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Critical Care Boards > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What is seen in EKG in ACS?

A

ST elevations above 1mm in 2 contiguous leads, new LBBB, ST depressions >0.5mm, TWI >1mm, Q waves

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2
Q

What is the timeline to fibrinolytics or PCI in STEMI patients?

A

Within 12 hrs of symptoms, or 12-24 hrs of clinical/EKG ischemia
30 min to fibrinolytics, 90 min to PCI

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3
Q

What are the guidelines if PCI is unavailable at the institution for STEMI patients?

A

If DIDO (door in, door out) is <30min and FMC to device is <120min, then transfer for PCI. If there is no lytic contraindication and DIDO >30 min or FMC to device is >120 min, then lytics first then transfer

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4
Q

When are bare metal stents preferred over DES in AMI?

A

patients with high bleeding risk, unable to comply with DAPT for 1+ years, anticipated surgery within 1 year

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5
Q

What is the danger of receiving streptokinase?

A

High risk of allergic reactions if you’ve had it before

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6
Q

Which adjuncts are added for fibrinolytic therapy in AMI patients?

A

Heparin, ASA, and clopidogrel (300mg load then 75mg)

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7
Q

When should beta blockers be used in AMI?

A

Orally once revascularized, IV only if hemodynamically unstable from AMI

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8
Q

Is there a mortality benefit to revascularizing UA/NSTEMI patients?

A

Yes, but timeline is 24-48hrs

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9
Q

What is the PCI strategy for patients that receive fibrinolysis for STEMI?

A

If it works: non-invasive ischemic testing or transfer high risk patients for elective PCI within 24hr
If it doesn’t work (persistent ST elevation, persistent symptoms, develop shock, evidence of artery re-occlusion): PCI

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10
Q

When risk stratifying NSTEMI/UA patients, which patients get a conservative strategy?

A

No high risk features with plan to get more information (echo, stress test, etc) before proceeding with angio. Otherwise, angio within 24-72hr

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11
Q

What are some EKG changes seen in pericarditis?

A

Diffuse ST elevation in 8+ leads, PR elevation in aVR with ST depression, PR depression everywhere else

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12
Q

What are some EKG changes seen in cardiac tamponade?

A

May see RBBB, low voltage

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13
Q

How do you differentiate VT with SVT with aberrancy?

A

Starts wide then narrows (“warms up” the His bundle)

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14
Q

What are you suspecting when you see a shortened PR interval with slurring of the QRS complex?

A

An accessory pathway capable of antegrade pre-excitation, such as in WPW. Avoid AV nodal blocking agents

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15
Q

What happens when you give atropine to patients with ischemia to AV node?

A

Speed up the sinus node but infranodal conduction is worse so becomes more overt heart block

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16
Q

Which meds cause prolonged QT?

A

SSRI/SNRIs, abx (macrolides, fluoroquinolones, azoles), antiarrhythmics, antipsychotics, triptans, methadone

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17
Q

What are the EKG changes seen in Brugada syndrome?

A

ST elevations in V1-3 with a RBBB appearance, J point elevation and a gradually sloping or biphasic T wave. Sodium channel blocking antiarrhythmics (ie procainamide) can reveal this in some patients. Tx with amiodarone, AICD and quinidine, potentially ablation.

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18
Q

Which subgroup of afib patients should receive adjunctive digoxin and not CCB therapy?

A

LV dysfunction/HF. No chronic digoxin monotherapy as it has increased mortality

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19
Q

What EKG changes are seen with digoxin toxicity?

A

Bidirectional VT, atrial/junctional/ventricular VT, severe sinus bradycardia or heart block

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20
Q

What is a VVI pacemaker vs VOO?

A

VVI (vent/vent/inhibitor) blocks aberrant beats, while VOO is driving the pacing regardless of what the native heart is doing

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21
Q

What are some differences between sinus node dysfunction vs vagal-mediated bradycardia?

A

Favors SN dysfunction: meds or prior cardiac Sx, age, not related to position, has a tachy-brady picture

Favors Vagal-mediated: positional, situational (cough//micturition, stretching, etc), sinus brady with AV block

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22
Q

What doses of dopamine have more beta activity versus alpha activity?

