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CHEST SEEK Library > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

acute hypoxemia on ECMO; 3 possibilities

A
  • patient
  • MV
  • ECMO circuit
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2
Q

acute hypoxemia on ECMO if it’s the ECMO circuit

A
  • large clot in oxygenator
  • poor O2 source
  • significant recirculation
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3
Q

indications for surgery for tricuspid endocarditis

A
  • failure of medical therapy (persistent bacteremia or enlarging vegetation)
  • large vegetation, > 1 cm
  • fungal endocarditis
  • HF d/t TR
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4
Q

when should you worry about fungal endocarditis in IVDU?

A

delayed growth of Candida species in BCs

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5
Q

causes of dampened (smooth contours) arterial line waveform

A
  • air bubbles
  • catheter kinking
  • tubing kinking
  • intraluminal thrombus
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6
Q

what is a distinguishing feature of a properly functioning arterial line system?

A

presence of 1-3 beats of pressure overshoot or oscillation

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7
Q

four phases of myocyte action potential

A
  • phase 4 (repolarization) = resting potential
  • phase 0 (rapid depolarization) = Na+ influx
  • phase 1 = K+ efflux
  • phase 2 (plateau) = Ca++ influx
  • phase 3 (repolarization) = K+ efflux
  • phase 4 (repolarization) = resting potential
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8
Q

arrhythmias are initiated and maintained by what 3 main mechanisms?

A
  • automaticity
  • afterdepolarizations
  • reentry
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9
Q

which arrhythmias are a/w automaticity?

A
  • sinus tachycardia
  • atrial premature complexes
  • some atrial tachycardias
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10
Q

afterdepolarizations are a/w an increase in cellular

A

Ca++ accumulation

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11
Q

afterdepolarizations are a/w an increase in cellular Ca++ accumulation, leading to what?

A

repeated myocardial depolarization

  • EADs if between phase 2 and phase 3 of the action potential (prolongs action potential and QT on ECG)
  • DADs if between phase 3 and phase 4 of the action potential
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12
Q

which arrhythmia may be related to early afterdepolarization?

A

initiation of torsades de pointes

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13
Q

which arrhythmias may be related to delayed afterdepolarization?

A
  • digoxin toxicity
  • catecholamine-induced ventricular tachycardia
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14
Q

which arrhythmias are a result of reentry?

A

most supraventricular and ventricular tachycardias

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15
Q

class 1 antiarrhythmics
- work on what phase of the action potential
- block what channel

A
  • phase 0
  • Na+ channel blocker
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16
Q

what are the class 1A antiarrhythmics?

A
  • quinidine
  • procainamide
  • disopyramide
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17
Q

when are the class 1A antiarrhythmics used?

A
  • AF
  • AFl
  • SVT
  • ventricular tachyarrhythmias (VTs)
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18
Q

what are the class 1B antiarrhythmics?

A
  • lidocaine
  • tocainide
  • mexiletine
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19
Q

when are the class 1B antiarrhythmics used?

A

VTs

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20
Q

what are the class 1C antiarrhythmics?

A
  • flecainide
  • propafenone
  • moricizine
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21
Q

when are the class 1C antiarrhythmics used?

A

life-threatening SVT and VTs

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22
Q

quinidine distinguishing characteristic

A

moderate anticholinergic

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23
Q

quinidine AEs

A
  • cinchonism (blurred vision, tinnitus, headache, psychosis)
  • cramping and nausea
  • enhances digitalis toxicity
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24
Q

procainamide distinguishing characteristics

A
  • weak anticholinergic
  • relatively short half-life
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25
Q

procainamide AE

A

lupus-like syndrome (25-30%)

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26
Q

disopyramide distinguishing characteristic

A

strong anticholinergic

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27
Q

disopyramide AE

A

negative inotropic effect

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28
Q

lidocaine distinguishing characteristic

A

good efficacy in ischemic myocardium

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29
Q

tocainide distinguishing characteristic

A

orally active lidocaine analog

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30
Q

tocainide AE

A

pulmonary fibrosis

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31
Q

mexiletine distinguishing characteristic

A
  • orally active lidocaine analog
  • good efficacy in ischemic myocardium
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32
Q

flecainide used for

A

SVT

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33
Q

flecainide AE

A

can induce life-threatening VT

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34
Q

propafenone used for

A

SVT and VT

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35
Q

propafenone AE

A

can worsen HF d/t beta and Ca++ channel blockade

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36
Q

moricizine distinguishing characteristic

A

also has class 1B activity

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37
Q

what are the class 2 antiarrhythmics?

