the tricuspid valve. |
|
|
Term
| What are the two categories of Ventricular arrhythmias? |
|
Definition
Ventricular Tachycardia: Discrete wide QRS complexes. Treat w/ an implantable defibrillator. Ablation/drugs too.
Ventricular Fibrillation: Disorganized and chaotic. QRS not discrete. Cardiac arrest. |
|
|
Term
| What are the two types of ventricular tachycardia? What are their two subtypes? |
|
Definition
1. Monomorphic: A single consistent QRS morphology.
Idiopathic: Benign. Reentry circuit.
Associated w/ structural heart disease: Disease provides the substrate. When it's triggered you get the circuit.
2. Polymorphic: QRS morphology changes.
Normal QT: Due to automaticity of a part of the ventricle or a reentry circuit.
Long QT: Torsade de Points. Associated w/ some drugs. |
|
|
Term
| What are the 3 factors of pathogenesis of arrhythmias? Describe them. |
|
Definition
1. Substrate: MI, weird electrical things going on
2. Triggers: Premature ventricular contraction (PVC) - a focus in the ventricle decides to go off.
3. Modulating factors: Electrolyte imbalance, ischemia, autonomic tone. |
|
|
Term
|
Definition
One large functionally reentrant circuit that can “wander” or give off smaller wavelets.
A mechanism of Afib and Torsades. |
|
|
Term
| What are the two types of Ventricular Fibrillation and what are their causes? |
|
Definition
Primary: Due to non-reversible causes, i.e. heart disease, congenital abnormalities. Treat w/ implantable cardioverter defibrillator (ICD).
Secondary: Due to a stimulus, i.e. MI, Ischemia, electrocution, impact, drugs, severe electrolyte disturbances. |
|
|
Term
| What is the beta adrenergic system? What does it do? |
|
Definition
| It is the sympathetic nervous system - epinephrine and norepinephrine (catecholamines). It accelerates phase 4 depolarization. |
|
|
Term
What does the Class system measure for potential treatments?
Specifically what does Class I, IIa, IIb, and III mean? |
|
Definition
The class system measures the size of the treatment effect.
Class I: The benefit is much greater than the risk. Treatment should be performed.
Class IIa: Benefit is greater than the risk. Reasonable to perform.
Class IIb: Benefit is close to risk. May be considered.
Class III: Leads to little or no benefit with great potential harm. Should not be performed. |
|
|
Term
| What are the different levels of evidence? |
|
Definition
Level A: Multiple populations - multiple RCTs or meta analyses.
Level B: Limited populations - one RCT or non-randomized studies.
Level C: Very limited data - Expert consensus, case studies, standard of care. |
|
|
Term
| What are the three mechanisms of tachyarrhythmias that can be treated with pharmacologic agents? What mechanisms would be employed? |
|
Definition
1. Enhanced Automaticity: Decrease slope of phase 4 depolarization, lower resting potential, raise threshold.
2. Reentry: Slow the slow conduction until it stops, suppress premature beats which can set up slow conduction.
3. Triggered Activity: Modify the milieu. - Address the prolonged QT in early afterdepolarizations, address the high Ca in delayed afterdepolarizations. |
|
|
Term
| What are the 3 indications for Anti arrhythmic therapy? |
|
Definition
1. Disruption of reentrant SVTs. Eg: AVNRT, AVRT
2. Treatment of AFib, AFlutter, and ATach through rate control and rhythm control.
3. Suppression of VT and symptomatic PVCs (premature ventricular contractions). Special cases: Myocardial ischemia, torsades de pointes. |
|
|
Term
What is rhythm control?
What is rate control? |
|
Definition
Rhythm control: Modify atrial electrical properties (try to let the SA node take back over).
Rate control: Slow down the AV node. |
|
|
Term
What is the mechanism for class I anti-arrhythmic drugs?
Specifically 1a, 1b, and 1c? |
|
Definition
Na+ channel blocking. Only binds active or inactivated gates, not resting gates. More effect in tachycardia.
1a: Lengthens AP duration (K+ blocking side effects). Medium effects on phase 0.
1b: Shortens AP duration. Low effect on phase 0.
1c: Potent effects on Phase 0. |
|
|
Term
| What are the Class IA drugs and their uses/side effects? |
|
Definition
Procainamide: Use: VT after MI. Side effects: Drug induced Lupus (after long term oral administration), Torsades de Pointes.
Quinidine: Side effects: Cinchonism (CNS toxicity), Torsades, Heart Block.
Disopyrimide: Use: Hypertrophic Obstructive Cardiomyopathy. Side effects: Antimuscarinic (blocks parasympathetic nervous system - urinary retention, constipation, blurred vision, dry mouth), Torsades |
|
|
Term
| What are the Class IB drugs and their uses/side effects? |
|
Definition
Lidocaine: IV. Uses: Vtach in the setting of ischemia (post-MI). Side effects: CNS toxicity.
Mexelitine: PO. Uses: Chronic suppression of ventricular arrhythmias. Side effects: Same as Lidocaine - similar structure. |
|
|
Term
| What are the Class IC drugs and their uses/side effects/contraindications? |
|
Definition
Flecainide: Negative inotropic effects. Slows conduction. Uses: Acute conversion of AFib to sinus rhythm. Maintainence of sinus rhythm in AFib. Contraindications: LV systolic dysfunction (due to negative inotropic effects).
Propafenone: Same as above + Beta blocking effects. |
|
|
Term
What is the mechanism for class II drugs?
What are two examples and their uses/side effects? |
|
Definition
They are beta blockers. They prolong decrease the slope of phase 4 depolarization.
Eg: Metoprolol PO. Esmolol IV. Uses: Slow ventricular response in AFib, dirupt re-entrance arrhythmias, suppresses premature contractions. Side effects: Hypotension, Bradycardia, depression, sexual dysfunction, cognitive impairment. |
|
|
Term
| What is the mechanism for class III anti-arrhythmic drugs? |
|
Definition
| K+ channel blockers. They prolong the action potential. |
|
|
Term
| What is Amiodarone? What is special about it? |
|
Definition
| It is a class III (beta blocker) anti-arrhythmic agent. It also has class I, II, and IV properties. Toxicity: Liver, Lungs, Thyroid. Side effects: Bradycardia, heart block, prolongs QT (but rarely causes torsades). |
|
|
Term
| What are the other Class III drugs and their uses/side effects? |
|
Definition
Sotalol: Uses: Maintenance of sinus rhythm in AFib and AFlutter, VT, prevention of AVNRT & AVRT. Also has beta blocking effects.
