Term
| Are supraventricular or ventricular arrhythmias generally more serious? Why? |
|
Definition
| Ventricular, because the ventricles have a greater effect on cardiac output. |
|
|
Term
| What's the difference between regular and irregular arrhythmias? |
|
Definition
| Regular arrhythmias have a pattern eg skip every fourth beat. Irregular arrhythmias don't have a normal pattern. |
|
|
Term
| What are the four supraventricular tachycardias we talked about? |
|
Definition
| Sinus tachycardia, atrial fibrillation, atrioventricular nodal re-entry tachycardias, wolff-parkinson-white syndrome |
|
|
Term
| What is sinus tachycardia? |
|
Definition
| Increased rate of SA node firing. |
|
|
Term
| What are some normal (non disease) causes of sinus tachycardia? |
|
Definition
| Exercise, stress, tension, and conditions with enhanced catcholamine release (fear, fight or flight) |
|
|
Term
| What are three disease causes of sinus tachycardia? Why can each disease cause this? |
|
Definition
Anemia-because body not getting enough 02, tells heart to beat faster.
Hyperthyroidism-jacks up metabolic rate, increases heart rate also.
Heart failure-because body not getting enough 02, tells heart to beat faster (faint, fast heart beat) |
|
|
Term
| What is the treatment for sinus tachycardia? |
|
Definition
| First remove the underlying cause, or if that's not enough treat with drug to slow down SA node: Beta blockers or calcium antagonists. |
|
|
Term
| What happens in atrial fibrillation? |
|
Definition
"Irregularly irregular arrhythmia"
The heart is completely out of sync, no regularity.
Atria depolarize over and over with no pattern, 300-600 bpm. Ventricles contract at irregular rate also, 120-170 bpm. |
|
|
Term
| What are the three "classic" causes of atrial fibrillation? Are they the most common causes of atrial fibrillation? |
|
Definition
| Rheumatic heart disease, excessive alchohol, thryotoxicosis. They are NOT the most common causes of A-fib. |
|
|
Term
| What are the most common causes of atrial fibrillation? What are a few other less common causes? |
|
Definition
Hypertension and heart failure are most common.
Stress, smoking, and familial risk are possibly causes.
|
|
|
Term
| What is the treatment for atrial fibrillation? |
|
Definition
-First treat underlying causes.
-Use meds to slow ventricular contractions: Beta blockers
-Amiodarone or vernakalant (2011 drug can be used to prolong action potential
-Anticoagulative meds eg warfarin (coumadin) or dabigatran (2011 drug) to prevent clotting since the blood is not moving well in a-fib.
-Radiofrequency ablation: blast receptors of pulmonary veins going to atria to decrease signal to SA node and atria. Quite effective.
-Possibly need electrical cardioversion: shock to reset the heart and get back into normal rhythmn. |
|
|
Term
| What are the ocular SE of amiodarone? |
|
Definition
-90% develop iodine corneal microdeposits (within months). Whirl shape. Doesn't affect vision, subsides if stop meds.
-Disc edema: can affect VA, but will clear up is stop meds.
-Optic neuritis: will cause permenent vision loss. Rare.
-Lens opacities |
|
|
Term
| What are the ocular SE of warfarin (coumadin)? |
|
Definition
-Subconj hemorrhage
-Spontaneous hyphema
-Retinal hemorrhage
-Vitreous hemorrhage
-Cerebral hemorrhage |
|
|
Term
| What happens in AV nodal re-entry tachycardia? |
|
Definition
| -There are two functionally different paths through the AV node. Normally the fast side/signal of heart over-rules the slow signal, but when the slow signal hits at the right time, it will send a re entry (retrograde) signal causing an extra beat. The signal gets scrambled up and out of order. |
|
|
Term
| Does AV nodal re entry tachycardia occur in otherwise normal or abnormal pts? |
|
Definition
|
|
Term
| Is AV re entry tachy. more common in men or women, what are symptoms, and what is the heart rate? |
|
Definition
-more common in women
-Palpitations, chest pain, dyspnea, pre-syncope (dizzy spell before passing out) are symptoms
-heart rate is between 150 and 250 |
|
|
Term
| What is the treatment for AVNRT? |
|
Definition
Want the fast path to regain control, do this by slowing the heart down and getting back into normal rhythmn. Increase vagal tone to SA node to intercept and stop re entry. Do this by:
-Holding breath and bear down like weight lifting, carotid sinus massage of baroreceptors, stick head in cold water.
