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ABIM > Cardiology > Flashcards

Cardiology Flashcards

1
Q

cardiothoracic ratio of > 50% can indicate what?

A
  • cardiomegaly

- pericardial effusion

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2
Q

on the LATERAL view, any increase in the mass of the left ventricle extends the cardiac shadow ____

A

posteriorly and lower – closer to the diaphragm

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3
Q

on the LATERAL view, any increase in the mass of the right ventricle extends the cardiac shadow ____

A

anteriorly behind the sternum

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4
Q

CXR findings of coarctation of aorta

A
  • absence of normal aortic arch
  • “3” sign (prominent left subclavian artery, coarctation, poststenotic dilation of descending aorta)
  • “reversed 3” sign on barium swallow
  • intercostal rib notching
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5
Q

CXR findings of heart failure

A
  • cardiomegaly
  • pulmonary vascular redistribution (visibly thickened upper lobe pulmonary veins)
  • Kerley B lines
  • pleural effusions (usually right > left)
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6
Q

CXR finding of anomalous pulmonary vein that drains into the IVC

A

“scimitar sign” (curvilinear opacity in right lower lung field d/t associated lung hypoplasia)

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7
Q

CXR finding of aortic dissection

A

mediastinal widening on PA view

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8
Q

CXR finding of pericardial effusion

A
  • “WATER BOTTLE” or “water balloon” heart shape

- sometimes significant enlargement of cardiac silhouette

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9
Q

areas of CALCIFICATIONS on CXR:

  • aortic
A

think DISSECTION if separation between calcification and aortic border, especially if mediastinum appears wide

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10
Q

areas of CALCIFICATIONS on CXR:

  • myocardial
A

apical aneurysm

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11
Q

areas of CALCIFICATIONS on CXR:

  • valvular
A

commonly aortic

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12
Q

areas of CALCIFICATIONS on CXR:

  • annular (ring-shaped)
A

mitral annular calcification

if perfect ring, prosthetic valve likely

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13
Q

areas of CALCIFICATIONS on CXR:

  • pericardial
A
  • think constrictive pericarditis

- or think TB if clinical history suggests exposure

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14
Q

CXR finding of ventricular pacemaker

A

single lead in apex of right ventricle

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15
Q

CXR finding of implanted defibrillator

A

single lead in apex of right ventricle that is LARGER and WIDER than that of the pacemaker

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16
Q

CXR finding of atrioventricular (AV) sequential (dual-chamber) pacemaker

A

2 leads

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17
Q

CXR finding of biventricular pacemaker

A

3 leads

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18
Q
  • left ventricular structure and systolic function
  • right ventricular structure and systolic function
  • valvular heart disease
  • congenital heart disease
  • myocardial infarction (including post-MI complications)
  • cardiomyopathy (both loss of EF and hypertrophy of myocardium)
  • cardiac masses (tumor, thrombus, and vegetation)
  • diseases of aorta and pulmonary artery
  • estimation of pulmonary pressure
  • diastolic function
  • cardiac sources of emboli
A

BEST use of echocardiogram

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19
Q

echo performed w/ an esophageal probe

A

TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE)

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20
Q

HIGHER-RESOLUTION images compared to tranTHORACIC echocardiogram

A

TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE)

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21
Q
  • valvular structure and function
  • left atrium (including left atrial appendage)
  • cardiac masses
  • intracardiac shunts
  • endocarditis
  • aortic dissection
A

TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE) provides higher-resolution images than TTE

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22
Q

is used to evaluate intracardiac shunts

A

BUBBLE STUDY

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23
Q

measures the VELOCITY and DIRECTION of blood flow

A

doppler echocardiography

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24
Q

is useful in determining the severity of valvular stenosis or regurgitation, evaluating LV diastolic function, LV outflow tract gradients, and intracardiac shunts

A

doppler echocardiography

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25
Q

key factor in use of exercise testing as a diagnostic tool for coronary artery disease (CAD)

A

INCREASED DEMAND for myocardial oxygen

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26
Q

stress tests have an integral role in what 2 ways?

A
  • detection of CAD (DIAGNOSTIC tool)

- stratification of risk (PROGNOSTIC tool)

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27
Q

diagnostic testing is MOST VALUABLE when?