Dofetilide:
Ibutilide:
All prolong QT and can therefore cause torsades. |
|
|
Term
| What is the mechanism for class IV anti-arrhythmic drugs? |
|
Definition
| Ca2+ channel blockers. Prolongs Phase 4 depolarization and increases the duration of the action potential. (similar effects to beta blockers). |
|
|
Term
| What are the Class IV drugs and their uses/side effects? |
|
Definition
| Verapamil & Diltiazem: Side effects: Constipation and peripheral edema. Hypotension. |
|
|
Term
| What is the mechanism of Adenosine? What are its uses/side effects? |
|
Definition
A natural molecule. In high enough doses it causes a transient effective heart block through membrane hyperpolarization.
Uses: "Reset button" can terminate SVTs. Also helpful for diagnosis. |
|
|
Term
| What is the mechanism of Digoxin? What are its uses/side effects? |
|
Definition
Two mechanisms: 1. Inotropic effects by acting on the Na K exchanger 2. Vagomimetic effects (slow sinus rate, etc)
Uses: Control ventricular response to Afib & Aflutter.
Side effects: Narrow therapeutic window. Yellow vision, nausea diarrhea. Treat toxicity w/ anti-digoxin antibody. |
|
|
Term
| How do you disrupt reentrant SVT? |
|
Definition
| Anything that slows conduction through the AV node: Adenosine (stops it), Class II, Class IV, Amiodarone (Class III, but probably works through it's non-class III effects). |
|
|
Term
| What works well for rate control (in Afib Aflutter)? |
|
Definition
| Things that slow conduction through the AV node. Class II, Class IV, Digoxin. |
|
|
Term
| What drugs work well in rhythm control (Afib Aflutter)? |
|
Definition
| Class Ic (probably due to slowing conduction), Class III (probably by prolonging repolarization). |
|
|
Term
| What drugs can suppress VT and symptomatic PVC in MI? |
|
Definition
| Class II (slow conduction in sick tissue), Amiodarone (class III), Class 1b (interferes w/reentry by slowing conduction) |
|
|
Term
|
Definition
| This scheme can be helpful to understand how all the drugs fit together. |
|
|
Term
|
Definition
| Pressure gradient/resistance. |
|
|
Term
| What is Poiseuilli's Law? |
|
Definition
Q=[(P2-P1)*pi*r^4]/8nL
Q=flow r=radium n=viscosity L=length
Key point: radius change has a big effect on flow.
Only valid for laminar flow. |
|
|
Term
| What are the 3 general flow patterns? Describe them. |
|
Definition
Laminar: Usually in large vessels. Fluid moves in parallel layers, w/ fluid components staying in their layer. Velocity gradient w/ fastest in middle. Like a river.
Transitional: At branch points. Laminar flow will be reestablished after the critical distance.
Turbulent: High velocity, large diameter, low viscosity (internal friction) |
|
|
Term
| What is the "critical velocity"? |
|
Definition
| It is the point at which laminar flow becomes turbulent. Driving pressure is proportional to velocity up to that point, but then resistance increases (due to turbulence). |
|
|
Term
|
Definition
| Turbulent flow in a vessel. Like a heart murmur, but not around a heart valve. |
|
|
Term
| What is Reynold's number? |
|
Definition
=density*diameter*avg. velocity/viscosity
A number that describes how pressure changes varies with flow velocity. It defines the propensity for turbulent flow. Higher Re more likely turbulent flow. |
|
|
Term
| How do capillary beds in series affect TPR? |
|
Definition
|
|
Term
| How do capillary beds in parallel affect TPR? |
|
Definition
1/Total resistance = 1/R1 + 1/R2...
Opening one of these channels drops TPR
Total resistance is less than any individual resistance. |
|
|
Term
What is arborization and why does it matter?
How does velocity relate to flow? |
|
Definition
Branching in the vascular system. It matters because any change in resistance in one segment affects flow through the whole system.
Velocity * cross sectional area = flow. |
|
|
Term
| What do you call each division in the respiratory system? How many are there? |
|
Definition
| You call them generations. There are 23. 1-17 are conduction only - no gas exchange. |
|
|
Term
Flow has to be the same through each generation. That means that as cross sectional area goes up velocity must...
Where is the velocity the highest? |
|
Definition
Decrease.
Velocity is the highest in the segmental bronchi (gens 3-7) because that's where cross sectional area is the least. |
|
|
Term
| Where is airflow likely to be turbulent? Laminar? |
|
Definition
| It is most likely turbulent in the large airways due to the high velocities, and laminar in the small airways due to low velocity. |
|
|
Term
| What is the Starling Resistor? |
|
Definition
| It describes flow through collapsable tubing where external pressure matters. Application: Blood pressure measurements; Emphysema - air must be forced out of lungs due to decreased elasticity, but this compresses the bronchioles since they are structurally weaker inhibiting flow. Velocity is faster (to pass through smaller diameter) leading to turbulence which is heard as wheezing. |
|
|
Term
| What is one reason veins have very low total resistance? |
|
Definition
| They are arranged in parallel. |
|
|
Term
What is normal CO?
What % of blood volume is systemic? Pulmonary?
What % is arterial? Venous? |
|
Definition
5L/min.
Systemic 85%, Pulmonary 10%, Heart 5%
Arterial 20%, Venous 65% |
|
|
Term
| What are the 3 different types of pressures in the CV system? |
|
Definition
1. Transmural: Net pressure across the vessel wall. Usually net from in to out (otherwise vessels would collapse).
2. Hydrostatic: Pressure due to different elevations. Weight of the column of fluid above.
3. Pressure Gradient: Pressure decreases as blood flows. Driving force for flow. |
|
|
Term
| How do you determine total fluid energy? |
|
Definition
Potential energy: From cardiac contraction - stored in vessel walls. The pressure component.