A

Beta- 5-10 mcg/kg/min
Alpha- above 10 mcg/kg/min

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23
Q

Why do 50% of patients with AMI have sinus bradycardia?

A

Disruption of blood flow to SA node artery and increased vagal tone in the first 6 hrs after an inferior wall MI

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24
Q

How are bradyarrhythmias treated in setting of AMI?

A

Symptomatic, sinus pauses >3 sec, HR <40 + hypotension

Specifically transvenous pacing if the following:
asystole, alternating right and left bundle branch blocks, 2AVB with new BBB, 2AVB with fascicular block and RBBB, or 3AVB

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25
Q

Recall the pacemaker codes

A
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26
Q

What does a magnet do for a pacemaker?

A

Turns off the sensing

ie during surgery inappropriate sensing from Bovie doesn’t trigger or to stop pacemaker mediated tachycardia.

Placing a magnet over ICD inhibits shocks but not pacing

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27
Q

What are causes of appropriate and inappropriate ICD shocks?

A

Appropriate: arrhythmia not terminated with ICD shocks, terminated but recurs

Inappropriate: lead malfunction resulting in oversensing, EMI resulting in inappropriate shock, T wave oversensing, SVT/sinus tachy falling in VT zone (place magnet over ICD to inhibit shocks)

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28
Q

What can also elevate BNP levels?

A

Age, female gender, pressure overload, obesity, race (AA), treatment (carvedilol/spiro), anemia, cor pulmonale, critical illness, sepsis

Better for negative predictive value than diagnosis or for trends

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29
Q

How will HF vasodilators affect hemodynamics?
(nitroprusside is arterial vasodilator for better afterload reduction vs nitroglycerin is venous)

A
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30
Q

Recall the ionotropic drugs

A
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31
Q

Which patients will have survival benefit with defibrillator +/- cardiac resychronization therapy?

A

EF <35%, LBBB and wide QRS

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32
Q

How does an IABP work?

A

Inflates during diastole to augment pulsatile blood flow to increase mean aortic BP to augment coronary perfusion

Deflates during systole to reduce ventricular afterload leading to an increase in mean arterial pressure and augment ventricular stroke volume

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33
Q

What is considered a normal pulse pressure?

A

40
Low is around 20

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34
Q

What is one clue for cardiac tamponade?

A

Equalization of pressure (RA/CVP, PA diastolic, wedge, loss of y descent)

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35
Q

Recall the PA catheter findings in the different types of shock

A
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36
Q

On a waveform, where do you measure wedge pressure?

A

End-expiration
Also, don’t flush the cath when wedged- can cause vascular injury

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37
Q

Recall the difference in the PA waveforms

A
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38
Q

How do you differentiate RA waveform from wedge waveform?

A
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39
Q

Which scenarios can large V waves be seen in PAC waveforms?

A

TR, MR, can be confused with PA tracing, VSD, volume overload

PAOP/CVO estimation at should be at mean ‘a’ wave

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40
Q

How does mechanical ventilation affect LV/RV preload and afterload?

A

Increases preload and decreases afterload of LV

Decreases preload and increases afterload of RV

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41
Q

How do you calculate pulse pressure variation?

A

PPV= 100x (PPmax-PPmin)/PPmean

12-15% strongly associated with fluid responsiveness

**Patient must be passive on vent and in sinus rhythm, arterial catheter in place, 8-10cc/kg

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42
Q

What degree of IVC variation suggests fluid responsiveness?

A

above 12%

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43
Q

What are the benefits of passive leg raise?

A

CO increase by 10% predicts fluid responsiveness

Can be vent or non-vented, uses variety of CO assessment methods, not confounded by arrhythmia

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44
Q

Where on the arterial monitoring waveform do you measure the CVP?

A

Base of the C wave at end-expiration.

Can also take top and bottom of a wave (measured after p wave on ekg) and take the average

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45
Q

What are the arterial waveforms representing regarding chambers filling?

A
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46
Q

What waveforms on PAC can you see with aflutter?