A

pretest probability for CAD is INTERMEDIATE

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28
Q

what are the 2 general types of cardiac stress tests?

A
  1. exercise tolerance test (w/o imaging)
  2. stress imaging testing
    - “STRESS” is induced w/ exercise or pharmacologic stress
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29
Q

what is the associated IMAGING done w/ stress testing?

A
  • echocardiography (aka stress echo)

- myocardial perfusion imaging (MPI; nuclear stress test)

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30
Q

is the cornerstone of DIAGNOSTIC testing for ISCHEMIA and FUNCTIONAL CAPACITY and for determining PROGNOSIS (including post-MI)

A

exercise tolerance test (ETT)

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31
Q

level of maximal exercise achieved on the ETT is measured in?

A

metabolic equivalents (METS)

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32
Q

ETT WITHOUT imaging is NOT recommended in which 2 groups?

A
  1. pts unable to exercise sufficiently (MUST ACHIEVE 85% of age-predicted maximum heart rate (PMHR))
  2. pts w/ BASELINE ECG ABNORMALITIES
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33
Q

what BASELINE ECG ABNORMALITIES can interfere w/ ETT?

A
  • LVH
  • LBBB
  • WPW
  • ventricular pacing
  • resting ST depressing
  • taking digoxin
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34
Q

definition of a POSITIVE ETT

A

flat or down-sloping ST-segment depression > 1 mm at 80ms after the J-point in THREE consecutive beats

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35
Q

is an unusual finding suggestive of marked ischemia (can also be seen w/ coronary artery spasm)

A

ST elevation during an ETT in 3 contiguous leads w/o Q waves of prior MI

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36
Q
  • ST elevation > 1 mm in leads w/o Q waves from prior MI and excluding aVR, aVL, and V1
  • decrease in SBP > 10 mmHg when accompanied by any other evidence of ischemia or hypoperfusion
  • moderate-to-severe angina
  • CXS symptoms (ataxia, dizziness, near syncope)
  • signs of poor perfusion (cyanosis/pallor)
  • sustained 2nd or 3rd degree AV block
  • technical difficulties in monitoring ECG/BP
  • pt requests to stop
  • serious arrhythmia (eg sustained ventricular tachycardia)
A

absolute indications for termination of an ETT

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37
Q

what correlates w/ a good prognosis independent of degree of CAD?

A

excellent exercise tolerance (> 10 METS)

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38
Q

absolute CI to ETT

A
  • acute MI w/i 2 days
  • unstable angina not previously stabilized by medical therapy
  • uncontrolled arrhythmias causing symptoms or hemodynamic compromise
  • symptomatic severe aortic stenosis
  • uncontrolled symptomatic HF
  • acute PE or infarction
  • acute myocarditis or pericarditis
  • acute aortic dissection
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39
Q

when are stress imaging studies used as the initial diagnostic method?

A

pt is not a candidate for ETT d/t:

  • inability to exercise
  • or baseline ECG changes at rest
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40
Q

in which pts are stress imaging studies the preferred diagnostic method?

A

pts w/ prior revascularization

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41
Q

do stress imaging studies have greater sensitivity and specificity than regular ETT?

A

YES

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42
Q

when are stress imaging studies used?

A

to measure EJECTION FRACTION or MYOCARDIAL VIABILITY; in addition to identifying CAD

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43
Q

how is the “stress” portion of stress imaging studies done?

A
  • EXERCISE

- PHARMACOLOGIC agents

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44
Q

when is exercise stress imaging NOT used and why?

A
  • pts w/ PACEMAKERS
  • LBBB
  • can cause false-positive left ventricular anteroseptal perfusion defects
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45
Q

pharmocologic agent used for stress imaging that is both iontropic and chronotropic

A

dobutamine

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46
Q

is usually NOT used in stress imaging studies in pts w/ PACEMAKERS

A

dobutamine

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47
Q

dobutamine is used for pts who are not only unable to exercise, but also have what CI’s to vasodilators?

A
  • BRONCHOSPASM

- SEVERE CAROTID ARTERY STENOSIS

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48
Q

what are the main coronary vasodilators used in pharmacologic MPI stress tests?