-Medical Treatment: IV admin of drugs to slow heart |
|
|
Term
| Why do you get pre syncope is AVNRT? |
|
Definition
| - Because even though the heart is beating fast, its not filling enough so pt not getting good 02 flow to brain, so get dizzy spells. Signal keeps building on itself. |
|
|
Term
| What is happening in Wolff-parkinson-white syndrome? |
|
Definition
-An alternate pathway between atria and the ventricles independent of the sa node fires and jacks up heart beat.
-either random occurrence or inherited (male>female)
-can conduct impulses in both directions
-Men more pron to atrial fibrillation which can lead to life threatening ventricular fibrillation.
-macro reentry problem compared to micro reentry in AVNRT. |
|
|
Term
| What are treatments of Wolff-Parkinson-White syndrome? |
|
Definition
-Observation
-Medications
-Radiofrequency ablation of receptors in pulmonary veins. |
|
|
Term
| What are the two life threatening types of ventricular tachyarrhythmias we talked about? |
|
Definition
-Sustained ventricular tachycardia
-Ventricular fibrillation |
|
|
Term
| What happens in sustained ventricular tachycardia? |
|
Definition
-Regular rhythmn but b/w 120 and 220 bpm. Lasts more than 30 seconds.
-Occur paroxysmally: sudden, frequent.
-Cardiac relaxation is impaired
-Results in poor cardiac output |
|
|
Term
| What kind of pt does sustained ventricular tachycardia occur in more often? |
|
Definition
| Pts with underlying structural heart disease. |
|
|
Term
| What is treatment for sustained ventricular tachycardia? |
|
Definition
| -Usually need direct current cardioversion: shock to get rid of fast heart beat and return to normal. |
|
|
Term
| What happens in ventricular fibrillation? |
|
Definition
-Very rapid and irregular heart rate
-No oder to contraction of ventricles
-NO CARDIAC OUTPUT**which causes death w/o CPR or electrical defibrillation |
|
|
Term
| Survivors of ventricular fibrillation are at high risk of what? What is used to treat them? |
|
Definition
-SCD: sudden cardiovascular death.
-Implanted cardioverter-defibrillators used for treatment. |
|
|
Term
| What happens in premature ventricular contraction (PVC)? |
|
Definition
| -Extra heart beat directly from ventricles |
|
|
Term
| Does PVC have an effect on atria or the SA node? |
|
Definition
| No, the next sinus beat occurs normally. |
|
|
Term
| What things cause increased PVC's? |
|
Definition
| Increased freq with age, infection, emotional stress, caffeine, tobacco, alcohol. |
|
|
Term
| What are the consequences and treatment for PVC? |
|
Definition
| NONE unless the cause is heart failure. |
|
|
Term
| Is bradycardia from inadequate SA node activity or blocked conduction a concern? |
|
Definition
|
|
Term
| Sinus bradycardia may be a normal response to what? |
|
Definition
| Cardiovascular conditioning of athletes, hypothyroidism, drugs. |
|
|
Term
| If bradycardia is extreme, what might be used to treat it? |
|
Definition
-Meds to increase rinus rate: atropine
-Pacemaker implant |
|
|
Term
| What happens in AV block? |
|
Definition
Some impulses generated from the SA node are not conducted thru to the ventricles.
-can occur anywhere in system
-usually at level of AV node or His-Purkinje system |
|
|
Term
| AV block incidence increases with what? May be associated with what? |
|
Definition
-Increases with age
-May be associated with meds |
|
|
Term
| What happens in 1st degree AV block? Does it have symptoms or need treatment? |
|
Definition
-Prolongation of AV conduction time but impulse does get to ventricles.
