Chronic Cardio Flashcards
Self-Assessment Questions
Answers and explanations to these questions can be
found at the end of this chapter.
1. R.S., a 58-year-old woman with a history of hypertension
(HTN), coronary heart disease (CHD),
myocardial infarction (MI) 4 months ago, and dyslipidemia,
presents to the clinic for a follow-up.
She has no worsening signs or symptoms of dyspnea or edema compared with her baseline. An
echocardiogram reveals a left ventricular ejection
fraction (LVEF) of 35%. She is in New York Heart
Association (NYHA) class III. Her medications
include aspirin 81 mg/day, metoprolol succinate
150 mg/day, and atorvastatin 40 mg/day at night.
Her vital signs include blood pressure (BP) 138/80
mm Hg and heart rate (HR) 58 beats/minute. Her
lungs are clear, and laboratory results are within
normal limits. Given her history and physical
examination, what is the most appropriate modification
to R.S.’s current drug therapy?
A. Continue current therapy.
B. Initiate digoxin 0.125 mg/day.
C. Initiate spironolactone 25 mg/day.
D. Initiate lisinopril 5 mg/day.
- Answer: D
This patient has HFrEF (NYHA class III), probably
secondary to her MI 4 months ago, and is not receiving
optimal HF therapy with an ACE inhibitor and
β-blocker, making Answer A incorrect. ACE inhibitors
are considered a cornerstone of therapy for HFrEF
because evidence shows that they slow the progression
of HF and reduce symptoms, hospitalizations, and mortality
in this patient population. ACE inhibitors should
be initiated in all patients with HFrEF, unless there is
a contraindication. This patient has no contraindications
for using an ACE inhibitor; therefore, lisinopril
should be initiated (Answer D). Digoxin is not indicated
unless a patient is symptomatic on optimal HF therapy
(Answer B). This patient is not symptomatic and is
not receiving optimal therapy. Although the patient is
NYHA class III, no rationale exists for adding spironolactone
at this time because she is not receiving optimal
HF therapy (Answer C).
- J.O. is a 64-year-old woman with NYHA class II
nonischemic dilated cardiomyopathy (LVEF of
30%). She presents to the heart failure (HF) clinic
for a follow-up. She is euvolemic. Her medications
include enalapril 10 mg twice daily, furosemide
40 mg twice daily, and potassium chloride 20 mEq
twice daily. Her vital signs include BP 130/88 mm
Hg and HR 78 beats/minute. Her laboratory results
are within normal limits. What is the best way to
manage J.O.’s HF?
A. Continue current regimen.
B. Increase enalapril to 20 mg twice daily.
C. Initiate carvedilol 3.125 mg twice daily.
D. Initiate digoxin 0.125 mg/day.
- Answer: C
This patient is taking the target dose of enalapril; further
increases in the enalapril dose are unnecessary
unless the patient is hypertensive (Answer B). Adding
β-blocker therapy, initially at a low dose, together with
ACE inhibitor therapy, is recommended for further
reductions in morbidity and mortality and for slowing
the progression of HF (Answer C). Digoxin is indicated
only in symptomatic patients, despite optimal therapy,
and this patient’s pharmacotherapy has not been optimized,
making Answers A and D incorrect.
- J.M. is a 65-year-old woman with a history of
HTN who presents to her primary care physician
with shortness of breath and markedly decreased
exercise tolerance. An echocardiogram reveals
an LVEF of 65%, with diastolic dysfunction. J.M.
currently takes losartan 150 mg/day for HTN. Her
vital signs include BP 134/84 mm Hg and HR 68
beats/minute. Her lung fields are clear to auscultation,
and there is no evidence of systemic congestion.
Her laboratory results include SCr 1.1 mg/
dL and K 5.1 mEq/L. Which is the best change to
make to J.M.’s pharmacologic regimen today?
A. Add metoprolol succinate 50 mg/day.
B. Initiate furosemide 40 mg/day.
C. Add spironolactone 25 mg/day.
D. Add empagliflozin 10 mg/day.
- Answer: D
This patient has HFpEF, which is caused by a problem
with ventricular relaxation. Treatment of HFpEF
includes managing risk factors such as HTN and optimizing
HF pharmacotherapy. The most recent HF
guidelines recommend consideration of SGLT2 inhibitors
for patients with HFpEF and adequate renal function,
making Answer D correct. SGLT2 inhibitors might
result in slight reductions in the patient’s blood pressure,
but additional blood pressure control may be warranted
in the future. Answer A is incorrect because the
patient’s heart rate is not elevated, and metoprolol succinate
is not mortality reducing in HFpEF. Furosemide
is not warranted because of lack of volume overload,
making Answer B incorrect. Although spironolactone is an appropriate therapy for patients with HFpEF, especially
in the context of HTN, this patient’s potassium is
greater than 5.0 mEq/L, so MRA therapy should not be
initiated.
