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271 Cards in this Set

  • Front
  • Back
What are the findings of acute rheumatic fever?
Fever, arthritis, acute carditis, chorea, erythema marginatum.
What is the pathologic giveaway for acute rheumatic carditis?
Aschoff bodies - inflammatory infiltrates of mononuclear cells, mainly histiocyes.
What's the most common cause of mitral stenosis?
Chronic rheumatic heart dz.
What is the pathologic difference btw calcific senile aortic stenosis (+/- congenital bicuspid valve) and aortic stenosis as a result of chronic rheumatic heart dz?
Rheumatic dz yields a thickened aortic valve with commissural fusion where the others do not.
Dental procedures offer an avenue of opportunity for what heart dz to arise? In what kind of patients?
Bacterial endocarditis in patients with a pre-existing structural deformity in their valves.
Classic presentation: 30-yr old female presents with psychiatric problems, a personality disorder, and cardiac symptoms (chest pain, palpitations, dyspnea). On auscultation the heart demonstrates a mid-systolic click. Weeks later the click is absent.
Mitral valve prolapse progressing to regurgitation.
What are four broad types/causes of vegetative endocarditis?
Bacterial, rheumatic heart dz, (marantic) thrombotic (from cancer, sepsis, or hypercoagulable states), lupus (Libman-Sachs vegetations).
What is the most common benign tumor of the heart in adults? Kids?
Atrial myxoma. Rhabdomyoma.
What are three measurements used to determine severity of aortic stenosis? How are they measured?
1. Pressure gradient across valve by cardiac catherization (or echo using the modified Bernoulli P = 4v^2 eqn); 2. Cross-sectional area across stenotic valve and 3. Duration (time) of flow through the valve, both by echo.
Between acute and chronic mitral regurgitation, which one results in the higher LV end-diastolic pressure?
Acute MR -> very high LV EDP -> Acute left-sided CHF.
Valvular insufficiency causes ____ overload of the ____ heart chamber resulting in ____ hypertrophy.
Volume, left, eccentric.
What common valvular defect does NOT lead to left-sided CHF?
Mitral stenosis. This does not increase pressure within the LV, but still causes pulmonary edema and left atrial enlargement. Its latest course is RVH and eventual RV failure.
Which valvular dz predisposes patients to atrial fibrillation?
All of them. They can all cause LAE and thus predispose to atrial arrhythmias.
What is the classic valvular disease associated with sudden death due to cardiac arrhythmias?
Aortic stenosis, this one is the most likely to cause concentric LVH which is the greatest risk factor for ventricular arrhythmias like VT, even more so than CAD.
What is the most common cause of mitral regurgitation in the US?
Mitral valve prolapse.
Others: Ischemia or infarction of papillary muscles, CHF, rheumatic heart dz.
What are the three clinical presentations of aortic stenosis and which has the worst prognosis associated with it?
Chest pain (angina), syncope (skipped beats), and CHF (dyspnea), with median survival rates of 5, 3, and 1-2 yrs respective.
What are findings of auscultation of the carotids in someone with AS?
1. A slow slurred upstroke with 2. a delayed peak.
When is an S4 gallop indicative of heart disease?
In patients with AS, HOCM (IHSS), and LVH, where an exaggerated atrial kick is needed due to an elevated LV EDP. In normal aging, the S4 sound may be heard as a function of the atrial kick playing a larger role in the filling of the LV.
S3 gallops are characteristic of what general heart finding?
Decompensated congestive heart failure.
What happens to pressures in these places during acute MR? LA, pulmonary system, aorta, peripheral system, LV.
LA up, PCWP up, AO down, SBP down, LV compensatorily up significantly, esp LV EDP.
What kid of heart murmur presents in chronic MR?
Holosystolic murmur best heard at the apex radiating to the axilla.
What common valvular disease presents with bounding pulses, a wide pulse pressure, and a large carotid volume?
Chronic aortic insufficiency.
Why is the acute AI diastolic murmur shorter than the decrescendo murmur of chronic AI?
Because the murmur/regurgitation stops when aortic and LV pressures equalize, and in acute decompensated AI the pressures equalize very early in diastole.
What is a pharmacotherapeutic treatment for CHRONIC (but not acute) MR or AI?
IV vasodilators. By reducing peripheral vascular resistance, afterload is reduced and forward flow is favored over regurgitation.
What is the key auscultatory finding in MS?
Diastolic rumble beginning after an opening mitral sound (opening snap OS which decreases with progressive calcification) and accentuated immediately prior to S1 due to the atrial kick.
What is the most common cause of aortic stenosis in patients below age 70?
1. Congenital bicuspid valves
2. Chronic rheumatic heart dz
3. Senile calcific degenerative
Which cardiac disease presents with the same clinical triad as aortic stenosis (angina, syncope, dyspnea)?
HOCM (IHSS)
What causes acute and chronic AI?
Acute - dissection, infection (syphilis)
Chronic - Marfan's, congenital bicuspid valve, chronic rheumatic heart dz.
What are pharmacologic therapies for MS?
Drugs that slow the heart rate (beta-blockers, CCB's) to increase LV filling time, anticoagulants to decrease thromboembolytic risk.
What are some right to left shunts in CHD?
Tetralogy of Fallot, Transposition of the Great Arteries, Truncus Arteriosus, Tricuspid Valve Atresia
Relate arterial and venous hypertension and their effects on preload or afterload.
Arterial hypertension causes increased afterload in the heart chamber behind it. Venous hypertension causes increased preload (and edema) in the heart chamber ahead of it.
What part of broader diseases is an ASD at the ostium primum considered to be? What valves are malformed in these defects?
An endocardial cushion defect where atrial and ventricular septa don't connect. Mitral and tricuspid valves malform.