-Rarely has symptoms or needs treatment |
|
|
Term
| What happens in 2nd degree AV heart block and what is the treatment? |
|
Definition
-Intermittent failure of the impulse to get from atrium to ventricles
-May need pacemaker |
|
|
Term
| What happens in 3rd degree/complete AV heart block? What is the treatment? |
|
Definition
-no atrial impulses reach the ventricles, so AV node takes over job as pacemaker, or ventricles start to contract due to spontaneous depolarization.
-Severe bradycardia can occur, 15-40 bpm!!
-Pacemaker implant for treatment. |
|
|
Term
| Is it possible to present with 2nd or 3rd degree AV block w/o previous issues? |
|
Definition
| Yes, but more likely to progress from 2nd degree to 3rd degree. |
|
|
Term
| What is heart failure? (formerly known as congestive heart failure) |
|
Definition
| Continuum of disorders that eventually prevent the heart from meeting the needs of peripheral organs for blood flow without compensatory mechanisms. |
|
|
Term
| What's the epidemiology of HF? |
|
Definition
| affects 5 mil, kills 260,000, half or more die within 5 yrs of diagnosis. |
|
|
Term
| What are risk factors for heart failure? |
|
Definition
| Age, obesity (poor diet, lack of exercise), smoking, alcohol abuse, DM especially with retinopathy, high-sensitivity C-reactive protein (hs-CRP), HTN, Dyslipidemia, poor dental health. |
|
|
Term
| What happens in stages A-D in heart failure? |
|
Definition
-Stage A: pts with risk factors but w/o structural heart disease or symptoms.
-Stage B: pts with structural heart disease, but no signs or symptoms of failure
-Stage C: pts with current or past symptoms of heart failure such as shortness of breath (SOB)
-Stage D: pts with refractory heart failure who might be eligible for specialized treatment strategies, eg heart transplant. |
|
|
Term
| Common causes of heart failure? |
|
Definition
-Ischemic heart disease (35-50%)-not enough blood flow to heart.
-Cardiomyopathy (30-34%)- heart walls get really stretched out.
-HTN (15-20%)-has to work hard to overcome resting blood pressure. |
|
|
Term
| Less common other causes of heart failure? |
|
Definition
| Valvular disease, drugs, alchohol, arrhythmias, pericardial disease, hypertrophic cardiomyopathy |
|
|
Term
|
Definition
-Terms used in practice to mean heart failure.
-Left heart failure
-Right heart failure
-High-output vs. low-output heart failure
-Systolic vs. diastolic heart failure |
|
|
Term
| What happens in right heart failure? |
|
Definition
| Left heart failure occurs, causing back up into the right side of the heart, which is weaker and can't handle it leading to right side heart failure. |
|
|
Term
| What is most common cause of right heart failure? |
|
Definition
|
|
Term
| What happens in low output heart failure? |
|
Definition
| Heart tissue not working well, not relaxing and therefore not filling all the way, can't put out enough blood. |
|
|
Term
| What happens in diastolic heart failure? |
|
Definition
| The heart has a general INability to fill. |
|
|
Term
| What happens in diastolic heart failure? |
|
Definition
| The heart has a general INability to fill. |
|
|
Term
| Describe the progressive breathlessness (dyspnea) associated with HF. |
|
Definition
-Exertional dyspnea-eg when walking around
-Orthopnea-SOB in supine position/on back. Need extra pillows at night to breath well, indicates disease worsening.
-Paroxysmal nocturnal dyspnea-sudden spasmodic episode of SOB while sleeping.
-Dyspnea at rest: disease bad
-Acute pulmonary edema: pulmonary congestion and rales. Nocturnal cough-might have bloody sputum.
- |
|
|
Term
| Second slide of signs and symptoms of HF (after dyspnea)? |
|
Definition
-Fatigue
-Reduced renal perfusion and increased blood volume b/c kidney not getting enough blood and start renin pathway. Good during day for 02 but at night the blood is processed and causes nocturia.
-Nocturia
-Cerebral symptoms from hypoxia: confusion, anxiety, nightmares, memory loss dizziness, and even delirium.
-Cardiac edema |
|
|
Term
| 3rd slide of signs and sympt of HF? |
|
Definition
-Peripheral edema b/c heart not pushing well, blood hangs out.
-Anorexia-loss of appetite, unknown cause, possibly poor blood supply to liver?