A

F waves

47
Q

What waveforms on PAC can you see with PVCs?

A

Cannon a waves (atrial systole when tricuspid valve is closed by PVC)

48
Q

What does overwedging look like on PAC and how do you fix it?

A

Flattening of the line looking upwards, catheter is pressed up against the wall

Deflate and retract a bit

49
Q

What does an overdamped waveform look like on PAC and how do you fix it?

A

loss of amplitude and c wave, can be due to air bubbles or small thrombi

Rapid flush

50
Q

What does catheter whip look like on PAC and how do you fix it?

A

Looks like Vtach, seen in high cardiac output causing reverberations in the transducer

Can refloat catheter but otherwise fix underlying issue

51
Q

What are the stages of heart failure?

A

A- at risk but without structural disease or symptoms (ex HTN, DM, FHx)
B- Structural without symptoms
C- Structural with symptoms
D- Refractory symptoms at rest

52
Q

What blood pressure is HTN urgency/emergency?

A

180/110

53
Q

What are the traits of posterior reversible encephalopathy syndrome?

A

Symptoms: headache, seizures, altered mental status
Etiology: loss of cerebral auto-regulation, endothelial dysfunction
Dx: MRI>CT, hyperintensity on T2 FLAIR (vasogenic edema in parietal/occipital)

54
Q

What is the recommended rate of reduction of MAP in HTN emergencies?

A

10-20% quickly, then another 5-15% in the following hours

55
Q

What is the disadvantage of nitroprusside?

A

Gets converted to cyanide and then liver converts to thiocyanate.
Cyanide and thiocanate toxicity–> lactate and AMS. Toxic level 1mg cyanide and >10 ug/dL thiocyanate. Give IV thiosulfate

56
Q

What is the disadvantage of fenodolpam?

A

Beware in glaucoma.
Better though for patients with renal failure than nitroprusside

57
Q

What are the principles of management of an acute aortic dissection?

A

Lower BP, avoid tachycardia to decrease the steepness of pulse wave (dP/dT) and PV contractility. Prefer BBers over vasodilators to avoid reflex tachycardia. Goal SBP 100-110 and MAP 60-70

58
Q

Which drugs put you at risk of hypertensive crisis (catecholamine overload)?

A

MAO inhibitor + tyramine (Chianti, cheeses, fava beans), Pheos, meth, cocaine

Treat with pure alpha blocker (like phentolamine). Get flushing/headaches

59
Q

Recall the criteria for the 4 classes of hemorrhage

A
60
Q

What are the causes of distributive shock?

A

Sepsis, hepatic failure, pancreatitis, trauma/SIRS, thyroid storm, AV fistula, Paget’s disease, Thiamine deficiency

61
Q

Is there any benefit to maintaining MAP at 65 vs 85?

A

One trial suggested less RRT in chronic HTN patients but more afib, but otherwise had no difference in mortality

62
Q

What tests are used in septic shock for adrenal insufficiency?

A

Free AM cortisol level (<5) or ACTH stim test

63
Q

Which has better outcomes in septic shock- early goal directed, protocol driven therapy or usual care?

A

None, they’re equal

64
Q

Recall the vasopressors and their targets and effects

A
65
Q

How often are there post-MI tachyarrhythmias?

A

10-20%, most commonly SVT (afib/aflutter), also PVCs, NS-VT, less than 5% with sustained VT/VF

66
Q

Recall the cardioversion energy levels for each arrhythmia

A

Afib RVR- 120-200J biphasic or 200J monophasic
VT regular- synch 100J
VT irregular- defib 200J

67
Q

What are the treatments of choice for acute stable afib RVR?

A

BBers, CCBers, or digoxin
in HF- amiodarone or digoxin
Accessory pathway- Ibutilide, procainamide, but NO digoxin/amio/CCBers

68
Q

What is the incidence and treatment for post heart surgery afib?

A

25-40% after heart surgery, peak onset POD2, self resolves in 90% in weeks 6-8 postop, treat the same as regular afib

69
Q

What are the risk factors for multifocal atrial tachycardia?