What is a sinus venosus usually an abnormal communication between?
The pulmonary veins and the sinus venosus portoin of the right atrium.
Atrial septal defects induce what kind of overload on which side of the heart?
Volume AND pressure overloads with the risk of pulmonary hypertension and right-sided CHF.
What is the junction point for the embryologic tissues of the heart and last part of the ventricular septum to close? What valve attaches to its upper border?
The membranous septum, the site of 90% of all VSD's. The tricuspid valve is attached to its upper border.
What other characteristic problem is associated with infundibular (conal septal) VSD's?
Insufficiency of aortic/pulmonic valves because its support point is absent.
Which VSD can present as a multitude?
Muscular VSD's with trabecular openings.
In a VSD what happens to the right ventricle, left ventricle, pulmonary vascular pressure, and systemic vascular pressure?
The right ventricle experiences a pressure overload, the pulmonary circulation increases bloodflow and pressure, the left ventricle experiences increased preload, and the systemic BP goes down due to a decreased cardiac output.
What is the main risk in a child with a left-to-right shunt that would preclude defect repair and mandate a heart transplant?
Irreversible pulmonary hypertension manifested as a late "shunt reversal" where pulmonary pressure exceeds systemic and cyanosis results. Unlikely in children under the age of 2yrs.
What are the four components of a Tetralogy of Fallot?
Sub-PA stenosis (RVOT)
VSD
Aortic override of VSD
RV hypertrophy
What kind of shunting in a tetralogy of Fallot is more serious? What are the symptoms when the dz gets to this point? What can a child with this and an acute spell of paroxysmal hypoxia (and RVOT spasms) do to relieve this?
Right to left. Cyanosis that worsens with exercise and clubbing. Children can squat, it kinks their aorta increasing PVR and forcing more blood flow to the lungs.
In a tetralogy of Fallot, where is preload increased? Where is afterload increased?
Both increased in the RV, potentiating eccentric and concentric hypertrophy ("boot-shaped heart") and right-sided CHF.
T/F: A patent ductus arteriosus makes an aortic coarctation worse.
False. The patent ductus provides blood more space to navigate around the "juxtaductal" coarctation.
What other congenital heart defects are also associated with an aortic coarctation?
Congenital and acquired aortic stenosis, bicuspid aortic valve, tubular hypoplasia of arch.
What's the most common congenital anomaly causing death in the neonate?
Hypoplastic left heart syndrome
T/F: A patient with transposition of the great arteries will benefit from the presence of a VSD.
True. Anything to increase communication between the two circuits (such as a PFO or PDA) will help.
A spike-and-dome (bisferiens) arterial pulse is distinctive of which cardiomyopathy?
Hypertrophic cardiomyopathy.
A pt presents with tachycardia, hypotension, and Arrhythmia X. What do you do?
SHOCK HIM.
What is the histologic appearance of idiopathic dilated cardiomyopathy?
Nonspecific myofiber changes with ATTENUATION, stretching, irregularities of orientation. Interstitial and endocardial fibrosis.
What is the histologic appearance of hypertrophic cardiomyopathy?
Disproportionate thickening of the ventricular septum with 1. myocyte hypertrophy, both of the nucleus and transverse myofibers; 2. disarray of myocyte bundles; and 3. interstitial fibrosis.
How does salt ingestion affect systemic blood pressure?
It induces hypervolemia, increasing intravascular volume, venous return, and thus preload. Preload affects cardiac output which then determines the mean arterial pressure, so BP goes up with increased salt intake.
What is the equation for mean arterial pressure as a function of cardiac output?
MAP = CO X SVR -or-
V = iR
What are the standard limits of pre-hypertension, stage I/II hypertension, and hypertensive crisis? What is the optimal blood pressure for minimizing risk? What is the BP increase necessary to double the risk of stroke and ischemic events?
Pre-hypertension: 120-140/80-90
SI Hypertension: 140-160/90-100
SII Hypertension: 160+/100+
Hypertensive crisis: 200+/120+
Ideal: 115/75

Doubling: 20 mmHg in systolic
What does essential hypertension mean? What are the main causes of secondary hypertension.
Hypertension of unknown origin. Renal artery stenosis, renal parenchymal lesions, oral contraceptive use, primary aldosteronism, pheochromocytoma, coarctation of the aorta.
Is drug therapy recommended in pre-hypertensive patients?
Only in diabetics or pts with kidney dz. Threshold for treatment of those pts is 130/80 and goal is to reduce below that number.
Elderly patients with decreased diastolic blood pressures but hypertensive systolic levels have what?
Isolated systolic hypertension (ISH) found in >2/3 of elderly hypertensive pts.
What is the difference in side effect profile between ACE inhibitors and angiotensin receptor blockers and why is this?
ACE-I's have cough as an SE because they also inhibit bradykinin breakdown, which accumulates to induce a dry cough. ARB's don't do this.
Hypertension commonly leads to progressive LVH and what kind of heart disease?
LV diastolic heart failure with a normal systolic function.
What separates emergency and urgency hypertensive crises?
The presence of secondary physical signs like papilledema, retinal hemorrhages, encephalopathic altered consciousness, acute pulmonary edema, MI, renal failure, aortic dissection.
For patients with target SBP's 20mmHg below their current BP, therapy should consist of what?
Two or more anti-hypertensive drugs, one of which must be a thiazide-type diuretic. Stage II mandates multiple drugs over Stage I.
After someone has an MI, what drugs should you put them on before discharge?
Aspirin, beta-blocker, statin, ACE-I
Pts with diabetes or chronic kidney disease, even in the absence of hypertension, have a compelling indication to be placed on:
An ACE-I or ARB. They help to reduce end-stage renal failure, CAD, stroke, and LVH.