-Peripheral cyanosis-toes blue b/c poor perfusion in extremities
-Tachycardia b/c of sympathetic tone and increase speed of heartbeat (body not getting enough blood, tells heart to beat faster) but weak beat.
-Additional heart sounds |
|
|
Term
| What are the normal heart sounds? |
|
Definition
S1: closure of mitral and tricuspid valves.
S2: closure of pulmonic and aortic valves. |
|
|
Term
| What are the abnormal heart sounds? |
|
Definition
S3: early diastolic sound. Rapid filling of dilated, large left ventricle eg in young athletes.
S4: Late diastolic sound. Loss of compliance of chamber walls. Blood from atria being pushed into thickened, stiff ventricles. Causes heart to to push against the chest. |
|
|
Term
| What can you do to diagnose heart failure? |
|
Definition
-EKG may be helpful is MI is cause.
-Chest radiograph to check for enlargement and lung congestion.
-Echocardiogram-to check for enlargement, valvular disease
-Cardiac catheterization for assessing valves. |
|
|
Term
| Treatments for all "stages" of heart failure? |
|
Definition
-Pt and family education, especially stage A b/c have all the risks, close to heart failure.
-Correct underlying cause. Statins to reduce inflammation and sympathetic stimulation.
-Vaccination against pneumococcal disease and influenza for pts over 65.
-Dietary salt restriction
-Adequate rest and avoidance of exertion
-Some regular exercise to improve exercise capacity |
|
|
Term
| Therapy for Stage B Heart Failure? |
|
Definition
-ACEI's-lower systemic vascular resistance and venous pressure (easier for heart to pump blood). Decrease levels of circulating catecholamines-Captopril, lisinopril, enalapril.
-A2RBs-similar to ACEI except do not produce a cough. Valsartan, candesartan..
-ACEI or A2RB in all stage B pts with B-blockers toward the end of stage B because it has negative inotropic (decrease force of contraction) and negative chronotropic effect (slows heart)-less work for heart. |
|
|
Term
| Therapy for stage C heart failure? |
|
Definition
Stage A and B therapies, but ACEI and beta blockers in all pts, carvedilol, metoprolol, bisoprolol.
-Diuretics-start with thiazide, move to loop if dyspnea and edema persist. Aldosterone antagonists (spironolacton, eplerenon) decrease mortality by decreasing fibrosis of heart.
-Cardiac glycoside to increase contractility in certain pts, Digoxin |
|
|
Term
| Therapy for stage D heart failure (refractory heart disease)? |
|
Definition
-Inotropes (increase strength of contraction). Beta-adrenergic agnonists (dobutamine) used as a "bridge" until transplant available. Keep pt alive. Dopamine has been used.
-Biventricular pacemaker-in pts with conduction defects or those not responding to treatment
-Implantable cardioverter-defibrillator
-left ventricular assist device (LVAD) as bridge to transplantation
-Cardiac transplantation
-Stem cell repair (future) |
|
|
Term
|
Definition
| progressive inflammation of INTIMA (not endothel) or large and medium sized arteries. Vessel narrow and predisposes overlying thrombosis. |
|
|
Term
| What's the most common cause of heart disease? And what heart diseases does it cause? |
|
Definition
| Atherosclerosis by causing ischemic heart disease, myocardial infarction. |
|
|
Term
| Atherosclerosis causes what? |
|
Definition
| heart disease, stroke, and associated with increased risk of dementia. |
|
|
Term
| What are non-modifiable risk factors for atherosclerosis? |
|
Definition
-Increased age: men>45, women>55
-Genetic predisposition
-Male gender |
|
|
Term
| What are modifiable risk factors of atherosclerosis? |
|
Definition
-Hypercholesterolemia
-hypertension
-smoking-damage to endothelial cells
-Diabetes/insulin resistance-problem/damage to endothelium |
|
|
Term
| "Soft" risk factors of atherosclerosis? |
|
Definition
-lack of physical activity: exercise increases LDL's
-obesity
-type A personality-strung a little tight.
