Cardiology Flashcards

1
Q

What are the complications of infective endocarditis?

A

Cardiac: valvular insufficiency (common cause of death), perivalvular abscess, conduction abnormalities, mycotic aneurysm
Neurologic: embolic stroke, cerebral hemorrhage, brain abscess, acute encephalopathy or meningoencephalitis
Renal: renal infarction, glomerulonephritis, drug induced acute interstitial nephritis from therapy
MSK: vertebral osteomyelitis, septic arthritis, MSK abscess

NO chronic diarrhea or flushing.

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2
Q

What is the most common cause of mitral regurgitation?

A

Mitral valve prolapse, which occurs due to myxomatous degeneration of the mitral valve leaflet and chordae; causes a mid-systolic click followed by a mid-to-late systolic murmur

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3
Q

What is the relationship between peripheral artery disease and cardiovascular disease?

A

CVD is the major cause of morbidity and mortality in pts with PAD.
Only 1-2% of pts with PAD progress to develop critical limb ischemia with risk of limb amputation.

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4
Q

What are clues to renovascular disease/renal artery stenosis?

A

HTN related sxs:
-resistant HTN (uncontrolled despite 3-drug regimen -one being a diuretic)
-malignant HTN (w/end organ damage)
-onset of severe HTN (>180.120) after 55
-severe HTN w/ diffuse atherosclerosis
-recurrent flash pulmonary edema w/ severe HTN
Supportive evidence: physical exam (asymmetric renal size >1.5cm, abdominal bruit*), labs (unexplained rise in serum creatinine >30% after starting ACE inhibitors or ARBS, imaging results (asymmetric kidney size/unexplained atrophic kidney)
Dx: renal duplex doppler u/s, CT angio, or MR angiography

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5
Q

What is sudden cardiac death?

A

Pt w/ prior MI complicated by LV systolic dysfunction w/ ejection fractioin <30% are at increased risk of sudden cardiac death due to ventricular arrhythmia (ie ventricular tachycardia, ventricular fibrillation)
ICD indicated in pts who fail medical therapy

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6
Q

What is the most important predisposing risk factor for aortic dissection?

A

Systemic hypertension in older pts (>60)
Marfan’s in younger pts (<40)
Tx: IV beta blockers (labetalol, propranolol, esmolol) - decrease HR, SBP, and LV contractility
Hydralazine + nitroprusside can cause reflex sympathetic stimulation w/ consequent rises in HR, LV contractility, and aortic wall stress which might propagate aortic dissection.

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7
Q

What is the 4th heart sound?

A

Due to left atrial kick against stiff LV
Low frequency sound heard at the end of diastole just before S1 that is commonly associated with LVH from prolonged hypertension
Often heard during the acute phase of MI due to LV stiffening and dysfunction induced by MI

Seen in : decreased LV compliance - hypertensive heart diseae, aortic stenosis, HOCM, acute phase of MI

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8
Q

What is vasospastic angina?

A

Pathogenesis: hyper-reactivity of coronary smooth muscle
Clinical presentation: young pts (<50), smoking (minimal other CAD risk factors), recurrent chest discomfort (occurs at rest or during sleep, spontaneous resolution <15m)
Dx: ambulatory ECG - ST elevation, coronary angio - No CAD
Tx: ccb (preventive), sublingual nitro (abortive)
ASA should be avoided b/c it can inhibit prostacyclin production and worsen coronary vasospasm

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9
Q

What is non-cardiac chest pain suggestive of esophageal origin?

A

Prolonged episodes lasting more than an hour, postprandial symptoms, associated heartburn or dysphagia, and relief of pain by anti-reflux therapy

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10
Q

What is the relationship between aspirin, beta blockers, and asthma?

A

Aspirin and beta blockers are common medications that can trigger bronchoconstriction in patients with asthma.

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11
Q

What is fibromuscular dysplasia?

A

Pts to screen: women age <50 w/ 1 of the following - severe or resistent HTN, onset of HTN before age 35, sudden increase in BP from baseline, increase in cr >0.5-1 after starting ACE inhibitor or ARB and w/o significant effect on blood pressure, systolic -diastolic epigastric bruit
Presentation: resistent HTN, sxs of brain ischemia, carotid or vertebral artery involvement (HA, pulsatile tinnitus, dizziness)
Dx and f/u: ct angio, duplex us, BP and cr f/u, renal us q6-12mo

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12
Q

What is the association between AR and LV volume?

A

In severe, chronic AR, the LV responds to volume overload with eccentric hypertrophy to increase both LV compliance and contractility, allowing for an increase in SV to maintain CO.
This allows for a temporary asymptomatic period.
Overwhelming wall stress eventually leads to symptomatic, decompensated heart failure.

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13
Q

What is beta blocker poisoning?

Beta adrenergic agonists - cause bronchoDILATION

Dobutamine is an inotropic agent that can cause significant vasodilation and worsen hypotenson. Not recommended in this setting.

A

Presents with bradycardia, hypotension, wheezing, hypoglycemia, delirium, seizures, and cardiogenic shock.
Tx: IV fluids and atropine are 1st line; IV glucagon if there is profound or refractory hypotension
Glucagon also used to treat ccb toxicity as well

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14
Q

What is heart failure with preserved ejection fraction (HFpEF)?

A

Form of diastolic heart failure; Common cause of decompensated heart failure.
Causes: LV diastolic dysfunction, valvular disease (AS/AR, MS/MR; impaired myocardial relaxation or increased LV wall stiffness (decreased compliance), leading to increased LVEDP, which is transmitted to LA and pulmonary veins and capillaries
Presentation: exertional dyspnea, orthopnea, bibasilar rales, LE edema, normal EF on echocardiography
Tx: ctrl BP and HR, address afib and myocardial iscihemia, treat volume overload w/ diuretics, exercise training/cardiac rehabilitation

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15
Q

Where does high output heart failure occur?