A
  • nadolol
  • propranolol
  • sotalol
  • timolol
  • acebutolol
  • atenolol
  • betaxolol
  • bisoprolol
  • esmolol
  • metoprolol
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38
Q

nadolol distinguishing characteristic

A

long acting

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39
Q

propranolol distinguishing characteristic

A
  • membrane stabilizing activity
  • prototypical beta-blocker
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40
Q

timolol distinguishing characteristic

A

primary used for glaucoma

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41
Q

acebutolol distinguishing characteristic

A

intrinsic sympathomimetic activity

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42
Q

betaxolol distinguishing characteristic

A

membrane stabilizing activity

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43
Q

esmolol distinguishing characteristic

A

ultra-short acting

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44
Q

metoprolol distinguishing characteristic

A

membrane stabilizing activity

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45
Q

class 3 antiarrhythmics
- work on what phase of the action potential
- block what channel

A
  • phase 3
  • K+ channels
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46
Q

what are the class 3 antiarrhythmics?

A
  • amiodarone
  • dronedarone
  • bretylium
  • sotalol
  • ibutilide
  • dofetilide
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47
Q

amiodarone therapeutic uses

A
  • VT
  • VF
  • AF and AFl (off-label)
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48
Q

amiodarone distinguishing characteristic

A
  • very long half-life (25-60 days)
  • has class 1, 2, 3, and 4 activity
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49
Q

amiodarone AEs

A
  • pulmonary fibrosis
  • hypothyroidism
  • bradycardia and AVB
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50
Q

dronedarone therapeutic uses

A
  • AF (non-permanent)
  • AFl
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51
Q

dronedarone distinguishing characteristic

A
  • structurally related to amiodarone
  • CI in severe or recently decompensated symptomatic HF
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52
Q

dronedarone AE

A

risk for severe liver injury

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53
Q

bretylium therapeutic uses

A

life-threatening VT and VF

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54
Q

bretylium distinguishing characteristic

A

initial sympathomimetic effect (NE release) followed by inhibition which can lead to hypotension

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55
Q

sotalol therapeutic uses

A
  • VT
  • AF
  • AFl
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56
Q

sotalol distinguishing characteristic

A

also has class 2 activity

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57
Q

ibutilide therapeutic uses

A
  • AF
  • AFl
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58
Q

ibutilide AE

A

can cause life-threatening ventricular arrhythmias

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59
Q

dofetilide therapeutic uses

A
  • AF
  • AFl
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60
Q

dofetilide distinguishing characteristic

A
  • very selective K+ channel blocker
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61
Q

dofetilide AE

A

can cause life-threatening ventricular arrhythmias

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62
Q

what are the class 4 antiarrhythmics?

A
  • verapamil
  • diltiazem
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63
Q

what are the 3 classes of CCBs?

A
  1. dihydropyridines
  2. phenylalkylamine (non-dihydropyridine)
  3. benzothiazepine (non-dihydropyridine)
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64
Q

what are the dihydropyridine CCBs?

A
  • amlodipine
  • felodipine
  • isradipine
  • nicardipine
  • nifedipine
  • nimodipine
  • nitrendipine
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65
Q

which CCB is the phenylalkylamine class?

A

verapamil

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66
Q

which CCB is the benzothiazepine class?

A

diltiazem

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67
Q

how do CCBs work as antiarrhythmics?

A
  • decrease firing rate of aberrant pacemaker sites w/i the heart
  • decrease conduction velocity, especially at AV node
  • prolong repolarization, especially at AV node
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68
Q

initial treatment of RV infarction

A

ivf w/o overdistention of RV

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69
Q

treatment of RV infarction if no improvement w/ ivf

A

inotrope

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70
Q

clinical findings of primary RCM

A

skeletal myopathy

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71
Q

What causes endomyocardial fibrosis (EMF)

A

h/o parasitic infestation, hematologic malignancy, or AI d/o

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72
Q

clinical findings of amyloidosis

A
  • macroglossia
  • periorbital ecchymosis
  • orthostatic hypotension
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73
Q

clinical findings of drug-induced

A

h/o chloroquine or hydroxychloroquine use

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74
Q

What causes post-radiation RCM?