-Oral contraceptives
-Depression-feels not contributing to society
-Fructose intake, damage to endothelium
-Trans fat intake |
|
|
Term
| Are "soft" risk factors proven to be associated with atherosclerosis? |
|
Definition
|
|
Term
| Cholesterol can't dissolve in blood so it's carried by what? |
|
Definition
| Lipoproteins: LDL's and HDL's |
|
|
Term
| What are LDL's and what do they do? Do they increase or decrease risk of atherosclerosis? |
|
Definition
| Take lipid from liver to the body. Circulate for 2-4 days. High levels increase risk of atherosclerosis. |
|
|
Term
| What are HDL's, what do they do, and do they increase or decrease risk of atherosclerosis? |
|
Definition
| High density lipoproteins. Take lipid from cells to liver for excretion in bile. High levels are considered protective against athero. |
|
|
Term
| What is the disease process of atherosclerosis? |
|
Definition
-Localized trauma
-Injury increases wall permeability and LDL's accumulate/stick to the site of damage.
-Endothelial cells oxidize LDL's, starting inflamm process, attracting WBC's, especially monocytes
-activated monocytes are macrophages, eat the oxidized LDL, then become foam cells (bigger).
-Foam cells accumulate to form fatty streak and more convex surface
-increased shear stress (stress on cells as blood rushes by)
-as inflamm process continues, enzymes and toxic substances released by foam cells injure the site more.
-adhesion of platelets to site
-growth factors released by platelets and macrophages cause migration and prolif of smooth muscle cells
-causes either fibrotic lesion of intima or a fibrous cap over lipid rich core
-Decreases vessel lumen size
-Can calcify
-can be sheared off and release atheromatous material into the blood
-can result in embolus, possibly leading to MI or stroke. |
|
|
Term
| Does early atherosclerosis often have symptoms? |
|
Definition
| No. Begins early, in childhood. progesses slowly. More common in diet rich in cholesterol. Most ppl have evidence of it by 5th decade. |
|
|
Term
| The first symptoms of atherosclerosis occur during what? Why? What symptom occurs? |
|
Definition
First symptoms often on exertion. Occur because oxygen need is greater than the supply.
-Intermittent claudication in tissue with limited oxygen occurs. Means lameness/weakness with associated pain due to ischemia. |
|
|
Term
| What are symptoms of more advanced atherosclerosis? |
|
Definition
PVD, MI, kidney disease, aneurysm, angina, sudden death, stroke.
-25% of people with advanced atherosclerosis have no idea they have it until they die from it! |
|
|
Term
| What can be done to diagnose atherosclerosis? |
|
Definition
-Pt history for risk factors
-Symptoms
-Physical exam
-Lab testing-
1)measure fasting total serum cholesterol and HDL in all adults 20 years old or older every 5 years.
2)Eval of serum highly sensitive C-reactive protein (hs-CRP) in pts with 10 yr CHD risk of 10% or more. hsCRP released by liver in response to systemic inflammation eg atherosclerosis. Not normal.
-imaging studies |
|
|
Term
| What is a desirable cholesterol level? |
|
Definition
-<200 mg/dL total cholesterol
-at least 40 HDL
-less than 160 LDL (even less wanted for those with more risk factors) |
|
|
Term
| Increased levels of what indicate systemic inflammation? What does it increase risk of? |
|
Definition
| Hs-CRP. Causes higher risk of cardiovascular disease. |
|
|
Term
| What are the risks for CVD and associated levels of hs-CRP? |
|
Definition
<1.0 mg/L -- low risk
1.0-3.0 mg/L-- average risk
>3.0 mg/L-- high risk |
|
|
Term
| What can be used to get an image of the lumen of blood vessels? Where are athromatous lesions more likely to be seen by this? |
|
Definition
Doppler ultrasonography. Adds sound to ultrasound, provides image of lumen of vessel, allows image of stenosis and blood slow.
-Athromatous lesions more likely to form at bifurcations of vessels b/c of great shear stress. |
|
|
Term
| What is the management for atherosclerosis? |
|
Definition
1)Prevention is most important:
-control risk factors, which slows progression and may even allow regression.
-Lose weight
-Modify diet
-Increase physical activity
2)Pharmaceutical intervention for cholesterol and inflammation
3)Surgical intervention |
|
|
Term
| What are statins used for, and what is the mechanism of action? |
|
Definition
-Statins- used for atherosclerosis, -Interferes with production of cholesterol by inhibiting HMG CoA reductase.
