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Cardiology > Cardiology Combined > Flashcards

Cardiology Combined Flashcards

1
Q

Which artery supplies the SA and AV nodes?

A

RCA

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1
Q

When do coronary arteries fill?

A

During diastole

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2
Q

What inhibits the Na/K ATPase creating less extracellular Ca and more intracellular thus increasing contractility?

A

Digoxin/digitalis

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3
Q

How to calculate EF?

A

What heart can pump out over what can hold. SV/EDV.

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4
Q

2 Equations for CO

A

CO = SV X HR. CO= rate of O2 consumption / (arterial O2 - Venous O2)

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5
Q

Equation for SV

A

EDV-ESV

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6
Q

Do polycythemia, hyper proteinemic states, hereditary spherocytosis increase or decrease resistance in vessel?

A

Increase resistance because increase viscosity.

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7
Q

S3 heart sound

A

rapid ventricular filling. Dilated cardiomyopathy(ventricles) CHF, Mitral regurg, Left to right shunt.

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8
Q

S4 heart sound (right before S1)

A

High atrial pressure. LVH with atrial kick. Hypertrophic cardimyopathy, aortic stenosis, chronic HTN with LVH, after MI.

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9
Q

At Carter’s Xing Vehicles Yield

A

JVP Pulse order.

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10
Q

Normal S2 splitting happens with….

A

inspiration because it causes more venous return to right ventricle (negative pressure in chest due to diaphragm lowering) so pulmonic valve takes longer to close than aortic

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11
Q

Phase zero of cardiac action potential

A

Upstroke, voltage gated Na+ channels open. Sodium channel blockers would affect this.

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12
Q

Phase one of cardiac action potential

A

inactivation of sodium channels, K+ channels begin to open.

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13
Q

Phase 2 of cardiac action potential

A

Calcium influx through voltage gated calcium channels. Plateau.

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14
Q

Phase 3 of cardiac action potential

A

Rapid repolarization with massive efflux of K+ with opening of voltage gated slow K+ channels and closing of Ca2+ channels. Potassium channel blockers would affect this.

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15
Q

Phase 4 of cardiac action potential

A

RMP with K+ permeability.

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16
Q

Pacemaker action potential

A

Phase 4- RMP (K+ permeable). Na+ channels gradually open until threshold causes opening of voltage gated Ca2+ channels and phase 0 happens (upstroke). No plateua and now Potassium brings it back down in phase 3.

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17
Q

What inhibits phase zero of pacemaker action potential?

A

Calcium channel blockers.

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18
Q

What suppresses the slope of phase 4 in pacemaker action potential.

A

Beta blockers.

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19
Q

4 classes of antiarrhythmics

A

No Bad Boy Keeps Clean. 1- Na+, 2- Beta Blockers. 3-K+. 4- Calcium channel blockers.

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20
Q

Sodium channel blockers

A

Class 1 antiarrhythmics. Increase slope of phase 0 for cardiac action potential (sodium depolarization) so increase refractory period thus decreasing heart rate

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21
Q

Sodium channel blocker used for Wolf Parkinson White

A

Procainamide. Can cause SLE (antihistone antibodies).

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22
Q

Quinidine toxicity

A

Cinchonism (headache and tinnitus), thrombocytopenia, torsades (arrhythmia).

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23
Q

Beta blockers

A

Class 2 antiarrhythics. Suppress abnormal pacemakers by decreasing slope of phase 4 (Calcium influx).

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24
Q

Sotalol and amiodarone

A

Class 3 antiarrhythmics. Potassium channel blockers. Used for atrial fib. Amiodarone for WPW.

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25
Q

Pulmonary fibrosis, hepatotoxicity, hypo/hyperthryoidism are side effects of……

A

Amiodarone. Check PFTs, LFTs, TFTs

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26
Q

Class 3 antiarrhythmics

A

K+ channel blockers. Class 3 phase 3…. (repolarization due to K+)

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27
Q

Verapamil and diltiazem

A

Class 4 antiarrhythmics, Calcium channel blockers. Non-Dihydropyridine CCB’s. Prolong phase 0 of pacemaker cells (depolarization due to calcium).

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28
Q

Adenosine

A

Pushes K+ out of cells hyperpolarizing the cell and preventing depolarization causing flat line. Diagnose and abolish supraventricular tachycardia.

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29
Q

Conduction delay through AV node on ECG

A

PR Segment

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30
Q

Mechanical contraction of ventricles on ECG

A

QT interval

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31
Q

T wave inversion on ECG

A

Indicative of MI

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32
Q

QRS complex

A

Depolarization of ventricles. Less than 3 little boxes (120 msec).

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33
Q

Drugs which can prolong QT interval (possibly leading to torsades)

A

Macrolides (erithromycin), haloperidol and risperidone, methadone, protease inhibitors, chloroquine and primaquine, antiarrhythmics.

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34
Q

How to treat torsades

A

magnesium

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35
Q

Electrical signal not going through AV node

A

Wolf Parkinson White

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36
Q

Early ventricular depolarization with a delta wave on ECG

A

Wolf Parkinson White can lead to reentry current and supraventricular tachycardia.

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37
Q

How to treat WPW

A

Procainamide (NA channel blocker), Amiodarone (calcium channel blocker)

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38
Q

Irregularly irregular ECG with no discrete P waves how do you treat?

A

Atrial fibrillation and treat with Digoxin with beta blocker or CCB

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39
Q

Sawtooth appearance on ECG how do you treat?

A

Atrial flutter so use Na+ channel blocker or K+ channel blocker (Sotalol and amiodarone).

