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UWorld > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the indications for Amlodipine?

A

Amlodipine is a dihydropyridine Calcium antagonist (CCB).

First line for isolated systolic HTN (often seen in elderly)

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2
Q

What are the side effects of Amlodipine?

A

Flushing and peripheral edema

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3
Q

What are the symptoms of brachiocephalic obstruction?

A

Brachiocephalic vein drains the ipsi jugular and subclavian veins >

One sided face and arm swelling + engorgement of subcutaneous veins on that side

Much like SVC syndrome, but one-sided

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4
Q

What part of the heart is closest to the esophagus?

A

Left atrium.

  • Most of the posterior surface
  • TEE visualizes LA well
  • LA enlargement > dysphagia
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5
Q

EKG shows A-V dissociation with narrow QRS complex. What location is responsible for pacing the patient’s ventricles?

A

AV node.

Blockage between SA and AV in complete heart block. But if the QRS are narrow (normal), the AV has taken over (not the His Purkinje system, which would produce wider QRS).

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6
Q

What are fatty streaks?

A

The earliest lesion of atherosclerosis.

Lipid filled foam cells (macrophages that have engulfed lipoproteins).

Some progress to atherosclerotic plaques, but the location doesn’t predict location of atherosclerosis.

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7
Q

What are three drugs commonly used for invasive MRSA (ex. causing bacterial endocarditis)?

A

Vancomycin

Daptomycin

Linezolid

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8
Q

Which drug used to treat MRSA can cardiac side effects?

A

Daptomycin

  • Myopathy and CPK elevation
  • Also inactivated by pulm surfactant
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9
Q

What does ‘a’ indicate in the JVP?

A

R atrial contraction

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10
Q

What does ‘c’ indicate in the JVP?

A

Bulge of tricuspid into R atrium during RV contraction

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11
Q

What does ‘x’ indicate in the JVP?

A

R atrial relaxation

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12
Q

What does ‘v’ indicate in the JVP?

A

Continued venous blood (R atrium filling)

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13
Q

What does ‘y’ indicate in the JVP?

A

Passive emptying of R atrium after tricuspid valve opens

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14
Q

When does an S4 heart sound occur, and what does it indicate?

A

Right before S1.

Inidcates reduced ventricular compliance (hypertensive heart disease, aortic stenosis, hypertrophic cardiomyopathy).

This is diastolic dysfunction. Atrium is contracting against a a ventricle with reduced compliance.

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15
Q

What does an abnormal S4 sound like?

A

Low frequency, late diastolic sound (right before S1).

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16
Q

Why does mean arterial pressure only rise a little bit during strenuous exercise?

A

Adaptive decrease in systemic vascular resistance.

Exercising muscle releases local vasodilatory factors.

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17
Q

Does coronary blood flow occur during systole or diastole?

A

Diastole.

In systole, the open aortic valve partially blocks coronary blood flow.

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18
Q

What is the major side effect of drugs that relax arterioles but not veins (minidoxil and hydralazine)?

A

Sodium and fluid retention

Vasodilation > reduced arterial pressure > baroreceptors > RAAS

Causes reflex tachycardia and edema

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19
Q

What is holiday heart syndrome?

A

AFib (irregular tachyarrhythmia) precipitatied by binge alcohol.

EKG shows absent P waves because there are no coordinated atrial contrations

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20
Q

What is a drug that increases arteriolar dilation, increases renal perfusion, and promotes natriuresis?

A

Fenoldopam

  • D1 receptor agoinst
  • Improves renal perfusion and lowers BP
  • Indicated for short term management of severe HTN
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21
Q

What is the mechanism of action of nitroglycerin?

A

Dilates large VEINS, leading to decreased preload, lessening myocardial O2 demand.

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22
Q

What is a good alternative to ASA in case of allergy?

A

Clopidogrel

Antithrombotic agent that binds & irreversibly blocks the platelet surface ADP receptors needed for platelet activation

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23
Q

What is the mechanism of isoproterenol?

A

Increases cardiac contractility through action on B1 adrenergic receptors. (high doses)

Relaxation of vascular smooth muscle through action on B2 receptors. (low doses)

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24
Q

What is the most common cardiac anomaly in Turner’s Syndrome?

A

Bicuspid aortic valve.

  • May occur w aortic coarctation
  • Aortic ejection sound: early systolic, high frequency click over R 2nd intercostal space
  • Risk for stenosis, insufficiency, and infection
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25
Q

What does a tall (upsloping) left atrial ‘v’ wave during cardiac cath indicate?

A

Mitral Regurge

V wave measure atrial filling in systole.

Atrial pressure is increased if blood is entering from across the ventricle in addition to passive filling.

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26
Q

A class of medications used to treat depression cannot be taken with foods such as aged cheeses and wines, or else will cause severe hypertension and other signs of sympathetic hyperactivity.

What is this class of drugs? How do they work?

A

MAO inhibitors (traylcypromine, phenelzine)

They prevent monoamine degradation, including that of tyramine.

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27
Q

What adverse effect is associated with taking beta blocker and non-dihydropyridine CCBs (verapimil, diltiazem) together?

A

Negative chronotropy (decreased HR)

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28
Q

Cardiac assoc. with Down’s Syndrome?

A

Endocardium cushion defects:

  • ASD
  • AV valve regurge
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29
Q

Cardiac assoc. with DiGeorge?

A

Tetralogy of Fallot

Aortic arch abnormalities

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30
Q

Cardiac assoc. with Friedreich’s Ataxia?

A

Hypertrophic cardiomyopathy

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31
Q

Cardiac assoc. with Marfan’s?

A

Cystic medial necrosis of the aorta

  • Aortic dissection
  • Aortic aneurysm

Mitral valve prolapse

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32
Q

Cardiac assoc. with Tuberous Sclerosis?

A

Valvulvar obstruction due to cardiac rhabdomyomas

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33
Q

Cardiac assoc. with Turner’s Syndrome?

A

Aortic coarctation

Bicuspid aortic valve

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34
Q

Changes to myocardium 0-4hrs post MI:

A

Minimal change/none

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35
Q

Changes to myocardium 4-12hrs post MI:

A

Early coagulation necrosis
Edema
Hemorrhage
Wavy fibers

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36
Q

Changes to myocardium 12-24hrs post MI:

A

Coagulation necrosis

Marginal contraction band necrosis

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37
Q

Changes to myocardium 1-5days post MI:

A

Coagulation necrosis

Neutrophilic infiltrate

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38
Q

Changes to myocardium 5-10days post MI:

A

Macrophage phagocytosis of dead cells

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39
Q

Changes to myocardium 10-14days post MI:

A

Granulation tissue

Neovascularization

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40
Q

Changes to myocardium 2wks-2mo post MI:

A

Collagen deposits

Scar formation

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41
Q

In which types of vasculitis are giant cells found?