A

Severe anemia, hyperthyroidism, beriberi, Paget disease, and arteriovenous fistulas

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16
Q

What is alcoholic cardiomyopathy?

A

Diagnosis of exclusion in patients with dilated cardiomyopathy and history of alcohol abuse.
Presentation: dyspnea, 3rd heart sounds, bibasilar crackles, low ejection fraction
Tx: complete abstinence from alcohol use associated with improvement or normalization of LV function over time

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17
Q

What is HOCM?

A

Presentation: syncope, dyspnea, and chest pain
Due to interventricular septal hypertrophy
Primary mitral valve abnormality is presence of systolic anterior motion of mitral valve leading to anterior motion of mitral valve leaflets toward the interventricular septum
Contact b/n mitral valve and thickened septum during systole leads to LVOT obstruction
Dx: crescendo-decresendo systolic murmur along L sternal border w/o carotid radiation
Tx: BB (atenolol, metoprolol) or CCBs (verapamil)

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18
Q

What is a premature ventricular contraction?

A

QRS duration >.12s, bizarre morphology not resembling any conduction abnormality (eg BBB), T wave in opposite direction of QRS axis, compensatory pause
Tx: (for frequent symptomatic PVCs) escalating doses of BBs (metoprolol) or CCBs are 1st line

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19
Q

What is the indication for placement of an automatic implantable cardioverter-defibrillator (AICD)?

A

Recommended for primary prevention of sudden cardiac death due to ventricular arrhythmias (eg ventricular tachycardia) in pts with a LVEF =35 (and those with prior MI and LVEF <= 30.

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20
Q

What is situational syncope?

A

A form of reflex or neurally mediated syncope associated with specific triggers (eg micturition, defecation, cough)
These triggers cause an alteration in the autonomic response and can precipitate a predominant cardioinhibitory, vasodepressor, or mixed response.
-increased PNS: bradycardia, AV block, asystole
-decreased SNS: vasodilatioin, hypotension, or syncope

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21
Q

What is CHF due to LV systolic dysfunction?

A

Characterized by decreased cardiac output/index, increaed systemic vascular resistance (SVR), and an increase in LVEDV.

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22
Q

What does angiotensin II do?

A

Vasoconstriction of both the afferent and efferent glomerular arterioles, leading to an increase in renal vascular resistance and a net decrease in renal blood flow.
Preferential vasoconstriction of efferent renal arterioles, which increases intraglomerular pressure in attempt to maintain adequate GFR
Direct stimulation of Na resorption in the proximal tubules and increased secretion of aldosterone from the adrenal glands, which promotes further Na resorption in the cortical collecting tubule. Leads to decreased Na delivery to distal tubule and increase in extracellular fluid volume

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23
Q

What is aortic stenosis?

A

Common cause of angina, syncope, and HF - but these are rare until symptoms become severe
Mild to severe: early peaking systolic murmur
Severe: valve area <1cm squared
Severe AS restricts SV and leads to low pulse pressure (<25)
-delayed (slow rising) and diminished (weak) carotid pulse (“pulses parvus and tardus”),
-presence of single and soft S2,
-mid-to-late peaking systolic murmur w/ maximal intensity at 2nd ICS radiating to the carotids

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24
Q

What is cardiac tamponade?

A

Early cases due to large pericardial effusion
Presentation: recent URI, dyspnea, elevated JVP, clear lung fields
Diminished heart sounds + Inability to palpate point of maximal apical impulse = pericardial effusion; decrease in SBP>10 w/ inspiration = pulsus paradoxus
Beck’s triad: hypotension, elevated JVP, muffled heart sounds
Does not cause dramatic hypoxia
Sxs are due to an exaggerated shift of the interventricular septum toward the LV cavitiy, which reduces LV preload, stroke volume, and cardiac output.
Imaging: enlarged, globular cardiac silhouette (water bottle heart shape)
CXR: enlarged and globular cardiac silhouette (water bottle heart), clear lungs
Unable to palpate the point of maximal impulse due to large pericardial effusion
Pericardial metastasis common in lung cancer and lymphoma, rare in colon cancer
B/c R-sided heart chambers are principally affected, the lungs remain clear and there is usually no evidence of pulmonary edema (eg, orthopnea, crackles on lung auscultation)

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25
Q

What is uremic pericarditis?

A

Occurs in 6-10% of renal failure patients, typically in those w/ BUN >60mg/dl
Most pts doe not present with classic electrocardiogram changes of pericarditis (eg diffuse ST segment elevations)
Tx: hemodialysis leads to rapid resolution of chest pain and reduces size of any associated pericardial effusion

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26
Q

What is chronic venous insufficiency?

A

A common cause of LE edema.
Presentation: varicose veins, skin discoloration, and medial skin ulceration, pitting edema is most common PE finding
Initial treatment: conservative measures w/ leg elevation, exercise, and compression stockings

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27
Q

What is the indication for an exercise stress ECG?

A

It is recommended as an initial stress test for diagnosis and risk stratification of most pts with suspected stable ischemic heart disease.
Coronary angiography is performed in pts with high-risk findings on initial stress testing.

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28
Q

What is dilated cardiomyopathy?

A

Hx of URI followed by sudden onset of cardiac failure
Etiology: coxsackievirus B, parvovirus B19, HSV6, adenovirus, enterovirus
Dx: echocardiogram - dilated ventricles with diffuse hypokinesia resulting in low EF (ie systolic dysfunction)
Tx: supportive

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29
Q

What is cardiac sarcoidosis?