A
  • ADENOSINE
  • DIPYRIDAMOLE
  • REGADENOSEN
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49
Q

vasodilators should be used cautiously in stress imaging studies in pts w/ h/o?

A

BRONCHOSPASM

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50
Q

which vasodilator for stress imaging studies is a more selective A2A receptor activator, has less bronchospasm effect, and allows for a faster stress test?

A

REGADENOSEN

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51
Q

pharmacologic agent of choice for stress imaging studies for pts w/ h/o BRONCHOSPASM

A

DOBUTAMINE

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52
Q

unlike ETT, exercise stress echo and stress MPI can be used in which pts?

A
  • resting ECG changes
  • WPW syndrome
  • on digoxin therapy
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53
Q

do pts w/ the following:

  • resting ECG changes
  • WPW syndrome
  • on digoxin therapy

require chemical stress?

A

NO, if they can exercise, CLASS I indication to do stress echo WITH EXERCISE or MPI WITH EXERCISE

(i.e. they need the IMAGING, not the chemical stress)

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54
Q

what is the stress test of choice for pts w/ PACED VENTRICULAR RHYTHM?

A

MPI w/ vasodilators

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55
Q

how is the target heart rate achieved for stress echo?

A
  • EXERCISE, or

- DOBUTAMINE

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56
Q

what does the stress echo evaluate? (3)

A
  • changes in WALL MOTION
  • systolic WALL THICKENING
  • systolic EJECTION FRACTION w/ stress
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57
Q

abnormal wall motion of failure of the wall to thicken (contract) appropriately during a stress echo suggests what?

A

myocardial ischemia to that region

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58
Q

are NOT used for stress echo

A

vasodilators

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59
Q

MPI uses which radioisotopes with single-photon emission computed tomography (SPECT)

A
  • TECHNETIUM-99m (99mTc)

- THALLIUM-201 (201TI) (less frequently)

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60
Q

in MPI the radioisotope tracers distribute in heart tissue in proportion to _____ which is recorded by a gamma camera and compared visually between resting and stressed states

A

blood FLOW

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61
Q

in MPI preserved myocardial perfusion at REST, but decreased during STRESS is suggestive of

A

ischemia (“REVERSIBLE defect”)

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62
Q

in MPI matched reduction in perfusion between rest and stress images is suggestive of a

A

myocardial infarction (“FIXED defect”)

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63
Q

determining best cardiac stress test:

  • resting ECG normal
  • able to exercise
A

ETT

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64
Q

determining best cardiac stress test:

  • resting ECG normal
  • NOT able to exercise
A
  • dobutamine echo
  • dobutamine MPI
  • vasodilator MPI
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65
Q

determining best cardiac stress test:

  • > 1 mm resting ST depression
  • WPW
  • LVH
  • on digoxin
  • able to exercise
A
  • exercise echo (preferred)

- exercise MPI (preferred)

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66
Q

determining best cardiac stress test:

  • > 1 mm resting ST depression
  • WPW
  • LVH
  • on digoxin
  • NOT able to exercise
A
  • dobutamine echo
  • dobutamine MPI
  • vasodilator MPI
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67
Q

determining best cardiac stress test:

  • LBBB
  • able to exercise
A

N/A

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68
Q

determining best cardiac stress test:

  • LBBB
  • NOT able to exercise
A
  • vasodilator MPI (preferred)

- dobutamine echo

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69
Q

determining best cardiac stress test:

  • pacemaker
  • able to exercise
A

N/A

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70
Q

determining best cardiac stress test:

  • pacemaker
  • NOT able to exercise
A

vasodilator MPI

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71
Q

which cardiac stress test is ALWAYS PREFERRED is pt has no limitations and what are the only 2 exceptions?