Kinetic energy: In direction of flow. Proportional to velocity.
Gravity energy: Gravity can change pressure depending on position relative to heart.
**Flow is down an ENERGY gradient. Not always pressure.** |
|
|
Term
| Where is pressure controlled? Where is flow controlled? |
|
Definition
| Pressure is controlled centrally. Flow is controlled locally (due to metabolic needs of the area.) |
|
|
Term
|
Definition
| "lack of slipperiness". It is a measure of internal friction between the different lamina in laminar flow. |
|
|
Term
What happens to apparent viscosity as area increases?
As velocity increases? |
|
Definition
It goes up. There are more layers so more friction. In small vessels there may only be one lamina, so interlaminal friction (viscosity) isn't significant.
As velocity increases apparent viscosity goes down. This is because the rapid movement pushes things to the center of the stream decreasing friction. |
|
|
Term
What is axial streaming?
What is Plasma skimming? |
|
Definition
Axial streaming: High velocity flow pushes RBCs to the center leaving plasma on the outside. Leads to lower viscosity.
Plasma skimming: Tendency of branching vessels to have relatively less RBCs (pulling from that outside area). This is a good thing in the kidney, since we want to filter the plasma. |
|
|
Term
| Why are arterioles important in pressure control? |
|
Definition
| They are the inflection point. Arteriole constriction increases pressure in the arterial system, and effectively decreases the pressure in the capillaries, etc. This creates a larger pressure gradient. |
|
|
Term
| What is the critical opening (or closing) pressure? |
|
Definition
| It is the pressure gradient required for conductance. You can have a positive pressure gradient and no conductance if you haven't reached this critical pressure. |
|
|
Term
| What is the mechanism of atherosclerosis? |
|
Definition
| Damage to the endothelium leads to entrance and proliferation of monocytes and smooth muscle cells in the tunica intima. Smooth muscle cells proliferate making ECM. Plaque forms. |
|
|
Term
|
Definition
1. Atrial Systole
2. Isovolumetric contraction
3. Rapid ejection
4. Decreased ejection
5. Isovolumetric relaxation
6. Rapid ventricular filling
7. Decreased ventricular filling
A. Mitral valve closes
B. Aortic valve closes
C. Aortic valve opens
D. Mitral valve opens |
|
|
Term
|
Definition
a wave: atrial contraction
c wave: Rise in pressure due to ventricular contraction pushing valves into the atrium
v wave: valve opens and pressure drops due to emptying into ventricle |
|
|
Term
| What is the dicrotic notch? |
|
Definition
| The bump in aortic pressure that occurs just after the closure of the aortic valve. It is due to recoil of the aorta (from being stretched). |
|
|
Term
|
Definition
A. a wave caused by atrial contraction.
B. c wave caused by ventricular contraction (tricuspid valve pushes into RA).
C. x descent. Fall in atrial pressure corresponding to ejection of blood into the pulmonary artery.
D. v wave. Due to atrial filling while the tricuspid valve is still closed.
E. y descent. Drop in pressure due to tricuspid valve opening. |
|
|
Term
| How does the right ventricle contract? The left ventricle? |
|
Definition
Right: Contracts like a bellows. It pushes toward the septum which bulges out due to LV contraction too.
Left. Squeezing all walls together, and vertical shortening. |
|
|
Term
| What is a measure of ventricular function that can be seen on the Wiggers diagram? |
|
Definition
| dP/dt. How much pressure change the ventricle can generate per unit time (slope of upstroke). |
|
|
Term
| What valve actually closes first - Mitral or tricuspid? Aortic or pulmonic? |
|
Definition
Mitral closes first as the first part of S1. Then tricuspid closes quickly after.
Aortic closes first then pulmonary creating S2. These will split with inspiration. |
|
|
Term
| Why does S2 split during inspiration? |
|
Definition
| The negative pressure draws blood into the RA, leading to greater filling of the RV which takes longer to empty delaying the closure of the pulmonary valve. |
|
|
Term
What is normal cardiac index?
Systemic venous pressure?
RA pressure?
RV systolic?
Pulmonary diastolic?
Pulmonary wedge?
LA pressure?
LV systolic?
Right brachial artery? |
|
Definition
Cardiac Index: 3.1 (2.5-4 at rest). =CO/body surface area
Venous: 5
RA: 2
RV: 25
Pulmonary diastolic: 10 (systolic 25 of course)
Wedge: 6
LA: 6
LV: 120 (diastolic 6 of course)
Right brachial: 95 |
|
|
Term
| How do you determine mean arterial pressure? |
|
Definition
(Systolic pressure + 2*diastolic pressure)/3
A weighted average, since 2/3s of the time the heart is in diastole. |
|
|
Term
| What are the three parts of the troponin complex and what do they do? |
|
Definition
Troponin T: Anchoring point
Troponin C: Calcium activated. Moves tropomyosin, uncovering myosin binding sites on actin.
Troponin I: Inhibitor - holds tropomyosin over the myosin binding sites on actin. |
|
|
Term
| What is titin and what are it's three functions? |
|
Definition
A molecule in the myocardium.
1. Tethers end of myosin to the z line.
2. Acts as a spring in systole and diastole (streches)
3. May transduce sustained stretch into a growth signal (hypertrophy) |
|
|
Term
| What happens with catecholamines? |
|
Definition
| The activate beta receptors. Leads to cAMP, which phosphorylates Phospholamban allowing Ca uptake into the SR to occur, Troponin I encouraging blockage of the binding sites on actin. It also phosphorylates the Ca channel. This leads to greater contraction, but also greater relaxation. |
|
|
Term
What is the Dihydropyridine receptor?
What is the Ryanodine receptor? |
|
Definition
It is the L-Ca++ channel in the T-tubule. It is what allows the initial calcium influx.
It is in close association w/ the Ryanodine receptor which is the Ca release channel for the SR. |
|
|
Term
What is the T Ca channel?
the L Ca channel? |
|
Definition
T - transient. Primarily found in atrial tissue. Unaffected by beta agonists. Open at more negative voltage.