A

Takayasu

Giant Cell Arteritis

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42
Q

In which types of vasculitis is segmental fibrinoid necrosis found?

A

Leukocytoclastic vascultis:
-MPA, microscopic polyarteritis, hypersensitivity vasculitis

PAN

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43
Q

What are the steps in forming an atheroma?

A
  1. Endothelial cell injury
    - HTN, hyperlipidemia, smoking, diabetes, homocysteine, toxins (alcohol), viruses, immune
  2. Monocyte and lymphocyte adhesion and migration to the intima
  3. Exposure of subendothelial collages promotes platelet adhesion.
  4. Growth factors from monocytes and platelets stimulate medial smooth muscle cell migration and proliferation in the intima
  5. Increased endothelial cell permeability allows LDL cholesterol into the intima, where it accumulates in macrophages and SMCs to produce foam cells
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44
Q

What are the sequelae of severe aortic stenosis?

A
  1. Impaired LV output
  2. LV hypertrophy
  3. Atrial contraction necessary to fill LV

AFib!

  • Reduced LV filling >
  • Hypotension &
  • Pulm edema
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45
Q

What type of cell responds to endothelial injury through fibrosis?

A

Smooth muscle cells

  • Reactive cells that migrate from the media to the intima
  • Produce collagen
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46
Q

When there is a PE, what do you expect to find in terms of:

  • pH
  • PaO2
  • PaCO2
  • Plasma HCO3-
A

Respiratory alkalosis (hyperventilation)

  • pH: high
  • PaO2: low
  • PaCO2: low
  • Plasma HCO3-: normal or low to compensate
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47
Q

What are the effects of dobutamine?

A

Dobutamine is a selective B1 agonist:

  • Increases HR (chronotrophy
  • Increases conduction velocity (inotropy)
  • Increases myocardial O2 consumption because of positive inotropy
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48
Q

What type of nitrate has the highest oral bioavailability?

A

Isosorbide mononitrate (metab in the liver)

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49
Q

In what form are each of the following nitrates administered?

NTG
Isosorbide dinitrate
Isosorbide mononitrate
Amyl nitrate
Sodium nitroprusside
A

NTG: sublingual
Isosorbide dinitrate: PO, but parent compound to mono
Isosorbide mononitrate: PO, metab in liver
Amyl nitrate: inhalant
Sodium nitroprusside: IV

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50
Q

What is statin myopathy?

A

Statins are lipid lowering agents commonly prescribed after MI because they lessen incidence of 2nd MI.

Myalgia occurs at lower doses of statins.

Myopathy including elevated creatinine kinase occurs at higher doses.

Myopathy increased when fibrates and/or niacin are used at same time.

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51
Q

Is nifedipine useful in brady or tachycardia?

A

Bradycardia.

Nifedipine causes peripheral vasodilation (and has minimal effect on AV conduction).

Vasodilation results in reflex tachycardia.

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52
Q

What is normal P in RA?

A

0-8

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53
Q

What is normal P in the RV

A

4-25

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54
Q

What is normal P in the PA

A

9-25

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55
Q

What is normal P in the LA?

A

2-12

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56
Q

What is normal P in the LV?

A

9-130

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57
Q

What is normal P in the aorta?

A

70-130

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58
Q

What is nonbacterial thrombotic endocarditis?

A

NBTE is small, sterile, non-destructive, fibrinous cardiac valve vegetations that often involve a hypercoagulable state.

  • May be the result of procoagulants circulating as products of a cancer
  • Strong association with adenocarcinomas of the pancreas and lung
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59
Q

What causes coronary sinus dilation?

A

Coronary sinus is the confluence of deoxygenated blood that has supplied the heart and drains into the RA.

Anything dilating the RA will dilate the sinus.
- Most common = pulmonary HTN

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60
Q

What organs are associated with vessel damage from PAN?

A

Kidneys
Liver
GI
Heart

NOT lungs

Think: what parts of an animal can be eaten? What would you cook in the PAN? Kidney, liver, intestines, and heart, but NOT LUNGS

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61
Q

What is the conduction velocity of the various cardiac tissues?

A

Fast > Slow =

Purkinje > Atrial Muscle > Ventricular Muscle > AV node

Mnemonic: Park at Ventura Avenue

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62
Q

What are 2 formulas to calculate cardiac output?

A

CO = SV x HR

CO = O2 consumption/arteriovenous O2 difference

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63
Q

What maneuvers increase the murmur associated with left ventricular outflow tract (LVOT) obstruction?

A

Sudden standing, Valsalva, or NTG will decrease preload, thereby decreasing chamber size, increasing the LVOT, and increasing the murmur

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64
Q

What maneuver decrease the murmur associated with LVOT obstruction?

A

Sustained hand grip or passive leg raise increase preload, thereby increasing chamber size, decreasing the LVOT and the murmur

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65
Q

What is hyperplastic arteriosclerosis?

A

Result of malignant hypertension.

Onion-like concentric thickening of arteriolar walls.

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66
Q

What is hyaline arteriosclerosis?

A

Associated with low level HTN.

Homogenous, acellular thickening of arteriolar walls.

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67
Q

When does ventricular free wall rupture generally occur after an MI?

A

3-7 days after, when coagulative necrosis, neutrophilic infiltration, and enzymatic degradation of connective tissue have weakened the infarcted myocardium

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68
Q

What is the most common cause of in-hospital death due to MI?

A

LV failure/cardiogenic shock

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69
Q

What is pulsus paradoxus?

A

Defined by decrease in systolic BP of > 10 mmHg with inspiration

Occurs in the setting of acute cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, and restrictive cardiomyopathy

Path:

  • More volume returns to the R heart with inspiration
  • If the heart can’t expand more (restriction) the BP falls
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70
Q

This triad of symptoms:

  • Hypotension
  • JVD (or distended neck veins)
  • Distant/muffled heart sounds

indicates…?

A

Cardiac Tamponade

(beck’s triad)

Other sx:

  • Tachycardia
  • Pulsus Paradoxus (drop of BP > 10 on inspiration)
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71
Q

What are the changes in preload and afterload expected in the case of an AV fistula?