A
  • EXERCISE STRESS TEST
  • LBBB
  • pacemaker
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72
Q

which cardiac stress test to choose:

if the pt is simply unable to walk and has no other issues

A

pharmacologic stress test

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73
Q

which cardiac stress test to choose:

if the pt has bronchospasm or severe carotid artery stenosis

A

DOBUTAMINE

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74
Q

which cardiac stress test to choose:

if the pt has severe HTN or prior ventricular tachycardia (VT)

A

use a VASODILATOR (adenosine, dipyridamole, or regadenoson), NOT dobutamine

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75
Q

which cardiac stress test to choose:

if the pt has a paced ventricular rhythm

A

use a VASODILATOR (adenosine, dipyridamole, or regadenoson), NOT dobutamine

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76
Q

is useful in evaluating pts w/ systolic HF, undergoing a pretransplant assessment, and for pts w/ unexplained exertional dyspnea

A

cardiopulmonary exercise testing (CPX)

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77
Q

is the GOLD STANDARD for diagnosis of CAD

A

coronary ANGIOGRAPHY

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78
Q

can also assess EF during coronary angiography

A

contrast VENTRICULOGRAPHY

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79
Q
  • noninvasive modality for imaging the heart
  • requires IV CONTRAST
  • HR must be < 60 BPM and regular
  • pts must be able to HOLD their BREATH
A

coronary computed tomographic angiography (CTA)

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80
Q

reasonable diagnostic test for symptomatic pts who are at INTERMEDIATE risk for CAD after initial risk stratification, including pts w/ equivocal stress test results

A

coronary computed tomographic angiography (CTA)

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81
Q

this test’s usefulness is reduced in pts w/ pronounced coronary calcification

A

coronary computed tomographic angiography (CTA)

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82
Q

is an excellent test for evaluation of pts w/ congenital coronary anomalies

A

coronary computed tomographic angiography (CTA)

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83
Q

can be used to assess:

  • right and left filling pressures
  • CO
  • RV and PA pressures
  • systemic and pulmonary vascular resistance
A

pulmonary artery catheterization (PAC)

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84
Q

what is pulmonary artery catheterization (PAC) used for?

A
  • determine pt’s volume status
  • causes of shock
  • existence of pericardial disease
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85
Q

is the dampened LA pressure that reflects left ventricular end-diastolic pressure (LVEDP) in most cases, which reflects LVED volume

A

pulmonary capillary wedge pressure (PCWP)

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86
Q

normal pressures:

RA

A

< 8 mmHg

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87
Q

normal pressures:

RV

A

15-30/1-7 mmHg

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88
Q

normal pressures:

PCWP

A

4-12 mmHg

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89
Q

jugular venous distention in the upright pt which indicates an elevated RA pressure

A

> 7 cm H2O (5 mmHg)

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90
Q

what happens to PCWP w/:

  • LV systolic failure
  • LV diastolic failure
  • mitral stenosis
  • aortic insufficiency
  • mitral insufficiency
  • tamponade
  • constrictive pericarditis
A

INCREASES

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91
Q

at what PCWP should LV failure be considered?

A

> 15-18 mmHg

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92
Q

at what PCWP do you have dyspnea on exertion (DOE)?

A

15-25 mmHg

93
Q

at what PCWP do you have dyspnea at rest, orthopnea, and interstitial edema

A

25-35 mmHg

94
Q

at what ACUTE PCWP do you have frank pulmonary edema?

A

> 35 mmHg

95
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 0-5
  • PA pressure: (13-28)/(3-13)
  • PCWP: 3-11
  • BP: 110/70
A

normal

96
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 18
  • PA pressure: 32/18
  • PCWP: 19
  • BP: 70/50
A

tamponade or constrictive pericarditis

97
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 15
  • PA pressure: 21/11
  • PCWP: 10
  • BP: 70/50
A

RV failure to RV infarct

98
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 18
  • PA pressure: 30/20
  • PCWP: 20
  • BP: 70/50
A

biventricular failure

99
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 18
  • PA pressure: 90/32
  • PCWP: 30
  • BP: 110/70
A

mitral stenosis

100
Q

pulmonary artery catheterization scenarios:

  • RA pressure: 18
  • PA pressure: 90/32
  • PCWP: 10
  • BP: 110/70
A

pulmonary HTN

101
Q

diastolic pressure in all 4 chambers is equalized in both ____ and ____

A
  • pericardial tamponade

- constrictive pericarditis

102
Q

when is endomyocardial biopsy used?