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40
Q

Completely erratic rhythm with no identifiable waves

A

Ventricular fibrillation. Leads to death.

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41
Q

Which baroreceptor (and which nerve is it on) responds to only increase in BP

A

Aortic arch (vagus nerve)

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42
Q

Which baroreceptor (and which nerve is it on) responds to both increase or decrease in BP

A

Carotid sinus (glossopharyngeal nerve)

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43
Q

HTN, bradycardia, respiratory depression. Also what kind of receptors are this sensed by.

A

Cushing triad due to Increased ICP sensed by CHEMORECEPTORS.

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44
Q

What releases NO which can lead to vasodilation?

A

Endothelial Cells.

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45
Q

What stimulates endothelial cells to release NO leading to vasodilation?

A

Bradykinin, Ach, alpha 2 agonist, histamine, serotonin, shear stress

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46
Q

Inhibits cGMP phosphodiesterase

A

Sildenafil. Leading to more cGMP and thus more vasodilation.

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47
Q

Which drug do you give for HTN but patient has renal stones?

A

Thiazide diuretics because thiazides retain Ca. Loops lose calcium so don’t give with renal stones.

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48
Q

Which drug increases cGMP (decreasing afterload because it works on arterioles>veins) for use for HTN in pregnancy

A

Hydralazine

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49
Q

What drug is a K+ channel opener relaxing hyperpolarizing and relaxing vascular smooth vessels for use in HTN?

A

minoxidil (hypertrichosis side effect)

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50
Q

Calcium channel blocker for use in HTN (reduces vascular smooth muscle contraction)

A

Nifedipine (verapamil and diltiazem are antiarrhythmics at the heart).

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51
Q

With smooth muscle spasm (prinzmetal’s angina, raynaud’s) what kinds of drug do you use?

A

Dihydropyridine Ca Channel Blocker (-dipines)

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52
Q

Releases NO in endothelial cells of smooth muscles (increasing cGMP) dilating veins more than arteries and decreasing preload.

A

Nitroglycerin

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53
Q

What drug can cause cyanide toxicity and vasodilates both arterioles and veins for use in malignant HTN?

A

Nitroprusside. (Labetolol also used in malignant HTN)

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54
Q

What antihypertensive drug has a first dose orthostatic hypotension?

A

Alpha Blockers (-zosins)

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55
Q

What anti-HTN drugs are ototoxic (especially with aminoglycosides)?

A

Loop Diuretics. And loops lose calcium.

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56
Q

What class of anti-HTN drugs can cause angioedema (swollen lips, eyes, face)?

A

ACE inhibitors

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57
Q

Anti HTN drugs that can result in hypercalcemia, hypokalemia?

A

Thiazide diuretics. Thiazides DON’t lose CA2+.

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58
Q

First line treatment for aortic dissection?

A

Beta blockers.

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59
Q

Tearing chest pain radiating to the back (or scapula), CXR shows mediastinum widening?

A

Aortic Dissection

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60
Q

Main risk factor for AAA?

A

Atherosclerosis of descending aorta (most common site)

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61
Q

To have angina must have narrowing of at least…..

A

75% of Coronary Artery

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62
Q

What drugs lower LDL the most?

A

HMG-CoA Reductase inhibitors (statins)

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63
Q

Side effects of statins?

A

Rhabdomyolysis (muscle breakdown), hepatotoxicity (increased LFT’s), myositis (muscle inflammation), myalgia (muscle pain)

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64
Q

What drug raises HDL the most?

A

Niacin

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65
Q

Red, flushed face, hyperglycemia, hyperuricemia side effects

A

Niacin

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66
Q

Drug that tastes really bad and lowers LDL

A

Bile acid resines(cholestyramine)

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67
Q

What drug causes liver to use more cholesterol?

A

Bile acid resins (block intestinal reabsorption of bile acids so liver must use cholesterol to make more)

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68
Q

What drug can cause cholesterol gallstones?

A

Bile acid resins

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69
Q

Which drug blocks cholesterol absorption? (Blocks at small intestine brush border.)

A

Ezetimibe.

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70
Q

Which drugs decrease triglycerides most?

A

Fibrates

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71
Q

Which drug upregulates LPL?

A

Fibrates

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72
Q

What can lead to pancreatitis?

A

Increased TG’s.

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73
Q

Which lipid lowering drug binds to C. Dificile?

A

Cholestyramine (bile acid resin)

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74
Q

How can you prevent the flushing reaction of Niacin?

A

Aspirin

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75
Q

Which anti-HTN drug can cause hyperkalemia?

A

ACE inhibitors. Don’t have us much aldosterone which helps excrete potassium.

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76
Q

Chest pain at rest (secondary to coronary artery spasm) with ST elevation on ECG?

A

Prinzmetal’s angina

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77
Q

How to treat prinzmetal’s angina?

A

Nifedipine (dihydropyridine ca channel blockers.

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78
Q

What most commonly leads to aortic dissection?

A

HTN

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79
Q

What can lead to sharp chest pain that is relieved by sitting forward?

A

Pericarditis which can be caused by Rheumatic fever among other conditions. Also fibrinous pericarditis from an MI (presents with friction rub).

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80
Q

Best treatment for angina?

A

Nitrates + Beta blockers

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81
Q

Contraction bands seen…….

A

at least 2 hours since MI.

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82
Q

What are the cells of acute inflammation in an MI (2-4 days)

A

Neutrophils

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83
Q

What kind of necrosis occurs in an MI?