A

Communication between the arterial and venous systems causes blood to rush from A to V.

  • Increased preload (more volume in the venous bed)
  • Decreased afterload (less resistance in the arterial bed)

On a PV loop, this would cause a wider, shorter box.

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72
Q

What are the 3 major cyanotic heart diseases that can be caused by abnormal migration of neural crest cells through the primitive truncus ateriosus and bulbus cordis?

A

Tetralogy
TGA
Truncus Arteriosus

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73
Q

What is the effect of dopamine (on the kidney and heart) at low, medium, and high doses?

A

Low: stimulate D1 receptors in renal and mesenteric vasculature > vasodilation and increased blood flow

Medium: stimulate B1 receptors in the heart > increased cardiac contractility

High: stimulate a1 receptors > vasoconstriction

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74
Q

What is indicated by a mid-systolic click followed by a murmur during systole?

A

Mitral valve prolapse

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75
Q

What are the main causes of mitral valve prolapse?

A

Myxomatous degeneration

Some connective tissue disorders:

  • Marfan’s
  • Ehler Danlos
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76
Q

What does a prolonged QT indicate in terms of the cardiac action potential (what phase and channels are affected)?

A

QT corresponds to ventricular repolarization
This is phase 3, marked by K+ efflux

Class III antiarrythmics (and Sotalol, a beta blocker with III activity) can cause this effect.

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77
Q

What is a strawberry hemangioma and what is it’s natural progression?

A

Unencapsulated aggregate of closely packed blood vessels, common in children

Will increase in size as the child grows and usually regress spontaneously between 1-3 years of age, completely gone by age 7

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78
Q

What do siderophages indicate?

A

Siderophages are macrophages that have ingested hemosiderin, leaked from erythrocytes in a pulmonary capillary bed

They indicate pulmonary congestion and edema, consistent with chronic left sided heart failure

Test: hemosiderin turns blue with Prussian blue stain

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79
Q

What are the most lethal arrhythmias in patients with acute MI?

A

Vtach and Vfib

Atrial flutter and fib do not result in sudden cardiac death

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80
Q

What is the mechanism of nitrates?

A

Conversion into NO at vascular smooth muscle cell
Stimulates guanylate cyclase to convert CTP to CGMP
Increased cGMP
Decreased Ca
Decreased myosin light chain kinase
Myosin dephosphorylation
Smooth muscle relaxation

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81
Q

What is indicated by a holosystolic murmur best heard at the apex of the heart and radiating to the axilla?

A

Mitral regurge

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82
Q

What indicates the severity of mitral regurge?

A

High regurge and left ventricular volume overload is marked by a left-sided S3 gallop

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83
Q

A child has severe chest pain and is diagnosed with MI. Labs show increased serum methionine. What is the condition?

A

Homocystinuria

Homocysteine cannot be converted to cysteine because of a complete lack of cystathione beta synthetase.

Homocysteine comes from methionine, so both of these build up.

Sx: premature atherosclerosis, lens subluxation, osteoporosis, mental retardation

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84
Q

What is the treatment for prosthetic valve endocarditis?

A

Staph epidermiditis is the most common pathogen.

Assume it is methicillin resistant –> Vancomycin.

If it’s not resistant, nafcillin or oxacillin. Few strains are susceptible to penicilin!

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85
Q

Where are the leads placed on a 2 lead pacemaker?

A

Right atrium, right ventricle

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86
Q

Where are the leads placed on a 3 lead pacemaker?

A

RA, RV, and the LV lead in a “biventricular” pacemaker goes through the coronary sinus to rest in the atrioventricular groove.

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87
Q

What is the most common cardiac neoplasm?

A

Myxoma

  • Most commonly in the LA
  • Scattered cells within a mucopolysaccharide stroma
  • Abnormal bvs and hemorrhage
  • Produce VEGF –> angiogenesis
  • Produce IL-6 –> weight loss, fever
  • Look gelatinous, pedunculated, large
  • Present with emboli or CV sx secondary to valve obstruction by the myxoma
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88
Q

How do Class IA antiarrhythmics change the AP?

A

Phase 0 inhibition: intermediate

Length of AP: prolonged

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89
Q

How do class IB antiarrhythmics change the AP?

A

Phase 0 inhibition: weak

Length of AP: shortened

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90
Q

How do class IC antiarrhythmics change the AP?

A

Phase 0 inhibition: strong

Length of AP: no change

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91
Q

What does S4 sound like?

A

Low frequency sound heard at the end of diastole, just before S1

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92
Q

What conditions is S4 associated with?

A

S4 is the atrial kick, so it is due to decreased left ventricular compliance:

  • Restrictive cardiomyopathy
  • LVH
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93
Q

What is the sodium channel binding strength of Class I antiarrhythmics?

A

IC > IA > IB

This reflects “use dependence,” the idea that higher rates of depolarization lead to increased sodium channel blockade due to the channels spending less time in the resting state.

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94
Q

What is the differential for holsystolic murmurs?

A

Mitral regurge
Tricuspid regurge
VSD

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95
Q

A holosystolic murmur that increases with inspiration is likely:

A

Tricuspid regurge

  • Increased venous return during inspiration
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96
Q

A tricuspid regurge murmur is best heard in what location of the heart?

A

Left lower sternal border

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97
Q

A mitral regurge murmur is best heart in what location of the heart?

A

Apex, best heard in left lateral decubitus

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98
Q

What is the pattern of mitral stenosis murmur?

A

Mid-DIASTOLIC, low pitched murmur that starts after S2 and ends before S1

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99
Q

What is the pattern of aortic stenosis murmur?

A

Mid-SYSTOLIC ejection murmur that starts after S1 and ends before S2. Crescendo-decrescendo pattern.

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100
Q

What is the pattern of pulmonic regurge murmur?

A

Early diastolic murmur.
Crescendo-decrescendo config. May increase in intensity during inspiration.
High-pitched blowing sound over 2nd and 3rd intercostal spaces.

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101
Q

What does deficiency of LPL cause?

A

Familial chylomicronemia

  • LPL binds chylomicrons and releases FFAs into tissues
  • Without LPL, body cannot hydrolyze chylomicrons or release lipid loads

Symptoms:

  • Acute pancreatitis
  • Lipemia retinalis (milky retinal vasculature)
  • Eruptive xanthomas
  • Not at increased risk for premature CAD!
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102
Q

What does deficiency/defects of LDL receptor cause?

