Pharma Co-therapy Of Heart Failure Quiz
Understanding the pharmacotherapy of heart failure requires understanding most of the drugs and fundamentals of cardiology so far in this course. Ideally, you should be able to tie together the pathophysiology and recommend appropriate pharmacotherapy to treat the patient.
Questions and Answers
- 1.
Which of the following may describe the pathophysiology of heart failure? Check all that may apply.
- A.
Structural impairment of heart
- B.
Functional impairment of heart
- C.
Decreased ventricular filling of blood
- D.
Decreased ventricular ejection of blood
Correct Answer(s)
A. Structural impairment of heart
B. Functional impairment of heart
C. Decreased ventricular filling of blood
D. Decreased ventricular ejection of bloodExplanation
The definition of heart failure is a clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Basically, the heart is unable to deliver enough blood to oxygenate the circulation. This could be due to a structural impairment, such as left ventricular hypertrophy, or simply a functional impairment. The heart may not be filling appropriately due to elevated resistance, or it may not be ejecting blood properly due to an inability to properly contract. Knowing what is wrong, the pathophysiology, permits you to predict which therapies will be of benefit.Rate this question:
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- 2.
Which of the following may cause heart failure? Check all that apply.
- A.
Myocardial infarction
- B.
Untreated hypertension
- C.
Stroke
- D.
Diabetes
Correct Answer(s)
A. Myocardial infarction
B. Untreated hypertensionExplanation
A myocardial infarction may contribute to heart failure due to the death of viable cardiac muscle cells. Fewer muscle cells means a reduced ability for the heart to do its job: pumping blood!
Untreated hypertension can lead to atherosclerosis, and increased resistance. This means the heart must work harder on each beat to overcome the resistance to pump blood into the circulation. Over time, the heart will wear out.
A stroke does not affect the heart's ability to pump, and diabetes has no direct link to causing heart failure.
As a side note, the thiazolidinediones (TZDs), pioglitazone and rosiglitazone, are used to treat diabetes and have been shown to worsen and cause new onset heart failure by increasing fluid retention, and should be avoided in patients with advanced (Stage III or IV) heart failure.Rate this question:
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- 3.
Which of the following appropriately describes SYSTOLIC dysfunction? Check all that apply.
- A.
The contractility of the left ventricle is reduced
- B.
The rate of filling of the ventricles during diastole is slowed
- C.
The ventricle is dilated
- D.
The preload (end diastolic volume) is increased
- E.
The preload is not increased
- F.
The ejection fraction is decreased
- G.
The ejection fraction is not decreased
Correct Answer(s)
A. The contractility of the left ventricle is reduced
C. The ventricle is dilated
D. The preload (end diastolic volume) is increased
F. The ejection fraction is decreasedExplanation
The contractility of the left ventricle is reduced and the heart cannot pump as well during systole, hence the term systolic dysfunction.
The rate of filling of the ventricles during diastole is not slowed, since the filling is not dependent on the ability of the heart to constrict. The filling during DIASTOLE is slowed in DIASTOLIC dysfunction, usually due to a stiffening of the walls of the ventricular chambers, which increases the pressure when the blood enters.
The ventricle is dilated as a result of not ejecting the blood that filled the chambers.
The preload is increased since the ventricle is dilated and the heart can fill with more blood.
The ejection fraction is decreased since the heart fills with more blood, but the ventricle cannot contract enough to eject all the blood.Rate this question:
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- 4.
Which of the following appropriately describes DIASTOLIC dysfunction? Check all that apply.
- A.
The contractility of the left ventricle is reduced
- B.
The rate of filling of the ventricles during diastole is slowed
- C.
The ventricle is dilated
- D.
The preload (end diastolic volume) is increased
- E.
The preload is not increased
- F.
The ejection fraction is decreased
- G.
The ejection fraction is not decreased
Correct Answer(s)
B. The rate of filling of the ventricles during diastole is slowed
E. The preload is not increased
G. The ejection fraction is not decreasedExplanation
Please keep in mind that systolic dysfunction and diastolic dysfunction are not entirely separate entities. Patients may present with signs and symptoms of both type of heart failure, and the end result is a decrease in cardiac output.
In diastolic dysfunction, the contractility of the ventricle is not necessarily decreased, as it is in systolic dysfunction.
However, the filling is slightly decreased, due to increased resistance from thickened walls in the heart.
The ventricle is not dilated, but it is more difficult to fill due to the stiff walls, so it fills less.
The preload is not increased since the heart fills with slightly less amount of blood, and the pressure caused by the slightly less amount of blood is greater, due to the inability to expand.