A

Coagulative necrosis

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84
Q

Compression of heart by blood leaking into pericardium

A

Cardiac Tamponade.

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85
Q

Cells of inflammation in an MI 5-10 days after?

A

Macrophages come in and degrade things.

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86
Q

After 10 days from an MI at risk for……..

A

Ventricular aneurysm at bulging scar.

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87
Q

When does toponin I rise after an MI?

A

After 4 hours and elevated 7-10 days.

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88
Q

ECG changes of ST elevation can indicate what type of MI?

A

Transmural infarct

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89
Q

ECG changes of ST depression can indicate what type of MI?

A

Subendocardial infarct/

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90
Q

ECG changes of t wave inversion can indicate what type of MI?

A

Transmural infarct

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91
Q

What persists on ECG weeks after MI?

A

Q wave

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92
Q

Most specific marker of an MI (gold standard).

A

Troponin I

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93
Q

Severe MI then five days later have mitral regurg what happened?

A

Macrophages came and degraded things and we had rupture of the papillary muscle.

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94
Q

What drugs directly aid conversion of plasminogen to plasmin (which degrades fibrin)?

A

Thrombolytics. Streptokinase, Urokinase, tPA.

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95
Q

When do you use thrombolytics?

A

STEMI MI.

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96
Q

What do you treat thrombolytic toxicity?

A

Aminocaproic acid

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97
Q

What does aspirin do?

A

Irreverisbly inhibits COX-1 and COX-2 to prevent conversion of arachidonic acid to thromboxane A2 (clotting).

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98
Q

How do you treat aspirin toxicity?

A

NaHCO3

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99
Q

What do Clopidogrel and Ticlopidine do?

A

ADP receptor blockers which inhibits platelet aggregation. Inhibits figrinogen binding by preventing glycoprotein IIb/IIIa expression

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100
Q

Which drugs inhibit platelet aggregation by preventing glycoprotein IIb/IIIa expression? (what other drug also does this)

A

Clopidogrel and Ticlopidine. Abciximab is the other drug (monoclonal ab binds glycoprotein Iib/IIIa receptor).

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101
Q

Which drug inhibits platelet aggregation by binding to the glycoprotein IIb/IIIa receptor on activated platelets?

A

Abciximab

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102
Q

Balloon appearance on x ray of heart (big and circular)?

A

Dilated Cardiomyopathy.

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103
Q

Most common cause of US of myocarditis?

A

Coxsackie Virus. (also eckovirus and influenza virus)

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104
Q

Lymphocytes with myocyte necrosis?

A

Myocarditis (viral infection).

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105
Q

Cause of sudden death in young athletes?

A

Hypertrophic cardiomyopathy

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106
Q

Disoriented, tangled, hypertrophied myocardial fibers?

A

Hypertrophic cardiomyopathy

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107
Q

What can you hear with hypertrophic cardiomyopathy?

A

S4 heart sound.

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108
Q

Endomyocardial fibrosis with eosinophilic infiltrate?

A

Loffler’s Syndrome

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109
Q

How to increase contractility and cardiac output?

A

Digoxin/digitalis

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110
Q

Which artery supplies the SA and AV nodes?

A

RCA

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111
Q

Which artery supplies the inferior portion of the left ventricle and posterior septum?

A

Posterior descending (80% off the RCA, 20% off the circumflex)

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112
Q

Where does coronary artery occlusion occur most commonly?

A

LAD

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113
Q

What does the LAD supply?

A

apex and anterior interventricular septum

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114
Q

When do coronary arteries fill?

A

during diastole

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115
Q

Where is the most posterior portion of the heart and what can it cause?

A

The LA, can cause dysphagia because of compression of the esophageal nerve or hoarseness by compressing the the recurrent laryngeal nerve

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116
Q

What supplies the posterior left ventricle?

A

CFX (left circumflex coronary artery)

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117
Q

stroke volume x HR =?

A

CO

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118
Q

rate of 02 consumption/ arterial 02 - venous 02 ccontent=CO

A

fick principle

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119
Q

CO x Total peripheral resistance

A

mean arterial pressure

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120
Q

2/3 diastolic + 1/3 systolic

A

MAP

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121
Q

systolic - diastolic

A

pulse pressure

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122
Q

EDV - ESV

A

stroke volume

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123
Q

SV CAP means?

A

Stroke volume affected by contractility, afterload, and preload

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124
Q

How do catecholamines increase contractility?

A

Increasing activity of Ca pump in SR

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125
Q

What does increasing intracellular Ca do?

A

increase contractility

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126
Q

What happens with a decrease of extracellular Na

A

decrease in activity of Na/Ca exchanger and increase in contractility

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127
Q

How does digitatlis increase contractility?

A

Increase intracellular Na, resulting in increased Ca

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128
Q

How do beta blockers decrease contractility?

A

decrease in cAMP

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129
Q

Why is contractility decreased in heart failure?

A

systolic dysfunction

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130
Q

How does acidosis affect contractility?

A

decreased

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131
Q

Do dihydropyridine or non-dihyrdropyridine Ca channel blockers decrease contractility

A

Non

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132
Q

What cardiac change occurs in pregnancy?

A

increased SV

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133
Q

What 4 things drive myocardial 02 demand?

A

inc afterload, inc contractility, inc heart rate, inc heart size (inc wall tension)

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134
Q

If HR is too fast (V tach) what happens during diastole?

A

filling is incomplete and CO falls

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135
Q

EDV is also known as

A

Preload

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136
Q

MAP is also known as

A

Afterload (proportional to peripheral resistance)

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137
Q

Which class of drugs decrease preload

A

venodilators (nitrogylcerine)

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138
Q

Which class of drugs decreases afterload?