A

A disease of noncaseating granuloma infiltration of the myocardium.
Can result in serious arrhythmia (complete AV block*), cardiomyopathies, heart failure, and sudden cardiac death

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30
Q

What is the 3rd heart sound?

A

Due to inflow from LA striking blood already in the LV causing reverberation of blood between LV walls.
A low frequency diastolic sound heard just after S2 that is associated with LV failure.
IV diuretics provide symptomatic benefits to patients with decompensated heart failure.

Can be seen in viral myocarditis (+ pulmonary vascular congestion)

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31
Q

What is aortic regurgitation?

A

Due to aortic root dilation or congenital bicuspid valve
Produces early diastolic decrescendo murmur
It leads to increased LV end diastolic volume due to leakage of blood from the aorta back in the LV.
Presentation: wide pulse pressure, “water hammer” pulse - rapid, abrupt upstroke followed by rapid collapse of the peripheral pulse, and LV enlargement
L lateral decubitus position brings the newly enlarged LV closer to the chest wall and causes pounding sensation and increased awareness of the heartbeat

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32
Q

What is a diastolic murmur?

A

Diastolic and continuous murmurs are usually due to an underlying pathologic cause. Presence should prompt further evaluation w/ a transthoracic echocardiogram.

Midsystolic murmurs in otherwise young, asymptomatic adults are usually benign and do not require further evaluation.

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33
Q

What is atrial fibrillation?

A

Commonly caused by ectopic foci w/in the pulmonary veins.

Tx: radiofrequency ablation in the PVs

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34
Q

What is atrial flutter?

A

Commonly involves a reentrant circuit around the tricuspid annulus.

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35
Q

What is atrioventricular nodal reentry tachycardia?

A

Results from a reentrant circuit formed by 2 separate conducting pathways within the AV node.

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36
Q

What is peripartum cardiomyopathy?

A

An uncommon cause of dilated cardiomyopathy characterized by the development of heart failure during the last month of pregnancy (>36w) or w/in 5 months following delivery.
Rapid onset systolic HF (dyspnea, cough, pedal edema)
A fib with rapid ventricular rate is relatively rare in PPCM.

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37
Q

What has the greatest sensitivity for diagnosing heart failure?

A

An elevated plasma BNP level has high sensitivity (>90%) for the diagnosis of CHF.

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38
Q

What does acute limb ischemia after an MI suggest?

A

An arterial thrombus from the LV.

[Acute limb ischemia: Arterial occlusion due to: embolus from cardiac source (LA thrombus due to a fib; LV thrombus following MI), infective endocarditis (septic emboli), thrombus from prosthetic valves]

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39
Q

What is the presentation of a venous thromboembolism?

A

Warmth, erythema, swelling, and tenderness.

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40
Q

What is an abdominal aortic aneurysm?

A

Dx: preverterbral aortic calcifications on XR
Confirm with an abdominal CT scan

In pts w/ HD instability and signs and sxs consistent w/ an abdominal aortic aneursym (AAA) but w/o a known hx, a focused bedside u/s should be performed.
A CT scan is helpful in symptomatic pts who are stable, while those who are unstable w/ a known history of AAA should undergo emergent repair.

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41
Q

What is exertional syncope?

A

Portends underlying pathologic cause including ventricular arrhythmias (due to MI) and outflow tract obstruction (eg aortic stenosis, HOCM)
Presents with dyspnea on exertion, fatigue

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42
Q

What is subclavian steal syndrome?

A

Due to severe atherosclerosis of the L subclavian artery proximal to origin of vertebral artery; leads to reversal of blood flow in ipsilateral vertebral artery
L more commonly affect than the R
Presentation: ischemia in affected UE, vertebrobasilar ischemia (dizziness, ataxia, dysequilibrium)
Lower brachial SBP (>15mm Hg) in affected arm, systolic bruit in supraclavicular fossa on affected side; 4th heart sound due to LVH from systemic HTN
Dx: Dopper u/s or MRA
Tx: statins, smoking cessation, stent placement

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43
Q

What is wound dehiscence after CABG?

A

Common complication.
Presentation: sternal wound drainage
Soft tissue dehiscence occurs when superfical tissues (skin, muscle) separate. No signs of sternal instability or systemic illness. Local wound care/debridement with primary closure is indicated.
Sternal dehiscence occurs w/ separation of edges of approx. sternum, may occur w/ or w/o soft tissue dehiscence; sternal instability + nonunion = “clicking” or “rocking” on sternal palpitation. surgical emergency requiring sternal rewiring to prevent cardiac trauma
Dx: chest and sternal imaging

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44
Q

What is amyloid cardiomyopathy?

A

Should be suspected in pts w/ unexplained CHF, proteinuria, and LVH in the absence of hx of HTN.
Presentation: proteinuria (>300mg/d), nephrotic syndrome (>3.5g/d), waxy skin, anemia, easy bruising w/ ecchymosis, early satiety, enlarged tongue, peripheral or autonomic neuropathy
Increased ventricular wall thickness w/ normal or nondilated LV cavity

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45
Q

What is nitroprusside?

A

Parenteral vasodilator w/ quick onset and offset of action
Metabolized to nitric oxide and cyanide ions
Cyanide toxicity occurs in pts receiving prolonged infusion or higher doses of nitroprusside, most common in pts w/ renal insufficiency
Presentation: altered mental status, lactic acidosis, seizures, and coma

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46
Q

What is a PDA murmur?

A

Continuous flow murmur

Mildly accentuated peripheral pulses can occur

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47
Q

What are the murmurs of tetralogy of fallot?

A

Pulmonary stenosis leads to harsh, crescendo-decrescendo systolic ejection murmur over LUSB
RVH
Over-riding aorta: single S2 due to normal aortic and inaudible pulmonary component
VSD

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48
Q

Medical tx shown to improve morbidity + mortality in pts w/ known coronary artery disease.