A

h/o mediastinal radiation

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75
Q

clinical findings of hemochromatosis

A
  • hyperpigmentation
  • liver failure
  • DM
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76
Q

What causes Anderson-Fabry

A

reduced alpha-galactosidase

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77
Q

clinical findings of Danon/Pompe/PRKAG2

A

skeletal myopathy

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78
Q

clinical findings of Friedreich’s ataxia

A
  • ataxia
  • DM
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79
Q

clinical findings of constrictive pericarditis

A
  • fluid overload; ranges from peripheral edema to anasarca
  • decreased CO in response to exertion
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80
Q

if;
- fever
- AMS
- AF w/ RVR
- HF
after coronary angiography, consider what condition?

A

thyroid storm

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81
Q

Jod-Basedow syndrome

A

thyroid storm in a patient w/ subclinical hyperthyroidism precipitated by administration of iodinated contrast

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82
Q

clinical hallmarks of cardiac amyloidosis

A
  • biventricular HF
  • pAF
  • carpal tunnel syndrome
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83
Q

3 main types of amyloidosis

A
  1. amyloid light-chain (AL) amyloidosis
  2. amyloid A (AA) amyloidosis
  3. amyloid transthyretin (ATTR) amyloidosis
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84
Q

AL amyloidosis diagnosis

A

measuring serum immunoglobulin light chains and finding a monoclonal spike

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85
Q

what test is highly sensitive for ATTR amyloidosis in the presence of HF w/ a compatible TTE?

A

technetium-labeled bone scintigraphy compared w/ the bone signal

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86
Q

what class of medications used to treat non-small cell lung cancer can cause myocarditis?

A

checkpoint inhibitors, eg pembrolizumab

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87
Q

how to distinguish between true aortic stenosis and pseudostenosis?

A

dobutamine stress test

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88
Q

if dobutamine increases CO and the aortic valve gradient is unchanged, then calculated valve area will INCREASE, indicating what?

A

pseudostenosis

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89
Q

if dobutamine increases CO and the aortic valve gradient increases PROPORTIONALLY, then what is confirmed?

A

true aortic stenosis

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90
Q

if dobutamine does NOT increase CO (that is, the patient lacks contractile reserve), the test is what?

A

indeterminate regarding the severity of aortic stenosis

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91
Q

if a dobutamine stress test is indeterminate regarding the severity of aortic stenosis, what does that mean regarding prognosis?

A

POOR prognosis with or w/o valve replacement

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92
Q

what test is contraindicated in the presence of critical aortic stenosis?

A

exercise stress testing

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93
Q

dipyridamole administration w/ myocardial perfusion imaging may be used to diagnose what?

A

myocardial ischemia

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94
Q

is TEE good at evaluating AS?

A

no

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95
Q

how is aortic valve gradient calculated?

A

flow/AVA

  • AVA = aortic valve area
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96
Q

what tachyarrhythmia should be considered when these 3 criteria are present?

  1. wide complex tachyarrhythmia
  2. irregularly irregular rhythm
  3. varying widths of QRS complexes
A

preexcited AF or AF in a patient w/ an accessory conduction pathway AKA WPW syndrome

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97
Q

patients w/ WPW syndrome have an accessory conduction pathway that directly connects what to what?

A

atria w/ ventricles and bypasses the AV node

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98
Q

treatment for patients w/ preexcitation AF if signs/symptoms of hemodynamic instability; hypotension, chest pain, or confusion

A

urgent electrical cardioversion

99
Q

treatment for patients w/ preexcitation AF w/o hemodynamic instability

A

medical treatment w/ ibutilide (class 3) or procainamide (class 1a)

100
Q

what ETCO2 level is often the first indication that ROSC has been achieved?

A

abrupt increase to > 35 to 40 mmHg

101
Q

normal aortic valve area

A

3 to 4 cm2

102
Q

severe AS AVA (aortic valve area)

A

typically ≤ 1 cm2

103
Q

what are the lateral leads?

A

1, aVL, v5-v6

104
Q

what coronary arteries are a/w the lateral leads?

A

LCx or diagonal of LAD

105
Q

what coronary arteries are a/w leads 1, aVL, v5-v6?

A

LCx or diagonal of LAD

106
Q

what are the inferior leads?

A

2, 3, aVF

107
Q

what coronary arteries are a/w the inferior leads?