A

Vasodilators, (hydrAlAzine)

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139
Q

Exercise, overtransfusion and excitiment causes and increase in…?

A

Preload

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140
Q

What does the starling curve show?

A

changes in CO as a function of preload

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141
Q

When does EF decrease

A

in HF

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142
Q

What is the formula for EF?

A

SV/ EDV

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143
Q

What is a normal EF

A

at least 55%

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144
Q

Given P = QR, what factors influence resistance?

A

proportional to viscosity and inversely proportional to the radius to the 4th power

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145
Q

Which vessels account for the most total peripheral resistance

A

arteriorles

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146
Q

Which lab value indicates blood viscosity?

A

hematocrit

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147
Q

In what disease states is blood viscosity increased?

A

polycythemia, hyperproteinemic states (multiple myeloma), hereditary spherocytosis

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148
Q

In the cardiac and vascular function curves, in what instance is the vascular curve shifted to the left?

A

hemorrhage

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149
Q

In the cardiac and vascular function curves, in what instance is the vascular curve shifted to the right?

A

transfusion

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150
Q

What is indicated when CO and venous return are equal?

A

The operating point of the heart

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151
Q

What causes the CO curve to shift upwards?

A

pos inotropy, exercise

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152
Q

what causes the CO curve to shift downwards?

A

neg inotropy, HF, narcotic overdose

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153
Q

In the cardiac cycle, which period has the highest 02 consumption?

A

isovolumetric contraction

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154
Q

On the cardiac cycle graph, on which corners do the opening and closing of the aortic and mitral valves occur?

A

lower right, MC, upper right, AO, upper right AC, lower left MO

155
Q

What is the S1 sound?

A

mitral and tricuspid closure

156
Q

What is the S2 sound?

A

Aortic and pulmonary closing

157
Q

When and why is the S3 sound heard?

A

normal in children and pregs, assoc with inc filling pressures, early in diastole during rapid ventricular filling

158
Q

When and why do you hear the S4 sound

A

late in diastole, high atrial pressure, pushing against a stiff LV wall, associated with ventricular hypertrophy

159
Q

in the JVP, what is the a wave?

A

atrial contraction

160
Q

in the JVP, what is the c wave?

A

RV contraction (closed tricuspid valve bulging into atrium

161
Q

in the JVP, what is the v wave?

A

inc RA pressure, due to filling against closed tricupsid valve

162
Q

In normal S2 splitting, which valve closes first? What increases it?

A

the aortic before pulmonic, inspiration increases diff

163
Q

What is the association with wide S2 splitting?

A

pulmonic stenosis and RBBB

164
Q

What is association with fixed S2 splitting, does not increase with inspiration

A

ASD

165
Q

What is associated with paradoxical spliting of S2

A

Aortic stenosis or LBBB

166
Q

with what heart sounds do ASD usually present?

A

pulmonary flow murmur and diastolic rumble

167
Q

Does blood flow across the actual ASD account for abnormal heart sounds? What is the reason?

A

No, no pressure gradient

168
Q

Inspiration causes an increase in which sided heart sounds?

A

Right sided

169
Q

Expiration causes an increase in which sided heart sounds

A

Left sided

170
Q

What are the systolic heart sounds

A

aortic/pulmonic stenosis and mitral/tricuspid regurg

171
Q

What are the diastolic heart sounds?

A

aortic/pulmonic regurg and mitral/tricuspid stenosis

172
Q

Which murmur is characteristic of mitral/tricuspid regurg?

A

holosystolic

173
Q

What are common causes of mitral regurg?

A

ischemic heart dz, mitral valve prolapse, LV dilation

174
Q

What causes the murmur heard in MR to enhance?

A

inc TPR and LA return (expiration)

175
Q

What causes the murmur heard in tricuspid regurg to enhance

A

in RA return (inspiration)

176
Q

Which murmur is heard in aortic stenosis?

A

crescendo-decrescendo systolic ejection murmur following ejection click

177
Q

What causes the ejection click in the Cres-decres murmur?

A

aburpt halting of valve leaflets

178
Q

What is the characteristic pulse in aortic stenosis?

A

pulsus parvus and tardus, weak, can lead to syncope

179
Q

What causes aortic stenosis

A

age related calcifications or bicuspid aortic valve

180
Q

Which murmur is heard with VSD?

A

holosystolic, harsh sounding murmur, loudest over tricuspid area

181
Q

Which murmur is heard with mitral prolapse?

A

late systolic crescendo murmur with a midsystolic click

182
Q

what causes the midsystolic click

A

sudden tensing of chordae tendinae

183
Q

What does mitral prolapse predeispose to?

A

infective endocarditis

184
Q

What can cause mitral prolapse?

A

myxomatous degeneration, RF, chordae rupture

185
Q

What murmur is heard with aortic regurg?

A

immediate high pitched blowing diasystolic murmur with a wide pulse pressure

186
Q

What causes aortic regurg

A

aortic dilation, bicuspid aortic valve, RF,

187
Q

Which class of drugs decrease the murmur heard in aortic regurg?

A

Vasodilators

188
Q

Which murmur do you hear in mitral stenosis?

A

late diastolic murmur following an opening snap

189
Q

Chronic mitral stenosis can lead to what changes in size of the LA

A

dilation

190
Q

Mitral stenosis is most often secondary to which condition?