L - long-lasting. Opens at less negative voltage (-40). Effected by Ca antagonists, effected by Beta agonists. |
|
|
Term
| What is an Inotrope, Lusitrope, Chronotrope, Dromotrope? |
|
Definition
Inotrope: Affects contractility.
Lusitrope: Affects relaxation.
Chronotrope: Affects heart rate.
Dromotrope: Affects conduction. |
|
|
Term
|
Definition
| It is the the Calcium uptake pump in the SR. 75% of Ca goes back into the SR via this pump. 25% goes out via the Na Ca exchanger. A small amount goes into the mitochondria (can be problematic in heart disease). |
|
|
Term
| What molecules bind Ca within the SR? |
|
Definition
| Calsequestrin, Sarcalumenin and Calmodulin. |
|
|
Term
| What is the ascending staircase or Treppe? |
|
Definition
| With increasing frequency of contraction, there is less time for Ca to be removed from the cell. As it accumulates, the contraction gets stronger. |
|
|
Term
| What is rest potentiation? |
|
Definition
| If the heart pauses amount of time between beats it can build up a larger store of Ca in the SR. The next contraction will be more forceful. |
|
|
Term
| What is Post-Extrasystolic Potentiation (PESP)? |
|
Definition
| If a premature depolarization occurs, the beat will be weaker due to less Ca being stored in the SR. However, the next beat will be stronger since the cell will have higher Ca levels from that excitation. |
|
|
Term
| What are the 4 determinants of cardiac muscle performance? |
|
Definition
| 1. Preload: Passive stretching of the muscle) 2. Afterload: load opposing shortening (arterial pressure) 3. Contractility 4. Heart Rate. |
|
|
Term
| What is an auxotonic contraction? |
|
Definition
| Term not really used. Contraction against a changing load. What the heart does during ejection. Heart also undergoes isometric contraction (isovolumetric contraction). |
|
|
Term
| Why does is tension development increased with a greater preload? |
|
Definition
1. Increased Ca sensitivity of troponin C at greater initial muscle lengths.
2. More crossbridges are formed. |
|
|
Term
| What is contractility? What is it proportional to? |
|
Definition
| It is the change in force development by the heart independent of length changes (preload, afterload, etc.) It is proportional to calcium influx. |
|
|
Term
| Increasing preload holding afterload and contractility constant does what 4 things? |
|
Definition
1. Decreases time to onset of shortening.
2. Increased amount of shortening.
3. Increased shortening velocity.
4. Doesn't affect max tension. |
|
|
Term
| Increasing afterload at constant preload and contractility does what 3 things? |
|
Definition
1. Decreases the velocity of shortening.
2. Decreases the amount of shortening.
3. Increases the total tension developed. |
|
|
Term
| Increasing contractility does what? |
|
Definition
| Increases tension developed. Increases the amount of shortening. |
|
|
Term
| What the Ejection Fraction? |
|
Definition
| EF = [(EDV-ESV)/EDV). Normal is about 60%. |
|
|
Term
| What is systolic reserve? |
|
Definition
| It is the ability of the heart to pump more blood out by either increasing contractility or decreasing afterload. |
|
|
Term
| How would you tap into the diastolic reserve? |
|
Definition
| You increase preload. That will increase stroke volume. |
|
|
Term
| What factors affect preload? |
|
Definition
| Pressure gradient, time for ventricular filling, ventricular compliance, and atrial function. |
|
|
Term
| What factors affect contractility? |
|
Definition
| Neurotransmitters (beta agonists), drugs (inotropic agents), and disease (loss/dysfunction of myocardium). |
|
|
Term
| What factors affect the afterload? |
|
Definition
| Aortic pressure, and outflow tract resistance. |
|
|
Term
| What happens to right atrial pressure as CO drops? As it increases? |
|
Definition
| If CO drops, RAP increases. This is due to pressure equilibration across the whole system. If CO rises, RAP drops. It's all about volume distribution. |
|
|
Term
| What is mean systemic filling pressure? |
|
Definition
| It is the pressure that would exist in the circulation if the heart were stopped. It is 7mmHg. |
|
|
Term
| What is the pressure gradient for venous return? |
|
Definition
|
|
Term
| What is the vascular function curve? |
|
Definition
| The relationship between venous return and right atrial pressure. Increasing volume shifts the curve, while vasoconstriction rotates it (only affects venous return, not RAP). |
|
|
Term
| What is Starling's law of the heart? |
|
Definition
| Increase the preload, increase the output. Or "What goes in should come out." |
|
|
Term
|
Definition
| A condition in which the heart fails to provide a cardiac output sufficient to meet the needs of the body. |
|
|
Term
| What is a junctional rhythm? |
|
Definition
| A heart rhythm, where the AV node does the pacing. Leads to a retrograde p wave. |
|
|
Term
| What is a Cardiomyopathy? |
|
Definition
| A disease of the heart muscle that causes abnormal myocardial performance and is not the result of disease or dysfunction of other structures (i.e. not MI, not hypertension, not regurg, or valvular stenosis) |
|
|
Term
| What are the 3 types of cardiomyopathies? |
|
Definition
1. Dilative
2. Restrictive (obliterative) - amyloid.
3. Hypertrophic - can treat w/ myomectomy. |
|
|
Term
| Why do you see on a microscopic level with hypertrophic cardiomyopathies? |
|
Definition
| Some fibrosis with myocyte hypertrophy and disarray (not orderly anymore). |
|
|
Term
What happens to the heart during dynamic exercise training?
What happens to the heart during static exercise training? |
|
Definition
Dynamic: The heart will grow, but proportionally. Mass to volume ratio stays the same.
Static: The heart hypertrophies. Mass to volume ratio increases. Due to increased blood pressure during training. |
|
|
Term
| What is idiopathic dilated cardiomyopathy? |
|
Definition
| LV dilation and systolic dysfunction. Increased heart size and weight, increased fibrosis. |
|
|
Term
What are some of the microscopic features of dilated cardiomyopathy?