- B.W. is a 78-year-old man with a history of HTN,
peripheral arterial disease (PAD), gastroesophageal
reflux disease, and asymptomatic atrial fibrillation
(AF) for the past month. His therapy includes
aspirin 325 mg/day, lansoprazole 30 mg every
night, atenolol 50 mg/day, lisinopril 10 mg/day, and
atorvastatin 20 mg/day. His vital signs include BP
132/72 mm Hg and HR 68 beats/minute. Which is
the best therapy for B.W. at this time?
A. Add diltiazem and rivaroxaban.
B. Add digoxin and increase lisinopril to 20 mg/
day.
C. Discontinue atorvastatin and add warfarin.
D. Add apixaban and decrease aspirin to 81 mg/day.
- Answer: D
This patient’s CHA2DS2-VASc score is 4 (risk factors
are HTN, PAD, and age greater than 75 years), making
him a candidate for an oral anticoagulant, such as
rivaroxaban, because of his AF. Use of an oral anticoagulant
will greatly decrease his risk of stroke from
about 5% per year to about 1% per year. Because his
HR is less than 110 beats/minute with atenolol therapy,
there is no reason to discontinue atenolol. In addition,
there is reason to add an additional rate control drug,
such as digoxin (Answer B) or diltiazem (Answer
A). With his PAD, atorvastatin therapy is necessary,
making Answer C incorrect. In addition, his BP is
well controlled; therefore, increasing the lisinopril
dose is not warranted, making Answer B incorrect.
To derive the beneficial antiplatelet effects for CV
event prevention, aspirin 81 mg is adequate. Aspirin
325 mg/day is also effective, but has a greater risk of
bleeding with concomitant apixaban. Therefore, adding
apixaban and decreasing the dose of aspirin to 81 mg/
day (Answer D) is correct.
- Z.G. is a 61-year-old man with AF, HTN, and dyslipidemia.
His medications include digoxin 0.125
mg/day, warfarin 5 mg/day, amlodipine 10 mg/day,
and pravastatin 20 mg every night. He comes to the
clinic with no complaints except for palpitations
and shortness of breath when doing yard work. His
vital signs include BP 138/80 mm Hg and HR 100
beats/minute. His international normalized ratio
(INR) is 2.4, and his digoxin concentration is 1.1
ng/mL. All other laboratory results are within normal
limits. Which is the best option to help with
Z.G.’s symptoms?
A. Add metoprolol succinate 50 mg/day.
B. Increase digoxin to 0.25 mg/day.
C. Add verapamil 240 mg/day.
D. Continue current regimen and advise the patient
to avoid activities that cause signs or symptoms.
- Answer: A
This patient is experiencing a rapid ventricular response
with exercise or strenuous activity, causing the sensation
of palpitations and dyspnea. Digoxin alone poorly
controls the ventricular rate during times of high sympathetic
influence (e.g., exercise). Additional therapy is
usually necessary to control the ventricular rate adequately.
A β-blocker such as metoprolol succinate is a
good choice to maintain HR during activity (Answer
A). Using verapamil with digoxin in this patient could
result in signs or symptoms of toxicity, given his current
digoxin concentration. In addition, he is already
taking a CCB, making verapamil a less desirable
choice (Answer C). Similarly, doubling the digoxin
dose would almost double the current serum concentration
to 2.2 ng/dL, which should be avoided (Answer B).
Instructing the patient to avoid activity is undesirable
because physical activity should be encouraged and
supported in all patients, especially in those with risk
factors for CV disease (Answer D).
- R.P. is an 69-year-old African American man with
a history of HTN and gout. His medications include
allopurinol 300 mg/day, amlodipine 10 mg/day,
and aspirin 81 mg/day. His vital signs include BP
145/85 mm Hg and HR 82 beats/minute. His laboratory
values are normal and his 10-year ASCVD
risk is 22.4%. Which is the best therapy for R.P.?
A. Add hydrochlorothiazide 25 mg/day to achieve
a systolic blood pressure (SBP) goal of less
than 130 mm Hg.
B. Add lisinopril 40 mg/day and titrate to achieve
an SBP goal of less than 140.
C. Add atenolol 50 mg/day to achieve an SBP less
than 130 mm Hg.
D. Make no changes to his current medications
because his SBP is at goal.
- Answer: A
According to the ACC/AHA guidelines, this patient’s BP
should be treated to a goal of less than 130/80 mm Hg
because he has no clinical CVD and a 10-year ASCVD
risk ≥10%, making answers B and D incorrect. Beta blockers
are not recommended first-line for HTN management
in the absence of coronary artery disease, heart failure,
or atrial fibrillation, making answer C incorrect. Answer
A includes a first-line HTN medication which also maintains
efficacy in the African American population.
- J.T. is a 58-year-old man who presents to his primary
care provider for the first time in 10 years.
He has smoked 2 packs/day for the past 30 years
and takes no medication. A fasting lipid panel
shows total cholesterol (TC) 222 mg/dL, lowdensity
lipoprotein cholesterol (LDL-C) 105 mg/dL,
triglycerides (TG) 330 mg/dL, and high-density
lipoprotein cholesterol (HDL-C) 51 mg/dL. His
vital signs include BP 140/75 mm Hg and HR 80
beats/minute. His pooled cohort equation reveals
a 10-year atherosclerotic cardiovascular disease
(ASCVD) risk of 14.6%. Which would be the best
pharmacologic therapy to initiate in J.T.?