What does the x descent in the atrial pressure curve represent?
Early systole - atrial relaxation and filling during ventricular contraction.
If a CXR shows a cardiac to thoracic width ratio of greater than 1.55, what is in your differential?
If it is chronic, think ventricular hypertrophy or other dilation etiologies (myocarditis, dilated cardiomyopathy). Otherwise suspect cardiac tamponade caused by pericardial effusion. Use an echo to confirm.
What does a steep x descent mean?
It signifies that atrial relaxation and diastolic filling is being impaired, generally nonspecific, could be cardiac tamponade or constrictive pericarditis or restrictive cardiomyopathy.
During inspiration, the negative inspiratory pressure surrounding the heart leads to exaggerated splitting of the S2 sound. Why does this happen?
Greater RV filling occurs during inspiration, requiring greater systole times to pump it all out. The pulmonic valve closure becomes delayed, but the aortic valve closure ALSO becomes earlier due to lesser LV filling. Finally, the septum shifts to the left during inspiration, reducing the LV cavity size/CO and increasing the RV.
How does SBP get reduced (by >10mmHg) in pulsus paradoxus?
The physiologic response to inspiration (reduced LV cavity size and stroke volume) becomes exaggerated due to the excess pericardial fluid, leading to lower BP since SBP = SVxHRxSVR.
What happens to the following in cardiac tamponade?
JVP
Systolic BP
Heart size
JVP increases
Blood pressure decreases
Heart size gets smaller except in cases of large pericardial effusions.
In the JVP curve, which descent is associated with constrictive pericarditis?
The x and y descent both.
What are the three specific signs of constrictive pericarditis?
1. The dip-and-plateau RV pressure waveform (square-root sign)
2. Kussmaul's sign- JV distension refuses to go down or even gets worse during inspiration.
3. Pericardial knock extra sound (K) in diastole, resembles S3.
Is amount of fluid or pericardial pressure the determinant of cardiac tamponade severity?
Pericardial pressure increase.
What is the good news in a patient with MI-associated V-fib?
The recurrence rate of the V-fib is low. An AICD is not recommended in pts with these "secondary VF's".
How do you differentiate a V-tach and an Accelerated Idioventricular Rhythm (AIVR)? What is a "sustained" VT?
V-tach consists of at least 3 consecutive PVC's (wide QRS, no P) at a rate of over 110bpm and potentially life-threatening. AIVR is anything below that and is a benign finding. "Sustained" is anything lasting over 30s.
What is the rate of patients with VF having primary VF? What is the rate of resuscitation of patients experiencing sudden cardiac death? What properties of the VF dictate survival rate?
85% have primary. 1/3 survive. VF's longer than 12 beats and faster than 160bpm are associated with poorer prognoses.
T/F: You see a P wave in V-tach but not V-fib.
False. All ventricular arrhythmias imply the absence of atrial depolarization.
What is the most common (arrhythmia) cause of SCD in adults? Outpatients? What about etiologies?
Ventricular fibrillation. Primary ventricular fibrillation. 80% have CAD as their etiology. Other causes: tamponade, cardiac rupture, IHSS (most common in young adults during exercise), AS.
What cardiac complication is described by an EKG with a polymorphic VT (R-on-T syndrome) and wide QRS, and is more likely to occur in patients with hypokalemia?
Torsades de pointes.
T/F: Plasma norepinephrine levels during CHF predict a better prognosis, since the sympathomimetic response is stronger in response to the insult.
False. The higher the norepinephrine levels, likely the worse the condition of failure.
T/F: In the setting of acute CHF, drugs of choice increase the load on the heart.
True for the most part. Beta-agonists and PDE inhibitors do this. Diuretics and vasodilators reduce the heart load.
How does digoxin work?
It inhibits the Na/K pump, increasing intracellular calcium transiently and increasing myocardial contractility.
In settings of increased afterload, does the LV end-systolic or end-diastolic volume change?
The LVESV goes up reducing stroke volume.
In settings of digoxin administration, does the LV end-systolic or end-diastolic volume change?
The LVESV goes down via increased contractility. The systolic pressure also increases.
Why is digoxin preferred over digitalis?
Increased bioavailability, more rapid onset of action, shorter half-life (more specific sx).
T/F: Digoxin is useful for ventricular arrhythmias.
False. Only supraventricular arrhythmias.
What drugs are contraindicated in conjunction with digoxin use?
Non-potassium-sparing diuretics - thiazide diuretics, loop diuretics; also corticosteroids, amiodarone, erythromycin, quinidine, tetracycline, verapamil.
What can you administer to counteract digoxin toxicity?
Anti-arrhythmics (lidocaine, phenytoin, atropine), potassium IV, antiglycoside antibodies to bind digoxin.
What effect does increased cAMP have upon the myocardium? What about smooth muscle wall? What drugs increase this?
Increases contractility of myocardium, relaxes SMC in blood vessels, beta-agonists, nitrates, and PDE3 inhibitors do this.
What are the effects of beta-2 and alpha-1 adrenergic stimulation in the heart?
Alpha-1 increases contractility, beta-2 does this as well as inc heart rate. Neither are as important as beta-1's.
What are Milrinone and Amrinone?
PDE3 inhibitors, Milrinone is the oral one.
What is hydralazine? What is an important SE?
An arterial vasodilator used to treat acute CHF. It can cause lupus-like sx.
What is nitroprusside? What is an important SE?
A nitrate that induces balanced arterial and venous dilation. It cannot be administered for too long due to the cyanide toxicity that builds up causing renal failure.
Which diuretics do you want to choose for treating hypertension? CHF?