A

Familial hypercholesterolemia

  • Defects in LDL receptor or its ApoB-100 ligand
  • Super elevated LDL

Sx:

  • Ischemic chest pain
  • Tendon xanthomas
  • Xanthalesmas
  • High risk for accelrated CAD
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103
Q

What pathologic processes are associated with an S3?

A
  1. Forceful, rapid filling of ventricle that has normal or elevated compliance
  2. Normal or even decreased filling rate when ventricular compliance is low
  3. Blood flowing into an overfilled ventricle with high end-systolic volume

Basically, associated with left ventricular systolic failure.

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104
Q

What is a contraindication for ACEI?

A

Bilateral renal artery stenosis or unilateral with only 1 fx kidney

  • Need ACE mediated efferent arteriolar constriction to maintain renal perfusion and GFR
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105
Q

What are the signs of Digitalis toxicity?

A

Hyperkalemia

Bradycardia

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106
Q

What is the Kussmaul sign?

A

JVP usually drops during inspiration, but it rises paradoxically in patients with constrictive pericarditis.

This is because the volume-restricted Rv is unable to accommodate the inspiratory increase in venous return.

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107
Q

What is a side effect of varicose veins?

A

Skin ulcerations!

Also painful thromboses, stasis dermatitis, poor wound healing, superficial infections

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108
Q

What is phelgmasia alba dolens?

A

“Painful white leg” or “milk leg” result of iliofemoral venous thrombosis

  • Occurs in peripartum women
  • Pregnancy predisposes to DVT because of pressure of the gravid uterus on deep pelvic veins
  • Also increased hyeprcoagulability
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109
Q

What is the greatest risk factor for aortic dissection?

A

Hypertension is the single most important risk factor for the development of intimal tears leading to aortic dissection.

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110
Q

What is the genetic cause of HCM?

A

AD mutations in cardiac sarcomere proteins
- Mostly a single point missense mutation in the genes for beta-myosin heavy chain.

The dystrophin gene is associated with DCM.

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111
Q

What are signs specific to left heart failure?

A

Orthopnea
- Supine dyspnea relieved by sitting up (Because of lung congestion)

Productive cough, wheezing, chest tightness (nonspecific)

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112
Q

What are signs specific to right heart failure?

A

Bilateral lower extremity edema

Congestive hepatomegaly

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113
Q

What kind of drug is dofetilide?

A

Class III antiarrhythmic that blocks K efflux from cardiac myocytes and prolongs phase 3 of the mycoyte AP

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114
Q

In AFib, what determines the number of atrial impulses that reach the ventricle?

A

AV node refractory period

In AFib, the AV node is stimulated a lot. Each time it’s excited, it enters a refractory period in which additional atrial impulses are not transmitted to the ventricles. So the majority of atrial impulses do not reach the ventricles.

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115
Q

What does the PR interval on the EKG correspond to in terms of depolarization?

A

The time between atrial depolarization and ventricular depolarization.

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116
Q

How do beta blockers affect the EKG?

A

They prolong the PR interval because they slow AV conduction (increasing the time between atrial depol and ventricular depol).

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117
Q

What is the most common cause of death in acute rheumatic fever?

A

Severe myocarditis.

Death due to ARF is rare.

  • ARF occurs 10 days - 6 weeks post Strep pharyngitis
  • 3% of patients get ARF
  • 1% of those with ARF die from it
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118
Q

What are 3 factors that distinguish heart circulation from blood flow to skeletal muscle and viscera?

A
  1. Volume: heart muscle consumes 5% of cardiac output (a lot!)
  2. Local regulation by metabolic factors (like hypoxia and adenosine)
  3. Diastolic perfusion

VoLoDiasto

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119
Q

What does pulsus alternans indicate?

A

Left ventricular dysfunction

Beat to beat variation in the magnitude of pulse pressure

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120
Q

What does dicrotic pulse indicate?

A

Severe systolic dysfunction

The pulse has two distinct peaks, one during systole, another during diastole

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121
Q

What does pulsus parvus et tardus indicate?

A

Aortic stenosis

Pulse of low magnitude with delayed peak

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122
Q

What does a hyperkinetic pulse indicate?

A

Rapid ejection of large stroke volume against decreased afterload

  • Exercise in normal subjects
  • High output conditions (PDA, AV fistula)
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123
Q

What is pulsus paradoxus associated with?

A

Cardiac tamponade

Decrease in systolic BP of 10mmHg or more during inspiration

(Radial pulse disappears on inspiration)

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124
Q

What is the effect of nitroprusside?

A

Balanced venous and arterial vasodilator

  • Decreases preload
  • Decreases afterload
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125
Q

What kind of study simultaneously measures exposure and outcome?

A

Cross sectional

“snapshot”

126
Q

What is indicated with mycocytes of the cardiac ventricles express mRNA for natriuretic peptides generally made by the atria?

A

Hypertrophy

  • Ventricular hypertrophy means not only morphological changes but also changes in gene transcription
  • Volume overload increases release of ANP (usually atria, now also ventricles) and BNP (usually ventricles)
127
Q

Describe LVEDP, LVEDV, and EF in diastolic heart failure.

A 
LVEDP = increased
LVEDV = normal
EF = normal

Diastolic failure is due to decreased ventricular compliance, so pressure has to increase more to maintain EF.

128
Q

Describe LVEDP, LVEDV, and EF in systolic heart failure.

A 
LVEDP = increased
LVEDV = increased
EF = decreased

Systolic failure is due to impaired contractility, so pressure and volume must both rise to improve stroke volume.

129
Q

What is the cause of endocarditis caused by gram + cocci that are catalase - and able to grow in hypertonic saline and bile?

What procedure is this associated with?

A

Enterococcus

Cytoscopy (gut colonizers)

130
Q

What type of cell provides the major proliferative stimuli for the cellular components of atherosclerotic plaques?

A

Platelets

- Release of PDGF promotes migration of SMCs from media to intima and their subsequent proliferation

131
Q

What type of heart medication has been shown to slow the progression of heart failure and lessen all-cause mortality in CHF?

A

Beta blockers, esp. Carvedilol (B1, B2, a1)

  • Decrease cardiac work by slowing ventricular rate and decreasing afterlodad
132
Q

What medication used to treat PAD inhibits platelet aggregation and directly dilates arteries?

A

Cilostazol

  • Decreases activity of platelet PDE
  • Also direct ation
133
Q

What substance causes the cutaneous flushing associated with niacin treatment?