A. Initiate simvastatin 20 mg/day and gemfibrozil
600 mg twice daily.
B. Initiate rosuvastatin 2.5 mg/day.
C. Initiate pravastatin 20 mg/day and fenofibrate
160 mg/day.
D. Initiate atorvastatin 20 mg/day.
- Answer: D
This patient has been identified as being at risk of
ASCVD, according to his pooled cohort equation result
of 14.6%. Therefore, the patient falls into one of the four
patient management groups (age 40–75 years with an
LDL-C of 70–189 mg/dL and a 10-year ASCVD risk
of 7.5-19.9% without DM or ASCVD) and thus should
be initiated on statin therapy. According to the guidelines,
this patient should be treated with moderate- to
high-intensity statin therapy. Although simvastatin
20 mg is considered a moderate-intensity dose, adding
gemfibrozil to this patient’s regimen would be inappropriate
because gemfibrozil is contraindicated in combination
with simvastatin; also, his TG concentrations
are less than 500 mg/dL and need not be specifically
targeted (Answer A). Using pravastatin 20 mg would
be inappropriate because this is considered a lowintensity
dose, and it would not provide the more than
30%–50% reduction in LDL-C that is recommended.
In addition, fenofibrate would not be needed because his
TG concentrations are lower than 500 mg/dL (Answer
C). Rosuvastatin 2.5 mg is a low-intensity dose and
would not be appropriate (Answer B). Atorvastatin 20
mg is considered a moderate-intensity dose, and it will
provide a 30%-50% reduction in LDL-C, as is recommended
(Answer D).
- J.S. is a 43-year-old man with HTN who presents
for an annual physical examination. His family
history is significant for his father having HTN.
His only medication is lisinopril 10 mg/day. His
BP is 145/90 mm Hg. A fasting lipid profile shows
TC 238 mg/dL, TG 95 mg/dL, LDL-C 176 mg/dL,
and HDL-C 43 mg/dL. His calculated 10-year
ASCVD risk according to the pooled cohort equation
is 3.9%. Which best describes the next step for
management in J.S.?
A. Initiate high-intensity statin therapy.
B. Initiate fenofibrate 130 mg/day.
C. Initiate moderate-intensity statin therapy.
D. Do not initiate statin therapy and reevaluate
risk in 4–6 years.
- Answer: D
This patient is 40–75 years of age and does not have
ASCVD, severe hypercholesterolemia, or DM.
Therefore, he is in the statin treatment group of primary
prevention. His 10-year ASCVD risk of 3.9% indicates
he is considered at low risk. Statin therapy is not indicated
at this time (Answers A and C are incorrect), and
only lifestyle modifications are indicated. He should
be reassessed in 4–6 years (Answer D is correct). The
patient’s TGs are normal, so treatment with a fibrate is
not necessary at this time (Answer B is incorrect).
- J.C. is a 62-year-old man (height 70 inches, weight
135 kg [1 month ago 143 kg]) with a history of
diabetes mellitus (DM), chronic kidney disease
(CKD), bipolar disorder, CHD, and hypertriglyceridemia
that, in the past, has resulted in pancreatitis.
His family history is significant for his
father having CHD and hypertriglyceridemia. He
is not a smoker, but admits drinking a 6-pack of
beer daily. Pertinent laboratory findings include a
hemoglobin A1C of 11.6% and a serum creatinine
(SCr) of 2.6 mg/dL. He currently takes atorvastatin
40 mg every evening, aspirin 81 mg/day, metformin
1000 mg twice daily, olanzapine 10 mg/day, metoprolol
tartrate 50 mg twice daily, and coenzymeQ10
200 mg/day. His fasting lipid profile is TC 402 mg/dL,
LDL-C unable to calculate, HDL-C 48 mg/dL, and TG
1500 mg/dL. His other laboratory values are within
normal limits. Which best describes potential secondary
causes of elevated TG concentrations that
should be considered in J.C.?
A. Obesity, poorly controlled diabetes, olanzapine,
metoprolol, coenzyme Q10.
B. Alcohol consumption, poorly controlled diabetes,
weight loss, metoprolol.
C. Obesity, calcium channel blockers, hyperthyroidism,
alcohol consumption.
D. Alcohol consumption, obesity, poorly controlled
diabetes, olanzapine, metoprolol.
- Answer: D
Secondary causes of hypertriglyceridemia should be
ruled out when TG concentrations are greater than
500 mg/dL or when LDL-C is greater than 190 mg/dL.
Different medications, conditions, and diet can affect
these lipid values. Although obesity, poorly controlled
DM, olanzapine, and metoprolol can increase TG concentrations,
coenzyme Q does not affect TG; therefore,
Answer A is incorrect. Alcohol consumption, poorly
controlled DM, and β-blockers can all increase TG,
but weight loss does not increase TG. Weight loss can
actually lower LDL-C and TG; therefore, Answer B is
incorrect. Although obesity and alcohol consumption
can elevate TG, neither CCBs nor hyperthyroidism are
expected to have this effect (Answer C is incorrect). All
the conditions, medications, or disease states in Answer
D can increase TG, making this option correct.