What is a common cause? |
|
Definition
Myocyte hypertrophy and attenuation. Interstitial fibrosis. Endocardial fibrosis.
Cause: Alcohol |
|
|
Term
| What is the hallmark of restrictive cardiomyopahties? |
|
Definition
| Abnormal diastolic function. Stiff ventricular wall, with impaired filling. |
|
|
Term
|
Definition
| A disease characterized by an inflammatory infiltrate of the myocardium. Can be caused by infections, toxins, and hypersensitivity. |
|
|
Term
| What can cause pericardial inflammation? |
|
Definition
1. Contiguous spread - from lungs, esophagus, etc.
2. Hematogenous spread - from blood stream.
3. Lymphangetic spread
4. Traumatic or irradiation |
|
|
Term
| Why is Chaga's disease important in heart disease? |
|
Definition
| It is the most common cause of congestive heart failure in the world. |
|
|
Term
| What is important about the Coxsackie viruses (A&B)? |
|
Definition
| They have a tropism for the heart and cause a dilated cardiomyopathy. |
|
|
Term
| What is the acronym to remember the common causes of acute pericarditis? |
|
Definition
Trauma
Uremia
MI/Medications
Other infections
Rheumatoid, radiation. |
|
|
Term
| What is Dressler's syndrome? |
|
Definition
| Fever, pericarditis, and pleuritis after MI or heart surgery. Treat w/ high dose aspirin. |
|
|
Term
| What is cardiac tamponade? |
|
Definition
| Constriction of the heart due to filling of the pericardial space. When constriction is sufficient that central venous return is impeded you have tamponade. |
|
|
Term
|
Definition
3 features of acute tamponade.
1. Decline in systemic arterial pressure.
2. Elevation in systemic venous pressure.
3. A small, quiet heart. |
|
|
Term
| What are some common pathophysiologic features of cardiomyopathy? |
|
Definition
1. Elevated LV diastolic filling pressures
2. Reduced SV and CO
3. Mitral regurgitation
4. Supraventricular and ventricular arrhythmias. |
|
|
Term
| What are the mechanisms of disease in Dilated Cardiomyopahties? |
|
Definition
1. LV systolic dysfunction.
2. Arrhythmias. |
|
|
Term
| What are the disease mechanisms in restrictive cardiomyopathies? |
|
Definition
1. Impaired LV diastolic filling
2. LV systolic dysfunction
3. Arrhythmias |
|
|
Term
| What are some findings of constrictive pericarditis? |
|
Definition
1. Kussmaul's sign - a rise in jugular venous pressure on inspiration.
2. Jugular venous distension
3. Pericardial knock - when ventricles fill they hit the hard pericardium creating a knocking sound. |
|
|
Term
| What is a common cause of pericardial effusion? |
|
Definition
| Procedures done by doctors. Bumping things, perforating things, etc. |
|
|
Term
| What do you use a PA catheter for? |
|
Definition
| Determine if pulmonary venous congestion is present. Determine CO. Determine central venous oxygenation. |
|
|
Term
|
Definition
| The difference between systolic and diastolic pressures. |
|
|
Term
What drugs affect preload?
What drugs affect afterload? |
|
Definition
Pre: Venodilators increase it. IV fluids increase it.
After: Vasodilators increase it.
Vasopressors decrease it. |
|
|
Term
What are some side effects of an increased HR?
Of a decreased HR? |
|
Definition
Increased: decreased diastolic filling, increased myocardial oxygen consumption.
Decreased: Increased coronary perfusion, decreased myocardial oxygen consumption. |
|
|
Term
| Why can't you increase preload forever? |
|
Definition
You get increased back pressure - increased congestion.
You get resistance to subendocardial flow. |
|
|
Term
| What are three things that influence ventricular compliance? |
|
Definition
1. Filling volume (higher volume, lower compliance)
2. Wall thickness (higher thickness, lower compliance)
3. Ventricular size (higher size, higher compliance) |
|
|
Term
| What does the catheter measure directly? |
|
Definition
|
|
Term
| How do you solve for systemic vascular resistance (SVR)? |
|
Definition
V=IR so R=V/I. Therefore SVR = (MAP-CVP/CO)*80
MAP = mean arterial pressure
CVP = central venous pressure = RAP = right atrial pressure |
|
|
Term
Know the normal values for:
RA, RV, PA, PCWP
the "rule of 6's" |
|
Definition
RA<6
RV<24/6
PA<24/12
PCWP<12 |
|
|
Term
What does high RAP indicate? Low RAP?
High PCWP? Low PCWP? |
|
Definition
High RAP and low SV indicates RV failure.
Low RAP usually reflects hypovolemia if SV is low.
High PCWP and low SV indicates LV failure.
Low PCWP usually reflects hypovolemia if SV is low. |
|
|
Term
What would cause tall A waves?
Cannon A waves?
No A waves? |
|
Definition
Tall: Tricuspid stenosis, pulmonic stenosis, pulmonary hypertension, cor pulmonale (RVH).
Cannon: 3rd degree AV block
No A waves: A fib. |
|
|
Term
What is the Fick method to determine CO?
The thermodilution method? |
|
Definition
Fick: Treat O2 like a dye. More dilution means more time circulating, and low output.
Thermodilution: Cold sailine injected into RA, measure temp at distal port to monitor function. |
|
|
Term
| What is the normal range for SvO2? |
|
Definition
| 60-80%. Outside this value suggests abnormal cardiac output. |
|
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Term
| When are PA lines useful? |
|
Definition
| Differential Dx of pulmonary edema, differential dx of shock, pulmonary hypertension, right sided HF (to find etiology). |
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Term
| What are some contraindications for use of a PA line? |
|
Definition
| Vascular access issues, LBBB (could cause complete block), acute PE, prosthetic valves, RV/RA mass or thrombus. |
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Term
| How do you diagnose shock? |
|
Definition
1. Touch the pt: Warm (high CO - think sepsis) or cool (low CO).
2. Look at JVP: Elevated (think cardiogenic shock), decreased (think hypovolemic shock) |
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Term
Is Heart Failure a disease?