A

Digoxin toxicity, CAD, MI, cor pulmonale, hypokalemia, pulmonary disease

Cardioversion is not effective

70
Q

Where do you see P waves in AV node reentry tachycardia?

A

buried at the end of the QRS because of the slow pathway hitting the fast pathway in the AV node

71
Q

How is AV node reentry tachycardia treated?

A

AV nodal blocking agents (adenosine, CCBers, BBers), digoxin, amio, procainamide, vagal maneuvers, DC cardioversion, or atrial/ventricular overdrive pacing

72
Q

In accessory pathway mediated tachycardia (aka WPW), where is the delta wave?

A

In front of the QRS in NSR, tachycardia
In orthdromic reciprocating tachycardia (95%), narrow QRS and AV nodal blocking helps block the reentry pathway
In antidromic reciprocating tachycardia (5%), see a wide complex tachycardia and still treat with AV nodal blocking

73
Q

What is the increased risk of sudden death due to in WPW?

A

Afib with rapid ventricular conduction through the reentry pathway leading to VT

Will see different QRS morphologies and width along with rapidly conducting rate (short RR interval)

74
Q

How do you treat Afib in WPW?

A

Rate control with procainamide + BBers
Chemical conversion with Ibutilide or procainamide
DC cardioversion (120-200J)

75
Q

How do you treat atrial flutter?

A

Rate control may be more difficult
DC CV 50-100J
Atrial pacing may be effective

76
Q

How do fusion beats occur in VT?

A

A random narrow QRS within a bunch of wide ones because a normal beat occasionally makes it down the other bundle

77
Q

How do you differentiate VT with SVT with aberrancy?

A

VT- a focus arising from the ventricle. Will have fusion beats, QRS concordance in precordial leads (all pointing in the same direction from V1-6), AV dissociation, QRS >140 in RBBB/>160 LBBB, left axis deviation

SVT + aberrancy- as it goes through the AVN, gets delayed in one of the bundles. Terminates with vagal tone, a critical rate which widens QRS, alternating BBB, long-short sequence (Ashman’s phenomenon)

78
Q

Identify a strip of Ashman’s phenomenon

A
79
Q

How is stable VT treated?

A

Adenosine if wide and regular just in case if its SVT with aberrancy
Procainamide or amio bolus

80
Q

What are the etiologies and treatments of torsades?

A

Prolonged QT, metabolic (low K/Mg), CNS injury, cardiomyopathy, MI

MgSO4, Isuprel, lidocaine, atrial pacing or defibrillation

81
Q

What are the indications for CTS consult in endocarditis?

A

Failure of medical therapy, large (>1cm) vegetations, fungal, heart failure due to tricuspid regurg

82
Q

How do you distinguish constrictive pericarditis and restrictive pericarditis?

A

Negative intrathoracic pressure decreases left-sided filling (as this pressure is not transmitted intracardiac) and increases RV volume at the expense of LV volume. In constriction- increased RV volume leads to increased RAP. Will see respiratory changes in RV/LV pressures

83
Q

What are the causes of acquired long QT?

A

hypokalemia, hypomagnesemia, meds, ETOH withdrawal, hypocalcemia (but no increased risk of torsades)

84
Q

What can be a complication of receiving iodinated contrast (such as with cardiac cath)

A

Thyroid storm in a patient with subclinical hypothyroidism (Jod-Basedow syndrome)

85
Q
A
86
Q

Describe the therapies for thyroid storm

A

PTU (decrease hormone synthesis and T4–>T3 conversion)
Steroids (decrease conversion and modulates autoimmunity and relative adrenal insufficiency)
Exogenous iodine (inhibits preformed hormone release: Wolff-Chaikoff effect)
Bile acid sequestrants (may interfere with enterohepatic recirculation and enhance clearance)
Lithium (blocks release of hormone)

87
Q

What are symptoms of cardiac amyloidosis?

A

Biventricular heart failure, previous carpal tunnel, renal failure, neurologic deficits, afib, restrictive cardiomyopathy

88
Q

When do you see accelerated idioventricular rhythmn?

A

Reperfusion arrhythmia, rate 60-100
Not sinus but usually transient and only requires observation

89
Q

How do hemodynamics change with a hemothorax?