Questions 10 and 11 pertain to the following case.
A.M. is a 32-year-old woman with type 1 DM and HTN.
Her current medication regimen is as follows: ramipril
10 mg/day, chlorthalidone 25 mg/day, amlodipine
10 mg/day, ethinyl estradiol 20 mcg/norethindrone
1 mg daily (for the past 2 years), and insulin as directed.
Her vital signs today include BP 145/83 mm Hg,
repeated BP 145/81 mm Hg; HR 82 beats/minute; height
66 inches; weight 70 kg. A.M. would prefer not to take
any more drugs, if possible.
10. Which option is the best clinical plan for A.M.?
A. No change in therapy is currently warranted.
B. Advise weight loss and recheck her BP in
3 months.
C. Change chlorthalidone to hydrochlorothiazide.
D. Discuss changing her contraceptive method.
- Answer: D
Oral contraceptives, specifically estrogen, can increase
BP, especially with a longer duration of use. An alternative
contraceptive without estrogen would be less
likely to contribute to her HTN (Answer D is correct).
Answers A and B are incorrect because her BP
requires better control, but weight loss is unlikely to
help because her BMI is normal. Answer C is incorrect
because hydrochlorothiazide is no more potent than
chlorthalidone.
- A.M. and her husband have decided they are ready
to have children. What is the best medication
option for A.M.?
A. No change in therapy is warranted.
B. Discontinue ramipril and replace with labetalol.
C. Increase chlorthalidone to 50 mg/day.
D. Discontinue all antihypertensive therapy.
- Answer: B
ACE inhibitor therapy is contraindicated in pregnancy,
and discontinuing ramipril is the most important next
step, making Answers A and C incorrect. Answer D is
incorrect because this patient will require good BP control
during her pregnancy. Labetalol is a good choice of
therapy because it is a preferred antihypertensive drug
in pregnancy (Answer B is correct
- A 66-year-old African American man (height 70
inches, weight 91 kg) with AF and CHD (non–
ST-segment elevation MI and stent placement 3
years ago) presents with palpitations. Rate control
therapy, including trials of β-blockers and nondihydropyridine
calcium channel blockers, has
been unsuccessful in controlling his symptoms. He
currently takes metoprolol succinate 50 mg/day,
aspirin 81 mg/day, atorvastatin 80 mg/day, lisinopril
5 mg/day, and warfarin 4 mg/day. His laboratory
results show INR 2.2, potassium 4.8 mEq/L,
SCr 1.2 mg/dL. His BP is 110/70 mm Hg, and his
HR is 95 beats/minute. Which is the best antiarrhythmic
therapy for him?
A. Disopyramide.
B. Flecainide.
C. Propafenone.
D. Sotalol.
- Answer: D
Because the patient has CHD, his options for antiarrhythmic
therapy are limited. Class Ic antiarrhythmic
drugs are contraindicated in patients with CHD;
therefore, flecainide and propafenone cannot be used
(Answers B and C are incorrect). Disopyramide, a class
Ia antiarrhythmic, is not a preferred therapy for AF;
therefore, Answer A is incorrect. Sotalol, a class III
antiarrhythmic, can be used in patients with CHD and
good renal function; therefore, Answer D is correct
Patient Cases
1. L.S. is a 48-year-old woman with alcohol-induced cardiomyopathy. Her most recent LVEF is 20%; her daily
activities are limited by dyspnea and fatigue (NYHA class III). Her medications include lisinopril 40 mg
daily, furosemide 40 mg twice daily, carvedilol 12.5 mg twice daily, spironolactone 25 mg/day, and digoxin
0.125 mg/day. She has been stable on these doses for the past month. Her most recent laboratory results
include sodium (Na) 140 mEq/L, potassium (K) 4.0 mEq/L, chloride 105 mEq/L, bicarbonate 26 mEq/L,
blood urea nitrogen 12 mg/dL, SCr 0.8 mg/dL, glucose 98 mg/dL, calcium 9.0 mg/dL, phosphorus 2.8 mg/
dL, magnesium 2.0 mEq/L, and digoxin 0.7 ng/mL. She weighs 69 kg, and her vital signs include BP 112/70
mm Hg and HR 72 beats/minute. In the clinic today, she has concerns for increased shortness of breath and
fatigue. On physical examination, you note 2+ bilateral lower extremity pitting edema and hear crackles on
inspiration. What is the best approach for maximizing the management of her HF?