A

ACE-i/ARBs
Aldosterone antagonists (spironolactone, eplerenone)
Beta blockers
Aspirin + p2y12 receptor blockers (clopidogrel, prasugrel, ticagrelor)
Statins

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49
Q

Perivalvular abscess.

A

Development of AV block in pt w/ infective endocarditis should raise suspicion for perivalvular abscess extending into adjacent cardiac conduction tissues.
Aortic valve endocarditis is assoc. w/ an increased risk of periannular extension of endocarditis.

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50
Q

Viridans group streptococci infectious endocarditis treatment.

A

Highly susceptible to pencillin and should be treated w/ IV aqueous penicillin G or IV ceftriaxone for 4 weeks.
Oral abx are not recommended.

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51
Q

Risk of systemic thromboembolism.

A

Warfarin or non-vit. K antagonist oral anticoagulants (eg apixaban, dabigatran, rivaroxaban) should be used to reduce the risk of systemic thromboembolism in pts w/ a fib and moderate to high risk of thromboembolic events (CHADVASC score >2).

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52
Q

Interventricular septum rupture.

A

Occurs 3-5d after an acute MI
Presentation: sudden onset cardiogenic shock w/ sudden onset hypotension, biventricular failure, VSD-new harsh holosystolic murmur w/ palpable thrill at the L sternal border
Does not cause rapid decompensation

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53
Q

What is papillary muscle rupture?

A
Occurs 3-5d after an acute MI
Leads to acute, severe MR
Presentation: sudden onset hypotension, dyspnea, pulmonary edema
Does not cause rapid decompensation 
Systolic murmur of MR is soft
There is NO palpable thrill present
54
Q

Diagnosis of aortic dissection.

A

Transesophageal echocardiogram has excellent sensitiivty and specificity for the dx of aortic dissection and is preferred diagnostic study in pts w/ hemodynamic instability or renal insufficiency.
CT angio and MR angio should be avoided in pts w/ moderate to severe kidney disease.
Antiplatelet or anticoag therapy can increase the bleeding complications assoc. w/ aortic dissection (eg hemothorax, hemopericardium, propagation of dissection).
NO FEVERS present.

55
Q

What is direct current cardioversion?

A

Energy delivery is synchronized to the QRS complex to minimize the likelihood of the shock occurring during repolarization, which can precipitate ventricular fibrillation.
Need a QRS complex present.

56
Q

Defibrillation.

A

Provides a high-energy shock at a RANDOM point in the cardiac cycle (unsynchronized shock) and is indicated in pts w/ v fib or pulseless v tach.

57
Q

What is Jervell + Lange Nielsen syndrome?

A
AD congenital long QT syndrome caused by molecular defects in K channels
Pts are at high risk of syncope, torsade de pointes, and sudden death
Tx: refraining from vigorous exercise, avoiding meds that can lengthen the QT interval, maintaining normal levels of Ca, K, + Mg
Beta blockers (propranolol) are class 2 antiarrhythmics and the TOC to blunt exertional HR and shorten the QT interval
Syptomatic pts (lightheadness, palpitations) or those w/ a hx of syncope require beta blocker tx + long-term pacemaker placement.
58
Q

Right-sided heart failure + restrictive cardiomyopathy.

A

Fatigue, exertional dyspnea, and LE swelling in the absence of pulmonary edema are consistent w/ right sided HF, the predominant manifestation of restrictive cardiomyopathy.
Amyloidosis can cause a restrictive cardiomyopathy.

59
Q

1 episode of resolved a fib.

A

“Lone AF” is occasionally used for pts w/ paroxysmal, persistent, or permanent AF w/ no evidence of cardiopulmonary or structural heart disease.
Pts w/ lone AF are generally <60y and have a CHADsVASc score of 0.
Risk of systemic embolization in pts is low and anticoag therapy is not indicated.

60
Q

Myxomas.

A

Most common primary cardiac neoplasm, usually arises in the LA.
Fragments of the tumor can dislodge and lead to systemic embolization (eg stroke, acute limb ischemia)
Tumors may cause position-dependent obstruction of the mitral valve, leading to a middiastolic murmur and sxs of decreased cardiac output (eg dyspnea, syncope)
Constitutional sxs (fever, wt loss) may be present.

61
Q

What is dobutamine?

A

A potent inotropic agent w/ a strong affinity for beta1 receptors and a weak affinity for beta2 and alpha1 receptors.
Stimulates increased myocardial contractility leading to improved ejection fraction, reduced LV end systolic volume, and symptomatic improvement of decompensated HF.
Increase in myocardial contractility allows for forward ejection of a higher volume of blood and results in decrease in LV end systolic volume.

62
Q

What is a vascular ring?

A

Congenital malformation of the great vessels that encircle and compress the trachea and/or esophagus
Respiratory symptoms incldue biphasic stridor that improves w/ neck extension
Esophageal sxs: dysphagia, vomiting, difficulty feeding
Dx: CT scan, all pts require direct laryngoscopy, bronchoscopy, and echocardiogram
Tx: surgical division of structures creating the ring

63
Q

Acute decompensated HF

A

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bibasilar crackles, hypoxemia = pulmonary edema due to acute decompensated HF
Due to LV systolic or diastolic function, uncontrolled HTN
Tx: supplemental O2, IV furosemide

64
Q

What is norepinephrine-induced vasopasm?

A

Alpha1 agonist which causes vasoconstriction
In pts w/ decreased blood flow, vasoconstriction can result in ischemia and necrosis of distal fingers and toes
Can also occur in intestines (resulting in mesenteric ischemia) or kidney (causing renal failure)

65
Q

Raynaud’s phenomenon.