A
  • to monitor cardiac transplant rejection

- to evaluate the cause of CARDIOMYOPATHY or MYOCARDITIS if cause is unclear or therapy isn’t working

103
Q

decreased pulse amplitude w/ INSPIRATION seen as absence of Korotkoff sounds during inspiration

A

pulsus PARADOXUS

104
Q

can be observed by auscultating BP and listening for an exaggerated decrease in SBP (> 10 mmHg) during inspiration

A

pulsus PARADOXUS

105
Q

pulsus PARADOXUS is present w/? (4)

A
  • cardiac tamponade (especially)
  • constrictive pericarditis
  • asthma
  • tension pneumothorax
106
Q

what is the paradox in pulsus PARADOXUS?

A

you can hear a heartbeat, but not feel a pulse during inspiration

107
Q

bifid w/ 2 systolic peaks per cardiac cycle

A

pulsus BISFERIENS

108
Q

pulsus BISFERIENS is present w/? (2)

A
  • aortic regurgitation (w/ or w/o stenosis!)

- HCM

109
Q

varying pulse pressure w/ a regular pulse rate

A

pulsus ALTERNANS

110
Q

what is pulsus ALTERNANS seen w/?

A

severely depressed systolic function of any cause that leads to DECREASED STROKE VOLUME

111
Q

what is pulsus PARVUS ET TARDUS and when is seen?

A
  • parvus = LOW amplitude
  • tardus = slow upswing
  • aortic stenosis
112
Q

what is BRACHIOFEMORAL DELAY and when is seen?

A
  • femoral pulse occurs AFTER brachial pulse

- coarctation of aorta

113
Q

what is pulse ASYMMETRY and when is seen?

A
  • good UE pulses, but diminished or absent LE pulses, OR asymmetry between right and left extremities
  • aortic dissection
114
Q
  • DECREASED OR ABSENT peripheral pulses

- possible BRUIT over proximal artery (such as femoral artery)

A

peripheral artery disease (PAD)

115
Q

maneuvers to differentiate murmurs:

passive straight-leg raise (to 45 degrees, listen after 15 sec)

A

increases venous return

116
Q

maneuvers to differentiate murmurs:

Valsalva (hold for 20 sec, listen just before end)

A

decreases venous return

117
Q

maneuvers to differentiate murmurs:

standing (squat for > 30 sec then quickly stand; listen during first 15 sec after standing)

A

decreases venous return

118
Q

maneuvers to differentiate murmurs:

transient arterial occlusion (BP cuff on both arms, inflated > 20 mm above systolic pressure)

A

increases systemic vascular resistance

119
Q

maneuvers to differentiate murmurs:

handgrip (isometric; listen at end of 1 min max grip)

A

increases systemic vascular resistance

120
Q

maneuvers to differentiate murmurs:

squatting

A

increases venous return and increases systemic vascular resistance, but preload effect is stronger than afterload effect

121
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use

  • standing (from squat)
A

(95%) INCREASED murmur

122
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use

  • Valsalva (if cannot do squat-to-stand)
A

(65%) INCREASED murmur

123
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use

  • passive straight-leg raise
A

(85%) DECREASED murmur

124
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use

  • handgrip
A

(85%) DECREASED murmur

125
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use

  • standing and Valsalva
A

click-murmur moves EARLIER

126
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use

  • transient arterial occlusion
A

(80%) click-murmur moves LATER

127
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use

  • handgrip
A

(70%) click-murmur LATER

128
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use

  • standing and Valsalva
A

DECREASED murmur

129
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use

  • transient arterial occlusion
A

(80%) INCREASED murmur

130
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use

  • handgrip
A

(70%) DECREASED murmur

131
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for AS use

  • transient arterial occlusion
A

DECREASED murmur

132
Q

maneuvers for increasing/decreasing specific systolic murmurs:
- for AS use

  • handgrip
A

DECREASED murmur

133
Q

what happens to the ALL valve murmurs when blood INCREASES across the valve?

A

INCREASES murmur

134
Q

how does STANDING and the strain phase of VALSALVA effect most most valve murmurs, and what are the 2 exceptions?

A
  • DECREASES intensity of murmur

- MVP and HCM

135
Q

how does STANDING and the strain phase of VALSALVA effect right and left cardiac filling?