A

RCA and/or LCx

108
Q

what coronary arteries are a/w leads 2, 3, aVF?

A

RCA and/or LCx

109
Q

what are the septal and anterior leads?

A

v1-v2 = septal
v3-v4 = anterior

110
Q

what coronary arteries are a/w the septal/anterior leads?

A

LAD

111
Q

what coronary arteries are a/w leads v1-v4?

A

LAD

112
Q

what is the key to distinguishing AF in a patient w/ LBBB from VT?

A

irregular R-R interval

113
Q

complications of aortic dissection

A
  • rupture into pericardium
  • acute MI, 3%
  • aortic insufficiency, 32%
  • stroke, 5%
  • BP differential, 15%
  • paraplegia, 1%
  • mesenteric ischemia, 5%
  • renal ischemia, 8%
  • lower extremity ischemia, 3%
114
Q

which P2Y12 inhibitor is a/w dose-related episodes of dyspnea (unknown mechanism), and ventricular pauses?

A

ticagrelor

115
Q

AF, in patients, w/ what condition can have profound effects on hemodynamic stability?

A

structural heart disease

116
Q

most reliable view on pocus to measure RV size

A

apical 4-chamber view

117
Q

what is a normal RV size?

A

≤ 2/3 LV

118
Q

what is the most appropriate sequence of resuscitation for cardiac arrest in a patient w/ pulseless VT or VF and is w/i 10 days of cardiac surgery?

A
  • shock x 3
  • check for rhythm and pulse
  • CPR
  • call cardiac surgeon for sternotomy
  • amiodarone 300 mg iv
  • prepare chest for resternotomy
  • repeat shock every 2 min
  • perform resternotomy w/i 5 min by any trained personnel
119
Q

VF is the cause of cardiac arrest in what percentage of cardiac surgery patients?

A

25 to 50%

120
Q

what causes of cardiac arrest should be considered in post cardiac surgery patients, especially in patients in whom a SBP > 60 mm Hg is not achieved during effective CPR?

A
  • cardiac tamponade
  • intrathoracic bleeding
121
Q

what dose of epinephrine should be given during a cardiac arrest in a post cardiac surgery patient?

A

50 to 300 mcg iv (0.05-0.3 mg)

122
Q

why should reduced doses of epinephrine be given during cardiac arrest in a post cardiac surgery patient?

A

the usual dose, 1 mg iv, can precipitate severe HTN and bleeding in patients who regain ROSC

123
Q

90% of Duchenne muscular dystrophy (DMD) patients > 18 yoa have what heart problem?

A

dilated cardiomyopathy

124
Q

treatment for DMD-related cardiomyopathy

A

glucocorticoids

125
Q

what percentage of mitral and tricuspid flow velocities indicates cardiac tamponade, reflecting ventricular interdepence?

A
  • > 30% variation in mitral
  • > 60% variation in tricuspid
126
Q

how to calculate pulmonary vascular resistance (PVR)?

A

mean pulmonary artery pressure - pulmonary artery wedge pressure / CO

mPAP - PAWP / CO

PAWP = left atrial pressure (LAP)

127
Q

how to calculate systemic vascular resistance (SVR)?

A

mean arterial pressure - right atrial pressure / CO

MAP - RAP / CO

128
Q

CHB a/w IWMI is located where in 90% of patients?

A

proximal to the His bundle

129
Q

CHB a/w AWMI is more often located where?

A

distal to the AV node

130
Q

CHB a/w AWMI is usually symptomatic and a/w?

A

high mortality rate

131
Q

normal intracardiac and vascular pressures (mm Hg)

  • RA
A

0-4 (varies w/ respiration)

132
Q

normal intracardiac and vascular pressures (mm Hg)

  • RV
A

25/4

133
Q

normal intracardiac and vascular pressures (mm Hg)

  • PA
A

25/10

134
Q

normal intracardiac and vascular pressures (mm Hg)

  • LA
A

8-10

135
Q

normal intracardiac and vascular pressures (mm Hg)

  • LV
A

120/10

136
Q

normal intracardiac and vascular pressures (mm Hg)

  • aorta
A

120/80

137
Q

normal TAPSE (tricuspid annular plane systolic excursion)

A

> 16 mm

138
Q

treatment of RVMI

A
  • antiplatelet therapy
  • reperfusion therapy
139
Q

treatment of shock d/t RVMI is aimed at raising RV stroke volume by doing what?