A

Prostaglandins

Can be prevented by ASA pretreatment

134
Q

What tumor marker is liver angiosarcoma associated with?

A

CD 31, an endothelial cell marker

CD21 is PECAM1 (platelet endothelial cell adhesion molecule)

135
Q

What do myxamatous changes in large arteries predispose?

A

These are found in cystic medial degeneration

Predisposes to development of aortic dissection and aneurysms

136
Q

What valve is associated with LVOT in HCM?

A

Mitral valve

  • Abnormal systolic anterior motion of the anterior leaflet of the mitral valve towards the hypertrophied IV septum
137
Q

What vessels does atherosclerosis most commonly affect?

A

Abdominal aorta > coronary arteries > popliteal arteries > internal carotid arteries > Circle of Willis

138
Q

What other symptom is congenital long QT usually associated with?

A

Neurosensory deafness (congenital)

Jervell and LAnge-Nielsen syndrome is one of the most common congenital long-QT syndromes.
- AR condition

139
Q

What chamber/part of the heart is most affected in DCM?

A

Left ventricle becomes dilated

140
Q

What chamber/part of the heart is most affected in HCM?

A

Asymmetrical septal hypertrophy is common, and may lead to LVOT

141
Q

What underlying condition is indicated by signs of renal failure, toe gangrene, or livedo reticularis following an invasive vascular procedure?

A

Atherosclerotic renal disease

- Light microscopy shows cholesterol emboli obstructing renal arterioles

142
Q

What pattern is indicated by polymorphic QRS complexes that change in amplitude and cycle length?

A

Torsades

143
Q

What drugs cause Torsades?

A

Antiarrhythmics

  • Disopyramide, Quinidine, Procainamide
  • Ibutilide, dofetilide
  • Sotalol

Also phenothiazines and TCAs

144
Q

What is a diastolic, low frequency heart sound heard in patients with heart failure?

A

S3, signifying LV systolic failure or restrictive cardiomyopathy

145
Q

What does S3 indicate?

A

Low frequency heart sound heard just after S2

  • Physiologic in young people
  • Pathologic in older adults, indicating LV systolic failure or restrictive cardiomyopathy
146
Q

Where is type 1 collagen found?

A

bONE, dermis, tendons, ligaments, dentin, cornea, bvs, scar tissue (including heart!)

assoc. disease: osteogenesis imperfecta

147
Q

Where is type 2 collagen found?

A

cartilage, vitreous humor, nucleus pulopsus

148
Q

Where is type 3 collagen found?

A

skin, lungs, intestines, bvs, bone marrow, lymphatics, granulation tissue

assoc. disease: Ehlers-Danlos

149
Q

Where is type 4 collagen found?

A

basement membrane

assoc. disease: Alport Syndrome

150
Q

What is the vascular derivative of the FIRST aortic arch?

A

Part of the Maxillary artery

151
Q

What is the vascular derivative of the SECOND aortic arch?

A

Hyoid artery

Stapedial artery

152
Q

What is the vascular derivative of the THIRD aortic arch?

A

Common Carotid

proximal Internal Carotid

153
Q

What is the vascular derivative of the FOURTH aortic arch?

A

(L) Aortic Arch

(R) proximal Right Subclavian artery

154
Q

What is the vascular derivative of the SIXTH aortic arch?

A

proximal Pulmonary Arteries

(L) Ductus Arteriosus

155
Q

Mnemonic for aortic arch vascular derivatives:

A

Max’s Helped Saved Carrie In Archery–the Sub Put Down!

1- Maxillary
2- Hyoid, Stapedial
3- Common Carotid, prox. Internal Carotid
4- Aortic Arch, prox. R Subclavian
5- prox. Pulmonary, Ductus Arteriosus
156
Q

What changes in the heart are associated with normal aging?

A
  • Decreased LV chamber size
  • Sigmoid shape of ventricular septum
  • Increased interstitial connective tissue
  • Lipofuscin pigment
157
Q

What is the cause of diGeorge Syndrome?

A

Maldevelopment of 3rd and 4th branchial pouches (due to a deletion on chr. 22)

158
Q

What heart defect causes wide, fixed splitting of S2 that does not change with respiration?

A

ASD

159
Q

What receptors does NE stimulate?

What are the effects of each?

A

a1: (Gq, increased IP3)
- peripheral vasoconstriction

a2: (Gi, decreased cAMP)
- decreased release of NE, insulin

b1: (Gs, increased cAMP)
- increased contractility

no effect on b2 (Gs), bronchodil.

160
Q

What causes the myocardial cell size increase that results from ischemia?

A

Intracellular Ca accumulation, because the solute draws free water into the cell, causing mitochondria to swell

161
Q

How do you calculate the number needed to treat?

A

NNT = 1/absolute risk reduction

ARR = event rate in group A - B

162
Q

What the drug of choice to treat PSVT?

A

Adenosine: rapid acting antiarrhythmic that quickly converts people out of PVST
- Half life of

163
Q

What are the side effects of adenosine?

A

Chest burning from bronchospasm
Flushing
High grade block

This drug is used for chemical stress tests.

164
Q

What is is a side effect of PDE inhibitors (like Milrinone)?

A

Vasodilation

  • PDE-Is stop the metab of cAMP
  • More Ca, more force of contraction

-More cAMP in vascular smooth muscle causes vasodilation

165
Q

What adult structure is derived from the common cardinal veins, and where is it located?

A

SVC, located to the right of the heart, posterolateral to the ascending aorta

166
Q

What is Osler-Weber-Rendu Syndrome?

A

Hereditary hemorrhagic telangiectasias

  • AD condition
  • Telangectasias in skin and mucous membranes of lips, oronasopharynx, respiratory tract, GI tract, and urinary tract
  • Rupture causes epistaxis, GI bleed, hematuria
167
Q

What is Sturge-Weber syndrome?

A

Encephalotrigeminal angiomatosis

  • Congenital neurocutaneous disorder
  • Cutaneous facial angiomas and leptomeningeal angiomas
  • Assoc. with mental retardation, seizures, hemiplegia, skull radiopacities
  • Skull radiograph shows tram track calcifications
168
Q

Are these CYP inducers or inhibitors?

Carbamazepine
Phenobarbital
Phenytoin
Rifampin
Griseofulvin
A

Inducers

- Decreased levels of other drugs using CYP system

169
Q

Are these cYP inducers or inhibitors?

