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int med exam 0828 > cardiology 1: General > Flashcards

cardiology 1: General Flashcards

1
Q

define the x-ray findings

A
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2
Q

define x-ray findings lateral view

A
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3
Q

Describe the sign?

A

this is the scimitar sign, which is a curvilinear opacity in the right lower lung field due to associated lung hypoplasia. It is an anomalous pulmonary vein

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4
Q

Describe the cxr finding

A

This is pericardial effusion, “water bottle” sign.

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5
Q

what are teh two types of cardiac stress tests?

A

exercise tolerance test and stress imaging test

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6
Q

what are the groups that you should not perform an exercise tolerance test?

A
  1. unable to achieve 85% of age-predicated max HR
  2. patients with baseline ECG abnormalities
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7
Q

what is the definition of a positive Exercise tolerance test?

A
  • flat or down-sloping ST-segment depression >1mm and 80ms after J-point in 3 consecutive beats.
  • ST depression does not correlate with anatomic location unlike ST elevation
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8
Q

what are the absolute indications for termination of ETT? (7)

A
  1. ST elevation >1mm in leads without q waves from prior MI excluding aVR, aVL, and V1
  2. the decrease in SBP >10mm Hg when accompanied by other evidence of ischemia or hypoperfusion
  3. moderate to severe angina
  4. CNS symptoms
  5. Sustained 2/3rd AV block
  6. Signs of poor perfusion (cyanosis/pallor)
  7. serious arrhythmia
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9
Q

what are the stress imaging studies you can do?

A

stress echo and myocardial perfusion imaging (MPI)

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10
Q

what is the general sensitivity/specificity of ETT?

A

60% sensitive, 70% specific

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11
Q

when are stress imaging tests done instead of ETT?

A

cannot exercise or ECG changes at rest

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12
Q

why is exercise tolerance tests not used in patietns that have pacemakers or LBBB?

A

produces false-positive left ventricular anteroseptal perfusion defects

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13
Q

what agents are used in cardiac imaging studies? How do they work?

A
  • Dobutamine acts as an inotropic/chronotropic and acts similarly as exercise
  • Vasodilatation increases blood flow but does not increase heart rate. They increase blood flow to normal vessels while doing no change to stenotic vessels. Thus, steal blood from stenotic vessels causing perfusion defects as seen on EKG.
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14
Q

what are the specific agents used for vasodilatation in cardiac stress testing?

A

Adenosine, dipyramadole, and regadenoson (nonselective A2 receptor activator)

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15
Q

what agent can you use for chemical stress test in patient w/history of bronchospasm?

A

dobutamine. Regadenoson has less effect.

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16
Q

when are exercise stress echo and MPI indicated instead of ETT? (5)

A
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17
Q

what cardiac test is indicated for patients with paced ventricular rhythm?

A

MPI with vasodilators

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18
Q

when do you use cardiopulmonary exercise testing?

A
  • patients with systolic heart failure
  • pre-transplant assessment
  • unexplained exertional dyspnea
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19
Q

what are the requirements prior to doing a coronary Computed tomographic angiography?

A
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20
Q

when do you choose CTA diagnostic test? when should you not use this test?

A
  • symptomatic patients who are at intermediate risk for CAD after initial risk stratification.
  • Patient with congenital coronary anomalies
  • It should not be used in asymptomatic patients or symptomatic patients with low/high probability for CAD.
  • Usefulness is reduced patients with pronounced coronary calcification
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21
Q

why do you use Coronary computed angiogrpahy in intermediate CAD risk?

A

high negative predictive value in excluding significant CAD

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22
Q

what is coronary artery calcium scoring?

A
  • use to scan for atherosclerosis and does not use IV contrast
  • Used to further risk stratification in asymptomatic, intermediate-risk patients
  • CAC score 0 is low
  • CAC score>400 indicates 3 fold risk for CAD
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23
Q

what is a cardiac MRI used for?

A

can be used for everything but the mainstay is infiltrative diseases, post-MI tissue viability

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24
Q

what is PCWP?

A

dampened LA pressure that reflects LV-EDP, which reflects LV-EDV

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25
Q

what are normal Right atrial, right ventricular and pcwp pressures?

A
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26
Q

In what conditions does PCWP elevate?

A
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27
Q

in what conditions are diastolic pressures equal in all 4 chambers?

A

pericardial tamponade and constrictive pericarditis

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28
Q

what is pulsus paradoxus?

A
  • decreased pulse amplitude with inspiration seen as absence of korotkoff sounds during inspiration
  • Can be observed clinically bu auscultating BP and listening for exaggeration of normal inspiratory decrease in SBP>10mm Hg
  • you can heart a heart beat but not a feel a pulse during inspiration
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29
Q

when do you see pulsus paradoxus?

A
  • cardiac tamponade
  • constrictive pericarditis
  • asthma
  • tension pneumothorax
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30
Q

what is pulsus bisferiens?

A

bifid with 2 systolic peaks during cardiac cycle

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31
Q

when do you see pulsus bisferiens?