What are the 3 criteria for heart disease? |
|
Definition
No, it is a clinical syndrome. It occurs when:
1. The heart can't generate enough output to meet the demands of the body; or
2. The heart can only produce enough output at the expense of high filling pressures; or
3. Both of the above. |
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Term
| How can you describe heart failure? Why? |
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Definition
| Heart Failure w/ reduced (40% or less) or preserved (50% or more) ejection fraction. It is determined by the structure and function of the heart. That's all you can say, because it is usually a combination of other issues. |
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Term
| What are the different stages of heart failure? |
|
Definition
Stage A: High risk for development. HTN, CAD, DM
Stage B: Asymptomatic HF - LV remodeling. MI, LVH
Stage C: Symptomatic HF. HFpEF HFrEF
Stage D: End-stage. HFrEF. Hospice, LV assist, or transplant. |
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Term
| What are the signs & symptoms of heart failure due to decreased output? |
|
Definition
Fatigue, dyspnea, exercise intolerance, end organ failure;
Hypotension, hypothermia, cool extremities, weak carotid upstroke. |
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Term
|
Definition
No! The heart often responds to stress by dilation. This decreases EF, but can maintain CO.
Also, you could have a maintained EF but low output due to not enough filling (stiff ventricle). |
|
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Term
| What are signs and symptoms of heart failure due to high filling pressures? |
|
Definition
LV: Pulmonary venous congestion, dyspnea, orthopnea, PND, pulmonary rales
RV: Systemic venous congestion, leg swelling, abdominal bloating, elevated JVP, ascites, hepatomegaly, edema.
Causes: Impaired relaxation, stiff ventricles, fluid retention. |
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Term
How are afterload and CO related?
In HF? |
|
Definition
Increasing afterload decreases CO.
In HF, output is more afterload sensitive than in a healthy heart. |
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Term
| What does vasopressin do? |
|
Definition
| It leads to vasoconstriction. It also leads to fluid retention. Both effects increase BP. |
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Term
| What are natriuretic peptides? |
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Definition
| They are peptides that are released when the myocardium is under stress. They are natural diuretics, and are beneficial proteins. |
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Term
How do you calculate cardiac wall stress?
Vessel wall stress? |
|
Definition
Cardiac wall stress = pressure*radius/2*wall thickness.
Vessel wall stress = pressure*radius/wall thickness. |
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Term
| What are 3 common electrical problems in HF? |
|
Definition
1. Scar formation - reentry
2. Atrial enlargement - atrial fibrosis - Afib, Aflutter
3. Electrical remodeling - dyssychrony. |
|
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Term
| What are the NYHA classes for? |
|
Definition
They are functional classifications for heart failure.
Class I: No limitation
Class II: Slight limitation; dyspnea and fatigue w/ moderate exertion
Class III: Marked limitation; dyspnea with minimal activity
Class IV: Severe limitation; symptoms at rest. |
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Term
| What are the two most common causes of acute HF events? |
|
Definition
1. Medication non-compliance
2. Dietary indescretion |
|
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Term
|
Definition
1. Improve Frank-Starling relationship
2. Neurohormonal antagonists
Devices etc. |
|
|
Term
|
Definition
| Find and treat underlying etiology. Treat HTN. Revascularization. Treat Afib/flutter. Treat by treating comorbidities. |
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Term
| How do you treat acute pulmonary edema? |
|
Definition
LMNOP
Loop diuretics
Morphine
Nitrates
Oxygen
Positive pressure ventilation |
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Term
| How do you treat acute decompensated HF? |
|
Definition
Diuretics
Venodilators
Inotropes
Natriuretic peptides
Ultrafiltration for volume removal |
|
|
Term
|
Definition
1. Diuretics
2. Vasodilators
3. Vasodilators + Inotropics
4. Inotropics |
|
|
Term
|
Definition
Cold: Poor perfusion. Wet: Signs of congestion
1. 28%, 1st vasodilators, 2nd inotropes - warm then diurese
2. 67%, Diurese and uptitrate HF meds
3. 5%, End stage HF, Vasodilators, inotropes, LVAD, transplant
4. Reconsider HF diagnosis |
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Term
What are signs of congestion?
What are signs of poor perfusion? |
|
Definition
Congestion: Orthopnea, elevated JVP, rales, ascites, leg swelling.
Perfusion: Cool extremities, low BP, low pulse pressure, sleepy/obtunded, worsening renal function, low urine output. |
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Term
| What are the main types of diuretics used in HF? |
|
Definition
Loop Diuretics: Improve symptoms, but increase neurohormones. Eg: Furosemide, torsemide, bumetanide, ethycrinic acid (ototoxicity).
Thiazide diuretics: Improve symptoms. Eg: HCTZ (low potency), Chlorthalidone (medium potency), Chlorthiazide, metolazone (high potency).
Potassium Sparing Diuretics: Aldosterone antagonists (Eg: Spironolactone - improve mortality), triamterene and amiloride (rarely used in HF). |
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Term
| What are some IV vasodilators? |
|
Definition
IV nitroglycerin: venodilator primarily
IV nitroprusside: best for COLD patients because it doesn't decrease preload too much.
IV nesiritide (recombinant BNP): Natriuretic, venous > arterial vasodilator. Do not use in hypotensive patients. |
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Term
| What are some oral vasodilators? |
|
Definition
Hydralazine: arterial vasodilator. Reduces SVR, can increase CO and even BP.
Nitrates: venodilator, increase pulmonary venous capacitance, decreasing pulmonary venous pressure, decrease hydrostatic pressure, decrease pulmonary edema. Use with caution in hypertensive patients who may be preload dependent.
Both of these can cause reflex tachycardia. |
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Term
| List some more oral vasodilators. |
|
Definition
ACE-Inhibitors (_pril): block deleterious effects of Angiotensin II. Also increase bradykinin (vasodilation, cough).
Angiotensin receptor blockers (ARBs, _artan): Block angiotensin II receptor. No cough, but no bradykinin vasodilation. |
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Term
| What drugs decrease mortality in HF? |
|
Definition
Hydralazine/nitrates.