A. Increase carvedilol to 25 mg twice daily.
B. Increase lisinopril to 80 mg/day.
C. Add empagliflozin 10 mg/day.
D. Increase digoxin to 0.25 mg/day.
- Answer: C
This patient has NYHA class III HFrEF with an LVEF
of 20%. The best option is to add empagliflozin 10 mg
orally daily to reduce CV mortality and HF hospitalizations
(Answer C is correct). Appropriate monitoring
would include signs and symptoms of hypotension
and genitourinary infections. Although increasing this
patient’s carvedilol dose (Answer A) is desirable long
term, the patient currently has signs and symptoms of
fluid overload; adding or increasing doses of ß-blockers
is not advisable in this setting. The ACE inhibitor is
already at the maximum recommended lisinopril dose
for HF; therefore, further increases are not warranted
(Answer B). Her digoxin concentration of 0.7 ng/dL is
within the desired range of 0.5–0.9 ng/mL; therefore,
no dose increase is warranted because this would not
improve efficacy and would only increase the risk of
toxicity (Answer D).
- J.T. is a 62-year-old man (height 72 inches, weight 85 kg) with a history of CHD (MI 3 years ago), HTN,
depression, CKD (baseline SCr 2.8 mg/dL), PAD, osteoarthritis, hypothyroidism, and HF (LVEF of 25%).
His medications include aspirin 81 mg/day, simvastatin 40 mg every night, enalapril 5 mg twice daily, metoprolol
succinate 50 mg/day, furosemide 80 mg twice daily, cilostazol 100 mg twice daily, acetaminophen 650
mg four times daily, sertraline 100 mg/day, and levothyroxine 0.1 mg/day. His vital signs include BP 128/74
mm Hg and HR 72 beats/minute. Pertinent laboratory results include K 4.1 mEq/L, SCr 2.8 mg/dL, and a
thyroid-stimulating hormone of 2.6 mIU/L. His HF is stable and considered NYHA class II. What is the best
approach for maximizing the management of his HF?
A. Discontinue metoprolol and begin carvedilol 12.5 mg twice daily.
B. Change enalapril to sacubitril/valsartan 24/26 mg orally twice daily.
C. Add spironolactone 25 mg/day.
D. Add digoxin 0.125 mg/day.
- Answer: B
An ACE inhibitor or ARB should be changed to an
ARNI in all patients with HFrEF, if possible (Answer B
is correct). This patient’s blood pressure and SCr safely
permit this change. Because the patient was taking a
low dose of enalapril, the appropriate starting dose for
sacubitril/valsartan is 24/26 mg orally twice daily. The
clinician should remember to allow a 36-hour washout
period between ACE inhibitor and ARNI doses. There
is no consensus that carvedilol is preferred to extended-
release metoprolol for patients with HFrEF (Answer
A is incorrect). Spironolactone is not appropriate to initiate
in this patient because his baseline SCr concentration
is greater than 2.5 mg/dL (Answer C is incorrect).
Digoxin should be added only in patients who continue
to have symptoms or hospitalizations despite optimized
therapy with an ACE inhibitor/ARB/ARNI, β-blocker,
MRA, SGLT2 inhibitor, and diuretic, and this patient’s
therapy is not considered optimal. In addition, digoxin
0.125 mg daily would likely be too high for a patient
with an SCr of 2.8 mg/dL. This patient’s ACE inhibitor
therapy is not considered optimal (Answer D is
incorrect).
Patient Case
3. Which drug that J.T. (from Patient Case 2) is currently taking would be best to discontinue because of his
HFrEF?
A. Acetaminophen.
B. Sertraline.
C. Cilostazol.
D. Levothyroxine.
- Answer: C
Cilostazol, a phosphodiesterase type 3 inhibitor, may be
associated with an elevated risk of ventricular arrhythmias
and death in patients with HFrEF (Answer C).
Acetaminophen is the drug of choice for mild to moderate
pain in patients with HF, because NSAIDs can
lead to water retention and worsening HF symptoms
(Answer A). The selective serotonin reuptake inhibitors
are not contraindicated in HF (Answer B). Properly
dosed thyroid replacement therapy, as evidenced by
his therapeutic thyroid-stimulating hormone concentration,
is also beneficial because both hypothyroidism
and hyperthyroidism have negative consequences in
patients with HF (Answer D).
Patient Case
4. P.M. is a 52-year-old man (height 70 inches, weight 116 kg) with a history of HTN and a transient ischemic
attack 2 years ago. He visits his primary care doctor with the chief concern of several weeks of a “fluttering”
feeling in his chest on occasion. He thinks the fluttering is nothing; however, his wife insists he have it
checked. His current medications include metoprolol tartrate 50 mg twice daily and aspirin 81 mg/day. He is
adherent to this regimen and has health insurance, but he does not like to make the 3-hour trip to his primary
care provider. His laboratory data from his past visit were all within normal limits. His vital signs today include
BP 130/78 mm Hg and HR 76 beats/minute. All laboratory values are within normal limits. An electrocardiogram
(ECG) reveals an irregularly irregular rhythm, with no P waves, and a HR of 74 beats/minute. A diagnosis of AF
is made. What is the best approach for managing his AF at this time?