Likewise, the ejection fraction is not decreased, since the heart ejects the same fraction, but was filled with less blood. For example, instead of ejecting 40ml out of 50ml, the heart with diastolic dysfunction is now ejecting 32ml out of 40ml. The ejection fraction in each case is identical at 0.8, but the heart is ejecting 8ml less with diastolic dysfunction.Rate this question:
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- 5.
Atrial fibrillation would have a more deleterious effect on which type of heart failure?
- A.
Systolic dysfunction
- B.
Diastolic dysfunction
Correct Answer
B. Diastolic dysfunctionExplanation
Hopefully you were able to reason your way through this one. Since atrial fibrillation would decrease the filling that occurs during diastole (see your notes on dysrhythmias), it would cause even more harm to a heart that has trouble filling, which is the heart with diastolic dysfunction. Likewise, tachycardia would worsen heart failure due to diastolic dysfunction since the fast heart rate would decrease the time in diastole and therefore decrease the ability of the heart to fill with blood.Rate this question:
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- 6.
To which of the following areas is blood flow MOST reduced in heart failure?
- A.
Brain
- B.
Heart
- C.
Kidneys
- D.
Lungs
Correct Answer
C. KidneysExplanation
The body has mechanisms for ensuring adequate blood flow to the brain and to the heart. These compensations result in decreased blood flow to the kidneys. Decreasing the blood flow to the kidneys is dangerous, and a vicious cycle that worsens the heart failure.
Due to the decreased filtration, more volume backs up in the body, and this increases the pressure in the veins, which raises the hydrostatic pressure in the capillaries (blood is trying to get through but there's too much blood on the venous side of the capillary), leading to leakage into the interstitial fluid space = EDEMA, which is a hallmark symptom of heart failure.
The reduced blood flow also activates the renin angiotensin aldosterone system, since aldosterone will retain more Na+ and water to fill the vasculature and constrict the vasculature to ATTEMPT TO INCREASE the renal pressure.
The decrease in blood pressure will also activate the sympathetic nervous system, to try to stimulate the heart and constrict the vasculature.
The secretion of vasopressin is also increased in order to stimulate water reabsorption and constrict the vasculature.
In case that was not enough, endothelin, a vasoconstrictor, is also produced in greater quantities.
Keep these pathophysiological changes in mind in order to justify drug therapy that targets each of these facts.Rate this question:
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- 7.
Which beta-blockers have been proven to have a morbidity and mortality benefit in heart failure? Check all that apply.
- A.
Metoprolol succinate
- B.
Metoprolol tartrate
- C.
Carvedilol
- D.
Propranolol
- E.
Bisoprolol fumarate
Correct Answer(s)
A. Metoprolol succinate
C. Carvedilol
E. Bisoprolol fumarateExplanation
These are the three beta-blockers that have been proven in trials to result in a decrease in all-cause mortality. These should probably be the beta-blockers you choose for your patient.Rate this question:
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- 8.
True or False: Diuretics have a mortality benefit in heart failure observed in studies.
- A.
True
- B.
False
Correct Answer
B. FalseExplanation
Diuretic therapy has no mortality (death) benefit observed in studies, but may improve symptoms of fluid retention (morbidity). Use them when necessary, but remember that it is not necessarily increased the life expectancy of the patient.Rate this question:
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- 9.
Which ARBs have a mortality benefit proven by clinical trials? Check all that apply.
- A.
Candesartan
- B.
Losartan
- C.
Irbesartan
- D.
Valsartan
Correct Answer(s)
A. Candesartan
B. Losartan
D. ValsartanExplanation
It is often difficult to tell if the mortality benefit may be a class effect, but the selected drugs (candesartan, valsartan, and losartan) have a proven mortality benefit as evidenced by clinical trials.Rate this question:
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- 10.
For a patient with acute renal insufficiency, which drug(s) would you want to avoid? Check all that apply.
- A.
Hydralazine
- B.
Isosorbide dinitrate
- C.
Lisinopril
- D.
Losartan
Correct Answer(s)
C. Lisinopril
D. LosartanExplanation
ACE inhibitors and ARBs are harmful in an acute renal insufficiency case because they can increase the serum creatinine. In such a situation, hydralazine with isosorbide dinitrate may be used. Exogenous nitrate therapy has beneficial effects for HF treatment at the cellular and hemodynamic level by enhancing endothelium dependent vasodilation, improving systolic function and exercise capacity, and inhibiting cardiac remodeling black and non-black HF patients. Both Vasodilator-Heart Failure Trials I and II showed improved ejection fraction and exercise tolerance with this therapy in whites and in blacks.Rate this question:
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- 11.