-Increases liver's ability to remove LDL's from blood by increasing number of LDL receptors on liver. |
|
|
Term
| Why are statins a first line treatment for lowering cholesterol? |
|
Definition
-Have a good safety profile
-Substantially reduce mortality and morbidity in pts with OR w/o coronary artery disease**
-Helpful in pts with normal cholesterol levels with prior MI
-May decrease blood pressure |
|
|
Term
| Do statins affect symp or paramsymp system? Do they have an anti inflammatory effect? |
|
Definition
Affect sympathetic nervous system.
Yes, they do have anti-inflammatory effect. |
|
|
Term
| What are adverse rxns from taking statins? |
|
Definition
-GI upset-diarrhea or constipation
-Possibly arrhythmias-can actually help pts with premature ventric contractions, but can cause pts with no history of problem to develop arrhythmia.
-myalgia, muscle cramps, and tendonitis
-abnormal liver function-can be fatal! need to make sure pt has good liver fxn when put on statins
-Rhabdomyolysis-skeletal muscle break down. Very rare, can be fatal |
|
|
Term
| What are contraindications for statin use? |
|
Definition
-Liver dysfunction
-Pregnancy |
|
|
Term
| What are bile acid binders, what do they do, and what are they often prescribed with in pts with heart disease? Any SE? |
|
Definition
-They bind with cholesterol-containing acids in intestine and are eliminated in stool
-Often prescribed with statin meds in pts with heart disease-additive effect.
-Few side effects, mostly GI. BUT, will bind other drugs pt is taking, so want to space out dosing of this with other meds. |
|
|
Term
| What are names of bile acid binders? |
|
Definition
| Cholestyramin, colestipol, colesevelam |
|
|
Term
| What do fibrates do? What receptors do they affect? They increase risk of what if used with statins? What are their side effects? |
|
Definition
-They inhibit development of cholesterol
-They affect PPAR-alpha receptors, causing more LDLs to be taken out of circulation and into cells. Raises HDLs.
-The increase risk of myopathy when used with statins
-Side effects: increased likelihood of gallstones, anemia, bleeding
-Can cause gas and bloating |
|
|
Term
| What are nicotinic acid agents and what do they do? What dose is given? |
|
Definition
-Niacin, water soluble B vitamin.
-Decrease production of LDLs (better than any other med*) and triglycerides. Increase effect of anti-HTN meds
-Dose started low and gradually increased to high levels. |
|
|
Term
| What are SE of nicotinic acid agents? |
|
Definition
-Flushing (decrease over time), hot flashes, and itching-kinda like menopause
-Nausea and vomiting
-Gas
-Liver damage
-Gout
-Hyperclycemia
-Toxic amblyopia
-Macular edema-due to taking too much. Affects VA. |
|
|
Term
| What are optometric consideration of statins? |
|
Definition
1)Have been shown to increase retinal blood circulation
-May be useful for ischemic retinal diseases?
-May protect against AMD?
2) May decrease incidence of diabetic neuropathy (35%) |
|
|
Term
| What are optometric considerations of fibrates? |
|
Definition
1) Increase retinal circulation-May protect against diabetic neuropathy (45% reduction)
2) Have been shown to decrease need for laser treatment in diabetic retinopathy |
|
|
Term
| What is ischemic heart disease? It's a leading cause of what in US? |
|
Definition
-Imbalance b/w cardiac need for oxygenated blood and its supply.
-Leading cause of death |
|
|
Term
| Risk factors for ischemic heart disease? |
|
Definition
-Genetic susceptibility -Advancing age
-Gender (M>F)* -Lipoprotein levels
-HTN and DM -Hs-CRP
-Cigarette smoking -Diet and obesity
-Sedentary lifestyle -Migraine HA with aura
-Psychosocial well-being: work stress, lack of social support, depression, and personality (hostility) |
|
|
Term
| What things are important about ischemic heart disease in women? |
|
Definition
-In younger pts, there are less women with it, but equal prevalence in older years.