A
  • AR
  • HCM
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32
Q

what is pulsus alterans?

A

varying pulse pressure with a regular pulse rate

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33
Q

when do you see pulsus alterans?

A

any cause pf decreased systolic function that leads to decreased stroke volume

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34
Q

what is pulsus parvus et tardus? condition seen?

A
  • parvus = low amplitude
  • tardus - slow upswing
  • aortic stenosis
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35
Q

what is and where do you see branchiofemoral delay?

A

this is femoral pulse occurring after brachial pulse

see this in coarctation of the aorta

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36
Q

what does standing do to valve murmurs?

A
  • decrease right and left cardiac filling and cause the sound of most murmurs to decrease
  • increase murmurs of MVP and HCM
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37
Q

what does strain phase of valsalva do to cardiac murmurs?

A
  • decrease right and left cardiac filling and cause the sound of most murmurs to decrease
  • increase murmurs of MVP and HCM
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38
Q

what does squatting do to cardiac murmurs?

A
  • increase cardiac volume
  • increase volume and after load
  • increase intensity of all murmurs except MVP and HCM
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39
Q

what does lying down or supine passive straight leg raise?

A
  • increase cardiac volume
  • increase volume and after load
  • increase intensity of all murmurs except MVP and HCM
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40
Q

what does sustained handgrip do?

A
  • boosts SVR and LV volume
  • decreases murmurs of HCM and aortic stenosis
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41
Q

what maneuever can you do to distinguish HCM and MVP?

A

handgrip prolongs murmur of MVP due to earlier prolapse of MV.

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42
Q

what maneuver can you use to differentiate between AS and MVP?

A
  • AS murmur decreases
  • MVP murmur increases in duration
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43
Q

what does inspiration/expiration do to heart murmurs?

A

inspiration increases right-sided sounds

Expiration increases left-sided sounds.

44
Q

S1 is caused by?

A

closing of mitral and tricuspid valves

45
Q

S1 is decreased when?

A
  • prolonged PR interval
  • Mitral regurgitation
  • acute aortic regurgitation (Increased LV pressure causes early LV closure)
  • severely calcified mitral valve
46
Q

S1 intensity is increased when?

A
  • (mitral valve slams shut)
  • short PR interval
  • mitral stenosis
  • hyperdynamic ventricular function
47
Q

what is S2 caused by?

A

closing by the aortic and pulmonic valves (A2 then P2)

48
Q

why do you have a physiologic split?

A
  • this is when P2 occurs after A2
  • Caused by the increased volume of blood in the RV prolonged RV systole, delays closure of the pulmonic valve.
  • Disappears during expiration
49
Q

what is a persistent/wide split S2? causes?

A
  • vary with respiration but does not disappear on expiration
  • anything that cause delay or prolonged contraction of the right ventricle
  • pulmonic stenosis, PE, RBBB,
50
Q

what is the classic presentation of a fixed split S2?

A

also see patient with systolic ejection murmur, ASD, and pulmonary vascular congestion on CXR

51
Q

what is paradoxical split S2?

A
  • P2 occurs before A2
  • hear split with expiration instead of inspiration
52
Q

what conditions do you see paradoxical split S2?

A
  • LBBB
  • pacemaker beat from RV
53
Q

what does a S3 indicate?

A

indicates end of rapid ventricular filling

54
Q

what conditions do you see a S3?

A

kids, patients with poor LV dysfunction.

55
Q

what is S4?

A
  • ventricular filling during atrial contraction
  • hear it in patients with decreased ventricular compliance
  • ischemic heart disease, aortic stenosis, HCM,
56
Q

what pathological conditions do you not hear a S4?

A
  • atrial fibrillation
  • mitral stenosis (ventricular inflow obstruction)
57
Q

when do you see large right sided v waves?

A
  • ventricular septal rupture
  • Tricuspid regurgitaiton
58
Q

when do you left sided v waves?

A

severe MR

59
Q

what do you see with constrictive pericarditis?

A

rapid x and y descents

60
Q

what do you see with tamponade?

A

rapid x descent only

61
Q

what do you see with mitral stenosis?

A

large, left sided a-waves

62
Q

when do you see cannon a waves?

A

anything with AV disassociation (times when atrium is contracting gainst a close TV)

63
Q

when do you see a slow y descent?

A

delayed atrial emptying as in from tricuspid stenosis

64
Q

what waveforms are seen during diastole?

A
  • A wave (atrium contracting, tricuspid valve open)
  • Y descent (atrium emptying, tricuspid open)
65
Q

what wave forms are seen during systole?

A
  • C notch
  • X descent (atrium relaxing then filling, tricuspid closed)
  • V wave (atrium tense and full, tricuspid close)
66
Q

what waveforms do you see in pulmonary HTN?

A

elevated A and V waves

67
Q

what waveforms are seen in tricuspid regurgitation?

A

large V waves

68
Q

what waveforms do you see with tricuspid stenosis?

A

slow y descent

69
Q

what waveforms do you see with restrictive cardiomyopathy?