A

Equalization of cardiac pressures (wedge and PA pressures increase, CO decreases)

90
Q

What can you suspect when you see a large coronary sinus on TTE?

A

Left sided SVC, elevated right atrial pressures
Usually an incidental finding

91
Q

How does one distinguish low CO AS versus pseudostenosis?

A

Stress echo, see if cardiac output increases without changing the gradient

92
Q

What triad should make you think of WPW?

A

wide complex tachycardia, irregularly irregular, varying QRS widths. Give Ibutilide or procainamide

Seen in pre-excited afib or afib with an accessory conduction pathway

93
Q

When does ETCO2 decrease?

A

Ineffective compressions, excessive ventilation
ETCO2 <10 after 20 minutes is low likelihood of neurologic recovery

93
Q

When should you avoid placing a PAC?

A

When patient has an LBBB (can induce a RBBB)

94
Q

What is underdamped vs overdamped?

A

Under- cath is too long causing whip effect. MAP is unchanged
Over- waveform is flattened due to air bubbles/clot/kink/stiffness/ against a vessel. Flush it to get 2 oscillations after square wave (0-1 overdamp, 3+ underdamp)

94
Q

How do you calculate PVR and mPAP?

A

(mPAP-PCWP)/CO

mPAP= 1/3 (systolic - diastolic) + diastolic

95
Q

How do you treat an electrical storm (refractory VT)

A

Bblocker to manage high sympathetic tone

96
Q

Which scenarios would you utilize stroke volume variability over pulse pressure variability in fluid responsiveness?

A

Vented patients, arrhythmias

97
Q

Which vessels supply the posteromedial papillary muscle?

A

RCA or LCx
May not hear a murmur with rupture due to low cardiac output, but otherwise early systolic from equalization of LA and LV

98
Q

Recall the SCAI SHOCK stages

A
99
Q

What can be done for refractory Vfib arrest?

A

Double sequential external defibrillation (DSED)

100
Q

What are the pad placements for DSED?

A
101
Q

How do you troubleshoot low flow on an LVAD?

A

Low JVP- hypovolemia (bleeding? overdiuresis?)
Septal shift to the left on TTE- underfilling of LV (hypovolemia? inflow cannula problem? RV dysfunction?)

Recommended MAP 65-80 to maintain pressure differential

Remember diuretics reduce preload and ACEi/ARB reduce afterload

102
Q

In which leads is it normal to have inverted Twaves? What is loss of balance in precordial leads indicative of?

A

Normal inversion in aVR and V1
When V1 is upright and taller than Twave in V6, sign of ischemia

103
Q

What scenarios can you see large Twave inversions with QT prolongation?

A

Cerebral Twaves, looks for catastrophic CNS injury like SAH

104
Q

How does carbon monoxide affect EKG?

A

ST depression or T wave inversion via myocardial stunning or ischemia

105
Q

When can a transcatheter edge-to-edge mitral repair be considered?

A

HFrEF with secondary MR with regurgitant volume >60cc, effective regurgitant orifice >0.4cm2

106
Q

What is the most effective treatment for severe malaria?

A

artemether-lumefantrine- fast onset and lower mortality

107
Q

PICC vs central line regarding CLABSI and DVT risk?

A

PICC has similar CLABSI and higher DVT

108
Q

What are the features of Fusarium infection?

A

Immunocompetent: keratitis, onchomycosis
Immunocompromised: sinusitis, endophthalmitis, PNA, fungemia, Gray macules with central ulceration vs black eschar.
Azoles have limited efficacy, echinocandins have none. Ampho B only and source control

109
Q

When are healthcare workers potentially infectious after VZV exposure?

A

Days 8-21

110
Q

Who cannot get the VZV vaccine?

A

Pregnant, immunocompromised. Get if exposed within 3-5d

Get immune globulin instead

111
Q

What are the features of hypervirulent K pneumoniae

A

Difficult to get source control, hyperviscous, more virulent, and often metastasizes. Strong >5mm

112
Q
A

Critical Care Boards (10 decks)

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