What is the target serum concentration of digoxin in heart failure?
- A.
0.1-0.5 ng/mL
- B.
0.3-0.7 ng/mL
- C.
0.5-0.9 ng/mL
- D.
0.7-1.1 ng/mL
Correct Answer
C. 0.5-0.9 ng/mLExplanation
The targeted therapeutic serum concentration is based off the clinical trial in which the greatest mortality benefit was seen in the range of 0.5-0.9 ng/mL, specifically 0.7 ng/mL. Target your dose to match this serum concentration, but monitor for adverse effects as well.Rate this question:
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- 12.
Digoxin has benefits in which of the following?
- A.
Decreasing hospitalizations
- B.
Decreasing mortality
- C.
Reducing symptoms of heart failure
- D.
Treating atrial fibrillation
Correct Answer(s)
A. Decreasing hospitalizations
C. Reducing symptoms of heart failure
D. Treating atrial fibrillationExplanation
Digoxin has no proven mortality benefit, but may be used to decrease symptoms and hospitalizations. These are the findings from trials that have evaluated digoxin. Digoxin is also indicated for treating atrial fibrillation. By increasing the contractility of the heart, digoxin increases cardiac output, which allows for a decreased heart rate and thus less chance of arrhythmia.Rate this question:
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- 13.
Which medication(s) should be avoided in heart failure patients? Check all that apply.
- A.
Acetaminophen
- B.
Diltiazem
- C.
Ibuprofen
- D.
Pioglitazone
- E.
Terazosin
Correct Answer(s)
B. Diltiazem
C. Ibuprofen
D. PioglitazoneExplanation
Acetaminophen is a safe option for OTC pain relief in heart failure patients. Recommend this option over the use of an NSAID.
Diltiazem and verapamil and both non-dihydropyridine calcium channel blockers, and slow down conduction in the AV node, which could be dangerous for a heart failure patient with already decreased cardiac output. If a calcium channel blocker is to be used for controlling hypertension or ischemic symptoms, then a dihydropyridine such as amlodipine or nifedipine should be used.
All NSAIDs should be avoided as they can lead to fluid retention and have negative effects on the kidney. They decrease the production of prostaglandins, which decreases pain but also vasodilation, thus resulting in vasoconstriction.
Pioglitazone (Actos) is a thiazolidinedione (TZD) and should be avoided as it can cause a worsening of heart failure. Rosiglitazone (Avandia) is another TZD and as such should be avoided.
Terazosin is an alpha-one antagonist and is beneficial due to reducing afterload and preload.Rate this question:
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- 14.
What is the primary reason for using dobutamine or dopamine in a heart failure patient?
- A.
Acute improvement in sodium levels to treat hyponatremia
- B.
Acute treatment of hypertension
- C.
Short-term support in acute decompensated heart failure
Correct Answer
C. Short-term support in acute decompensated heart failureExplanation
Dobutamine and dopamine are used in acute decompensated heart failure to increase the contractility and vasodilation in order to provide short term support for the patient.
Dobutamine is a beta-one agonist, which will stimulate the heart to increase contractility and inotropic activity--this is its primary reason for use.
Dopamine has dose-dependent effects at different receptors. Between 3-10 mcg/kg/min, dopamine is a beta-one agonist that increases heart rate and contractility, thus increasing cardiac output.
Thus, these agents are used to increase cardiac output, not for acutely treating hypertension, although blood pressure would be lowered by their use, due to the increased cardiac output requiring less vasoconstriction to maintain blood pressure.Rate this question:
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- 15.
BS is an acutely decompensated heart failure patient with a cardiac index of 2.0 L/min/2. Is BS at goal with regard to her cardiac index?
- A.
Yes
- B.
No
Correct Answer
B. NoExplanation
The cardiac index (CI) is a measure of cardiac output (CO) normalized for patient size in meters squared. To ensure adequate perfusion, a goal of greater than 2.2 L/min/m2 is supported. A normal human's cardiac index is 2.8-4.2 L/min/m2, but a heart failure may not achieve such a perfusion level in the acute setting, so the patient will be at goal if the CI is greater than 2.2 L/min/m2. Thus, at 2.0 L/min/m2, this patient is not at goal.Rate this question:
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- 16.
BS is an acutely decompensated heart failure patient. Her pulmonary capillary wedge pressure is 22 mmHg. Is BS at goal with regard to her pulmonary capillary wedge pressure?
- A.
Yes
- B.