A

Cause of finger ischemia that typically progresses from pallor to cyanosis to erythema.
Can be accompanied by pain and is usually due to cold exposure or stress.

66
Q

What is acute cardiac tamponade?

A

Due to rapid accumulation of a small amount of fluid w/in a stiff pericardium, causing a sudden rise in intrapericardial pressure.
Unlike subacute tamponade, the cardiac silhouette can be normal on CXR.

67
Q

Aortic rupter in collision.

A

Immediately fatal.
Rare instances: aortic rupture w/ bleeding into the L pleural space has been contained (by a hematoma) can present w/ L sided pleural effusion and hypotension.
However, it would cause hypovolemic (rather than obstructive) hypotension w/ flat (rather than distended) neck veins.

68
Q

Nitrates + CAD

A

Direct vascular smooth muscle relaxation causing systemic venodilation and an increase in peripheral venous capacitance
Primary anti-ischemic effect mediated by systemic vasodilation and decrease in cardiac preload resulting in a decrease in LV end diastolic and end systolic volume which leads to a reduction in LV systolic wall stressand a decrease in myocardial O2 demand, resulting in relief of anginal sxs
[coronary vasodilatoiin effect mechanism is not certain]

69
Q

Peripheral artery disease

A
Supervised graded exercise program is the most useful intervention to improve functional capacity and reduce symptomatic claudication in pts w/ PAD. 
Antiplatelet agents (aspirin, clopidogrel) reduce overal cardiovascular mortality. 
Lipid lowering therapy w/ statin should also be given to all pts w/ clinically significant atherosclerotic cvd.
70
Q

Right sided HF + PE

A

Chronic pulmonary emboli can lead to pulmonary HTN and subsequent right HF (cor pulmonale).
[COPD is the most common cause of cor pulmonale; distant heart sounds due to inflated lungs
Cor pulmonale = RHF from pulmonary HTN; gradual onset, but can present acutely (loud P2, tricuspid regurg, elevated JVP, peripheral edema, hepatomegaly due to hepatic congestion, ascites)]
Presentation: right-sided murmurs, elevated JVP, bilateral peripheral edema, and hepatojugular reflux
[XR: enlarged central pulmonary arteries and loss of retrosternal air space due to RVH
EKG: right axid deviation, R BBB, RAH
Right heart cath = gold standard for diagnosis; shows elevated CVP, mean arterial pressure >=25 w/o LH disease]

71
Q

IV atropine

A

Or external pacing
Indicated only for symptomatic bradycardia.
Sx include: lightheadedness, presyncope, or syncope

72
Q

What is cardiac sarcoidosis?

A

A disease of non-caseating granuloma infiltration of the myocardium.
Can result in serious arrhythmia (AV block most common), restrictive (early) + dilated (late) cardiomyopathy, valvular dysfunction, heart failure, and sudden cardiac death.
Should be suspected in any young pt (<55) w/ unexplained 2nd or 3rd heart block or when EKG changes occur in pts w/ known or suspected systemic sarcoidosis

73
Q

Ventricular aneursym post MI

A

EKG: persistent ST segment elevation after a recent MI and deep Q waves in the same leads.
Large VAs can lead to progressive LV enlargement, causing heart failure, refractory angina, vent. arrhythmias, mural thrombus w/ systemic arterial embolization or annular dilatioin w/ MR.
Dx: echocardiography

74
Q

Mitral stenosis

A

Loud S1
Commonly due to rheumatic heart disease and presents w/ gradual and progressively worsening dsypnea or orthopnea.
A fib is a common complication and can cause rapid decompensation in previously asymptomatic pts.
Longstanding mitral stenosis can cause severe LA enlargement leading to compression of recurrent laryngeal nerve to cause persistent cough or hoarse voice and elevation of the L main stem bronchus seen on CXR.

75
Q

What is sick sinus syndrome?

A

Inability of sinoatrial node to generate an adequate heart rate
Most common cause: age-related degeneration of the cardiac conduction system w/ fibrosis of the sinus node; ischemia and infiltrative cardiac disease (eg sarcoidosis, amyloidosis) are other potential causes
Exercise testing demonstrates chronotropic incompetence (inadequate heart rate response to exercise)
Mgmt: pacemaker
Once a pacemaker is placed, rate-control meds (beta blockers) can be administered in pts w/ persistent paroxysmal tachyarrhythmias

76
Q

Heart rate

A

Decreases w/ expiration

Increases w/ inspiration

77
Q

Mitral valve prolapse

A

Occurs due to myxomatous degeneration of the mitral valve leaflets and/or chordae tendinae.
Nonejection clcik w/ a mid to late systolic murmur
Third heart sound
Most common cause of chronic MR.

78
Q

Chronic heart failure

A

Meds shown to improve long-term survival in pts w/ LV systolic dysfunction: beta blockers, ACE-i, ARBs, mineralocorticoid receptor antagonists, and in AA pts a combo of hydralazine and nitrates.

79
Q

Acute heart failure + respiratory distress

A

Initial therapy of patients w/ pulmonary edema and hypoxemia due to acute decompensated heart failure includes aggressive IV diuresis, O2 supplementation, and possible assisted ventilation.

80
Q

What is vasospastic angina?

A

RF: smoking
Results from hyperreactivity of intimal smooth muscle, leading to intermittent coronary artery vasospasm.
Resolves spontaneously w/in 15min.
Commonly occurs during sleep.
CCB (diltiazem, amlodipin) cause coronary artery vasodilatioin and are the preferred treatment.

81
Q

Asprin and vasospastic angina

A

Aspirin (+statins) are standard therapy in pts w/ atherosclerotic CAD
Aspirin should be avoided in pts w/ vasospastic angina as it can inhibit prostacyclin production and worsen coronary vasospasm.
Propranolol can worsen coronary vasospasm as well.