A. Begin digoxin 0.25 mg/day.
B. Begin diltiazem CD 240 mg/day.
C. Begin warfarin 5 mg/day and titrate to a goal INR of 2.5.
D. Begin dabigatran 150 mg twice daily.
- Answer: D
This patient’s ventricular rate is well controlled with
his metoprolol tartrate therapy; therefore, an additional
AV nodal-blocking agent is unnecessary and would
increase the risk of adverse events and heart block. If
additional rate control is desired, the metoprolol dose
could first be increased, but the patient’s heart rate is
currently within the goal range (Answers A and B are
incorrect). This patient with AF would be considered
at high risk of a stroke because of his history of HTN
and TIA. Given these risk factors, this patient has a
CHA2DS2-VASc score of 3; therefore, anticoagulation
with an oral anticoagulant agent is indicated. Warfarin
titrated to a goal INR of 2.5 would be a potentially
appropriate option; however, this patient may be unable
to travel to his primary care provider’s office for weekly
INR checks, and DOACs are preferred to warfarin for
DOAC-eligible patients (Answer C). In this case, dabigatran
150 mg twice daily (Answer D) may be the best
choice because it does not warrant INR monitoring,
the patient has prescription insurance, he appears to be
adherent to a twice-daily medication regimen already,
and he does not have renal impairment.
Patient Case
5. H.D. is a 67-year-old man with a history of HTN and AF for 4 years. His medications include ramipril 5 mg
twice daily, sotalol 120 mg twice daily, digoxin 0.125 mg/day, and warfarin 5 mg/day. He visits his primary
care physician today after being discharged from the emergency department with increased fatigue on exertion,
palpitations, and lower extremity edema. His vital signs today include BP 115/70 mm Hg and HR 88
beats/minute, and all laboratory results are within normal limits; however, his lower extremity edema has
worsened. His INR is 2.8. His ECG shows AF. An echocardiogram reveals an LVEF of 35%–40%. H.D.’s
physician would like to continue a rhythm control approach. What is the best treatment option for managing
his AF?
A. Discontinue sotalol and begin metoprolol succinate 12.5 mg/day.
B. Discontinue sotalol and begin dronedarone 400 mg twice daily.
C. Discontinue sotalol and begin amiodarone 400 mg twice daily, tapering to goal dose of 200 mg/day for the
next 6 weeks.
D. Continue sotalol and add metoprolol tartrate 25 mg twice daily.
- Answer: C
With the new diagnosis of HFrEF, this patient can no
longer receive sotalol. Discontinuing this medication
is important so that his risk of arrhythmic death is not
increased. Adding metoprolol is a reasonable approach,
but not until his HF has been properly controlled, making
both Answers A and D incorrect. If rhythm control
is desired, amiodarone and dofetilide are the only two
antiarrhythmic drugs that have been proven safe and
effective in patients with HFrEF, making Answer C
correct. Of importance, drug interactions exist between
amiodarone, digoxin, and warfarin, which will need to be addressed. Dronedarone (Answer B) is not recommended
in patients with symptomatic HF with a recent
decompensation.
Patient Cases
6. W.D. is a 55-year-old white female who was recently admitted to the hospital with acute myocardial infarction
which was treated with a stent. She has a past medical history of HTN and GERD. She is visiting your
clinic today for management of her cardiovascular medications. Her vitals today include BP 152/86 mm Hg
and HR 82 beats/minute. Her labs are all WNL, including Na 140 mEq/L, K 4.3 mEq/L, and SCr 1.0 mg/dL.
Her current medication regimen includes clopidogrel 75 mg daily, aspirin 81 mg daily, and atorvastatin 40
mg daily. What is the most appropriate approach to manage her HTN?
A. Add carvedilol monotherapy
B. Add lisinopril and metoprolol
C. Add amlodipine and metoprolol
D. Add lisinopril monotherapy
- Answer: B
W.D.’s blood pressure falls into the stage 2 HTN category.
The ACC/AHA guidelines recommend two-drug
therapy for patients with stage 2 HTN, making answers
A and D incorrect. This patient recently suffered from
a myocardial infarction, and the ACC/AHA guidelines
recommend both β-blockers and ACE inhibitors or
ARBs for treatment of HTN in ischemic heart disease,
making answer B correct and Answer C incorrect.
- T.J. is a 58-year-old African American woman presenting for routine follow-up of her chronic obstructive
pulmonary disease. She has no other medical history. Her blood pressure today (average of 2 readings) is
138/88 mm Hg. Her HR is 77 beats/minute. Her BP at her last visit was 138/88 mm Hg. Her current medications
include tiotropium dry powder inhaler daily and an albuterol metered dose inhaler as needed. Her labs
include Na 140 mEq/L, K 4.0 mEq/L, Cl 102 mEq/L, bicarbonate 28 mEq/L, blood urea nitrogen 14 mg/dL,
and SCr 0.8 mg/dL. Her 10-year ASCVD risk is 12.0%. What is the best approach for managing her HTN?
