Part 9.3- HEART FAILURE

Proverbs 16:3

c. “Weakened” poorly contracting myocardium

The underlying pathophysiology of heart failure is:
a. Excess thyroid hormone production
b. Increased platelet aggregation
c. “Weakened” poorly contracting myocardium
d. Increased renal perfusion only

a. Increased cardiac workload (preload, afterload)

Which precipitating event may worsen heart failure?
a. Increased cardiac workload
b. Reduced preload
c. Reduced afterload
d. Increased venous return

b. Increasing strength of cardiac contraction

One management approach in heart failure is:
a. Increasing cardiac workload
b. Increasing strength of cardiac contraction
c. Increasing afterload
d. Increasing venous congestion

a. Inotropism

Pharmacologic management to improve cardiac contraction mainly involves:
a. Inotropism
b. Dromotropism
c. Chronotropism
d. Vasospasm

c. Cardiac transplantation

Surgical approach may be used in heart failure management
a. Appendectomy
b. Coronary thrombosis
c. Cardiac transplantation
d. Nephrectomy

c. Reduce cardiac workload

The main medical approach in heart failure management is to:
a. Increase afterload
b. Increase preload
c. Reduce cardiac workload
d. Increase myocardial oxygen demand

a. Reduce preload and afterload

“Unloader” medications in heart failure are used to:
a. Reduce preload and afterload
b. Increase preload and afterload
c. Increase platelet aggregation
d. Increase myocardial oxygen requirement

d. Improve functional capacity

One goal of heart failure management is to:
a. Reduce physical activity permanently
b. Increase myocardial stress
c. Increase preload and afterload
d. Improve functional capacity

c. NYHA Functional Classification

Functional improvement in heart failure is assessed using:
a. APGAR score
b. Glasgow Coma Scale
c. NYHA Functional Classification
d. JNC classification

a. Class I

[NYHA Functional Classification]

Symptoms with activities beyond regular activities

a. Class I

b. Class II

c. Class III

d. Class IV

b. Class II

[NYHA Functional Classification]

Symptoms with regular activities

a. Class I

b. Class II

c. Class III

d. Class IV

c. Class III

[NYHA Functional Classification]

Symptoms on less than regular activities

a. Class I

b. Class II

c. Class III

d. Class IV

d. Class IV

[NYHA Functional Classification]

Symptoms even at rest

a. Class I

b. Class II

c. Class III

d. Class IV

a. Cardiac glycosides

[Inotropics]

Digoxin belongs to which class of drugs?
a. Cardiac glycosides
b. Beta-blockers
c. Calcium channel blockers
d. ACE inhibitors

c. Na⁺/K⁺-ATPase inhibition → reduced Ca²⁺ expulsion and increased Ca²⁺ stored in sarcoplasmic reticulum

[Inotropics]

The mechanism of action of digoxin is:
a. AT1 receptor blockade
b. β1 receptor blockade
c. Na⁺/K⁺-ATPase inhibition
d. Inhibition of carbonic anhydrase

c. Increasing intracellular Ca²⁺ storage in the sarcoplasmic reticulum

[Inotropics]

Digoxin increases cardiac contractility primarily by:
a. Reducing preload
b. Blocking sodium channels only
c. Increasing intracellular Ca²⁺ storage in the sarcoplasmic reticulum
d. Increasing potassium excretion

a. Increased strength of cardiac contraction (positive inotropism)

[Inotropics]

The main mechanical effect of digoxin is:
a. Increased strength of cardiac contraction
b. Coronary vasospasm
c. Reduced myocardial contractility
d. Increased preload only

c. Increased AV node effective refractory period

[Inotropics]

Which of the following is an electrical effect of digoxin?
a. Reduced stroke volume
b. Increased myocardial contractility only
c. Increased AV node effective refractory period
d. Peripheral venodilation

a. Decreasing AV node conduction velocity

[Inotropics]

Digoxin affects AV node conduction by:
a. Decreasing AV node conduction velocity
b. Increasing AV node conduction velocity
c. No effect on AV conduction
d. Blocking all cardiac conduction

a. Arrhythmias due to increased automaticity

[Inotropics]

Digoxin may increase the risk of:
a. Arrhythmias
b. Bronchodilation
c. Hyperglycemia
d. Renal vasodilation

Hypokalemia

Hypomagnesemia

Hypercalcemia

Hypoxia

[Inotropics]

Condition enhances the effects of digoxin

Hyperkalemia or Hypokalemia?