Thiazide-type diuretics (hydrochlorothiazide, chlorthalidone). Loop diuretics (furosemide, bumetanide, torsemide).
T/F: Digoxin helps decrease mortality in patients experiencing CHF.
False, it improves quality of life but does not increase life expectancy.
Which CCB is the most cardio-specific? What is the most peripheral-specific? What's the one in btw?
Verapamil -cardiac. Dihydropyridines - peripheral. Diltiazem - in btw.
T/F: Beta-blockers and CCB's are indicated in pts with acute CHF.
False. These are contraindicated and worsen the condition by further depressing the CO.
T/F: ACE-I's and ARBs can actually induce remodeling of the heart to a more healthy condition.
True.
Why are ARBs statistically better than ACE-I's in treating chronic CHF pts?
1. ARB's are more thorough at blocking all angiotensin signaling at AT1. 2. ARB's do no block the beneficial effects of AT2 signaling.
In a chronic CHF pt, would you want to use a drug therapy that encourages cell growth and proliferation?
No. The point of ACE-I's and ARB's is to block cell proliferation signaling from the RAAS axis that induces hypertrophy and fibrosis of the myocardium.
What are the contraindications for ACE inhibitors and ARB's?
Pregnancy (crosses placenta), renal failure, renal artery stenosis.
What is Eplerenone?
An aldosterone antagonist like spironolactone, useful in CHF pts.
Treatment of diastolic dysfunction may be achieved by administration of what for hypertrophic or restrictive cardiomyopathy?
For hypertrophy use a CCB ie verapamil. For restrictive CM use diuretics+preload reducing agents like nitrates or ACE-I (vasodilation).
What heart murmurs actually get louder when you ask the patient to bear down (Valsalva maneuver) or stand up from a sitting position?
Mitral valve prolapse and HOCM. These maneuvers increase thoracic pressures, reducing venous return/preload and thus flow. Most murmur intensities are proportional to flow but these aren't for some reason.
Does SL NTG work on unstable angina?
Usually not.
What effect do CCB's have on the heart rate, contractility of a myofiber?
Reduce both, thereby reducing oxygen demand.
What effect does increasing cAMP have in the heart myofibers and peripheral vascular system endothelial cells?
It increases the contractility of myofibers but relaxes smooth muscle by activating MLC-phosphatase.
NO transiently increasing what secondary messenger molecule resulting in vascular smooth muscle relaxation?
cGMP.
What signal messengers drive endothelial cells to synthesize NO using eNOS?
Ach or bradykinin naturally. Nitrates pharmacologically.
What are drugs you can use to treat angina?
Drugs that either reduce HR/contractility of the heart or vasodilate, or both: Nitrates, beta-blockers, CCB's ACE-I's, ARB's, K channel openers, alpha-1 antagonists, ETa/b antagonists, PDE5 inhibitors.
Are nitrates as a drug class easily absorbed in the gut? How are they degraded?
Poor bioavailability, that's why NTG is SL. Metabolized in liver, excreted in kidneys.
Phosphodiesterase inhibitors have what effect upon the lungs and heart?
Like nitrates they increase cGMP. Inc contractility in the heart. Dilate SMC where they have specific activity, so bronchioles dilated in some PDE-I's. Remember Sildenafil dilates blood vessels in the penis.
Why does nitrate tolerance occur?
1. Decreased activity of the enzyme that converts the nitrate to a usable form to make NO with. 2. Reflex activation of the RAAS system to constrict vessels.
What drug can't be taken on top of Viagra?
Nitrates- there's a synergistic effect, induces hypotension and reflex tachycardia.
What are two populations you would want to avoid beta-blockers in?
Pts with severe asthma (bronchoconstriction) and bradycardic conduction problems in the heart (exaggerated arrhythmias).
What is endothelin? How is it manipulated pharmacologically?
It is a peptide secreted by endothelial cells to induce vasoconstriction. Block ETa receptors on SMC's to vasodilate. Ex: Bosentan, used mainly for severe pulmonary hypertension.
What are risk factors for abdominal aortic aneurysm?
1. Hypercholesterolemia, 1a. Severe hypertension, 3. obesity, 4. smoking. Also, poorly controlled DM, not normal DM!
What is a good marker for disease in Wegener's granulomatosis?
C-ANCA, cytoplasmic anti-neutrophil antibodies.
What is the classic triad of Wegener's granulomatosis?
1. Glomerulonephritis; 2. Necrotizing granulomas characteristically in the upper and lower respiratory tract; 3. Non-granulomatous vasculitis
Aortic aneurysms due to atheromatosis (cholesterol build-up under the setting of hypertension) tend to occur where?
In the infrarenal region of the abdominal aorta.
Where do aortic dissections tend to occur?
Within the thoracic aorta, usu less than 10cm distal to the aortic valve, between the layers of the media.
T/F: Aortic dissection is directly corrolated to atherosclerosis.
False. Dissections typically do not have atherosclerotic plaques on the aortic walls. Hypertension is the predominating cause.
What is a common cause of aortic dissection or cystic medial degeneration at a young age?
Marfan's syndrome.
What is it called when blue basophilic mucin-type material accumulates in the tunica media of the aorta?
Cystic medial degeneration, occurs in old age or in Marfan's syndrome pts.
What causes obliterative endarteritis (inflammation of the vasa vasorum) and tunica media destruction of the ascending aorta?
Syphilis.
Which form of vasculitis is seen in classically young male smokers with gangrene of the extremities?
Beurger's dz (thromboangiitis obliterans)
What form of vasculitis is seen in young women with dizziness and decreased upper extremity pulses?
Takayasu's arteritis.
The difference btw an aortic dissection and aneurysm is:
Dissections involve separation of the vessel layers usu w/in the tunica media, where aneurysms involve dilation of the entire weakened wall.