A. Begin diet and lifestyle modifications only
B. Begin lifestyle modifications and add amlodipine 5 mg daily
C. Begin lifestyle modifications and add lisinopril 2.5 mg daily
D. Begin lifestyle modifications and add lisinopril 2.5 mg daily plus hydrochlorothiazide 12.5 mg daily
- Answer: B
T.J.’s blood pressure falls into the stage 1 HTN category.
Because the patient’s 10-year ASCVD risk is 10%
or greater, her blood pressure treatment threshold is
130/80 mm Hg or greater. Therefore, pharmacologic
treatment is warranted, making Answer A incorrect.
Because she has stage 1 HTN, she should be started
on a single drug regimen, making answer D incorrect.
According to the ACC/AHA guidelines, patients
without medical conditions that direct drug therapy
choices can be initiated on ACE inhibitors, ARBs, thiazide
diuretics, or calcium channel blockers. However,
because this patient is African American and she does
not have heart failure, CKD, or type 2 diabetes with
albuminuria, her initial HTN regimen should include a
calcium channel blocker or a thiazide diuretic because
these agents are more effective at lowering BP than
ACE inhibitors and ARBs. Therefore, answer C is
incorrect and answer B is the best choice.
Patient Cases
8. M.M. is a 63-year-old white woman who just finished 6 months of diet and exercise for dyslipidemia. She has
a history of hypertension, DM, and asthma. She smokes one pack of cigarettes and drinks three beers per day.
Her mother had HTN and suffered an MI at age 42 years. Her father had HTN and DM. Her medications are
albuterol metered dose inhaler, lisinopril, metformin, linagliptin, and calcium carbonate antacids. Her vital
signs include BP 134/84 mm Hg and HR 75 beats/minute. Her laboratory results are as follows: HDL-C 38
mg/dL, LDL-C 134 mg/dL, TG 186 mg/dL, TC 209 mg/dL, and hemoglobin A1C 8.6%. Her pooled cohort
equation estimates a 10-year ASCVD risk of 27.8%. What is the most appropriate next step for M.M.?
A. Initiate a low-intensity statin
B. Initiate a moderate-intensity statin
C. Initiate a high-intensity statin
D. Initiate a high-intensity statin plus ezetimibe
- Answer: C
This patient falls into the patient management group
of patients with diabetes and age 40-75 years. Because
she has multiple ASCVD risk factors including smoking,
low HDL-C, and HTN, this patient would benefit
from high-intensity statin therapy (answer C). Answer
B would be correct if M.M. did not have additional
ASCVD risk factors. Low-intensity statins are not recommended
for initial therapy for any patient in the 2018
ACC/AHA Cholesterol guidelines (answer A). This
patient should receive maximally tolerated statin therapy
and be assessed for response before the addition of
ezetimibe (Answer D).
- According to the ACC/AHA blood cholesterol guidelines, which is best described as a high-intensity statin dose?
A. Pravastatin 20 mg/day.
B. Lovastatin 20 mg/day.
C. Atorvastatin 40 mg/day.
D. Rosuvastatin 10 mg/day.
- Answer: C
A high-intensity statin should provide a ≥50% reduction
in LDL-C. Atorvastatin 40 mg is considered a highintensity
statin because it will lower LDL by more than
50% (Answer C is correct). Pravastatin 20 mg (Answer
A) and lovastatin 20 mg (Answer B) are considered
low-intensity statins because they will lower LDL by
less than 30%. Rosuvastatin 10 mg will reduce LDL
30%–50%; therefore, it is considered a moderateintensity
statin (Answer D).
- Which best describes a potential secondary cause of high TG concentrations?
A. Amiodarone.
B. Biliary obstruction.
C. Sirolimus.
D. Saturated fats.
- Answer: C
If fasting TG concentrations are 500 mg/dL or greater
or LDL-C is greater than 190 mg/dL, patients should
be assessed for potential secondary causes of their dyslipidemia.
Secondary causes of elevated TG include
high intake of carbohydrates, excessive alcohol intake,
oral estrogens, glucocorticoids, protease inhibitors,
sirolimus (Answer C), thiazides, anabolic steroids, raloxifene,
β-blockers, nephrotic syndrome, CKD, lipodystrophies,
poorly controlled DM, hypothyroidism,
pregnancy, and obesity. Amiodarone (Answer A), biliary
obstruction (Answer B), and saturated fats (Answer
D) are all secondary causes of increased LDL-C.
Patient Case
11. A 66-year-old man with a medical history of HTN and acute coronary syndrome with a drug-eluting coronary
stent placement 14 months ago presents to the primary care clinic. Current medications include aspirin 81
mg/day, prasugrel 10 mg/day, nitroglycerin 0.4-mg sublingual tablets as needed for chest pain, metoprolol
succinate 75 mg/day, ramipril 10 mg/day, and atorvastatin 20 mg/day. He asks you how long he will need to
take prasugrel. What is the best answer?
A. Call your physician because you may be able to stop prasugrel now.
B. Your prasugrel should have been discontinued 6 months after acute coronary syndrome; discontinue
it now.