A

decreases filling

136
Q

sustained handgrip (20-30 seconds) boosts systemic _____ and _____, and therefore decreases the murmurs of _____ and _____

A
  • systemic vascular resistance

- HCM and aortic stenosis (AS)

137
Q

sustained handgrip (20-30 seconds) boosts systemic _____, which prolongs the murmur of _____ d/t earlier prolapse of the valve

A
  • systemic vascular resistance

- MVP (mitral valve prolapse)

138
Q

right-sided murmurs and heart sounds are louder during

A
  • INSPIRATION

- anything that increases VR

139
Q

left-sided murmurs and heart sounds are louder during

A

EXPIRATION

140
Q

what is the only semi-exception to right-sided murmurs sounding less loud during inspiration?

A

right-sided ejection click d/t pulmonic stenosis

141
Q

what happens to S1 intensity when there is:

  • prolonged PR interval
  • MR
  • acute AR (increased LV pressure cause early valve closure)
  • severely calcified mitral valve
A

DECREASES

142
Q

what happens to S1 intensity when there is:

  • short PR interval
  • mitral stenosis
  • hyperdynamic ventricular function
A

INCREASES

143
Q

what causes S1?

A

closing of mitral and tricuspid valves

144
Q

what causes S2?

A

closing of aortic and pulmonic valves at the end of systole

145
Q

when does P2 occur?

A

right after A2

146
Q

what is PHYSIOLOGIC SPLITTING of S2?

A

A2 followed by P2

147
Q

when does PHYSIOLOGIC SPLITTING INCREASE, and why?

A
  • during INSPIRATION

- increased volume of blood in RV, which prolongs systole and delays pulmonic valve closure

148
Q

causes for PERSISTENTLY (or WIDELY) split S2

A
  • pulmonic stenosis
  • acute PE
  • ectopic or pacemaker beats originating in the LEFT ventricle
  • RBBB
149
Q

why do pulmonic stenosis, acute PE, actopic or pacemaker beats originating in the LEFT ventricle, and RBBB cause PERSISTENTLY (or WIDELY) split S2?

A

they cause DELAYED or PROLONGED CONTRACTION of the RIGHT VENTRICLE

150
Q

cause for FIXED splitting of S2

A

atrial septal defect (ASD)

151
Q

other cause for fixed splitting of S2 besides ASD

A

RV failure when SV is unable to increase w/ inspiration

152
Q

cause for PARADOXICAL split S2 w/ P2 coming before A2

A
  • LBBB
  • ectopic or pacemaker beats originating in the RIGHT ventricle
  • advanced HCM
153
Q

indicates end of rapid ventricular filling; is the first part of diastole

A

S3

154
Q

when is the S3 gallop normal?

A
  • children

- high CO, such as pregnant women

155
Q

when is the S3 gallop abnormal?

A

pts > 40 yoa

156
Q

causes for abnormal S3 gallop

A
  • acute ventricular decompensation
  • severe aortic regurgitation
  • severe mitral regurgitation

(anything that increases early LV filling rate or volume)

157
Q

S3 in a pt w/ KNOWN left ventricular dysfunction, means what?

A

POOR prognostic indicator

158
Q

both S3 and S4 are best auscultated how?

A

left lateral decubitus position using the bell

159
Q

when is S3 heard?

A

just after S2 (lub-dub-huh)

160
Q

when is S4 heard?

A

just before S1 (huh-lub-dub)

161
Q

is caused by ventricular filling during atrial contraction

A

S4

162
Q

is heard in pts w/ decreased ventricular compliance

A

S4

163
Q

causes for abnormal S4 gallop

A
  • ischemic heart disease
  • aortic stenosis
  • HCM
  • diabetic cardiomyopathy
  • hypertensive heart disease w/ concentric hypertrophy
164
Q

when do you NOT hear an S4 gallop?

A
  • during atrial fibrillation (no atrial contraction!)

- mitral stenosis

165
Q

which side is the jugular venous pulse assessed?