Hypomagnesemia or Hypermagnesemia?

Hypercalcemia or Hypocalcemia?

Hypoxia or Hyperoxia?

a. Digoxin

[Inotropics]

For symptomatic LV dysfunction in patient with concomitant atrial fibrillation (AF)

a. Digoxin

b. Dobutamine

c. Milrinone

d. Milrinone

a. Digoxin

[Inotropics]

For control ventricular rate in pc with AF and HF

a. Digoxin

b. Dobutamine

c. Milrinone

d. Milrinone

a. Digoxin

[Inotropics]

Adjunct if with persistent signs and symptoms of HF despite ACEi or ARB

a. Digoxin

b. Dobutamine

c. Milrinone

d. Milrinone

c. K⁺, Mg²⁺, and Ca²⁺

[Inotropics]

Before starting digoxin therapy, serum levels of which electrolytes should be within normal range?
a. Glucose, insulin, and calcium
b. Na⁺, Cl⁻, and phosphate
c. K⁺, Mg²⁺, and Ca²⁺
d. Iron, zinc, and potassium

a. Tablet

[Inotropics]

digoxin preparation has approximately 70–75% bioavailability (BA)
a. Tablet
b. Soft gel capsule
c. Injection
d. Spray

b. Soft gel capsule

[Inotropics]

digoxin preparation has approximately 100% bioavailability
a. Tablet
b. Soft gel capsule
c. Injection
d. Spray

a. <1 mg/mL

[Inotropics]

Digoxin adverse effects are less likely when serum digoxin level is:
a. <1 mg/mL
b. >5 mg/mL
c. >10 mg/mL
d. >20 mg/mL

a. Arrhythmias

[Inotropics]

A major cardiac adverse effect of digoxin is:
a. Arrhythmias
b. Bronchospasm
c. Hyperglycemia
d. Gingival hyperplasia

a. Junctional arrhythmias
&
c. Ventricular arrhythmias

[Inotropics]

Digoxin toxicity may cause which cardiac rhythm disturbance? (2)
a. Junctional
b. Bronchodilation
c. Ventricular
d. Peripheral edema

a. Digoxin

[Inotropics]

Extracardiac ADRs of this drug are N&V, visual disturbances

a. Digoxin

b. Dobutamine

c. Milrinone

d. Milrinone

a. Correct electrolyte abnormalities

[Inotropics]

Initial management of digoxin toxicity includes:
a. Correct electrolyte abnormalities
b. Increase digoxin dose
c. Give calcium immediately in all patients
d. Stop monitoring electrolytes

b. DigiFab or DigiBind

[Inotropics]

antidote used for severe digoxin toxicity
a. Naloxone
b. DigiFab or DigiBind
c. Protamine sulfate
d. Flumazenil

a. Beta-1 agonists

[Inotropics]

Dopamine

a. Beta-1 agonists

b. Phosphodiesterase Inhibitors

c. Calcium sensitizers

a. Beta-1 agonists

[Inotropics]

Dobutamine

a. Beta-1 agonists

b. Phosphodiesterase Inhibitors

c. Calcium sensitizers

a. Beta-1 agonists

[Inotropics]

Isoproterenol

a. Beta-1 agonists

b. Phosphodiesterase Inhibitors

c. Calcium sensitizers

a. Binding to Gs protein → activation of adenylyl cyclase → ATP to cAMP

[Inotropics]

The mechanism of action of β1 agonists involves:
a. Binding to Gs protein
b. Blocking Na⁺/K⁺-ATPase
c. Inhibiting ACE enzyme
d. Blocking calcium channels

c. Acutely decompensated chronic HF

[Inotropics]

β1 agonists are commonly used in:
a. Chronic gout prophylaxis
b. Stable osteoarthritis
c. Acutely decompensated chronic HF
d. Hypertension maintenance therapy

a. Tachyarrhythmias

[Inotropics]

A major adverse effect of β1 agonists is:
a. Tachyarrhythmias
b. Gingival hyperplasia
c. Dry cough
d. Hyperuricemia

b. Phosphodiesterase Inhibitors

[Inotropics]

Milrinone

a. Beta-1 agonists

b. Phosphodiesterase Inhibitors

c. Calcium sensitizers

b. Inhibition of PDE-III

[Inotropics]

The mechanism of action of milrinone is:
a. Inhibition of PDE-V
b.Inhibition of PDE-III
c. Na⁺/K⁺-ATPase inhibition
d. AT1 receptor blockade

d. Increasing inotropism and causing vasodilation

[Inotropics]