ACE-inhibitors/ARBs: even better than above.
Beta blockers
Spironolactone (by decreasing fibrosis). |
|
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Term
| What are the IV inotropes? When should they be used? |
|
Definition
Only to be used in Class IV patients. Improve symptoms, but may increase mortality.
Beta 1 agonists: dobutamine, dopamine, norepinephrine
Phosphodiesterase inhibitors: Milrinone - directly increase cAMP.
Digoxin: Blocks Na/K ATPase. |
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Term
| What are beta blockers? When are they recommended? |
|
Definition
Indicated for all classes of HF. Start low.
If they need an inotrope use Milrinone (bypasses beta receptor).
Beta blocker |
|
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Term
| What is some non pharmacologic therapy recommended in HF? |
|
Definition
| Exercise, low Na diet, decreased fluid intake, daily weights and BP, treat comorbidities, ICD/cardiac resynchronization therapy, Surgical: LVAD, transplant. |
|
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Term
| What is ventricular dyssynchrony? |
|
Definition
| The ventricles aren't firing/beating together. (LBBB affects 20% of HF patients). Cardiac resynchronization therapy improves mortality. |
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Term
|
Definition
| The change is volume associated with a given pressure change. |
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Term
| What is the Windkessel effect? |
|
Definition
| It is the second pump system. Healthy vessels store energy in their walls. They return this to the system during diastole. Helps convert the pump into a continuous output. |
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Term
| What factors determine BP? |
|
Definition
| CO, SVR, blood volume, arterial compliance. |
|
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Term
| What happens to pulse pressure in the femoral artery? |
|
Definition
| It is actually higher than in the aorta. Due to distortion, harmonic amplification, and dampening of different parts of the waveform. |
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|
Term
|
Definition
| Spontaneous contraction and relaxation of precapillary sphincters, modulated by metabolic activity of the tissue itself. |
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Term
| What happens to capillary hydrostatic pressure if arteriolar resistance increases? If vascular resistance increases? |
|
Definition
| If arteriolar resistance increases, capillary pressure drops. If vascular resistance increases capillary pressure increases. |
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Term
| What is another name for osmotic pressure? What is it due to? |
|
Definition
| Oncotic pressure. It is the pressure due to proteins drawing water toward the blood (albumin) or into the interstitium (proteoglycans). |
|
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Term
| What is Starling's law for capillary fluid movement? |
|
Definition
An equation describing the movement of fluid in/out of a capillary. It is determined by:
1. Capillary hydrostatic pressure 2. Interstitial hydrostatic pressure 3. Blood osmotic pressure 3. Interstitial osmotic pressure. |
|
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Term
| What are the sites for local control of blood flow? |
|
Definition
1. Arteriolar resistance
2. Precapillary resistance
3. Metarteriolar resistance
4. Venular resistance |
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|
Term
Where are beta 2 receptors? What do they do?
Where are alpha 1 receptors? What do they do? |
|
Definition
Beta 2s are located in blood vessels. They are vasodilators.
Alpha 1s are located in blood vessels. They are vasoconstrictors.
Veins don't really express Beta 2s, just alpha 1s. |
|
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Term
| What is EDRF and what does it do? What about endothelin? |
|
Definition
EDRF - endothelium derived relaxation factor (NO). Release triggered by increased velocity.
Endothelin - a vasoconstrictor released by damaged endothelium. |
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Term
| How does the renin-angiotensin system work? |
|
Definition
Renin (secreted by the kidney) converts angiotensinogen (secreted by the liver) to angiotensin I (a vasoconstrictor). This is converted to angiotensin II (another vasoconstrictor) by angiotensin converting enzyme (ACE). AII leads to aldosterone production (and Na retention). It also leads to vasopressin secretion, and cardiac remodeling among other things.
Note: Renin release is triggered by the sympathetic nervous system. |
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Term
| Name and describe the 3 theories for autoregulation of blood flow. |
|
Definition
1. Myogenic: Vascular muscle contracts with stretch and relaxes with less stretch.
2. Metabolic: Some metabolite is vasoactive (dilation). Possibly adenosine, oxygen, etc.
3. Tissue Pressure: A change in perfusion changes the interstitial pressure and thus the external force on the vessel. Requires limited compliance of the interstitium. |
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Term
What is the opposite of ischemia?
What is reactive ___(answer to above)? |
|
Definition
Hyperemia (a relative abundance of blood flow).
Reactive hyperemia is a compensatory period of overabundant flow that follows a period of restricted flow. |
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|
Term
|
Definition
| It is a vasodilator released by endothelium that acts similar to nitric oxide (NO). |
|
|
Term
| What are adrenergic receptors? |
|
Definition
| Those that are stimulated by epinephrine, norepinephrine, etc. Include alpha receptors and beta receptors (B1- myocardium, B2 - vessels) |
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Term
| What is special about norepinephrine vs epinephrine? |
|
Definition
Norepi binds preferentially to alpha receptors (vasoconstriction). Alpha blockers would make it bind to beta 2 receptors leading to vasodilation. Epi has a greater affinity for beta 2 receptors.
Norepi is a perfect pressor agent, while epi is a good agent to increase cardiac performance. |
|
|
Term
|
Definition
| It is a synthetic activator of beta receptors (1&2), but not alpha receptors. Increases heart performance through inotropic and chronotropic effects. |
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Term
| What is interesting about the interaction of the sympathetic and parasympathatic nervous systems? |
|
Definition
| Ach inhibits the release of norepi, norepi inhibits the release of ach. |
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|
Term
| What is the effect of acetylcholine on blood vessels? |
|
Definition
| Vasodilation. There is a sympathetic pathway (skeletal muscle, sweat glands) and primarily the parasympathetic pathway. |
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|
Term
|
Definition
| Non-neural factors. Ions, vascular filling etc, lead to some basal tone. Resting tone has some sympathetic activity. Allows for movement in both directions (vasodilation by removal of NE first). |
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Term
| What are the short term controls over arterial BP? |
|
Definition
| Baroreceptors & chemoreceptors. Short term is seconds to minutes. Hormonal action takes hours to days. |
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|
Term
Where are baroreceptors?