What form of vasculitis is assoc with arteritis and coronary artery aneurysm?
Kawasaki's dz, typically in children <4y.o.
How do you treat Kawasaki's dz?
IVIg, high dose aspirin(one of the few times you give this to children irrespective of Reye's risk) for 6 weeks with EKG on admission and at 2 and 6 weeks to rule out coronary artery aneurysm.
What form of vasculitis is assoc with Hepatitis B?
Polyarteritis nodosa.
Where does Wegener's tend to cause granulomaous inflammation?
In the small vessels of the upper and lower respiratory tract, the vasculitis is not granulomatous itself but the necrotizing effect from proximity to granuloma causes the dmg.
What is the histological difference between temporal arteritis and Takayasu's arteritis?
Temporal involves granulomatous inflammation of the inner half of the media, destroying the internal elastic lamina, where Takayasu's involves granulomatous inflammation of the outer half of the media.
Which ANCAs are associated with vasculitides?
C-ANCA -> Wegener's
P-ANCA -> Churg-Strauss and microscopic polyangiitis
All ANCA-assoc vasculitides involve small vessels.
What are risk factors for development of thrombophlebitis?
Pregnancy, obesity, immobility.
This malignant vascular neoplasm is assoc with arsenic, Thorotrast, and PVC.
Angiosarcoma.
What is another name for a "ventricular gallop"?
An S3 gallop.
What is the differentiating histological feature between polyarteritis nodosa and microscopic polyangiitis (leukocytoclastic vasculitis)?
PAN presents with vasculitis in a spectrum of phases, where all of LCV's vasulitides are in the same phase of injury. Also, LCV presents in lungs and kidneys where PAN doesn't.
What vasculitis is associated with smoking?
Buerger's dz (thromboangiitis obliterans).
Which vasculitis destroys the inner elastic lamina?
Giant cell (temporal) arteritis.
What arteries does temporal arteritis typically target?
Temporal, ophthalmic, and vertebral arteries, causing unilateral headache and blindness.
Where does Takayasu's arteritis typically induce inflammation?
Large vessels like the aortic arch and its immediate bifurcations. Leads to a "pulseless" arteritis.
What are the characteristic features of Kawasaki's dz?
High fever, general erythematous papular rash, conjunctivitis, edema (pedal and periorbital), diffuse skin desquamation, cardiomegaly, pericardial effusion, coronary artery aneurysms, ischemia, acute MI, sudden death syndrome.
What happens to the LVEDV and LVEDP during angina?
Both increase. Wall stress also increases.
A pt has diastolic heart failure from chronic hypertension. What class of drugs would you not want to give this person to treat the progressive heart failure?
Nitrates because they reduce preload upon which those patients depend to sustain their cardiac output.
How does nitric oxide act in the vasculature?
1. It induces cGMP formation in SMC leading to MLCP action and relaxation. 2. It binds to potassium channels, opening them and hyperpolarizing the cell to prevent contraction. 3. It inhibits platelet aggregation.
What kind of drugs are Monoxidil, Pinacidil, and Nicorandil, and what do they treat?
They are potassium channel openers in arterioles, and they treat severe/refractory hypertension +/- angina. Minoxidil = Rogaine, treats baldness.
In chronic MR, LVEF is expected to decrease after valve replacement because:
Afterload increases.
What classes of drugs are indicated for angina treatment?
Drugs that reduce the load and oxygen demand of the heart--nitrates/PDE-I's for venodilation, BB's and CCB's to decrease HR, contractility, K-channel openers, arteriodilators, and ET-channel inhibitors for extreme cases.
What classes of drugs are indicated for acute cardiac decompensated heart failure?
Drugs that increase the cardiac output and reduce congestion--positive inotropic agents like digoxin, beta-agonists and PDE3 inhibitors to increase CO, diuretics and vasodilators to dec blood volume.
What classes of drugs are indicated for chronic heart failure?
Drugs that reduce the cardiac output and the load--1. loop diuretics to counteract the RAAS activation inherent in chronic heart failure conditions, 2. inotropic drugs like digoxin to reduce hospitalization, 3. beta-blockers and 4. ACE-I/ARBs to improve mortality; 5. vasodilators, 6. aldosterone antagonists to further decrease volume.
What effect does digitalis have upon LV pressure?
It decreases the LVEDP by reducing the sympathetic signaling to the heart in a compensatory effort to maintain CO.
What's the difference between Milrinone and Sildenafil?
Milrinone is a PDE3 inhibitor that acts preferentially in the heart to increase contractility (but also have peripheral effects). Sildenafil (Viagra) is a PDE5 inhibitor that works in the periphery as a vasodilator.
What is a primary and secondary effect of arteriodilators upon CO/HR?
Primary - increase CO by reducing afterload significantly. Secondary - reflex tachycardia due to BP drop.
T/F: CCB's are indicated in the treatment of chronic heart failure.
False. The non-DHP's are negative inotropes and increase the risk for hospitalization. The DHP's have not been shown to be as effective as the BB's/ACE-I/ARB's which have the same effect on vasodilation.
T/F: Beta-blockers are indicated in the treatment of acute heart failure.
False. Beta-agonists and positive inotropic drugs are used in acute heart failure.
ACE-I's/ARBs have what effect upon preload and afterload?
Decrease both.
What are the risk factors for coronary artery disease?
High LDL, low HDL, hypertension, diabetes mellitus, CURRENT cigarette smoking, male gender, old age, family history.
What is the first step in atherosclerosis?
Endothelial injury.
T/F: Atherosclerosis is a pediatric disease.
True. Fatty streaks have been known to form by age ten.