Milrinone improves cardiac function by:
a. Decreasing chronotropism and causing vasodilation
b. Increasing chronotropism and causing vasoconstriction
c. Decreasing inotropism and causing vasoconstriction
d. Increasing inotropism and causing vasodilation

a. Acutely decompensated chronic HF

[Inotropics]

Which condition is an indication for milrinone therapy?
a. Acutely decompensated chronic HF
b. Chronic gout prophylaxis
c. Osteoarthritis
d. Stable hypertension

b. Acute heart failure

[Inotropics]

Milrinone may be used in:
a. Stable rheumatoid arthritis
b. Acute heart failure
c. Hyperuricemia
d. Chronic asthma management

tachyarrhythmias

bronchospasm

hypokalemia

tremors

easy bruising

[Inotropics]

ADRs of Milrinone

tachyarrhythmias or bradyarrhythmias?

bronchospasm or hyperventilation

hypercalcemia or hypokalemia

seizures or tremors?

easy bruising or poor wound healing?

c. Calcium sensitizers

[Inotropics]

Levosimendan

a. Beta-1 agonists

b. Phosphodiesterase Inhibitors

c. Calcium sensitizers

c. Sensitization of troponin C to Ca²⁺ during systole

[Inotropics]

The mechanism of action of levosimendan includes:
a. β1 receptor blockade
b. Na⁺/K⁺-ATPase inhibition
c. Sensitization of troponin C to Ca²⁺ during systole
d. ACE inhibition

b. Improves contraction at low energy cost

[Inotropics]

During systole, levosimendan:
a. Blocks myocardial contraction
b. Improves contraction at low energy cost
c. Increases energy consumption markedly
d. Causes coronary thrombosis

a. Improved diastolic relaxation due to reduced Ca²⁺ sensitization

[Inotropics]

During diastole, levosimendan produces:
a. Improved diastolic relaxation due to reduced Ca²⁺ sensitization
b. Increased myocardial stiffness due to reduced Ca²⁺ sensitization
c. Increased preload due to reduced Ca²⁺ sensitization
d. Reduced ventricular filling due to reduced Ca²⁺ sensitization

a. Opening ATP-dependent K⁺ channels in myocytes and vascular smooth muscle cells → Vasodilation

[Inotropics]

Levosimendan causes vasodilation by:
a. Opening ATP-dependent K⁺ channels
b. Blocking β1 receptors
c. Inhibiting PDE-III only
d. Blocking calcium channels directly

c. No cardiac myocyte dysfunction, arrhythmia, or increased energy consumption

[Inotropics]

A major advantage of levosimendan is:
a. No myocardial depression, arrhythmia, or increased energy consumption
b. Marked decreased in myocardial oxygen demand, and bradycardia
c. No cardiac myocyte dysfunction, arrhythmia, or increased energy consumption
d. Permanent tachycardia

a. Inotropism + unloading effect

[Inotropics]

Levosimendan provides which combined benefit in HF?
a. Inotropism + unloading effect
b. Vasoconstriction + preload increase
c. Bronchodilation + antiplatelet effect
d. Renal vasospasm + arrhythmia prevention

a. Acute heart failure

[Inotropics]

Which condition is an indication for levosimendan?
a. Acute heart failure
b. Osteoarthritis
c. Acute gout attack
d. Stable hypertension

d. Acutely decompensated HF

[Inotropics]

Which condition is an indication for levosimendan?
a. RA
b. Osteoarthritis
c. Acute gout attack
d. Acutely decompensated HF

c. Levosimendan

[Inotropics]

ADRs include Headache, Dizziness, Nausea, and Hypotension

a. Milrinone

b. Digoxin

c. Levosimendan

d. Dobutamine

c. ACEis) and ARBs

[Non-inotropic]

Non-inotropic:

a. Cardiac Glycosides

b. PDEi

c. ACEis and ARBs

d. B1 agonists

a. Unloaders/neurohormonal controllers

[Non-inotropic]

ACE inhibitors (ACEis) and ARBs in HF are classified as:
a. Unloaders/neurohormonal controllers
b. Cardiac glycosides
c. Beta-1 agonists
d. Calcium sensitizers

c. First-line therapies for HF

[Non-inotropic]