A
  • optimizing preload
  • decrease afterload
  • RV contractility
  • RVAD
  • venoarterial extracorporeal support
140
Q

should fluid loading be used to treat shock d/t RVMI?

A

no, and it may even depress CO thru ventricular interdependence

141
Q

should MV w/ PEEP be used to treat shock d/t RVMI?

A

no, as it tends to increase RV afterload, which depresses SV, and may exacerbate shock

142
Q

type 1 MI

A

spontaneous MI

143
Q

type 2 MI

A

MI 2/2 ischemic imbalance

144
Q

type 3 MI

A

MI resulting in death w/o biomarkers

145
Q

type 4a MI

A

MI related to PCI

146
Q

type 4b MI

A

MI related to stent thrombosis

147
Q

type 5 MI

A

MI related to CABG

148
Q

In a patient who has unexplained dyspnea, what conditions are you looking for when doing a RHC?

A
  • RV dysfunction
  • biventricular dysfunction
  • congenital heart disease
  • pulmonary arterial HTN
  • pericardial disease
  • intracardiac shunting
149
Q

absolute CIs to RHC

A
  • mechanical TV
  • RVAD
150
Q

relative CIs to RHC

A
  • coagulopathy
  • arrhythmias
  • LBBB
151
Q

unusual pattern of ST elevation in leads v1 and v2

A

Brugada syndrome

152
Q

increased r/o

  • syncope
  • cardiac arrest
  • sudden death

often occurs during sleep, rest, or enhanced vagal tone

A

Brugada syndrome

153
Q

channelopathy w/ loss of function of cardiac sodium channels

A

Brugada syndrome

154
Q

syndrome of polymorphic VT a/w prolonged QT

A

torsades de pointes

155
Q

first-line tx for torsades de pointes

A

magnesium 1-2 g IV or IO diluted in 10 mL of fluid over 5-20 minutes

156
Q

AE if magnesium sulfate is administered too rapidly

A

hypotension

157
Q

electrolyte d/o’s that can contribute to prolonged QT and TdP

A
  • hypokalemia
  • hypomagnesemia
158
Q

medications a/w long QT syndrome and TdP (12 items listed)

A
  • methadone
  • procainamide
  • quinidine
  • sotalol
  • amiodarone
  • haloperidol
  • erythromycin
  • levofloxacin
  • trimethoprim-sulfamethoxazole
  • azole antifungals
  • vasopressin
  • tacrolimus
159
Q

other risk factors for TdP besides electrolyte d/o’s and medications

A
  • bradycardia
  • liver dysfunction
  • renal dysfunction
  • heart disease
  • recent AF
160
Q

genetic d/o characterized by myofibril disarray, fibrosis, and myocardial hypertrophy

A

hypertrophic cardiomyopathy (HCM)

161
Q

HCM patients are prone to dynamic outflow tract obstruction in the following settings

A
  • decreased preload
  • decreased afterload
  • increased contractility
162
Q

the best way to increase BP in HCM w/ outflow tract obstruction is to ensure the following

A
  • adequate volume repletion
  • selective alpha agonist, such as phenylephrine
163
Q

which medications can increase outflow tract obstruction and decrease BP?

A
  • epinephrine
  • norepinephrine
  • dobutamine
  • dopamine
164
Q

which medical therapy is counterproductive and inappropriate in patients w/ CHF d/t HCM?

A

diuresis

165
Q

what factors commonly affect recirculation in VV-ECMO?

A
  • cannula configuration
  • cannula positioning
  • pump speed
  • ECMO blood flow rate
  • direction of ECMO blood flow
  • changes in intrathoracic pressure
  • changes in intracardiac pressure
  • changes in intraabdominal pressure
166
Q

what will increasing pump speed or ECMO blood flow rates lead to in a patient on VV-ECMO w/ recirculation?

A

worsen recirculation

167
Q

besides recirculation, persistent hypoxemia on VV-ECMO can be d/t

A
  • small cannula size limiting ECMO blood flow rate
  • patient positioning
  • low ratio of ECMO flow to native CO (worse in septic patients)
  • metabolic rate/O2 consumption
  • malfunctioning components of the circuit (eg oxygenator)
168
Q

VA-ECMO is used in which patients?

A

hemodynamic instability from LV or RV cardiogenic shock

169
Q

dopamine is a/w increased risk of what compared to norepinephrine?