Is a calcified plaque with a large fibrous cap more likely to lead to a stable or unstable angina?
Stable. Unstable plaques characteristically have little calcification with a large lipid core and a thin fibrous cap are called "vulnerable".
What is the genetic defect in familial hypercholesterolemia?
The LDL receptor in the liver that serves to absorb and metabolize LDL particles. Heterozygotes get MI in their 30-40's, homozygotes as children.
T/F: Women have a higher HDL than men on average.
True.
What consists of a family history for heart disease?
A first degree relative (parent, sibling) suffering a cardiac event below the age of 55 in men, 65 in women.
When does most coronary blood flow occur?
During diastole.
What parts of the ventricles does the right coronary artery supply?
The entire right ventricle, the inferior aspect of both ventricles, and (usually) the posterior wall of the left ventricle (which dictates dominance).
Which layer of myocardium is most susceptible to ischemia?
The subendocardium, because it is the furthest away from the coronary arteries.
What is the mediator of coronary vasodilation during exercise?
Adenosine from ATP breakdown and local acidosis from anaerobic metabolism.
T/F: Coronary artery autonomic innervation assists in the vasodilatory response to increased oxygen demand.
False. Coronary arteries have very scant autonomic innervation. Circulating catecholamines may indirectly assist by increasing adenosine but that's it.
Does parasympathetic innervation exist in the heart? Where?
In the atria yes, none in the ventricles.
T/F: Myocardial metabolism normally derives energy from anaerobic metabolism.
False. This is not supposed to occur normally. It should be 70% FFA, 30% glucose, and 0% anaerobic.
What effect does the HR have upon the systolic/diastolic time ratio?
Inc HR -> inc systolic/diastolic ratio, i.e. more time proportionately is spent in systole.
What are the determinants of myocardial O2 consumption??
Heart rate is the major one. Others: Wall Tension (along with Fenn effect) and Contractility.
What is a differentiating factor in the clinical presentation between stable and unstable angina?
Unstable angina is denoted by intensification over the past 2 mo.s and need not occur with exertion. It varies in frequency, usu longer in duration, and is due to platelet aggregation and thrombus formation.
What is the most sensitive way to detect angina?
Running an exercise-induced stress test while testing for reduced wall motion with an echo. Using an EKG and looking for ST elevation/depression/downsloping or nuclear perfusion during exercise also work.
What are the indications for coronary artery bypass grafting?
Proximal complete block of the left main coronary artery, or occlusion of 2 arteries with EF<50%, or occlusion of 2-3 arteries with proximal LAD lesions and post-MI ischemia.
What clinical presentation in the case of acute prolonged chest pain is the most specific for a cardiac etiology?
Diaphoresis- cold sweats.
Approximately how long after the onset of infarction does it take for the wave of necrosis to develop from the subendocardium? After how long does it become transmural?
15-20 min. 3-5 hr.
What is the histopathological significance of a Q-wave vs. non-Q-wave MI?
Non-Q-wave MI does not involve full breadth of myocardium (not transmural).
Q-wave MI -> ST elevation or depression? Red or white clot? How long?
ST elevation, red clot. This denotes a completely coronary artery occlusion for >3h. Red denotes fibrin meshwork+trapped RBC over just platelets.
What are the time frames that differentiate ACS into its various etiologies?
Less than 15-20min
20m-3h - non-STEMI
Over 3h - STEMI
How long after an MI does it take to see a pathologic Q wave? What does this mean clinically?
8-12hr. Do NOT wait for this EKG finding to present itself before deciding your course of treatment. Generally, STEMI = Q-wave+.
What is the single-most life-saving therapy in acute MI?
Thrombolytic therapy, which can be used in the absence of (PCI) stenting if the cath lab is unavailable.
What is the final common pathway for platelet activation?
GPIIb-IIIa receptor activation.
What is the hallmark of treatment for acute coronary syndrome patients experiencing unstable angina?
Chronic angina therapies (nitrates/PDE5-inhibitors+BB/CCB's to vasodilate + reduce CO) along with ANTI-PLATELET / ANTI-THROMBIN THERAPY. This spectrum ranges from aspirin and clopidogrel (mild) to heparin/LMWH (strong) and IIb/IIIa receptor blockers (strongest).
What is the newest set of thrombolytic therapies and what makes them better?
r-PA and TNK-t-PA, they are bolusable, easier to administer.
What is the standard of care for treating acute STEMI?
1. Aspirin immediately, (2. NTG to exclude angina, check BP), 3. beta blocker (check BP), 4. heparin/LMWH (rule out history of bleeds), 5. EITHER cath lab PCI or thrombolytics (r-PA, t-PA), 6. ACE-I/ARB within 24hr.
During an MI, how long does it take before any pathologic findings can be detected in the heart?
4hr.
From 4-24 hrs after an MI, how does the heart look histologically?
Coagulative necrosis with acute inflammation, PMN's. Myofibers turn pink, nuclei fragmented, edema in the interstitium.
From 24-72 hrs after an MI, how does the heart look histologically?
PMN inflammation gets more severe, myocardium turns from dark red to tan/yellow in the center of infarction. Loss of nuclei and striations.
From 3-7 days after an MI, how does the heart look grossly and histologically?
Infarcted tissue is yellow from chronic inflammatory infiltrate (mononuclear). Collagen deposition in the interstitium begins. This is the weakest time point for the heart structurally, rupture is a risk leading hemopericardium/death.
Two weeks after an MI, how does the heart look histologically?
Phagocytosis of dead myofibers evident, formation of granulation tissue begins, early fibrosis and angiogenesis occurring.
Two months after an MI, how does the heart look histologically?
Collagen-based scar tissue has replaced the dead myocardium, no contractility but at least regains tensile strength. Adjacent muscle hypertrophies compensatorily.