82
Q

Acute massive pulmonary embolism

A

Hypotension and sycnope

83
Q

Recurrent cardiac ischemia (or post infarction angina)

A

Presents w/ recurrent chest pain and new or worsening EKG changes of ischemia (eg ST elevation)
Can cause ventricular tachycaredia/fibrillation, which can degenerate further into asystole.

84
Q

Right ventricular infarction post MI

A

Occurs in pts w/ acute inferior wall MI due to occlusion of the proximal R coronary artery.
Hypotension, shock, JVD, clear lung fields
EKG: either an inferior MI and/or ST elevation in leads V4R-V6R

85
Q

Ventricular aneursym post MI

A

Occurs as a late (weeks to months) complications of acute ST segment elevation
Characterized by scarred or fibrotic myocardial wall as a result of healed transmural MI
Presentation: HF, refractory angina, ventricular arrhythmias, or systemic arterial embolism due to mural thrombus formed w/in aneurysm.

86
Q

Ventricular wall rupture post MI

A

Mechanical complicatoin that usually occurs w/in 5d to 2w after an acute MI (usually anterior).
Leads to hemopericardium and eventually cardiac tamponade
Presentation: acute onset chest pain, profound shock, w/ rapid progression to pulseless electrical activity and death.

87
Q

MI tx + longterm prognosis

A

Prompt recognition and restoration of coronary blood flow w/ primary percutaneous intervention or fibrinolysis improves cardiovascular and overall long-term mortality in pt w/ ST elevation MI.

No evidence of improved long term outcomes w/ interventions aimed at decreasing cardiac afterload (nitrates, intra-aortic balloon pump)
Early use of beta blockers (w/in 24h) decreases myocardial contractility and can reduce myocardial O2 demand in MI, but immediate use of IV beta blockers (before PCI) does not improve outcomes and can exacerbate hemodynamic instability or HF.

88
Q

Alcohol + HTN

A

Excessive alcohol intake (>2 drinks/d) or binge drinking (>=5 drinks in a row) is assoc. w/ increased incidence of HTN compared to nondrinkers.

If medication for HTN is absolutely necessary CCB are preferred over beta blockers unless there are compelling indications for b (HF, axs LV dysfunction, post MI, hyperthyroidism, rate control in a fib).

89
Q

What is an arteriovenous fistula?

A

An abnormal connection between the arterial and venous systems that bypasses the capillary beds
Shunting of a large amount of blood through fistula decreases SVR, increases cardiac preload, and increases CO
Presentation: widened pulse pressure, strong peripheral arterial pulsation (eg brisk carotid upstroke), systolic murmur, tachycardia, flushed extremities
LV hypertrophies and PMI is displaced to the L
EKG: LVH
Pts have HF b/c circulation is unable to meet O2 demand of peripheral tissues

90
Q

What is septic shock?

A

A form of distributive shock
Leads to decrease in SVR (cardiac afterload) due to overal peripheral vasodilaton.
Decreased (or low normal) pulmonary cap wedge pressure due to capillary leakage, which causes decreased preload
Elevated mixed venous O2 saturation due to hyperdynamic circulatoin (as CO is increased in response to reduced SVR to maintain perfusion) w/ an inability of tissues to adequately extract O2 (may develop lactic acidosis from tissue hypoperfusions)

91
Q

Cardiogenic shock

A

Decreased cardiac contractility from LV dysfunction causing poor pump function; Low cardiac output leads to high LVEV (preload) and a compensatory increase in systemic vascular resistance (afterload)
Elevated RA pressures, PCWP due to volume overload and a compensatory elevation in SVR
Pts experience dyspnea and hypoxemia due to pulmonary edema, and lung exam reveals bilateral crackles
Decreased CO decreases tissue perfusion, which signals tissues to extract more O2 decreasing MvO2

92
Q

Neurogenic shock

A

A form of distributive shock in which CNS injury affects autonomic pathway and results in reduction in SVR.
Bradycardia is classic (impaired sympathetic response)
MvO2 is low (improved peripheral extraction due to lower flow)
No underlying infection

93
Q

Mineralocorticoid deficiency (due to primary adrenal infsufficiency)

A

A form of distributive shock that usually presents w/ hypotension from low aldosterone levels.
Pts have low SVR w/ assoc. hyperkalemia and hyponatremia

94
Q

What is mixed venous O2 saturation?

A

The percentage of O2 bound to hemoglobin in blood returning to the right side of heart.
Reflects the amount of O2 “left over” after tissues remove what they need.

95
Q

Bradyarrhythmia + syncope

A

Conduction system abnormalities, prolonged PR interval and intraventricular conduction delay (prolonged QRS complex duration) suggest bradyarrhythmia or high grade av block as cause of syncope
AV block w/ assoc. bradyarrythmia can be intermittent
Normal HR does not exlude bradyarrythmia due to intermittent nature of block

EKG findings suggesting an arrhytmia as cause of syncope: inappropriate sinus bradycardia, sinoatrial block, sinus pauses, av block, nonsustained ventricular arrhythmias, and short or prolonged QTc interval.

96
Q

HFpEF

A

Diastolic dysfunction caused by impaired myocardial relaxation or increased LV wall stiffness (decreased compliance) leading to increased LVEDP which is transmitted to the LA and pulmonary veins and capillaries = pulmonary congestion, dyspnea, and exercise intolerance.
Pt w/ HF w/ preserved ejection fraction, often due to hypertensive heart disease, have typical manifestation of CHF w/ a normal LV EF and objective evidence of diastolic dysfunction.
Impaired myocardial relaxation and/or increased LV wall stiffness leads to an increase in LVEDP.

97
Q

What is complete atrioventriciular septal defect?