Cimetidine
Cipro
Erythromycin
Azoles
Grapefruit juice
Isoniazid
Ritonavir (protease inhibitors)
A

Inhibitors
- Increase levels of other drugs using CYP system

Ex. Erythromycin + statin = increased statin = myopathy and rhabdo, possible renal failure

170
Q

What nerve carries afferent fibers from carotid sinus baroreceptors?

A

Glossopharyngeal (CN IX)

171
Q

What nerve carries afferent fibers from aortic arch baroreceptors?

A

Vagus (CN X)

172
Q

What type of cell is tryptase released from?

A

Tryptase is released from mast cells during degranulation (along with histamine)

173
Q

What aggregates in isolated atrial amyloidosis?

A

Deposition of ANP-derived proteins

Incidence of IAA increases with age, and is a form of senile cardiac amyloidosis

Risk of AFib

174
Q

What is Ebstein’s anomaly?

A

Apical displacement of the tricuspid valve leaflets

Decreased RV volume

Atrialization of the RV

175
Q

What maternal disorder is associated with Ebstein’s anomaly?

A

Bipolar disorder or other conditions associated with Lithium

176
Q

What does differential cyanosis restricted to the lower body in a child suggest in terms of congenital cardiac anomalies?

A

PDA

  • Late onset reversal of shunt flow (L to R goes R to L)
  • Lower body gets deoxy blood
  • Limits exercise tolerance but does not cause total cyanosis
177
Q

What murmur is best heard at the left sternal border with the patient leaning forward?

A

AR, because it brings the valve close to the chest wall, and is loudest at end-expiration

  • Early diastolic
  • High-pitched
  • Blowing
  • Descrescendo
178
Q

How does digoxin contribute to decreased HR?

A

Increases parasympathetic tone by action on the vagus nerve.

This causes decreased AV conduction.

179
Q

How does digoxin increase cardiac contractility?

A

Blocks the Na/K ATPase in cardiac myocytes, icnreasing intracellular Ca concentration

180
Q

What other arterial defect may aortic coarctation be associated with?

A

berry aneurysm

181
Q

What does the vascular endothelium secrete to inhibit platelet aggregation?

A

Prostacyclin (balances out TXA2)

182
Q

What is the most common cardiac abnormality predisposing to native valve bacterial endocarditis?

A

MVP

2nd is rheumatic valve dsiease

183
Q

An ASD is closed to prevent damage to what part of the heart?

A

The pulmonary vessels

- Can become very sclerosis because of the increased vol and pressure coming from extra blood shunted L to R

184
Q

Bicuspid aortic valve are associated with accelerated onset of…

A

Calcific stenosis.

Begins int he 6th decade vs. 8th for gen pop.

185
Q

What kind of hypertrophy results from long term hemodynamic compensation for aortic regurge?

A

Eccentric LV hypertrophy

NOT concentric! Which is a response to pressure overload, whereas this is volume.

Aortic regurge causes increase in LV preload.

186
Q

What vasculitis is associated with Hep B?

A

PAN

187
Q

What type of vascular damage is a finding of PAN?

A

Fibrinoid necrosis

188
Q

How does NO cause vasodilation?

A

Stimuli:

  • Ach on muscarinic receptors on endothelial cells
  • Also: bradykinin, substance P, serotonin, shear stress
NO synthase activated (eNOS) >
Converts arginine (+ NADPH, O2) to NO >
NO release into adjacent smooth muscle >
Increased GC > cGMP> PKG >
DECREASED Ca in cytosol >
Vasodilation
189
Q

How does nitroprusside cause toxicity?

A

Cyanide is a metabolite

Inhibits cytochrome c oxidase

190
Q

What are some findings of nitroprusside toxicity?

A

Bright red venous blood

Altered mental status, seizure, CV collapse, lactic acidosis

191
Q

How do you treat nitroprusside toxicity?

A

Sodium thiosulfate, sodium nitrate, hydroxycobalamin

192
Q

How does isoproterenol affect the heart?

A

B1 agonist: increased contractility
B2 agonist: decreased SVR

B1 > B2; no A activity

193
Q

How do appetite suppressants such fenfluramine and phentermine cause HF?

A

Increase pulmonary HTN >
Cor pulmonale >
RV hypertrophy >
Sudden cardiac death

194
Q

What is orthopnea and what does it signify?

A

Supine dyspnea, relieved by sitting up

Specific to LH failure
Acute exacerbation of pulmonary edema, resulting from increased filling P due to redistribution of blood that had pooled in extremities

195
Q

What is the limiting factor on pulmonary blood flow?

A

The length of diastole (not pressure!)

196
Q

In A Fib, what determines the ventricular rate?

A

AV node refractory period

197
Q

What are the main side effects of Statins?

A

Remember as HMG (coA reductase)

Hepatotox

Myopathies (main)

  • Myalgia at low dose
  • Myopathy with increased creatinine kinase at high dose
  • Myopathy exacerbated by combination with Fibrates

Gestational contraindication (teratogen)

198
Q

What are some signs of hyperchylomicronemia?

A 
Milky plasma
Acute pancreatitis
Lipemia retinalis
Eruptive skin xanthomas
HSM

All due to raised TGs!

199
Q

What are some signs of hypercholesterolemia?

A

Premature CAD
Corneal arcus
Tendon xanthomas
Xanthalesmas

All due to raised LDL!

200
Q

What is the cause of hyperchylomicronemia?

A

Lack of LPL

201
Q

What is the cause of hypercholesterolemia?

A

Lack of LDL-R

202
Q

What is the marker for the substance deficient in hyperchylomycronemia?

A

ApoC-II, a marker of LPL

203
Q

What is the marker for the substance deficient in hypercholesterolemia?

A

ApoB-100, marker of LDL-R

204
Q

What is the pathogenesis of reflex tachycardia to nitrates?

A 
Nitrates vasodilate >
Relative hypotension >
Catecholamien release >
Reflex tachy >
Increased O2 demand
205
Q

What medication is administered with nitrates to prevent reflex tachycardia?

A

Beta blockers, which slow conduction through the AV node

206
Q

What cardio drugs cause long QT and are associated with Torsades?

A 
Class Ia (Na blockers)
Class III (K blockers)
- Prolong the AP duration > long QT

All are associated with Torsades except Amiodarone

207
Q

What is the MOA of calcium channel blockers?

A

Slow rate through the AV node

208
Q

Which CCB is more selective for the heart?

A

Verapimil

209
Q

Which CCB is more selective for the vessels?

