Cardiovascular Critical Care I

Answer: B

Given this patient’s CAD, type 2 diabetes, dyslipidemia,

gastroesophageal reflux disease, hypertension, obstruc-

tive sleep apnea, and ischemic cardiomyopathy, only

Answer B consists of the three agents that reduce morbid-

ity and mortality among these comorbidities: carvedilol

(HF and potentially diabetes), spironolactone (HF pro-

gression post-MI), and lisinopril (HF and diabetes),

making Answer B correct and Answers A (Amlodipine,

clopidogrel, and sitagliptin.), C (Pravastatin, amlodip-

ine, and aspirin 325 mg), and D (Prasugrel, sildenafil,

and atenolol) incorrect.

Although many of these tests might be helpful in this

patient’s differential diagnosis, the most likely consid-

eration would be respiratory decompensation or an HF

decompensation, given the patient’s presentation; thus,

a chest radiograph, ECHO, BNP, and lactate would be

most appropriate, making Answer C correct. Answer A

is incorrect; although an infectious etiology cannot be

ruled out, it is less likely than noninfectious cardiore-

spiratory differentials. Answer B is not the best answer;

although serial troponins and an ABG could be argued

for, liver function tests are unlikely to provide addi-

tional insight into this patient’s differential. Answer D

also is not the best answer; although it provides addi-

tional information for hemodynamic assessment, it is

lacking in an assessment of cardiac function, which is a

likely contributor to the patient’s presentation.

Answer: D

Dobutamine would be the ideal choice, given the

patient’s acutely worsening cardiac index and malperfu-

sion and its rapid onset; this would facilitate β2 arterial

vasodilation (both SVR and PVR reduction) as well as

increase chronotropy and inotropy. Milrinone, although

likely beneficial for both cardiac index and PVR reduc-

tion, would be less favorable, given that its time to peak

effect will exceed 6 hours (the time required to achieve

greater than 87.5% of steady state, even in normal renal

function), and the dosing is rather high for safe initia-

tion of therapy. Neither norepinephrine nor epinephrine

would be favored (particularly at these doses) because

the patient’s MAP is currently elevated, and these agents

would contribute to increased α1-mediated afterload

increases, causing increased myocardial workload in

a patient who already has decompensated systolic HF.

Answer D (dobutamine 5 mcg/kg/min) is correct, and

Answers A (norepinephrine 0.08 mcg/kg/min), B (epi-

nephrine 0.08 mcg/kg/min), and C (Milrinone 0.75 mcg/

kg/min) are incorrect.

Answer: D

The patient’s troponin elevation is most likely a result of

the patient’s decompensated HF (especially considering

clinical evidence of acute HF, such as high BNP, CVP,

and low cardiac output) superimposed on chronic CAD

(Answer D is correct). Given the patient’s chemistry and

ABG results, chronic obstructive pulmonary disease

(Answer B) is highly unlikely. Although this presenta-

tion could be attributed to NSTEMI (Answer A), it is

less likely, given the lack of new ST-T changes on ECG

and the accompanying evidence of an HF exacerbation.

Sepsis (Answer C) is also a potential contributor to tro-

ponin elevation; by comparison, an infectious etiology

is less likely in this patient’s case.

Answer: A

Ticagrelor has been associated with adenosine-mediated

dyspnea and bradycardia; therefore, this medication

should be evaluated as a contributing cause. According

to the current ACC/AHA guidelines, this patient should

continue P2Y12 inhibitor therapy because his stent was

placed less than 12 months ago, and he should con-

tinue aspirin therapy indefinitely (Answer A is correct).

Conversely, it would not be appropriate to stop ticagre-

lor without switching to an alternative P2Y12 inhibitor

(Answer B is incorrect). A likely cause has been iden-

tified (Answer C is incorrect), and the patient has no

evidence of hyperkalemia (Answer D is incorrect).

Answer: A

Because of this patient’s hypotension and ongoing car-

diogenic shock, synchronized cardioversion would be

preferred (Answer A is correct). Metoprolol (Answer

B) would be unfavorable because of the patient’s con-

current dobutamine use and hypotension; similarly,

amiodarone 300 mg intravenous push (Answer D) could

contribute to further hypotension. The primary of role

of adenosine (Answer C) is to slow AV nodal conduction

when patients are tachycardiac with a regular rhythm