What is the bark-reflex? |
|
Definition
THE baroreceptor is at the carotid sinus. There are baroreceptors at other places, especially the aorta.
Baro-reflex: High BP - Open the pipes and turn down the pump. Low BP - shrink the pipes and turn up the pump. |
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|
Term
| Why don't the baroreceptors regulate chronic hypertension? |
|
Definition
| The target point shifts over time with chronic hypertension. |
|
|
Term
| What are A and B receptors in the atria? |
|
Definition
| They are like baroreceptors. As are associated w/ contraction. Bs are more associated w/ blood volume. |
|
|
Term
| What is the Bezold - Jarisch reflex? What does it tell us about ventricular anatomy? |
|
Definition
| It is a reflex where posterior wall ischemia leads to hypotension. Posterior wall has depressor reflex, anterior wall has pressor reflex. |
|
|
Term
| What is the Bainbridge reflex? |
|
Definition
| Atrial stretch increase HR. Baroreceptor should use this same stimulus and cause a decreased HR. |
|
|
Term
|
Definition
| It stimulates a chemoreceptor reflex that increases TPR (sympathetic) decrease HR (parasympathetic) and increase rate and depth of inspiration, which in turn inhibits vagal responses leading to a increased HR. |
|
|
Term
| What is the mechanism for vasovagal syncope? |
|
Definition
| An emotional stress triggers big parasympathetic output and decreased sympathetic output. This can lead to vasodilation and the drop in BP can be sufficient to underperfuse the brain leading to syncope. |
|
|
Term
| What is the critical blood volume loss where reflexes aren't sufficient to maintain BP? |
|
Definition
|
|
Term
| What amount of CO goes to the brain? What molecule has primary control over cerebral blood flow? |
|
Definition
| About 15% of resting CO goes to the brain. CO2 is the most important metabolite affecting blood flow (high CO2 high flow). |
|
|
Term
| What is the Cushing reflex? |
|
Definition
| A high CSF pressure can collapse the blood vessels in the brain blocking perfusion. The cushing reflex is the body's response to rising CSF pressures, which is to raise MAP to overcome the CSF pressure. |
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|
Term
What amount of CO goes to splanchnic circulation?
What are the 3 main sites of flow control?
What are the mechanisms of control? |
|
Definition
25% of resting CO goes to the splanchnic circulation.
Flow control occurs at 1. The Celiac artery (liver - hepatic artery, and stomach/spleen) 2. The superior mesenteric artery (pancreas) 3. The inferior mesenteric artery (intestine)
Control is primarily more or less vasoconstriction. Sympathetic - big vasoconstrictor here (blood reservoir). |
|
|
Term
|
Definition
| An obstruction in the outflow tract from the liver: IVC, hepatic vein, hepatic portal vein. Leads to pressure increases which drive fluid out of the blood and into the interstitium. |
|
|
Term
What amount of CO goes to skeletal muscle circulation?
What are the important control mechanisms here? |
|
Definition
| 15% of CO. Sympathetic adrenergic control (at rest), cholinergic control (exercise). Sympathetic adrenergic always dominates. Also metabolic control is important - can overcome sympathetic caused dilation that occurs in exercise. |
|
|
Term
| What is special about cutaneous blood flow? |
|
Definition
| It is very thermo-sensitive. Lots of metarterioles. High temps, body sends blood to skin to cool. Can be problematic if exterior temp is higher than body temp. |
|
|
Term
What is special about deep breathing?
What is unique about pulmonary flow? |
|
Definition
It compresses pulmonary blood providing a blast of preload to increase CO.
Pulmonary flow: High flow, low pressure, no auto regulation, distensible vessels. |
|
|
Term
| What happens to resistance in inspiration? |
|
Definition
| Alveolar resistance goes up, extraalveolar resistance goes down. Net: small increase in resistance. |
|
|
Term
| What does low O2 in the lung lead to? |
|
Definition
| Vasoconstriction. Elsewhere it leads to vasodilation. |
|
|
Term
| What is a good clinical measure of O2 demand on the heart? |
|
Definition
| The double product: Systolic BP*HR (directly related to coronary blood flow). Can easily triple in exercise conditions. |
|
|
Term
| What are the 3 components of coronary resistance? |
|
Definition
R1: Resistance in the surface arteries (low)
R2: Microvascular resistance (Where most regulation occurs. Large reserve is greater in epicardial surface). Resistance is controlled metabolically, neurohumorally, and through endothelial control.
R3: Compressive resistance (due to squeezing of walls).
R3: |
|
|
Term
| When in the cycle does the vast majority of coronary blood flow occur? |
|
Definition
|
|
Term
| What is coronary flow reserve? |
|
Definition
Ratio of flow during maximum vasodilation to resting flow. In a healthy person this is 4-5 times resting flow.
Total increase due to endothelium dependent (>100 microns) and endothelium independent factors (<100 microns) |
|
|
Term
| What happens to the pressure gradient across a stenosis? |
|
Definition
| It increases non-linerly. That is as the diameter decreases the pressure gradient can increase by a huge amount. This is due to turbulence on the back side, leading to lower pressure there, and higher pressure before. You have to use up your reserve in order to maintain the same flow. |
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|
Term
| Why does subendocardial ischemia occur? |
|
Definition
| The subendocardial vessels are already using up more of their reserve, to combat the higher R3 there. This means they can't adjust to lower flow as well as the higher up vessels, and they are the first effected in ischemic conditions. |
|
|
Term
| How do you treat coronary artery disease? |
|
Definition
Limit increases in O2 demand (HR*Systolic BP).
Augment flow by altering the mechanisms that affect resistance. |
|
|
Term
What are the sounds of systolic murmurs (aortic stenosis, mitral regurg)?
What are the sounds of the diastolic murmurs (aortic regurg, mitral stenosis)? |
|
Definition
Aortic stenosis: crescendo-decrescendo
Mitral regurg: Holosystolic, heard at apex radiates to axilla
Aortic regurg: blowing decrescendo along sternal border
Mitral stenosis: Low pitched rumble at apex. |
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