A

Nifedipine

210
Q

Which CCB has equal action on heart and vessels?

A

Diltiazem

211
Q

What defect is indicated by fixed, wide splitting of S2?

A

ASD

212
Q

Oxygen deprivation for … (amount of time) causes loss of contractility during MI.

A

60s

213
Q

Ischemia of greater than … (amount of time) causes irreversible dysfunction of heart.

A

> 30 mins

214
Q

If ischemia lasts less than … (amount of time), contractility can slowly return to normal

A
215
Q

… is a segmental, thrombosing vasculitis of medium and small arteries that can extend to contiguous nerves and veins, encasing them in fibrous tissue.

A

Thromboangiitis obliterans (Beurger’s Disease)

216
Q

Who gets thromboangiitis obliterans?

A

Heavy smokers

217
Q

What is the MOA of phenoxybenzamine?

A

IRREVERSIBLE ANTAGONIST of a1 and a2 receptors

Counteracts the action of NE

218
Q

What vessels drain into the brachiocephalic vein?

A

Ipsilateral jugular and subclavian

R brachiocephalic drains R lymphatic duct

219
Q

What are the clinical findings of brachiocephalic vein obstruction?

A

Like SVC syndrome but on one side of the body

220
Q

What is the common COD in adults with aortic coarctation?

A

HTN complications

  • LV failure
  • Ruptured dissecting aortic aneurysm
  • Intercranial hemorrhage
221
Q

Patients with aortic coarctation may also have what other congenital finding?

A

Berry aneurysm

222
Q

What defect is indicated by a holosystolic murmur, loudest of the the L mid-sternal border.

A

VSD

223
Q

What hormones does the heart secrete in volume overload?

A

ANP (atria) and BNP (ventricles)

224
Q

What hormone secreted by the heart is diagnostic of CHF?

A

BNP

225
Q

In cardiac hypertrophy, the ventricles may begin producing what hormone?

A

ANP

226
Q

What is a reperfusion arrhythmia?

A

Fibrinolytics (tPA, reteplase, tenecteplase) can cause arrhythmia after lysing the clot that lead to an MI
- Benign

227
Q

The following indicate diastolic or systolic HF?

Increased LVEDP
Normal LVEDV
Normal EF

A

Diastolic

228
Q

The following indicate diastolic or systolic HF?

Increased LVEDP
Increased LVEDV
Decreased EF

A

Systolic

229
Q

(Exudate/transudate) is characterized by low protein and low LDH.

A

Transudate

230
Q

What are the causes of transudate?

A

CHF > leak from pulmonary capillaries

231
Q

What are the causes of exudate?

A

Infection, malignancy

232
Q

What are the lab findings in an exudate?

A

Pleural: serum protein > .5
Pleural: serum LDH > .6
Or, pleural LDH > 2/3 upper lim of normal

233
Q

What meds cause Torsades?

A

Antiarrhythmics:

  • Quinidine, procainimide, disopyramide (class Ia)
  • Ibutilide, dofetilide, sotalol (class III)

Phenothiazines (ex. Chlorpromazine)

Tricyclics (ex. Amitryptiline, Imipramine)

aTAC the heart not once but three times!

  • Tricyclics
  • Antiarrhythmics (Ia, III)
  • Chlorpromazine
234
Q

What is the pathogenesis of arrhythmia in Rheumatic Fever?

A

Molecular mimicry between bacterial antigens and self-antigens causes autoimmunity against cardiac tissue

235
Q

What are the JONES criteria?

A 
Joints
Heart
Nodules
Erythema Marginatum
Syndenham's Chorea
236
Q

What type of collagen is found in final healing after MI?

A

Type I

237
Q

What is the MOA of Nitroprusside?

A

Arterial and venous vasodilator

  • Decrease afterload
  • Decrease preload
  • Maintain SV
238
Q

What bacteria can cause subacute endocarditis?

A

Strep bovis

239
Q

What work up (other than cardiac) must be done with Strep bovis endocarditis?

A

GI: colon cancer seen in 25%

240
Q

What defect is associated with a continuous murmur with S2 splitting on inspiration, best heart at the left infraclavicular border?

A

PDA

241
Q

What defect is associated with a holosystolic murmur heart best at the apex, radiating to the axilla?

A

Mitral regurge

242
Q

What is the treatment for mitral regurge?

A

Arterial vasodilator

- Decreasing afterload increases forward flow

243
Q

What cells mediate vascular injury?

A

Smooth muscle cells that migrate from the media to the intima–not fibroblasts!

244
Q

ANP and NO are vasodilators that both utilize the … intracellular cascade.

A

cAMP

245
Q

ANP has receptors located…

A

on the cell surface

246
Q

NO has receptors located…

A

in the cytosol

247
Q

What is a common complication of varicose veins?

A

Venous stasis ulcers (esp. over medial malleolus)

248
Q

What type of venous thrombosis can be seen with varicose veins?

A

Superficial VT, not DVT

249
Q

What is the drug of choice to convert PSVT?

A

Adenosine

250
Q

What is the half life of adenosine?

A

10s

251
Q

What are the adverse effects of adenosine?

A

Chest burning, flushing, high grade block

252
Q

What drug is used in chemical stress tests?

A

Adenosine

253
Q

From what location is the Great Saphenous Vein grafted?

A

Medial thigh

254
Q

When prescribing nitrates, provide a drug free interval to avoid…

A

Tolerance

Usually provide interval at night when cardiac work is low

255
Q

What is the pathogenesis of pulmonary HTN due to LH disease?

A

1) Increased diastolic filling P
2) Increased LAP
3) Pulmonary venous congestion (bc they empty into LA)
4) Increased PAP
5) Vasoconstriction
6) Intimal thickening + medial hypertrophy

256
Q

What is the most important risk factor contributing to aortic dissection?

A

HTN

Also assoc. with Marfan’s

257
Q

What are risk factors for aortic aneurysm?

A

HTN, smoking, DM, syphilis

258
Q

What is the pathogenesis of aortic dissection?

A

Begins with a tear in the intima

Blood dissects through the media

259
Q

What are two arterial selective vasodilators?

A

Hydralazine and Minoxidil

260
Q

What is the MOA of arterial selective vasodilators?

A

Decreased arterial P >
Baroreceptor reflex >
Reflex tachycardia

Increased renin >
Na + H2O retention

261
Q

What is the cause of an LVOT obstruction in HCM?