A

tachyarrhythmias

170
Q

most important thing to do when removing a central venous catheter

A

placing the patient in a Trendelenburg or flat position

171
Q

what are the deleterious consequences of LV not ejecting blood while on ECMO?

A
  • stasis in LVOT and proximal aorta which leads to risk of thrombosis and systemic embolism
  • LV continues to fill through the pulmonary and Thebesian veins which raises LV and pulmonary vascular pressure
172
Q

what happens when the LV is overdistended in a patient w/ cardiogenic shock on VA-ECMO?

A
  • pulmonary edema
  • delay in LV recovery
173
Q

treatment to decompress LV in cardiogenic shock on VA-ECMO

A
  • inotropes
  • intraaortic balloon counterpulsation (to reduce LV afterload)
  • reducing ECMO pump speed (which lowers LV afterload)
  • placement of LVAD
  • transvenous or transseptal cannula drainage
  • maintaining PEEP (reduces afterload)
174
Q

what happens to LV afterload when you increase PEEP?

A

decreases

  • increasing PEEP raises intrathoracic pressure
  • decreases venous return to right heart
  • overdistention of lungs can increase PVR –> RV failure –> decrease LV preload
175
Q

underdamping (SBP is overestimated and DBP is underestimated) can be caused by

A
  • excessively long tubing
  • tubing that’s too elastic
  • excessive pressure bag inflation
  • too many stopcocks
176
Q

overdamping (SBP is underestimated and DBP is overestimated) occurs when the pressure waveform is flattened, can be caused by

A
  • air bubbles in tubing
  • clot in the catheter
  • kinked tubing
  • tubing that’s too stiff
  • tubing that’s too short
  • a catheter positioned against a blood vessel wall
  • inadequate volume in pressure bag
177
Q

how many oscillations are optimal after the end of a square wave test?

A

1-2

178
Q

how many oscillations at the end of a square wave test represent overdamping?

A

no oscillations (response speed is too slow)

179
Q

how many oscillations at the end of a square wave test represent underdamping?

A

> 2

180
Q

LCx supplies

A

LA and LV

181
Q

RCA supplies

A

RA and RV

182
Q

LAD supplies

A

RV, LV, and interventricular septum

183
Q

classic physical findings of RV infarction

A
  • hypotension
  • JVD
  • clear lung fields
184
Q

hypotension in patients w/ RV infarction results from what?

A

failure of dysfunctional RV to deliver adequate preload to the LV

185
Q

what medications should be avoided in patients w/ RV infarction?

A

medications that decrease preload (eg nitrates, diuretics, morphine)

186
Q

besides murmur, what are the findings of severe MR?

A
  • pulmonary edema
  • crackles on lung exam
  • hypoxemia
187
Q

heart block early after acute IWMI is usually d/t

A

ischemia in the AV node

188
Q

when does heart block from acute IWMI usually resolve?

A

w/i 5 to 7 days

189
Q

which therapy in CHF patients w/ LBBB has been shown to improve LV systolic performance, decrease MR, reduce LV remodeling, improve symptoms, and improve mortality?

A

resynchronization w/ biventricular implantable cardiac defibrillator (ICD)

190
Q

guidelines recommend insertion of biventricular ICD in which patients?

A

EF < 35% and LBBB w/ QRS > 120 ms (optimally > 150 ms) who are symptomatic on guideline-directed medical therapy for HF

191
Q

which coronary artery lies in close proximity to the mitral annulus and can be injured by suturing, distortion of the artery, coronary laceration, subintimal hematoma, or coronary embolization during MV repair?

A

left circumflex coronary artery (aka circumflex coronary artery)

192
Q

when should an implantable defibrillator be placed for primary prevention after MI after revascularization if EF is < 40% on optimal medical therapy?

A

after 90 days to allow for potential ventricular recovery

193
Q

mPAP equation

mPAP = mean pulmonary arterial pressure

A

2/3rd PADP + 1/3rd PASP

PADP = end-expiratory PA diastolic pressure

PASD = end-expiratory PA systolic pressure

194
Q

hemopericardium in the setting of acute STEMI should suggest 1 of 2 diagnoses

A
  • Stanford type A (proximal) aortic dissection into the right coronary cusp w/ subsequent pericardial dissection
  • ventricular free-wall rupture
195
Q

is TEE sensitive for proximal, type A, aortic dissection?