C. You will need to take prasugrel indefinitely.
D. You will need to take prasugrel for at least 18 months after your MI and stent placement.
- Answer: A
After placement of a drug-eluting stent for acute coronary
syndrome, a P2Y12 inhibitor is indicated for 12
months in most patients (Answer A is correct). Answer
B is incorrect because 6 months of dual antiplatelet
therapy (DAPT) is only for patients at high risk of
bleeding, and this patient has no indication of being at
high risk of bleeding. No current data support DAPT
indefinitely (Answer C is incorrect). Answer D is incorrect
because the guidelines recommend DAPT for at
least 12 months, not 18, in most patients.
Which antiarrhythmic agents have the
greatest risk for causing QT prolongation?
class 1a and class 3 agents
What other medications are known to
cause
QT prolongation?
Any drugs which blocks Na & K channels, blocks phase 0 or III conduction
§ Diphenhydramine (Benadryl)
§ Metoclopramide (Reglan)
§ Lidocaine (local anesthetic)
§ Phenytoin (Dilantin)
§ Tricyclic antidepressants (TCAs)
What anticonvulsant should NOT be given
for seizures is suspected overdose?
§ Answer = Phenytoin (Dilantin)
§ Why?
– Tricyclic antidepressants (TCAs) and Benadryl blocks Na+
conductance in the heard during phase O àleading to QRS
widening
– Na+ blockade affects nerve conduction in CNS àseizures
– Phenytoin works by blocking the same Na+ channels &
phenytoin toxicity (i.e., levels > 20-30) àseizures!!!!
What is the primary treatment for TCA
overdose and why?
§ Answer = HYPERtonic Saline
§ Why?
– Tricyclic antidepressants (TCAs) block Na+ conductance
during phase O àleading to QRS widening prolongation
– Na+ blockade affects nerve conduction in CNS àseizures
– Give HYPERtonic saline to compete with TCAs and shorten
QRS and prevent/treat against seizures
T
What electrolyte abnormalities are known
to cause QT prolongation?
Hyponatremia (severe)
§ Hypokalemia
§ Hypocalcemia
§ Hypomagnesemia
How does calcium “stabilize the cardiac
membrane” when treating hyperkalemia?
Hyperkalemia Treatment:
* Ca2+ (gluconate or
chloride) à+ charges
outside cell
* Insulin, albuterol, or bicarb
to drive K+ inside the cell à
+ charges inside cell
* Attempts to maintain
“neutral” electro-chemical
potential or gradient across
cell membrane like seen
during phase 2
How does digoxin cause the classic
“Salvador Dali” sign or “Scooped ST
segments”?
§ ECG findings reported in the literature:
– Wide variety of dysrhythmias due to conduction delays
and increased automaticity
– Normal Dig Levels: classically see “scooped” ST segments
– Paroxysmal atrial tachycardia with AV nodal block
– PACs & PVCs
– Junctional rhythm
– Sinus bradycardia
– V-Tach & V-Fib
– Bradydysrhythmias
§ Why Increased Automaticity:
− Increased resting membrane potential
due to blocking of Na+/K+ ATPase
pump causing a rise in intracellular
Na+ in phase 4
§ Why the “scooped” or slurred ST
segment?
− Inhibition of phase I, 2, 3
How can digoxin overdose lead to
hyperkalemia
Answer = Blockade of Na+/K+ ATPase Pump
§ Why?
– Acute overdose with digoxin àblocks K+ from coming into the
cell during phase 4
– Phase 4 =
* The cardiac cell is trying to set everything back for next action potential
* Na+ being moved out of the cell
* K+ comes back inside the cell
* Ca2+ is being moved back out of the cell via Ca2+ /Na+ exchange pump
Should you give calcium in patients with
digoxin induced hyperkalemia?
Concern for calcium administration:
– Case reports of patients going into cardiac arrest
– Concerns for the “stone heart” mainly from animal
studies which received rapid levels of Ca2+ with high
serum levels of > 5 mmol/L or 20 mg/dL
– A 2011 retrospective study of 159 patients showed
that 23 of those patients received IV Ca2+ with 5
patients dying but none died within 1 hr of IV Ca2+
infusion. The mortality rate of group not receiving IV
Ca2+ was 20% (though no statistical significance).
Treatment of digoxin toxicity
Hyperkalemia in Digoxin Toxicity:
– Give digoxin immune Fab
– If still need consider dextrose + insulin (or) Na bicarb
– Ok to give IV Ca if pt with bradycardic, wide-complexrhythm and in whom whom it is not known if the pt
is on digoxin.
antiarrythmic overall pearls
§ Class I agents have greatest impact on QRS
widening
– TCAs, Benadryl, phenytoin have similar effects
§ Class II reduce both chronotropy and inotropy
§ Class III agents have greatest impact on QT
prolongation
§ Class IV reduce both chronotropy and
inotropy, work well for rate control and BP, but
do not inhibit remodeling
§ Adenosine increases K+ removal and slows
nodal conduction that can lead to cardiac
asystole or pause – thankfully it has a halflife of 10 sec
§ Digoxin is a narrow therapeutic index,
unique mechanism of action, but benefits
in reducing mortality in HF