ACEis and ARBs are considered:
a. Drugs used only in gout
b. Last-line therapies for HF only
c. First-line therapies for HF
d. Contraindicated in all HF patients

b. Reduced cardiac preload and afterload

[Non-inotropic]

The primary effect of ACEis and ARBs in HF is:
a. Reduced myocardial contractility
b. Reduced cardiac preload and afterload
c. Reduced heart rate
d. Coronary vasospasm

a. Start at low dose and titrate every 1–2 weeks to maximum tolerated dose

[Non-inotropic]

Which statement correctly describes ACEi dosing in HF?
a. Start at low dose
b. Start immediately at maximum dose
c. Increase dose daily regardless of BP
d. Stop titration after the first dose

a. Maximum tolerated dose with SBP ≥100

[Non-inotropic]

ACE inhibitor dose titration in HF should continue until:
a. Maximum tolerated dose with SBP ≥100
b. SBP <70
c. Immediate hypotension occurs
d. HR exceeds 150 bpm

a. Captopril

[Non-inotropic]

initial dose (ID) of 6.25 mg every 8 hours (q8h) in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

a. Captopril

[Non-inotropic]

maximum dose (MD) of 50 mg q8h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

b. Enalapril

[Non-inotropic]

initial dose (ID) of 2.5mg q 24h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

b. Enalapril & c. Lisinopril

[Non-inotropic]

maximum dose (MD) of 40mg q 24 h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

c. Lisinopril

[Non-inotropic]

initial dose (ID) of 5mg q 24h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

d. Perindopril

[Non-inotropic]

initial dose (ID) of 2-2.5 mg q 24h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

d. Perindopril

[Non-inotropic]

maximum dose (MD) of 16-20 mg q 24h in HF

a. Captopril
b. Enalapril
c. Lisinopril
d. Perindopril

a. Neprilysin inhibitor prodrug + ARB

[Non-inotropic]

Sacubitril/valsartan is classified as:
a. Neprilysin inhibitor prodrug + ARB
b. ACE inhibitor + beta-blocker
c. Cardiac glycoside + ARB
d. PDE-III inhibitor + nitrate

a. Inhibition of neprilysin enzyme and activation of BNP receptors

[Non-inotropic]

The mechanism of action of sacubitril/valsartan includes:
a. Inhibition of neprilysin enzyme and activation of BNP receptors
b. Na⁺/K⁺-ATPase inhibition
c. β1 receptor stimulation
d. Calcium channel blockade

b. First-line therapy for HF

[Non-inotropic]

Sacubitril/valsartan is used as:
a. First-line therapy for acute gout
b. First-line therapy for HF
c. Maintenance therapy for COPD
d. Primary treatment for bacterial infection

a. More efficacious in HF

[Non-inotropic]

Compared with enalapril, sacubitril/valsartan is:
a. More efficacious in HF
b. Less effective in HF

Hypotension

Hyperkalemia

Renal failure

Angioedema

[Non-inotropic]

ADR of Sacubitril Valsartan

Hypotension or Hypertension?

Hyperkalemia or Hypokalemia?

Liver failure or Renal failure?

Peripheral edema or Angioedema?

a. Preload and afterload unloading

[Non-inotropic]

The combination of hydralazine + ISDN primarily produces:
a. Preload and afterload unloading
b. Increased cardiac workload
c. Increased preload only
d. Coronary vasospasm

c. An alternative to ACEi or ARB

[Non-inotropic]

Hydralazine + ISDN is mainly used in HF as:
a. Acute gout treatment
b. First-line antibiotic therapy
c. An alternative to ACEi or ARB
d. Beta-blocker replacement in all patients

a. African descent

[Non-inotropic]

A that patient may benefit from hydralazine + ISDN added-on to ACEi or ARB
a. African descent
b. A patient with acute asthma
c. A patient with metabolic acidosis
d. A patient with drug induced hepatotoxicity

b. Activating guanylyl cyclase → vasodilation

[Non-inotropic]

Recombinant human BNP exerts its effect mainly by:

a. Blocking angiotensin II receptors
b. Activating guanylyl cyclase
c. Inhibiting beta-1 receptors
d. Increasing aldosterone secretion

b. Acute decompensated heart failure

[Non-inotropic]

Primary therapeutic use of Nesiritide is:

a. Chronic stable angina
b. Acute decompensated heart failure
c. Hypertension long-term control
d. Myocardial infarction prophylaxis

b. Hypotension

[Non-inotropic]