A

RF

191
Q

What is the machine like murmur? What is the heart pathology and the predisposing causes

A

patent ductus arteriosus, congenital rubella or prematurity

192
Q

When does extracellular calcium enter the cardiac muscle cells during contraction?

A

the plateau period

193
Q

What stimulates release of calcium from the SR?

A

extracellular calcium, calcium induced calcium release

194
Q

When during cardiac nodal cells depolarize?

A

during diastole

195
Q

How are cardiac myocytes electrically coupled?

A

gap junctions

196
Q

What happens in phase 0 of the cardiac ventricular action potential?

A

rapid upstroke, voltage gated Na channels open

197
Q

What happends in phase 1 of the ventricular cardiac action potential?

A

initial repol, inactivation of of voltage gated Na channels, voltage gated K channels begin to open

198
Q

What happens in phase 2 of the cardiac ventricular action potential?

A

plateau, influx of calcium through voltage gated ca channels, ca release from SR and contraction

199
Q

What happens in phase 3 of the cardiac ventricular action potential?

A

rapid repol, massive K eflux, opening of voltage gated slow K channels and closure of Ca channels

200
Q

What happens in phase 4 of the cardiac ventricular action potential?

A

resting potential high K perm

201
Q

Where are pacemaker cells?

A

SA and AV nodes

202
Q

What channels do the the pacemaker cells lack?

A

fast volatge gated Na channels

203
Q

What constitutes the upstroke in pacemaker cells?

A

volatage gated Ca channels

204
Q

What is the result of not having fast sodium channels in pacemaker cells?

A

Slow conduction velocity, used by AV node prolongs transmission from atria to ventrical

205
Q

Which channel accounts for automaticity of the SA and AV nodes?

A

If sodium channel

206
Q

What is the effect on the slope of phase 4 in pacemaker cells by Ach or adenosine?

A

decreases

207
Q

What is the effect on the slope of phase 4 in pacemaker cells by catecholamines and

A

increase, increase the chance the If are open

208
Q

In an EKG, what is the p wave?

A

atrial contraction

209
Q

In an EKG, what is the PR segment?

A

conduction delay through AV node, nl < 120 msec

210
Q

In an EKG, what is the QRS complex?

A

ventricular depolarization, nl < 120 msec

211
Q

In an EKG, what is the QT interval?

A

mechanical contraction of the ventricles

212
Q

In an EKG, what is the T wave?

A

Ventricular repolarization

213
Q

What does T wave inversion indicated?

A

MI

214
Q

What masks atrial repolarization?

A

QRS complex

215
Q

What does an isoelectric ST segment indicate?

A

ventricles are depolarized

216
Q

What does the U wave indicated?

A

hypoK and bradycardia

217
Q

What does prolonged QT predispose to?

A

torsades de pointes

218
Q

What is the danger of torsades to pointes?

A

can progress to V fib

219
Q

What other sign is often present with congenital long QT syndrome, why?

A

sensironeural deafness, defects in sodium and potassium channels, jervell and lange-neilsen syndrome

220
Q

Rank the following by speed of conduction, av node, atria, purkinjee, ventricles

A

purkingee>atria>ventricles>AV node

221
Q

Rank the pacemakers cells

A

SA>AV>bundle of His>ventricles

222
Q

delta wave on ECG, accesory conduction pathway from atria to ventricles, reentry leading to supraventricular tachycardia

A

Wolff-Parkinson white syndrome

223
Q

Irregularly irregular ECG, no p waves: dx and treatment

A

A fib, beta block or ca channel block, warfarin, thromboembolism prophylaxis

224
Q

sawtooth wave

A

Atrial flutter, identical back to back atrial depol’s, convert to sinus, cal IA, IC or III antiarrhythmics

225
Q

prolonged PR interval

A

1st degree AV block

226
Q

progressive lengthening of PR until beat is dropped, a p wave not followed by QRS

A

2nd degree AV block, mobitz type 1

227
Q

no change in PR interval followed by dropped beat

A

2nd degree AV block, mobitz type 2, may progess to 3rd degree block

228
Q

no relation between p waves and QRS intervals, treatment and predisposing factor

A

3rd degree block, pacemaker, Lyme disease

229
Q

Fatal arrhythmia

A

V fib

230
Q

What does the atria release in response to inc blood volume and atrial pressure

A

ANP

231
Q

Which two mechanisms sense decrease MAP?

A

medullary vasomotor center senses baroreceptors and JGA

232
Q

Which sympathetic receptors raise MAP

A

beta 1 inc HR and cont, alpha 1 venocxn, alpha 1 arteriolar vascxn

233
Q

How does angiotensin II raise MAP

A

vasocxn

234
Q

How does aldosterone raise MAP

A

inc blood volume

235
Q

The aortic arch receptors transmit along which nerve?

A

vagus to medulla

236
Q

The carotid sinus transmits along which nerve?

A

glossopharyngeal to soliary nucleus of medulla

237
Q

decrease stretch in baroreceptors leads to what response?

A

increased efferent SANS and decreased efferent PANS

238
Q

What do the carotid and aortic bodies respond to?

A

dec P02, inc PC02 and dec pH

239
Q

Central chemoreceptors do not respond directly to which parameter?

A

P02

240
Q

What is the cushing triad?