A

yes, very

196
Q

how much fluid bolus do patients w/ hypotension and tamponade physiology need if they are fluid responders?

A

250-500 mL

197
Q

what should you think of and look for in a patient that had VF cardiac arrest, or has sinus bradycardia with no backup rate initiated in a patient w/ an AICD?

A
  • failed AICD
  • fracture of the AICD lead which can be seen on cxr
198
Q

treatment for acute severe MR c/b cardiogenic shock 2/2 acute papillary muscle rupture 2/2 recent STEMI until surgical MVR

A

IABP insertion

199
Q
  • acute pulmonary edema
  • acute hypoxemic respiratory failure
  • cardiogenic shock
  • occurs 2-7 days after STEMI
A

severe acute MR from acute papillary muscle rupture

200
Q

management of acute papillary muscle rupture causing acute MR is aimed at what in order to direct blood flow across the aortic valve, which reduces MR, increases CO, and decreases pulmonary venous congestion?

A

reducing LV afterload

201
Q

infusion of vasodilators, such as nitroglycerin, nicardipine, or nitroprusside, to reduce afterload are limited by what?

A

systemic hypotension

202
Q

mitral valve transcatheter edge-to-edge repair to clip anterior and posterior leaflets of the MV is indicated in which patients?

A
  • chronic primary MR w/ severe symptoms w/ high surgical risk
  • chronic secondary (functional) MR
203
Q

the definition of “electrical storm” varies, but in general the common definitions are

A
  • patients w/ an implantable cardiac defibrillator vs those w/o
  • recurrence of ventricular arrhythmias requiring treatment w/i a short period of time, usually > 2-3x w/i 24 hours
204
Q

what are the fundamental principles in treating electrical storm?

A
  • controlling the acute arrhythmia
  • addressing the underlying problem
  • managing the high sympathetic tone
  • rarely, urgent ablation may be attempted
205
Q

what are the usual antiarrhythmic therapies for sustained monomorphic VT?

A
  • amiodarone
  • dofetilide
  • lidocaine
206
Q

management for high catecholamine state observed in electrical storm (better than metoprolol)

A

propranolol

207
Q

recommended medication for electrical storm in patients w/ Brugada syndrome

A

isoproterenol

208
Q

what factors affect O2 delivery in patients on ECMO?

A
  • integrity of ECMO circuit
  • RV function
  • oxygenation by the lungs
  • O2-carrying capacity
209
Q

O2 delivery capability in patients on ECMO is determined by what?

A
  • blood flow
  • Hb concentration
  • inlet Hb saturation
  • membrane lung properties
210
Q

DO2 (rate of O2 delivery (mL/min)) formula

A

CO x (1.39 x [Hb] x SaO2 + (0.003 x PaO2))

CO = cardiac output (L/min)
1.39 = O2 binding capacity of Hb (1.39 mL/g)
SaO2 = Hb O2 saturation expressed as a decimal
0.003 = amount of dissolved O2 in the blood (mL)

211
Q

ECMO promotes lung rest by

A
  • minimizing shear stress and dynamic strain related to volutrauma (via low TV ventilation)
  • minimizing static strain and barotrauma (through the lowest PEEP necessary to reach critical opening pressure of the alveoli)
212
Q

a “spontaneous” wedge waveform indicates what?

A

incorrectly positioned catheter

213
Q

incorrect positioning of a pulmonary catheter can lead to what complications?

A
  • pulmonary infarction
  • pulmonary artery rupture
214
Q

what techniques can help predict volume responsiveness?

A
  • TTE to estimate EF and/or SV
  • change in IVC diameter
  • pulse pressure variability
  • SV variability
  • SV index (SVI)
215
Q

how can SV be measured?

A
  • TTE
  • flow analysis at the aortic root via Doppler US
  • chest wall electrical bioimpedance
  • flow-directed pulmonary artery catheter
  • arterial pulse contour analysis
216
Q

when techniques to predict volume responsiveness are combined w/ what, demonstrate high sensitivity and specificity?

A

passive leg raise maneuver or a 4 mL/kg fluid bolus

217
Q

variation in IVC diameter w/ inspiration is evaluated w/ US and is dependent on what factors?

A
  • CVP
  • intrapleural pressure
  • intraabdominal pressure
  • IVC distensibility (compliance)
218
Q

what is the formula for IVC diameter variation to predict volume responsiveness?