What are the various complications following acute MI?
Ventricular wall/septal rupture, hemopericardium, papillary muscle rupture or ischemia leading to valvular insufficiency (mitral usu), mural thrombus formation at dead wall, ventricular aneurysm, CHF->pulmonary edema, pleural effusion, arrhythmias, pericarditis.
Which cardiomyopathy involves impaired systolic function?
Dilated or congestive cardiomyopathy.
Which cardiomyopathy involves progressive dyspnea?
Dilated cardiomyopathy and hypertrophic cardiomyopathy.
What are the top causes of dilated cardiomyopathy? Irreversible DCM?
Alcohol, ischemia. Idiopathic, post-MI scarring, familial.
Alcohol has what effect upon risks of hypertension and MI?
It increases risk of hypertension (with heavy prolonged use), but it decreases risk of MI (in moderation).
What is the first therapy recommended to pts presenting with DCM?
A coronary angiography to confirm or exclude CAD since that is treatable and can lead to restoration of function.
What is the best way to confirm a diagnosis of DCM?
Echo to check for dilation and reduced EF.
On echo, how does HCM present?
LV hypertrophy with assymetric septal hypertrophy, and a SUPERNORMAL EF.
Which cardiomyopathy involves impairment of diastolic function?
Hypertrophic cardiomyopathy and restrictive cardiomyopathy.
What is the physical presentation of HCM?
Just like aortic stenosis, but in young patients +/- exertion. Dyspnea, palpitations, syncope, chest pain. Sudden death in youth.
Restrictive cardiomyopathy is typically accompanied by dilation of the ___. DCM? HCM?
Atria due to increase pressure requirements to pump blood in the noncompliant ventricle. DCM involves large dilations of all chambers, and HCM has larger LA with mildly dilated LV.
Restrictive cardiomyopathy presents with:
Dyspnea and edema, pulmonary venous congestion and elevated JVP. Fatigue and weakness later. May have S3 gallop. Right-sided CHF.
How can restrictive cardiomyopathy patients die?
Complete heart block primarily, also diastolic and right-sided CHF.
Which cardiomyopathy presents with angina and syncope?
HCM only.
Which cardiomyopathy presents with MR and TR holosystolic murmurs?
Dilated and restrictive cardiomyopathies, due to insufficiency of both AV valves.
Which cardiomyopathy presents with a low voltage ECG?
Restrictive mainly, but also dilated cardiomyopathy.
Which cardiomyopathy presents with loud S3 and S4 gallops?
Dilated cardiomyopathy.
Which cardiomyopathy presents with a prominent palpable S4?
Hypertrophic cardiomyopathy (think massive LVH).
What are the physical findings of HCM?
Spike-and-dome bisferiens arterial pulse. Triple apical impulse. Prominent palpable S4.
What's the Brockenbrough-Morrow-Braunwald phenomenon.
Post-extrasystolic cardiac output is not potentiated in HCM pts but rather decreased due to further obstruction due to increased contractility. The increased filling competes against this and loses out.
Which cardiomyopathy can lead to LBBB?
Dilated cardiomyopathy.
How do you treat dilated cardiomyopathy pts (with a non-ischemic etiology)?
Digitalis to increase contractility, diuretics and vasodilators to reduce preload on the heart. Think of it like heart failure.
How do you treat hypertrophic cardiomyopathy pts?
Beta blockers and CCB's to reduce contractility and improve the filling to reduce outflow obstruction.
Which cardiomyopathy presents with pathologic Q waves?
Hypertrophic cardiomyopathy.
Which cardiomyopathy mimics constrictive pericarditis in that it will carry the presence of Kussmaul's sign (stubborn JVD) and the dip-and-plateau RV pressure waveform?
Restrictive cardiomyopathy.
Define assymetric septal hypertrophy.
Ratio of septal to LV free wall thickness > 1.3.
What are some causes of restrictive cardiomyopathy?
1. Idiopathic. Amyloidosis, sarcoidosis, radiation and myocardial fibrosis after open-heart surgery. Initial hemochromatosis.
T/F: Afterload is measured just before contraction begins.
False. It's after contraction starts.
In young people, which phase of diastole induces the greatest filling of the ventricle?
Early rapid filling phase.
What are the four determinants of preload?
1. Intravascular volume
2. Venous return
3. Atrial contraction
4. Pericardial function
Which of the following is NOT a determinant of cardiac function?
Preload
Afterload
Wall stress
Contractility
None of the above. All contribute to determining CO, and wall stress while being similar to afterload is separate from it. Think about the internal resistance of an engine or battery.
Concentric hypertrophy is an attempt by the heart to ____ wall stress.
Reduce. Remember WS = P*r/(2h), so increasing thickness h will decrease WS.
What does a Swan-Ganz catheter measure?
CO and PCWP.
____ is a way to measure left atrial pressure and indirectly the left ventricular diastolic pressure.
Pulmonary capillary wedge pressure.
What do the a, c, x, v, and y parts of the atrial pressure waveform stand for?
a - atrial kick
c - closure of tricuspid valve
x - atrial relaxation and filling during systole
v - opening of the tricuspid valve
y - rapid early filling of the RV
Rapid early filling of diastole is preceded by which phase?
Isovolemic relaxation, following closure of the aortic/pulmonic valves but before opening of the tricuspid/mitral valves.
What is the cardiac index?
A normalization of cardiac output->CI = CO/(body surface area)
What's the difference between Doppler and Echo?
Echo is imaging and Doppler is measurements of fluid velocity and pressure. You get both performed when you go to the cath lab.
Between systemic and pulmonary vascular resistance, which one is greater and by how much?