A

HTN, bradycardia, and respiratory depression

241
Q

What causes the cushing reflex and why

A

inc ICP, cerebral ischemia, inc SANS tone (HTN) and reflex bradycardia

242
Q

Which organ gets the largest share of systemic cardiac output

A

Liver

243
Q

Which organ has ht highest blood flow per gram of tissue

A

Kidney

244
Q

Which organ has the largest arteriovenous difference

A

Heart, 02 extraction is always around 100%

245
Q

PCWP(Pulmonary Capillary Wedge Pressure) > LV Diastolic Pressure

A

Mitral Stenosis

246
Q

PCWP is an estimate of

A

Left atrial pressure

247
Q

What does hypoxia cause in the lung versus other tissues?

A

vasocxn, while other tissues it causes vasodilation

248
Q

What does autoregulation do?

A

maintain blood flow to organ over wide range of perfussion pressures

249
Q

What do the starling forces determine

A

fluid movement through capillaries

250
Q

In terms of starling forces, why does heart failure cause edema?

A

increase in Pc

251
Q

In terms of starling forces, why does nephrotic syndrome or liver failure cause edems

A

dec plasma proteins

252
Q

Why is there edema after burns or during infection

A

inc Kf, capillary perm

253
Q

what happens to capillaries in lymphatic blockage

A

inc interstitial osmotic pressure pulling fliud out of capillaries

254
Q

What are the 5 T’s of cyanoitc babies

A

tetralogy of fallot, transposition of great vessels, truncus arteriosus, tricuspid atresia, TAPVR

255
Q

what does TAPVR stand for

A

total anomalous pulmonary trunk venous return

256
Q

Right to left shunts are more common in babies or kids?

A

babies

257
Q

Left to right shunts are more common in babies or kids?

A

kids

258
Q

failure of truncus arteriosus to divide?

A

persistant truncus arteriosus

259
Q

absecnce of tricuspid valve, hypoplastic RV

A

tricuspid atresia, requires ASD and VSD

260
Q

pulmonary veins drain into right heart circulation (SVC, coronary sinus)

A

TAPVR

261
Q

L to R shunt becomes R to L due to increase pulm pressures from original congenital heart defect

A

Eisenmenger’s syndrome

262
Q

PROVe

A

tetrology of fallot - pulmonary stenosis, RVH, overiding aorta, VSD

263
Q

What causes the early cyanosis in Tet of Fallot?

A

R to L shunt caused by stenoic pulmonic valve

264
Q

What is the classic X ray finding for tet of fallot?

A

boot shaped heart

265
Q

What causes tet of fallot?

A

anterosuperior displacement of the infundibular septum

266
Q

How does a patient with Tet of fallot learn to improve symptoms?

A

squat. Compression of femoral arteries, inc TPR, dec

267
Q

What other congenital abnormality is necessary for life for a patient with transposition of the great vesses?

A

shunt, VSD, PDA or patent foramen ovale, due to failure of the aorticopulmonary septum to spiral

268
Q

Weak pulses, notching of the ribs on xray, HTN in upper extremeties and weak peripheral pulses

A

adult type aortic coarctation

269
Q

what is the difference between adult and infantile type aortic coarctation?

A

infantile is proximal to ductus arteriosus and adult is distal. Infantile IN and aDult is Distal to Ductus

270
Q

What other syndrom is associated with infantile aortic coarctation

A

turners

271
Q

machine murmer

A

PDA

272
Q

What is the difference between the fetal and neonatal direction of blood flow in a patent ductus arteriosus

A

fetal right to left, neonate left to right leading to RVH and failure

273
Q

which medications are used to maintain patency or close the ductus arteriosus?

A

indomethacin closes, and pge keeps it open

274
Q

congenital heart defect with 22q11

A

truncus, tet of fallot

275
Q

congenital heart defect withdown syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

276
Q

congenital heart defect with congenital rubella

A

septal defects, PDA, pulm art stenosis

277
Q

congenital heart defect with turner’s

A

coarcation of aorta

278
Q

congenital heart defect with marfan’s

A

aortic insuffic, late

279
Q

congenital heart defect in an infant with a diabetic mother?

A

transposition of great vessels

280
Q

What is the definition of HTN?

A

140/90

281
Q

which ethnic groups have higher association with HTN?

A

black > white > asian

282
Q

what percentage of HTN is secondary to renal disease?

A

10%

283
Q

What does HTN predispose to?

A

atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection

284
Q

What are tendinous xanthoma, atheromas, and corneal arcus signs of?

A

hyperlipidemia

285
Q

Hyperplastic onion skinning

A

arteriolosclerosis in malignant hypertension

286
Q

fibrous plaques and atheromas in intima of arteries

A

atherosclerosis

287
Q

moncekberg

A

calcification in media of arteries esp radial and ulnar, does not obstruct blood flow, intima not involved

288
Q

disease of elastic arteries and large and medium sized muscular arteries

A

atherosclerosis

289
Q

What is the progression of atherosclerosis?

A

endothelial cell dysfxn, mac and LDL accum, foam cell, fatty streaks, smooth muscle cell migration, fibrous plaque, comlex atheromas

290
Q

what are the complications of atherosclerosis?

A

aneurysms, ischemia, infarcts, peripheral vasc dz, thromboemboli

291
Q

what are the four most common locations for atherosclerosis?