A

Most common heart defect in Down Syndrome.
Clinical features: HF in early infancy, a fixed split S2 (ASD), holosytolic murmur (VSD), holosystolic apical murmur depending on degree of AV valve regurgitation, and a systolic ejection murmur due to increased pulmonary flow from the ASD.

98
Q

Diuretics and chronic venous insufficiency.

A

Likely to cause dehydration and are not recommended.

99
Q

Jugular venous pressure

A

Normal 6-8cm.

100
Q

WPW + A fib

A

Pt w/ WPW syndrome who develop a fib w/ a rapid ventricular rate should be treated w/ cardioversion or antiarrythmics such as procainamide.
AV nodal blockers such as beta blockers, calcium channel blockers, digoxin, and adenosine should be avoided as they can cause increased conduction through the accessory pathway.

101
Q

Digitalis toxicity

A

SEs: n/v/diarrhea, vision changes, arrhythmias
Pts chornically taking digoxin should have close and routine monitoring of their digoxin levels
Causes increased ectopy and increased vagal tone.
Atrial tachycardia w/ AV block occurs from the combination of these two effects, and is relatively specific for digitalis toxicity.

Digitalis toxicty does not cause atrial flutter, atrial fibrillation, Mobitz type II second degreee AV block (as this involves pathology of the conduction system below the AV node), and multifocal atrial tachycardia.

102
Q

What is peripartum cardiomyopathy?

A

Uncommon cause of dilated cardiomyopathy that develops during last month of pregnancy or w/in 5 months following delivery
dyspnea on exertion, LE edema, 3rd heart sound = decompensating HF due to PPCM
Often assoc. w/ MR (holosystolic murmur)
Dx: transthoracic echocardiogram shows dilated LV cavity w/ global systolic dysfunction and EF <45% can confirm dx
Urgent or immediate delivery should be considered for pts w/ advanced HF or hemodynamic instability.

103
Q

What is pulsus bisferiens (or biphasic pulse)?

A

Refers to 2 strong systolic peaks of the aortic pulse from the LV ejection separated by a midsystolic dip.
It can be palpated in patients w/ significant aortic regurgitation (w/ or w/o aortic stenosis), HOCM, and PDA.

104
Q

Right-side MI

A

Clear lungs on auscultation
Nitrates should be avoided as venous dilation causes an abrupt decrease in RV preload and can lead to profound hypotension; diuretics (volume depletion), opiates (venous dilation) can do this as well
To treat inadequate preload, give bolus w/ isotonic saline to increase RV preload and improve CO

Inotropic agents (dopamine, dobutamine) may be needed for RV MI pts w/ persistent hypotension despite adequate fluid resuscitation.

105
Q

Aortic coarctation

A

Narrowing of the descending aorta that leads to a proximal arterial pressure load.
Headaches, epistaxis
Pts typically present w/ upper extremity HTN and diminished femoral pulses w/ brachial femoral delay.
CXR reveals inferior notching of the 3-8th ribs due to pressure-induced enlargement of the intercostal arteries.
Can develop L-sided cardiac enlargement
Evaluate w/ simultaneous palpation of brachial and femoral pulses to asses for brachial-femoral delay
Bilateral UE (supine position) and LE (prone position) BP measurement to evaluate for U an LE BP differential
EKG shows sytemic long-standing HTN: high voltage QRS complexes, lateral ST segment depression, lateral T wave inversion
Dx: echocardiogram

106
Q

What is prominent right atrial contour?

A

Often seen in ebstein congenital abnormality (apical displacement of the tricuspid valve w/ atrialization of the RV).

107
Q

Chronic aortic regurg

A

In severe, chronic aortic regurg, the LV responds to volume overload w/ eccentric hypertrophy to increase both LV compliance and contractility, allowing for an increase in stroke volume to maintain cardiac output.
This allows for a temporary asymptomatic period.
However, overwhelming wall stress eventually leads to symptomatic, decompensated HF.

108
Q

Acute limb ischemia

A

Pain, pallor, poikilothermia (cool extremity), paresthesia, pulselessness, paralysis
Due to thromboembolic occlusion
ABI (ratio of SBP in ankle/arm) is used as a screening and/or diagnostic tool in pt w/ suspected peripheral arterial disease
Acute limb threatening complication should be treated with anticoagulation, heparin, which prevents further thrombus propagation and thrombosis in distal arterial and venous circulation

109
Q

Beta blockers and diabetes

Beta 2 actiativation increases insulin activity–> decreases glucose in the blood

A

Convential beta blockers (eg metoprolol, atenolol, propranolol) are assoc. w/ impaired glucose control and increased weight gain, likely via effects on skeletal muscle that lead to reduced insulin sensitivity.
Therefore, these drugs are an unfavorable option for HTN mgmt in pts w/ or at high risk for type 2 DM.

110
Q

Alpha blockers + DM

A

Alpha 1 stimulation causes vasocontriction which reduces glucose uptake into skeletal muscles

Alpha 2 decreases insuline release –> increased glucose levels in blood

111
Q

Temporary transvenous pacemaker

A

Can be used in pts w/ profound bradycardia
However, it fails to capture, and even adequate capture (w/ increases in HR) rarely results in improved cardiac output and BP in the setting of severe betablocker overdose.

112
Q

Hypovolemic shock

A

Loss of intravascular volume decreases LV preload which leads to decreased CO; LV, decreased in size due to low filling volume, compensates by increasing ejection fraction
Characterized by low BP and CO and a compensatory elevation in HR and SVR (in attempt to maintain CO).
Central venous pressure and pulmonary capillary wedge pressure are low due to decreased intravascular blood volume.
Cold extremities, flat neck veins

113
Q

What is constrictive pericarditis?