A

(Dmax - Dmin) / Dmin

D = measured IVC diameter

219
Q

what % change in IVC diameter predicts volume responsiveness?

A

> 18%

220
Q

what 2 variables are required when evaluating for volume responsiveness based on IVC diameter variation?

A
  • MV w/ > 8 mL/kg TV
  • passive variation
221
Q

how should a very high BMI be taken into consideration in regards to IVC diameter variation and volume responsiveness?

A

increased abdominal pressure could alter changes in IVC diameter

222
Q

do arrhythmias alter the respiratory changes in IVC diameter?

A

no

223
Q

what is a surrogate for SV variability that occurs w/ positive pressure ventilation?

A

pulse pressure variability

224
Q

reproducibility in SV variability and pulse pressure variability requires what conditions to ensure adequate intrapleural pressure swings to alter venous return?

A
  • TV of 10 mL/kg
  • absence of arrhythmia, especially AF
225
Q

what is the most frequent cause of pregnancy-related MI?

A

pregnancy-associated spontaneous coronary artery dissection (SCAD)

226
Q

preferred initial treatment for pregnancy-associated spontaneous coronary artery dissection (SCAD) if hemodynamically stable and no signs of ongoing ischemia?

A

conservative medical management w/ aspirin and nitroglycerin

227
Q

which patients w/ pregnancy-associated spontaneous coronary artery dissection (SCAD) should be considered for PCI?

A
  • p/w ongoing or recurrent ischemia
  • hemodynamic instability
  • ventricular arrhythmias
  • suitable coronary anatomy
228
Q

which patients w/ pregnancy-associated spontaneous coronary artery dissection (SCAD) should be considered for emergency CABG?

A
  • patients w/ left main dissections
  • extensive dissections involving proximal arteries
  • PCI failed
  • not anatomically suitable for PCI
229
Q

what is the only variable programmed by the operator in an LVAD (Heartmate 2)?

A

pump SPEED (rpm)

230
Q

which setting on an LVAD is a direct measurement of the number of watts required by the device to pump blood at the set rpm?

A

pump POWER

231
Q

what setting on the LVAD is a calculated number based on measured pump power and set pump speed?

A

FLOW

232
Q

the actual blood flow through the LVAD pump is dependent on what factors?

A
  • pump SPEED
  • preload
  • pressure differential between mean aortic pressure and LV chamber pressure
233
Q

what happens to LVAD pump POWER when LV pump thrombosis occurs?

A

increases in response to increased resistance to flow w/i the device

234
Q

what happens to flow if LVAD pump thrombosis is sufficiently severe?

A

can decrease

235
Q

what happens to the LVAD in RV failure?

A

LVAD output might decrease because of decreased preload

236
Q

the following indicate what issue?
- HF symptoms
- increased pump POWER
- low output LVAD alarms
- LV dilation
- aortic valve opening
- dark urine
- increased LDH

A

LVAD pump thrombosis

237
Q

management of LVAD pump thrombosis in a hemodynamically stable patient

A
  • fluid resuscitation
  • heparin gtt
  • +/- glycoprotein 2b/3a inhibitor
  • +/- thrombolytic agent
238
Q

when would LVAD pump thrombosis be managed w/ LVAD pump exchange?

A
  • hemodynamically unstable patients
  • failed medical therapy
239
Q
  • mechanical complication following acute MI
  • usually occurs 2 to 7 days after
  • pulmonary edema
  • hypotension
  • cardiogenic shock
  • V waves in PCWP tracing (increased LA diastolic pressure)
A

papillary muscle rupture

240
Q
  • mechanical complication following acute MI
  • pulmonary edema
  • shock
  • left-to-right shunt which increases pulmonary artery saturation
A

ventricular septal rupture

241
Q
  • mechanical complication following acute MI
  • a/w elevation and equalization of right-sided and left-sided diastolic pressure w/o a V wave
A

free-wall rupture w/ tamponade

242
Q

management of papillary muscle rupture

A
  • vasoactive support
  • afterload reduction if feasible
  • mechanical circulatory support as a temporizing measure
  • definitive therapy = surgical valve repair or replacement
243
Q

what percentage of patients suffering inhospital cardiac arrest survive to hospital discharge?

A

25%

244
Q

what are the essential components to achieve best components from inhospital cardiac arrest?

A
  • early recognition
  • highest quality BLS
  • optimal ACLS
  • optimal postcardiac arrest care (TTM)

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