A major adverse effect of Nesiritide is:

a. Hypoglycemia
b. Hypotension
c. Hyperkalemia
d. Bradycardia with AV block

a. Renal failure

[Non-inotropic]

Which of the following is also a reported adverse effect of Nesiritide?

a. Renal failure
b. Hearing loss
c. Liver cirrhosis
d. Pulmonary fibrosis

b. Atrial fibrillation and ventricular tachycardia

[Non-inotropic]

Serious arrhythmias associated with Nesiritide include:

a. Sinus bradycardia only
b. Atrial fibrillation and ventricular tachycardia
c. First-degree AV block only
d. Supraventricular tachycardia

d. Hypersensitivity

[Non-inotropic]

Adverse effect of Nesiritide

a. Pulmonary fibrosis
b. Hearing loss
c. Liver cirrhosis
d. Hypersensitivity

b. Evidence of fluid overload

[Non-inotropic]

Diuretics in heart failure are mainly indicated for patients with:

a. Severe bradycardia
b. Evidence of fluid overload
c. Hyperthyroidism
d. Stable angina only

a. Peripheral edema and pulmonary congestion

[Non-inotropic]

Which finding suggests fluid overload in heart failure?

a. Peripheral edema and pulmonary congestion
b. Dry skin and hypotension
c. Hyperactivity and tremors
d. Blurred vision and headache

b. Add-on therapy to reduce mortality and morbidity

[Non-inotropic]

Potassium-sparing diuretics are primarily used in heart failure as:

a. First-line monotherapy
b. Add-on therapy to reduce mortality and morbidity
c. Emergency antihypertensive drugs
d. Treatment for arrhythmias

d. Weight loss of ~1 kg/day or ≥4.5 kg in 5 days

[Non-inotropic]

The therapeutic goal of diuretic therapy in heart failure is approximately:

a. Weight gain of 1 kg/day or ≥4.5 kg in 15 day
b. No change in body weight in 10 days
c. Weight loss of 10 kg/day or ≥24.5 kg in 2 day
d. Weight loss of ~1 kg/day or ≥4.5 kg in 5 days

a. Failure to treat volume overload despite Furosemide dose of ≥80–160 mg

[Non-inotropic]

Diuretic resistance is defined as:

a. Failure to treat volume overload despite Furosemide dose of ≥80–160 mg
b. Severe dehydration after one dose of Furosemide dose of ≥80–160 mg
c. Immediate response to low-dose diuretics such as Furosemide dose of ≥80–160 mg
d. Development of hypertension during therapy

b. Thiazide + Loop diuretic

[Non-inotropic]

The recommended remedy for diuretic resistance is:

a. Beta blocker + ACE inhibitor
b. Thiazide + Loop diuretic
c. Calcium channel blocker + nitrate
d. Digoxin + aspirin

b. Reduce mortality and morbidity

[Non-inotropic]

A major benefit of beta blockers in stable CHF is:

a. Increase fluid retention
b. Reduce mortality and morbidity
c. Cause immediate diuresis
d. Increase myocardial oxygen demand

c. After at least 2 weeks of anti-HF treatment to stabilize CHF

[Non-inotropic]

Beta blockers in CHF should be started:

a. Immediately during acute decompensation
b. Only after surgery combined with other anti-HF treatment to stabilize CHF
c. After at least 2 weeks of anti-HF treatment to stabilize CHF
d. At maximum dose on day 1

b. Start at low doses and titrate slowly to maximum tolerated dose

[Non-inotropic]

The recommended dosing strategy for beta blockers in CHF is:

a. Start high dose then taper
b. Start at low doses and titrate slowly to maximum tolerated dose
c. Give only once during hospitalization
d. Maintain the same dose indefinitely without adjustment

c. Metoprolol

[Non-inotropic]

initial dose (ID) of 12.5 mg every 24 hours

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol

c. Metoprolol

[Non-inotropic]

maximum dose (MD) of 200 mg every 24 hours

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol

a. Carvedilol

[Non-inotropic]

initial dose (ID) of 3.125mg q 12h

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol

a. Carvedilol

[Non-inotropic]

maximum dose (MD) of 25-50mg q 12h

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol

d. Bisoprolol &

b. Nebivolol

[Non-inotropic]

initial dose (ID) of 1.25mg q 24h

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol

d. Bisoprolol &

b. Nebivolol

[Non-inotropic]

maximum dose (MD) of 10mg q 24h

a. Carvedilol
b. Nebivolol
c. Metoprolol
d. Bisoprolol