SVR about 10x > que PVR.
What are the right and left ventricular systolic and diastolic pressures?
R - 15-30/0-8 mmHg
L - 100-140/3-12 mmHg
Which atrium is depolarized first?
Right.
What is an RSR' in V2 indicative of?
RBBB.
What is an RSR' in V5 indicative of?
LBBB.
What is the main EKG criteria for LVH?
R5+S1>35mm
What are pathologic Q waves defined as?
Q waves wider than 0.04s and/or deeper than a third of the subsequent R wave. Other small q waves are just indicative of septal depolarization.
What lead should you examine to determine any P wave abnormalities?
Lead II because it is parallel to the P wave vector.
How is acute pericarditis diagnosed on EKG?
Diffuse ST elevation with PR segment depression. Physically pt will have sharp pains upon inspiration and be left to deep shallow breaths.
How does hyperkalemia manifest itself on EKG?
Peaked T waves.
What does a bifid P wave mean?
P-mitrale, delayed left atrial depolarization due to enlargement (late P wave peaking).
What does a tall P wave > 2.5mm mean?
P-pulmonale, due to right atrial enlargement (early P wave peaking).
What does a PR > 0.2s mean?
Delays in AV conduction, due to drugs (digoxin, BB, CCB), ischemia/infarction, or degenerative or calcific disease (Lev's or Lenegre's dz).
What are the EKG findings necessary to diagnose Wolff-Parkinson-White?
WPW is an accessory pathway dz, so:
1. Short PR interval
2. Delta wave (depolarization of accessory pathway)
3. QRS>0.12
What is the most common congenital disease presenting with RBBB?
ASD. It could be a RBBB or it could be delayed RV depolarization due to dilation.
What is a normal QTc?
360-440ms, calculated by dividing QT by the square root of the R-R interval.
What drugs prolong the QT interval?
Anti-arrhythmics, anti-psychotics, anti-depressants (TCA), anti-fungals. Also remember non-potassium sparing diuretics inducing hypokalemia!
What EKG findings are diagnostic for RVH?
RAD in the frontal plane with R>5mm or R>S in lead V1. Also, a persistent rS pattern from V1->V6.
What does an ST elevation in the setting of acute MI denote? ST depression?
Transmural infarction. Subendocardial ischemia.
What are all the causes of ST elevation?
Acute MI, coronary vasospasm, acute pericarditis, early repolarization.
What are the evolutionary signs of a myocardial infarction?
Inversion of the T wave then formation of the pathologic Q wave 8-12 post-MI.
What are the three phases of MI and what EKG findings denote them all?
Acute MI - ST elevation +/- T-wave inversion
Recent/evolving MI - ST elevation + T-wave inversion + pathologic Q waves
Old MI - Disappearance of the ST elevation w/in 14d of the MI. Q wave stays there for life.
What are the main regular narrow-QRS complex arrhythmias?
Sinus tach, A-tach, A-flutter, AVNRT, AVRT.
What are the main irregular narrow-QRS complex arrhythmias?
MAT, A-flutter with variable conduction, A-fib
What are the main wide-QRS complex arrhythmias?
Supraventricular Tachycardia with BBB, V-tach
What is effective in treating ectopic atrial tachycardia?
Since it is precipitated by inc sympathetic tone, drugs that diminish this and slow down conduction through the AV node are effective in treatment - beta blockers.
What is the typical cause of an atrial flutter?
A re-entrant circuit completely contained within the atria, brought about by diseased dilated atrial states as in MR or MS or DCM.
What is the typical atrial rate of depolarization during flutter?
300bpm.
What is the treatment for atrial flutter?
Cardioversion for the unstable pts and some of the stables. Quinidine or amiodarone as anti-arrhythmics. BB's/CCB's as second-line therapy, to reduce the ventricular response rate to 3:1 or 4:1. NOT digoxin.
What separates AVNRT and AVRT from other narrow complex tachycardias?
No P waves.
What is the standard treatment for a first-time acute AVNRT/AVRT?
Drugs that block AV node conduction like verapamil and adenosine.
What are the side effects of amiodarone?
Pulmonary fibrosis and thyroid dysfunction.
What diseases does MAT (multifocal atrial tachycardia) frequently arise from?
Pulmonary diseases like COPD exacerbations in which sympathomimetic drugs like beta-agonists and aminophylline are used.
What is the typical ventricular rate of depolarization in atrial flutter?
150bpm. (2:1 ratio of atrial to ventricular depolarizations).
Do you see P waves on atrial fibrillation?
No, the depolarization is too unorganized to yield a P wave.
How do you use P waves to discern between the irregular narrow complex tachycardias?
Multiple different P waves -> MAT
Irregular flutter waves -> Flutter w variable conduction
No P waves -> A-Fib
What is the treatment of a ventricular arrhythmia?
If stable - anti-arrhythmics like amiodarone or lidocaine.
Unstable - synchronized cardioversion.
Pulseless - defibrillation.
What causes Torsades de Pointes?
A pt on a QT-prolonging drug experiencing a PVC at the wrong time (R-on-T phenomenon).
Where is the best place to hear physiological splitting of S2?
At the aortic/pulmonic valve sites to each side of the sternal notch/2nd intercostal space.
What does wide and fixed (not increased on inspiration) splitting of S2 denote?
An ASD.
What treatment for acute MI may be harmful in acute pericarditis?
Thrombolytics (blood thinners)- inflammation of pericardium + blood thinner can lead to a rupture of blood in the pericardium leading to tamponade.
If a patient is positive for a delta wave on EKG, what drugs could lead to life-threatening conditions if administered?
Beta-blockers and CB's, because blocking conduction down the AV node could lead to complete anterograde accessory pathway conduction.