A

abdominal aorta>coronary artery>popliteal artery>carotid artery ACoPCa

292
Q

tearing chest pain radiation to the back, associated with marfan

A

aortic disecction, intraluminal tear forming false lumen

293
Q

retrosternal chest main with exertion, ST depression on ECG, likely due atherosclerosis

A

stable angina

294
Q

coronary artery spasm, ST elevation

A

prinzmetal angina

295
Q

thrombosis w/o necrosis, ST elevation, worsening chest pain at rest or with minimal exertion

A

unstable/crescendo angina

296
Q

What is the most common cause of MI

A

acute thrombosis of coronary artery

297
Q

What is sudden cardiac death most commonly due to

A

v fib arrhythima

298
Q

list the coronary vessels most likely to be occluded

A

LAD > RCA > circumflex

299
Q

diaphoresis, N/V, severe retrosternal pain, pain in left arm/jaw, SOB, fatigue, adrenergic symptoms

A

MI

300
Q

What is the time frame for arrhythmia risk in the evolution of MI

A

the first 4 days

301
Q

In an acute MI, are there any visible changes via LM in the first 2-4 hours

A

no

302
Q

In the evolution of an MI, when the risk for free wall rupture, tamponade, papillary muscle rupture, or interventricular septal rupture the hightest? Why?

A

5-10 days, macs have degraded structural components

303
Q

When do you see extensive coagulative necrosis in an MI

A

2-4 day, early coag necrosis on the first day

304
Q

When is the scar completely formed in an MI?

A

7 weeks

305
Q

Which enzyme rises after 4 hours and is elevated for 7 to 10 days after an MI?

A

troponin I

306
Q

What is the gold standard for dx of MI in the first 6 hours

A

EKG

307
Q

Which enzymes are useful for diagnosing reinfarction

A

CK-MB

308
Q

Which kind of infarct show ST elevation, and/or pathologic Q waves

A

transmural

309
Q

What kind of infarct show ST depression

A

subendocardial

310
Q

Which area of the endocardium is especially vulnerable to infarction? Why?

A

subendocardial, fewer collaterals and higher pressure

311
Q

In an anterior wall infarct, which artery is effected and which leads show Q waves

A

LAD, V1 -V4

312
Q

In an anteroseptal infarct, which artery is effected, and which leads show Q waves?

A

LAD, V1-V2

313
Q

In an anterolateral infarct, which artery is effected and which leads show Q waves

A

LCX, V4-V6

314
Q

In a lateral wall infarct, which artery is effected, and which leads show Q waves?

A

LCX, I, aVL

315
Q

In an inferior wall infarct, which artery is affected and which leads show Q waves,

A

RCA, II, III, aVF

316
Q

The 7 complications of MI

A

arrhythmia, LV failure and pulm edema, cardiogenic shock, free wall rupture, aneurysm, postinfarcation fibrinous pericarditis, dressler’s

317
Q

friction rub, 3-5 days post MI

A

postinfarction fibrinous pericarditis

318
Q

fibrinous pericarditis several weeks post MI

A

dressler’s, autoimmune

319
Q

S3, dilated heart on US, balloon appearance on CXR, eccentric hypertrophy

A

dilated cardiomyopathy

320
Q

What are the different etiologies of dialted cardiomyopathy

A

EtOh, wet Beriberi, Coxsackie B, cocaine, chagas, doxorubicin, hemochromatosis, peripartum cardiomyopathy

321
Q

How are the sarcomeres added in eccentric hypertrophy?

A

in series

322
Q

sudden death in young atheletes, S4, apical impulses, outflow obstruction

A

hypertrophied cardiomyopathy

323
Q

How are sarcomeres added in concentric hypertrophy?

A

in parallel

324
Q

Does eccentric hypertrophy or concentric hypertrophy cause systolic disfunction

A

eccentric, concentric hypertrophy causes diastolic disfunction

325
Q

Restrictive cardiomyopathy causes

A

sarcoid, amyloid, postradiation fibrosis, endocardial fibroelastosis, Loffler, hemochromatosis

326
Q

What kind of dysfunction ensues in restrictive cardiomyopathy

A

diastolic

327
Q

dyspnea, fatigue, edema and rales, multiple causes

A

CHF

328
Q

The cause of dyspnea on exertion?

A

failure of LV to in CO during exercise

329
Q

The cause of cardiac dilation?

A

greater ventricular EDV

330
Q

The cause of pulmonary edema, paroxysmal nocturnal dyspnea?

A

LV failure, pulm venous distention transudation of fluid

331
Q

When do you find hemosiderin laden macrophages in the lungs?

A

during HF from microhemorrhages from inc pulm cap pressure

332
Q

what causes orthopnea?

A

inc venous return exaccerbates pulm vasc congestion

333
Q

what causes hepatomegaly?

A

inc central venous pressure, inc resistance to portal flow

334
Q

What causes ankle, sacral edema, jugular venous distention

A

RV failure, in venous pressure

335
Q

What is the most common cause of right heart failure

A

left heart failure

336
Q

What does FROM JANE stand for in bacterial endocarditis?

A

fever, roth’s spots, osler’s nodes, murmur, janeway lesions, anemia, nail-bed hemorrhages, emboli

337
Q

Which valve is most commonly involved in bacterial endocarditis?

A

mitral valve

338
Q

Which valve is commonly involved in bacterial endocarditis from IV drug use and which bacteria are most common?

A

tricuspid, don’t tri drugs, S. aureus, pseudomonas, candida

339
Q

bacterial endocarditis, previously normal valves, rapid onset, which bacteria?

A

s. aureus

340
Q

smaller vegetations, congenitally abnormal or diseased valves, sequela of dental procedures. Insidious onset

A

viridans streptococci

341
Q

Which bacteria causes endocarditis in the presence of colon cancer

A

s. bovis

342
Q

which bacteria can cause endocarditis from prosthetic valves?

A

s. epidermidis

343
Q

What are the complications from bacterial endocarditis?