A

Mitral valve moving towards hypertrophied interventricular septum

262
Q

What murmur is caused by LVOT obstruction in HCM?

A

Systolic ejection murmur

263
Q

What is the blood supply to the diaphragmatic surface of the heart?

A

Inferior wall of LV, supplied by posterior descending (branch of RCA)

264
Q

What condition(s) is associated with Berry Aneurysm?

A

Ehler-Danlos, ADPCKD

265
Q

What condition(s) is associated with Charcot Bouchard Aneurysm?

A

HTN

266
Q

What is the pathogenesis of marantic endocarditis?

A

Tumor can release pro-coag factors >

Non-bacterial thrombotic endocarditis

267
Q

What is the MOA of Milrinone?

A

PDE-I >
Increased cAMP >
Vasodilation of smooth muscle

268
Q

What is an adverse effect of Milrinone?

A

Hypotension (contraindication)

269
Q

What is the MOA of Cilostazol?

A

PDE-I AND direct arterial vasodilator

270
Q

What is the indication for Cilostazol?

A

Peripheral Arterial Disease

271
Q

What abnormality of fetal development underlies failure of the aorticopulmonary septum to spiral?

A

Failure of neural crest migration

272
Q

What cardiac abnormalities may result from failure of the aorticopulmonary septum to spiral?

A

TGA, Truncus Arteriosus, Tetralogy

273
Q

What antiarrhythmic is selective for ischemic tissue?

A

Lidocaine

274
Q

What is the MOA of Lidocaine?

A

Class IB antiarrhythmic

- Targets depolarized Na channels

275
Q

What is Beck’s Triad and what does it indicate?

A
  • Muffled heart sounds
  • Pulsus Pardoxus (drop > 10 on inspiration)
  • JVD

> Cardiac Tamponade

276
Q

Describe the tricuspid regurge murmur.

A

Holosystolic

Increased intensity with inspiration (which is not true of other holosystolic murmurs like MR, AS, VSD)

277
Q

What is the effect of DA at low doses?

A

Targets D1 R > renal and mesenteric vasodilation

278
Q

What is the effect of DA at medium doses?

A

Targets b1 R > increased contractility

279
Q

What is the effect of DA at high doses?

A

Targets a1 R > vasoconstriction

280
Q

What is the MOA of Nitroglycerine?

A

Systemic vasodilation

281
Q

How does Nitroglycerine decrease O2 consumption by the heart?

A

Decreased ventricular volume

282
Q

What is an adverse effect of Nitroglycerine?

A

Reflex tachy

283
Q

What cardiac defects are associated with DiGeorge?

A

Conotruncal deformities

  • Tetralogy
  • Truncus Arteriosus
  • Interrupted aortic arch
284
Q

What is a COX inhibitor that can prevent thromboembolic events (and how)?

A

Aspirin

Irreversible COX1 inhibition > decreased TXA2 (platelet aggregator)

285
Q

What is a COX inhibitor that can increase thromboembolic events (and how)?

A

Celecoxib

COX2 inhibition > decreased PGI2 (vasodilator, inhibitor of platelet agg)

286
Q

Catheterization of the umbilical vein in a newborn can reach the R Atrium because of…

A

a patent Ductus Venosus

  • Functions to divert blood to the IVC in fetal circ
  • Dosen’t completely close for the 1st wk
287
Q

What type of angina is indicated by coronary vasospasm at rest or at night?

A

Prinzmetal/Variant angina

288
Q

Administration of what substance can diagnosed Prinzmetal/Variant angina?

A

Ergonovine, can provoke sx

- Ergot, stimulates a-adrenergic and 5HT Rs

289
Q

What is the Rx for Prinzmetal/Variant angina?

A

Nitrates

290
Q

What substances from endothelial cells opposes TXA2?

A

PGI2

  • Vasodilation
  • Decreased platelet agg
  • Increased vascular perm
291
Q

What is a CCB used for isolated systolic HTN?

A

Amlodipine

292
Q

What growth factor is triggered by decreased PO2?

A

VEGF

293
Q

How does palpation of sensitive baroreceptors cause fainting?

A

Palpation simulates increased BP >
Increased PS and decreased S >
Bradycardia

294
Q

What is the MOA of Verapamil?

A

CCB in phase 0 and 4
Slows depol of SA + AV nodes
Slows diastolic depolarization

295
Q

Under what conditions does dystrophic calcification occur?

A

Tissue necrosis, with normal serum Ca levels

296
Q

Under what conditions does metastatic calcification occur?

A

Normal tissue, with increased serum Ca levels

297
Q

What cardiac drug limits myocardial remodeling and deterioration of ventricular contractile fx?

A

ACE-I

  • Also decreases BP
298
Q

What are the most common causes of pre-hospital deaths in MI?

A

Arrhythmia

- VTach and VFib

299
Q

What cells are responsible for wound contracture?

A

Myofibroblasts

- Decrease size of wound by gripping edges and contracting wound bed, covering newly formed tissue

300
Q

What is the term that describes one hormone allowing another to exert max effect?

A

Permissiveness

301
Q

What is an example of permissiveness?

A

Cortisol upregulates a1 so NE effect increases

302
Q

How does cocaine cause cardiac arrest?

A

B2 blockade

- Never give B blocker if cocaine intox suspected

303
Q

What hydrostatic forces lead to edema in CHF?

A

Increased venous capillary pressure

Decreased plasma oncotic pressure

304
Q

What compensatory mechanism prevents edema in CHF

A

Collateral lymph drainage

305
Q

Pericardial friction rub indicates…

A

Acute pericarditis

306
Q

Kussmaul’s sign, Pericardial knock, and pulsus paradoxus indicate…

A

Chronic pericarditis

307
Q

Low pitched, rumbling, diastolic murmur
Heard at apex, better in lateral decubitus
+/- Diastolic thrill at cardiac apex

A

Mitral stenosis

308
Q

What is the result of ACE-I use in pregnancy?

A

ACE-I fetopathy

  • Need AT II for normal renal development
  • Oligohydramnios > lung hypoplasia (like Potter’s)
  • Calvarium defects
309
Q

What is the pathogenesis of cough syncope?

A 
Cough >
Increase intrathoracic pressure >
Decreased venous return >
Decreased CO >
Decreased cerebral perfusion
310
Q

What is the most common cardiac anomaly predisposing to Native Valve Bacterial Endocarditis?

A

MV prolapse

  • Myxomatous degeneration
  • The major cause of mitral regurge in the US

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