-women less likely to survive MI
-Different pathophysiology than men: smaller coronary arteries, and greater likelihood of endothelial dysfunction.
-Different risk factors: 1) low estrogen levels. 2) High testosterone levels and polycystic ovary syndrome |
|
|
Term
| What is different about the process of atherosclerosis in women relating to ischemic heart disease? Why does this cause IHD to be diagnosed less in women? |
|
Definition
When there is endothelial damage, nitric oxide is released, but women's arteries are not as able to dilate due to nitric oxide because the remodeling of the vessels tends to be outward. The vessel is now less able to dilate because there's nowhere to push out.
-Because of this, when they do imaging of blood vessels, the lumen seems to be wide open and the problem is not caught as easily. The blood flow seems normal. |
|
|
Term
| What prodromal symptoms for women with ischemic heart disease are different than in men? |
|
Definition
| Fatigue, sleep disturbance, and dyspnea. Usually NO previous history of chest pain* |
|
|
Term
| What can you do to diagnose ischemic heart disease in women? |
|
Definition
-Endotheial fxn (acetylcholine stress test)
-Stress echocardiography and SPECT
-Intravascular ultrasonography |
|
|
Term
| What is angina pectoris? Who does it usually happen to, what are the conditions where it typically happens? What is levine's sign? |
|
Definition
-It's chest pain that results from transient myocardial ischemia. May also have pain in neck and jaw
-Usually occur in men
-Usually happens in an older male exerting himself, often in cold weather.
-People will usually clench their fist and bring it to their chest: this is levine's sign |
|
|
Term
What is stable/typical angina?
What usually causes it?
How long does it take to present and how long does it last?
How can it be relieved? |
|
Definition
-Fixed atherosclerotic narrowing that decreases blood supply when demand is increasing
-usually provoked by exercise or emotional stress
-Presents over a few seconds or minuts
-Lasts 5 to 15 minutes
-Relieved with rest or sublingual NTG (vasodilator) |
|
|
Term
What is prinzmetal's/variant angina?
Who does is occur more in?
When is it common to happen?
Associated with?
May exhibit what other signs of arterial hypersensitivity?
Relieved how? |
|
Definition
-Vasospasm superimposed on fixes stenoses. Chest pain, vasospastic episode. Can occur AT REST***
-Occurs more in women
Common at night or early morning
-Associated with cigarette smoking
-May also exhibit migraines with aura and raynaud's phenomenon
-Relieved by NTG and possibly treated with Ca+ channel blockers. |
|
|
Term
| What is done in management of angina pectoris? |
|
Definition
-Activity guidelines and weight loss where appropriate
-warning signs that indicated need for med attention: discomfort not relieved with 2-3 NTG tablets given 5 min apart
-Control of risk factors: HTN, DM, hyperlididemia, smoking
-Treat underlying conditions: anemia, thyroid disease |
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Term
| What medical therapy can be used for management of angina pectoris? |
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Definition
-baby aspirin every day (81 mg). doesn't prevent first heart attack in women though. Prevents strokes in both sexes.
-Nitrates for venodilation: sublingual, oral, dermal, and i.v. are available
-Beta blockers to limit myocardial oxygen demand
-Calcium channel blockers to prevent coronary spasm and for vasodilation. |
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Term
| What surgical therapy can be done for AP? |
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Definition
-Percutaneous coronary intervention (PCI): less invasive, stenting almost always performed. Glycoprotein IIB/IIA inhibitors to prevent platelet aggregation
-Coronary-artery bypass grafting (CABG): transplant vessels to "bypass" blockage. Use internal mammary arteries or saphenous veins. |
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Term
| What is using PCI best for treating AP? What are the advantages of PCI? |
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Definition
PCI best when the disease involves less vessels.
-Advantage is pts back to work within a week or so. |
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Term
| What are acute coronary syndromes (ACS)? |
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Definition
Catch all term that includes
-unstable angina
-non-ST-elevation myocardial infarction
-ST-elevation myocardial infarction |
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Term
| What is the common mechanism to all ACS? |
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Definition
-Rupture or erosion of fibrous cap or coronary artery cap
-Platelet aggregation and adhesion
-Thrombus formation and vasoconstriction
-Embolization. |
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