A

chordae rupture, GN, suppurative pericarditis, emboli

344
Q

Wartlike, sterile vegetations occur on both sides of the valve, commonly causes mitral regurg. SLE causes it

A

Libman-Sacks Endocarditis

345
Q

Which bacteria causes rheumatic heart disease

A

group a beta hemolytic strep

346
Q

what do patients die early from in rheumatic heart disease?

A

early deaths from myocarditis

347
Q

Which heart valves are afected most in rheumatic heart disease

A

mitral>aortic>>tricuspid, high pressure valves affected most

348
Q

what is the early and late lesion in rheumatic heart disease

A

mitral valve prolapse

349
Q

What are aschoff bodies

A

granuloma with giant cells

350
Q

what are anitschkow’s cells

A

activated histiocytes

351
Q

Do you see elevated ASO titers in rheumatic heart disease

A

yes

352
Q

What does FEVERSS stand for in rheumatic heart disease

A

fever, erythema marginatum, valvular damage, ESR, red hot joints, subQ nodules, St. vitus dance (chorea)

353
Q

Equilibration of diastolic pressures in all 4 chambers, decreased CO from compression of heart by fluid in pericardium

A

cardiac tamponde

354
Q

exaggerated decrease in pulse during inspiration.

A

kussmaul’s sign, cardiac tamponade, pulsus paradoxus

355
Q

clinical signs of cardiac tamponade

A

hypotension, inc venous pressure, distant heart sounds, inc HR, pulsus paradoxus

356
Q

what conditions are associated with pulsus paradoxus

A

cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup

357
Q

disruption of the vasa vasorum of aorta, dilation of aorta and valve ring, tree bark appearance (calcifications on aortic root)

A

3rd degree syphillus, syphillit heart disease can lead to aortic valve incompetence

358
Q

most common primary cardiac tumor in adults, ball-valve obstruction in left atrium

A

myxoma

359
Q

most common primary cardiac tumor in children, associated with tuberous sclerosis

A

rhabdomyomas

360
Q

most common heart tumor

A

metastasis from melanoma or lymphoma

361
Q

dilated tortous veins due to chronically inc venous pressure, poor wound healing, varicose ulcers

A

varicose veins, thromboembolism rare

362
Q

decrease blood flow to the skin due to arteriolar vasospasm in cold temp, emotional stress, also in SLE and CREST

A

raynaud’s

363
Q

necrotizing granulomas in lung and upper airways, nectrotizing GN, small vessel vasculitis

A

Wegener’s

364
Q

Wegener’s presentation

A

hemoptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough dyspnea

365
Q

serum marker for wegener’s

A

c-ANCA

366
Q

Wegener’s tx

A

cyclophosphamide and corticosteroids

367
Q

p-anca

A

microscopic polyangiitis, like wegener’s without granulomas

368
Q

Churg Strauss, presentation and test

A

granulomatous vasculitis with eosinophilia. Asthma, sinusitis, skin lesions and periphereal neuropathy (wrist/foot drop) heart, GI, kidneys

369
Q

port wine stains on face, intracerebral AVM, siezures, early onset glaucoma, congenital

A

sturge weber, vasculitis of caps

370
Q

skin rash on buttocks and legs, arthralgia, intestinal hemorrhage, abdominal pain, melena. Follows URI, IgA immune complex, most common childhood systemic vasculitis

A

Henoch-Schlonlein purpura

371
Q

segmental thrombosing vasculitis of small and medium vessels in smokers with intermittent claudication, superficial nodular phlebitis, raynaud’s, gangrene and severe pain, autoamputation of digits is possible

A

Buerger’s disease

372
Q

acute, self limiting necrotizing vasculitis in children associated with fever, conjunctivitis, strawberry tongue, desquamatous skin rash, lymphadenitis, coronary sinus aneurysms. Seen in asians

A

kawasaki

373
Q

immune mediated transmural vasculitis with fibrinoid necrosis, small and medium vessels, renal and viscera, not pulm arteries, hep B seropos in 30% of pts,

A

polyarteritis nodosum

374
Q

pulseless disease, granulomatous thickening of the aortic arch and/or proximal great vessels - elev ESR, asian females > 40

A

takayasu’s arteritis

375
Q

what does FAN MY SKIN On Wednesday stand for?

A

Fever, Arthritis, Night sweats, Myalgia, SKIN nodules, Ocular disturbances, Weak pulses in upper extremities

376
Q

Unilateral headache, jaw claudication, impaired vision,

A

tempral arteritis, may cause irreversible blindness

377
Q

Most common vasculitis affecting medium and large arteries

A

Temporal arteritis

378
Q

benign cap hemangioma of infancy, spont regresses

A

strawberry hemangioma

379
Q

bening capillary hemangioma of elderly, does not regress

A

cherry hemangioma

380
Q

polypoid capillary hemangioma that can ulcerate and bleed

A

pyogenic granuloma, associated with trauma and pregnancy

381
Q

cavernous lymphangioma of the neck, associated with turner’s

A

cystic hygroma

382
Q

benign, painful, red-blue tumor under fingernails from smooth muscle cells

A

glomus tumor

383
Q

benign capillary skin papules in AIDS patients mistaken for kaposi sarcoma, caused by bartonella henselae

A

…

384
Q

highly lethal malignancy of the liver, associated with vinyl chloride, arsenic, and thorosrast exposure

A

angiosarcoma

385
Q

lymphatic malignancy associated with persistant lymphadema, post radical mastectomy

A

lymphangiosarcoma

386
Q

endothelial malignancy of the skin assocated with HHV-8 and HIV

A

kaposi’s sarcoma

Cardiology (10 decks)

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