A

right

166
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • pulmonary HTN
A
  • elevated a and v waves

- other physical exam findings of pulmonary HTN

167
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • tricuspid regurgitation
A
  • large v waves
  • TR murmur
  • pulsatile liver
168
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • constrictive pericarditis
A
  • rapid x and y descents
  • Kussmaul sign
  • pericardial knock
169
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • tamponade
A
  • rapid x descent
  • pulsus paradoxus
  • hypotension
170
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • tricuspid stenosis
A
  • slow y descent

- TS murmur

171
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • restrictive cardiomyopathy
A
  • rapid x and y descents
  • low-voltage ECG
  • echo
  • myocardial bx
172
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • tension pneumothorax
A
  • distended neck veins
  • dyspnea
  • U/L absent breath sounds
  • deviated trachea
  • CXR
173
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • superior vena cava syndrome
A
  • U/L distended neck veins
  • facial edema and cyanosis
  • dx of cancer
174
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • AV dissociation
A
  • irregular cannon a waves

- ECG

175
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • RV infarction
A
  • elevated a and v waves
  • acute inferior MI
  • Kussmaul sign
176
Q

venous waveforms in clinical setting:

  • neck vein appearance
  • other diagnostic features
  • ASD
A
  • large v waves and rapid y descent
  • fixed split S2
  • echo
177
Q

jugular waveform:

  • large, RIGHT-SIDED V WAVES
A
  • ventricular septal rupture

- TR

178
Q

jugular waveform:

  • rapid X and Y DESCENTS
A

constrictive pericarditis

179
Q

jugular waveform:

  • ONLY rapid x descent
A

tamponade (loss of y descent)

180
Q

jugular waveform:

  • large, RIGHT-SIDED Y WAVES
A
  • TS
  • severe pulmonic stenosis
  • severe noncompliant RVH
181
Q

jugular waveform:

  • “CANNON” A WAVES
A
  • complete heart block
  • ventricular tachycardia
  • asynchronous ventricular pacing
  • all conditions w/ AV DISSOCIATION (when atrium is contracting against CLOSED tricuspid valve)
182
Q

tall, LEFT-SIDED V WAVES are d/t

A

severe MR

183
Q

large, LEFT-SIDED A WAVES are d/t

A

mitral stenosis

184
Q

suspect SECONDARY causes of HTN in which pts?

A
  • onset before 30 yoa or after 55 yoa
  • drug-resistant HTN
  • development of uncontrolled HTN that was previously well controlled
185
Q

systolic abdominal bruits (w/o a diastolic bruit) suggests

A

renal vascular HTN

186
Q

what are noninvasive tests to diagnose RAS?

A
  • duplex US
  • CTA
  • MRA
187
Q

when should you think of primary hyperaldosteronism?

A
  • HTN
  • HYPOkalemia
  • LOW renin
188
Q

common cardiac medications:

  • digoxin

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. +
c. +
d. no
e. no
f. no
g. no
h. systolic HF, arrhythmias

189
Q

common cardiac medications:

  • BB

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. +++
b. +++
c. +++
d. no
e. yes
f. yes
g. yes
h. HTN, angina, HF, arrhythmias

190
Q

common cardiac medications:

  • carvedilol

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. ++
b. +++
c. +++
d. yes
e. yes
f. yes
g. yes
h. HTN, angina, HF, arrhythmias

191
Q

common cardiac medications:

  • nifedipine

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. ++
b. no
c. no
d. yes
e. yes
f. no
g. no
h. HTN, angina

192
Q

common cardiac medications:

  • amlodipine

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. +
b. no
c. no
d. yes
e. yes
f. no
g. yes (in DCM)
h. HTN, angina, DCM

193
Q

common cardiac medications:

  • diltiazem

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. ++
b. ++
c. ++
d. yes
e. yes
f. no
g. no
h. HTN, angina, arrhythmias

194
Q

common cardiac medications:

  • verapamil

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. +++
b. +++
c. +++
d. yes
e. yes
f. no
g. no
h. HTN, angina, arrhythmias

195
Q

common cardiac medications:

  • nitrates

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. yes
e. yes
f. no
g. yes (w/ hydralazine)
h. angina, HF

196
Q

common cardiac medications:

  • ACEIs

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. yes
e. no
f. yes
g. yes
h. HTN, HF

197
Q

common cardiac medications:

  • ARBs

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. yes
e. no
f. yes
g. yes
h. HTN, HF

198
Q

common cardiac medications:

  • hydralazine

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. yes
e. no
f. no
g. yes (w/ nitrates)
h. HTN, HF

199
Q

common cardiac medications:

  • spironolactone

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. no
e. no
f. no
g. yes
h. HTN, HF

200
Q

common cardiac medications:

  • eplerenone

a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications

A

a. no
b. no
c. no
d. no
e. no
f. yes (w/ HF)
g. yes (post-MI)
h. HF post-MI

201
Q

chest pain d/t “supply-demand” mismatch between coronary perfusion and cardiac workload

A

angina

202
Q

angina is either classified as

A

STABLE or UNSTABLE

203
Q

3 characteristics of UNSTABLE angina

A
  1. pain at rest
  2. new onset
  3. increased frequency
204
Q

most common underlying process triggering ACUTE coronary syndrome

A

plaque rupture or erosion w/ superimposed thrombus

205
Q

what are causes of INCREASED DEMAND in angina?

A
  • tachycardia
  • fever
  • thyrotoxicosis
206
Q

what are causes of DECREASED SUPPLY in angina?

A
  • hypotension
  • coronary vasospasm
  • anemia
  • hypoxia
207
Q

in what conditions can coronary blood flow be impaired, even in the ABSENCE of epicardial CAD?

A
  • severe aortic valve disease w/ LVH
  • HTN
  • idiopathic dilated CM
  • hypertrophic CM
208
Q

what percentage of pts actually have classic angina at the moment of ischemic ST changes?

A

20%

209
Q

silent ischemia is seen in what pts?

A
  • DIABETICS

- pts w/ prior ischemic events

210
Q

silent ischemia, MIs, and thrombotic strokes occur at what time during day w/ the highest incidence?

A

early morning hours

211
Q

what is the MOST IMPORTANT, easily determinable PROGNOSTIC factor in pts w/ CAD?

A

DEGREE of LV DYSFUNCTION

212
Q

severe LV dysfunction can be a reflection of what?

A

multi-vessel, or left main/left main-equivalent disease

213
Q

is an excellent, objective way to determine SEVERITY of angina and to determine prognosis

A

exercise tolerance test

214
Q

what is the 5-year survival rate for pts able to go to stage 4 of Bruce protocol?

A

nearly 100%

215
Q

what is the 5-year survival rate for pts NOT able to go to stage 1 of Bruce protocol?

A

only 50%

216
Q

coronary ANGIOGRAPHY is NOT REQUIRED to determine what?

A

prognostic factor for pt w/ ACS

217
Q

transient ST-elevation that occurs during stress testing

A

coronary artery SPASM

218
Q

what are causes of RESTING ST-segment elevation?

A
  • acute MI
  • coronary artery spasm
  • pericarditis
  • LV aneurysm
  • LBBB
  • ventricular pacing
  • LVH
  • benign early repolarization
219
Q

chronically underperfused myocardium WITHOUT irreversible myocyte injury

A

hibernating myocardium

220
Q

occurs when severely ischemic myocardium is reperfused after about 1 hour, causing further irreversible microvascular damage to myocytes

A

reperfusion injury

221
Q

d/t acute ischemia and takes 7-10 days for ventricle to return to normal

A

stunned myocardium

222
Q

treatment of all angina

A

modify risk factors and correct aggravating factors (anemia, HTN, smoking, drug abuse, noncompliance)

223
Q

what are the main drugs used to treat angina?

A
  • BB’s and nitrates; CCB’s can also help

- ASA +/- clopidogrel (if allergic to aspirin, or if indicated)

224
Q

which pts might benefit from ranolazine (Ranexa)?

A

pts w/ persistent angina on maximal standard therapy, or as a substitute for BB’s

225
Q

these meds ALL decrease myocardial O2 demand, and ALL decrease afterload

A

BB’s, nitrates, and CCB’s

226
Q

which meds decrease preload > afterload and can cause severe DECOMPENSATION in acute RIGHT ventricular MI?

A

nitrates

227
Q
  • cause sympathetic reflex tachycardia
  • degraded in LIVER
  • tachyphylaxis
A

nitrates

228
Q

how do BB’s decrease myocardial O2 demand?

A
  1. decrease HR
  2. decrease BP
  3. decrease contractility
229
Q

which medication can actually prolong vasospasm in pts w/ variant angina?

A

nonselective BBs

ABIM (9 decks)

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