A

RF: prior cardiac surgery (eg CABG, cardiac valve surgery), mediastinal irradiation, tuberculosis, malignancy, or uremia
-US: idiopathic or viral pericarditis, radiation tx, cardiac surgery, connective tissue disorders
-World: TB
Important cause of R HF
Presentation: progressive peripheral edema, ascites, elevated jugular venous pressure, pericardial knock (middiastolic sound)
Kussmal’s sing: lack of typical inspiratory decline in central venous pressure
Sharp x and y descents on central venous tracing
XR: pericardial calcifications

114
Q

Aortic aneursym

A

vague chest discomfort
Most thoracic aortic aneursyms are due to age related degenerative changes that lead to disruption of the aortic medial layer, resulting in loss of elasticity and consequent aortic dilation.
XR: widened mediastinum, enlarged aortic knob, tracheal deviation

115
Q

WPW

A

Characteristic EKG findings: short PR interval (<120s), slurred initial upstroke of the QRS complex (delta wave), and widening of the QRS complex w/ ST/T wave changes.
WPW is due to an accessor pathway that bypasses the AV node and directly connects the atria to the ventricles.

116
Q

Immediate post MI period

A

Ventricular arrhythmias, including ventricular premature beats, nonsustained or sustained ventricular tachycardia, and ventricular fibrillaton are quite common in the immediate post MI period.

Ventricular fibrillation is the most frequent underlying arrhythmia responsible for sudden cardiac arrest in the setting of acute MI. More than 50% occur in the 1st hour of sx onset.
Reentry is the predominant mechanism responsible for ventricular arrhythmias in the immediate post infarction period.

117
Q

Anticoagulants + aortic dissection

A

The use of anticoagulants in pts w/ suspected aortic disessction and possible hemopericardiuim is contraindicated.

118
Q

DM + statins

A

DM pt age 40-75 should be treated w/ statin therapy in addition to lifestyle modification and glucose control.
Those w/ a 10y risk of atherosclerotic cardiovascular disease <7.5% should receive moderate intensity statin therapy.
Those w/ a risk >7.5% should receive high intensity statin therapy.

119
Q

Signs of pulmonary hypertension

A

Widely split S2, increased intensity of the pulmonic component of S2

120
Q

What is electrical alternans?

URI can lead to pericarditis. Pericarditis causes extra fluid w/in pericardial cavity and leads to pericardial effusion.

A

Electrical alternans w/ sinus tachycardia is a highly specific sign for large pericardial effusion.
This is due to the swinging motion of the heart in the pericardial cavity causing a beat to beat variation in QRS axis and amplitude.
Pt w/ cardiac tamponade and HD compromise should have emergency pericardiocentesis.

121
Q

What is supravalvular aortic stenosis?

A

The second most common type of AS, usually refers to congenital LVOT obstruction due to discrete or diffuse narrowing of ascending aorta
Causes a systolic murmur similar to that seen in AS, but murmur is heard in R 1 ICS
Pts may also have unequal carotid pulses, differential blood pressure in the UE (high pressure jet in ascending aorta) and a palpabel thrill in the suprasternal notch
LVH and coronary artery stenosis
These changes with increased in myocardial O2 demand during exercise can lead to subendocardial or myocardial ischemia leading to angina during exericse

122
Q

What is an innocent murmur?

A

Results from normal blood flow from a structurally normal heart.
The intensity is typically grade I or II and decreases w/ standing and valsalva.
Valsalva and standing - decrease venous blood return
Benign murmurs are also early or mid-systolic in timing.
Mgmt: observation and reassurance

123
Q

Initial workup for HTN

A

Pt initially dx w/ HTN should have a detailed hx and physical.
In addition, the following basic testing should be performed:
u/a for occult hematuria and urine protein/creatinine ratio
chemistry panel
lipid profile (risk stratification for CAD)
baseline EKG (to evaluate for CAD or LVH)

124
Q

Renal ultrasound and HTN

A

It can identify asymmetrical kidney size or small atrophic kidneys, which suggests primary renal disease. Dupex dopper u/s is also helpful in screening for RAS in pts w/ severe or resistant HTN.
However, these imaging studies are done only if there is elevated serum creatinine or abnormal u/a.

125
Q

Temoral arteritis

A

ESR usually >50

126
Q

Complete heart block

A

Characterized by temporal dissociation of P waves and QRS complexes (atrioventricular [AV] dissociation).
Pts w/ symptomatic 3rd degree AV block should be managed w/ temporary pacemaker insertion while undergoing further evaluation to identify and correct reversible causes.
A permanent pacemaker is indicated if no reversible causes of heart block are found.

Adenosine, beta blockers, and digoxin are contraindicated in complete heart block.

127
Q

Bacterial endocarditis

A

IV abx decrease the risk of septic emboli in pts w/ native valve infective endocarditis.
Surgery can be considered in pts w/ significant valvular dysfunction, persistent/difficult to treat infection, or recurrent embolism.

128
Q

Central venous pressure

A
The pressure in the superior vena cava (SVC) where catheter tip is located. Approximates RA pressures
Low CVP (low preload): reflects hypovolemic or distributive shock 
Elevated CVP (high preload): reflects cardiogenic or obstructive shock 
Blunt cardic injury w/ myocardial dysfunction can cuase cardiogenic shock w/ elevated CVP and refractory hypotension
129
Q

VSD

A

Small VSDs close spontaneously in 75% of children by age 2 w/ no long term sequelae.

130
Q

Carotid artery stenosis

A

symptomatic: occurence of TIA or stroke in distribution of affected artery w/in previous 6mo. Carotid endarterectomy is recommended for symptomatic pts w/ high grade carotid stenosis (70-99% for symptomatic lesions)
Asymptomatic: carotid atherosclerosis w/o recent TIA or stroke. <80; managed medically (aspirin + statins)