No
Correct Answer
B. NoExplanation
The pulmonary capillary wedge pressure is a measure of the pressure in the lungs. If this pressure is elevated, it may lead to leakage of fluid. A normal human will have a PCWP of less than 12 mmHg, but an acutely decompensated heart failure patient has a goal of less than 18 mmHg. If the patient with heart failure has a PCWP of less than 18 mmHg, the patient is at goal. Therefore, this patient is not at goal.Rate this question:
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- 17.
A patient with a cardiac index of 2.0 L/min/m2 and a PCWP of 22 mmHg would be classified by the Forrester Hemodynamic Classification as which subset?
- A.
Subset 1: warm and dry
- B.
Subset 2: warm and wet
- C.
Subset 3: cold and dry
- D.
Subset 4: cold and wet
Correct Answer
D. Subset 4: cold and wetExplanation
This patient has both a CI and PCWP that are not at goal. The patient is cold due to inadequate perfusion, and is wet due to increased pressure in the lungs. The treatment for such a patient, who may be in cardiogenic shock and become hemodynamically unstable, is a combination of diuretics and inotropes, to get rid of the excess fluid and stimulate the heart to increase the cardiac output and cardiac index.Rate this question:
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- 18.
True or False: Beta-blockers should be discontinued for an acutely decompensated patient with a Forrester Hemodynamic Classification of stage II.
- A.
True
- B.
False
Correct Answer
B. FalseExplanation
The B-CONVINCED study found that the continuation of beta-blockers was not associated with a delayed improvement in dyspnea, and had better adherence 3 months post decompensation. However, the exceptions include to discontinue the beta-blocker and ACE-I/ARB if the patient is in cardiogenic shock (since the patient needs to have an adequate cardiac output) or has kidney dysfunction, and to discontinue the ACE-I/ARB if hyperkalemic.Rate this question:
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- 19.
For an acutely decompensated patient with an elevated PCWP, loop diuretics should be given at what dose relative to the patient's home dose?
- A.
Doubled home dose PO
- B.
Doubled home dose IV
- C.
Same home dose PO
- D.
Same home dose IV
Correct Answer
D. Same home dose IVExplanation
Even though furosemide has only 50% bioavailability and bumetanide and torsemide have greater than 90% bioavailability, current practice is to give the same dose in mg as the patient is on at home, but to give those mg IV.Rate this question:
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- 20.
True or False: Medications that show a benefit in studies in reducing all-cause mortality in HFrEF do not have the same benefit in HFpEF.
- A.
True
- B.
False
Correct Answer
A. TrueExplanation
This is true, but the focus remains on controlling symptoms and the CV comorbidities/ risk factors such as HTN, CAD, and atrial fibrillation. Controlling blood pressure may be the best option for patients with this condition.Rate this question:
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- 21.
What are potential serious adverse effects of beta-blockers? Check all that apply.
- A.
Rebound hypertension, if not tapered
- B.
Decreased cardiac output
- C.
Hepatotoxicity at therapeutic doses
- D.
Hypermagnesemia
Correct Answer(s)
A. Rebound hypertension, if not tapered
B. Decreased cardiac outputExplanation
Beta-blockers must be tapered when discontinuing, otherwise the patient will experience rebound hypertension. The mechanism is thought to be increased sensitivity and up-regulation of the beta-receptors, since they have been blocked by the beta-blocker. Thus, when the beta-blocker is discontinued, these receptors are now free to be extra sensitive to the effects of norepinephrine/epinephrine and thus hypertension is observed.
Keep in mind that beta-blockers decrease cardiac output. They decrease the heart rate and contractility. This allows the heart to decrease its workload and spend more time in diastole, which increases perfusion. However, this therapeutic mechanism can become dangerous, if the heart rate is decreased excessively, such as in cardiogenic shock.
Hepatotoxicity and hypermagnesemia are not particularly associated with beta-blockers.Rate this question:
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- 22.
Hypokalemia would have what effect on digoxin?
- A.
Decreased effect of digoxin
- B.
Effect that is not clinically significant
- C.
Increased effect of digoxin
- D.
No effect on digoxin
Correct Answer
C. Increased effect of digoxinExplanation
The monitoring of electrolytes, specifically potassium, is critical for patients on digoxin. Frequently, patients on digoxin are also on diuretics, which can result in hypokalemia. Less potassium means digoxin can bind with greater affinity to the Na+/K+ pump. This results in an increased effect of digoxin. This is definitely clinically significant.Rate this question:
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Oct 09, 2023Quiz Edited by
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Feb 22, 2014Quiz Created by
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