A

rapid x and y descents

70
Q

what waveforms do you see with RV infarction?

A

elevated A and V wave

71
Q

what waveforms do you see with ASD?

A

large V waves and rapid y descent

72
Q

when should you suspect secondary HTN?

A
  • age<30
  • drug resistant HTN
  • people who develop uncontrolled HTN that was previously well controlled
73
Q

physical exam finding that suggests renal vascular HTN?

A

systolic abdominal bruit without a diastolic bruit

74
Q

primary hyperaldosteronism basic script?

A

hypertension patient with hypokalemia and low renin

75
Q

which common cardiac medications prolong survival post - MI?

A
  • beta blockers
  • carvedilol
  • ACe/ARB
  • Epleronone
76
Q

which common cardiac medications prolong survival in HF?

A
  • Beta blockers
  • carvedilol
  • nitrates (with hydralazine)
  • Ace/ARb
  • spirinolactone
  • Epleronone
77
Q

what is a dromotrope?

A

affects the speed of the electrical impulses (SA node to purkinjie fibers)

78
Q

what is a inotrope?

A

affects the strength of contraction (ability to squeeze)

79
Q

what is chronotropic?

A

affects the heart rate

80
Q

what time of day does the highest incidence of spontaneous ischemic cardiac events occur?

A

circadian pattern with the highest incidence in the early morning hours.

81
Q

what type of cardiac medication is digoxin?

A

negative chronotropic and negative domotropic

82
Q

what type of cardiac medication are beta blockers?

A

negative inotropic

negative chronotropic

negative domotropic

anti-anginal

prolongs survival post - MI

prolongs survival in HF

Only coreg is a vasodilator

83
Q

generally, non-dihydropiridine CCB is what type of cardiac medication?

A
  • these are verapamidl and diltiazem
  • negative inotrope
  • negative chronotrope
  • negative dromotrope
  • vasodilator
  • antianginal
  • vasodilator
  • does not prolong survival
84
Q

generally, dihydropidine CCB is what type of cardiac medication?

A
  • These are nifedipine, amlodipine
  • negative inotrope
  • no chrono/dromotropic effects
  • vasodilator
  • anti-anginal
  • only amlodipine prolongs survival in DCM
85
Q

what type cardiac medication is ACE/ARB?

A
  • vasodilator
  • prolongs survival post mi and hF
86
Q

what type of cardiac medication do nitrates do?

A

vasodilator

anti-anginal

prolongs survival in HF with hydralazine

87
Q

what causes resting ST segment elevation?

A
  • acute MI
  • pericarditis
  • LV aneurysm
  • LBBB
  • LVH
  • ventricular pacing
  • benign early repolarization
88
Q

define hibernating myocardium?

A
  • chronically underperfused myocardium without irreversible myocyte injury
  • when perfusion restored to normal, contractility should return to normal
89
Q

define reperfusion injury?

A
  • severely ischemic myocardium is reperfused after 1 hour
  • causes further irreversible microvascular damage and myocardial cell damage
90
Q

define stunned myocardium?

A
  • result of acute ischemic
  • from time to reperfusion, takes 7-10 days for the ventricular function to return to normal
91
Q

what does ST-segment elevation suggest on an exercise ECG test?

A

suggest spasms of the coronary arteries

92
Q

what are the main drugs to treat angina?

A
  • beta-blockers and nitrates are staples
  • CCB can also help by decreasing coronary artery vasodilation, peripheral vasodilation, and negative chronotropic effect.
93
Q

which patient would benefit from ranexa?

A
  • maximal standard therapy or substitute for beta-blockers
  • inhibits late sodium current in cardiac myocytes reducing sodium and calcium overload that follows ischemia
  • improves myocardial relaxation and reduces LV diastolic stiffness, enhancing myocardial contractility and perfusion
94
Q

which antianginal drugs decrease preload?

A

nitrates decrease preload>afterload,

95
Q

which antianginals decrease afterload?

A
  • nitrates
  • beta blockers
  • CCB
96
Q

wat anti-anginal drugs do you NOT give to a patient with RV infarct?

A

Nitrates because acute preload reduction can cause severe decompensation

97
Q

what drugs decrease preload in general?

A
  • nitroglycerin
  • ACE/ARB
  • Morphine
  • Aldosterone blockers
98
Q

which drugs decrease afterload?

A
  • nitroprusside
  • milironine
  • CCB (pines)
  • ACE.ARB
99
Q

which drugs decrease heart rate?

A
  • beta blockers
  • CCB
  • Digoxin
  • adenosine
  • antiarrhythmics
100
Q

what 3 components make up SV?

A
  • preload
  • afterload
  • contractility
101
Q

what are the two pathologies of thoracic aortic aneurysms?

A
102
Q

when is surgery indicated for chronic thoracic aortic aneurysms?

A
103
Q

how to manage AAA?

A
104
Q

what is coarctation of the aorta?

A
105
Q
A

int med exam 0828 (24 decks)

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