[PCOL] Part 3.3 - Cardiovascular Drugs - Drugs for Congestive Heart Failure

c. Both

Congestive Heart Failure (CHF).

a. Results when the output of the heart is insufficient to supply adequate levels of oxygen for the body

b. Impaired Contractility of the Heart + Circulatory Congestion

c. Both

d. None

c. Both

Impaired Contractility of the Heart can be caused by:

a. Low contractility of the heart

b. Too much work load of the heart

c. Both

d. None

c. Both

Goals of Therapy and Agents for CHF.

a. Increase cardiac contractility

b. Reduce cardiac workload

c. Both

d. None

a. Increase cardiac contractility

Inotropic Agents.

a. Increase cardiac contractility

b. Reduce cardiac workload

b. Reduce cardiac workload

Afterload and Preload Unloaders.

a. Increase cardiac contractility

b. Reduce cardiac workload

d. a and b

Its PDE3 inhibitors not PDE5

PDE5 inhibitors (e.g. Sildenafil) → for erectile dysfunction and pulmonary HTN

Inotropic agents.

a. Cardiac glycosides

b. Beta agonist

c. PDE5 inhibitors

d. a and b

e. b and c

f. All

ACEi/ARBs

Beta-blockers

Diuretics

Vasodilators

Drug classes under unloader medications for HF.

Cardiac glycosides

Beta-1 agonists

PDE3 inhibitors (Bipyridine)

Drug classes under inotropic agents for HF.

a. Cardiac glycosides

Inhibit Na-K-ATPase Pump.

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

b. Beta1 agonist

increase cAMP → (+) inotropy

Increase adenylate cyclase increasing cAMP levels.

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

c. PDE3 inhibitors

Inhibit PDE3 increasing cAMP levels.

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

a. Cardiac glycosides

Digoxin

Digitoxin

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

b. Beta1 agonist

Dobutamine

Dopamine

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

c. PDE3 inhibitors

Inamrinone

Milrinone

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

a. Cardiac glycosides

(+) Inotropy

(-) Chronotropy

a. Cardiac glycosides

b. Beta1 agonist

c. PDE3 inhibitors

d. a and b

e. b and c

f. All

f. All

(+) Inotropy

(+) Chronotropy

a. Cardiac glycosides (toxic)

b. Beta1 agonist

c. PDE3 inhibitors

d. a and b

e. b and c

f. All

d. a and b

Cardiac glycosides are toxic with the effect:

a. (+) Inotropy

b. (+) Chronotropy

c. (-) Chronotropy

d. a and b

e. a and c

f. All

f. None

Cardiac glycosides MOA except:

a. Inhibition of Na-K-ATPase Pump

b. Increased intracellular Na+

c. Decreased intracellular K +

d. Indirect inhibition of sodium calcium exchanger → secondary increase in intracellular Ca2+

e. Positive Inotropism

f. None

f. All

Effects of cardiac glycosides.

a. Mechanical Effects

b. Electrophysiological Effects

c. Extracardiac Effects

d. a and b

e. b and c

f. All

b. Electrophysiological Effects

Dose dependent effect of cardiac glycosides.

a. Mechanical Effects

b. Electrophysiological Effects

c. Extracardiac Effects

d. a and b

e. b and c

f. All

a. Positive Inotropism

Cardiac glycosides mechanical effects:

a. Positive Inotropism

b. Negative Chronotropy Decreases

c. Baroreceptor Stimulation

d. Ventricular tachycardia

e. Sympathetic outflow is increased

f. Enhanced automaticity

a. Atria

Cardiac glycosides electrophysiological effects at therapeutic doses are observed in the

a. Atria

b. Ventricles

b. Ventricles

Cardiac glycosides electrophysiological effects at higher doses are observed in the

a. Atria

b. Ventricles

f. All

Cardiac glycosides electrophysiological effects at therapeutic doses.

a. Bradycardia

b. Vagus tone: Negative Chronotropy Decreases

c. Sympathetic tone: Baroreceptor Stimulation

d. a and b

e. b and c

f. All

f. All

Cardiac glycosides electrophysiological effects at higher doses.

a. Ventricular Tachycardia

b. Sympathetic outflow is increased

c. Enhanced automaticity

d. a and b

e. b and c

f. All

f. All

Cardiac glycosides Extracardiac Effects.

a. Anorexia, Nausea & Vomiting

b. Yellow green vision

c. Gynecomastia

d. a and b

e. b and c

f. All

b. Cardiac glycosides

Can cause yellow green vision.

a. Beta1 agonist

b. Cardiac glycosides

c. PDE3 inhibitors

d. ACEis and ARBs

e. Diuretics

f. None

Cardiac glycosides adverse effects and toxicity effects except:

a. Narrow Therapeutic Index

b. Induce virtually every type of arrhythmia

c. Hypokalemia

d. Hypomagnesemia

e. Hypercalcemia

f. None

f. None

Drugs that interact with cardiac glycosides except:

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

a. Cholestyramine and Neomycin

Decreased efficacy of Digoxin.

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

b. Phenobarbital

Lowers concentration of Digoxin.

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

c. Loop and Thiazide Diuretics

Causes hypokalemia with cardiac glycosides.

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

d. CCBs

Render digitalis less effective.

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

e. Quinidine

Prolonged half-life of Digoxin because of decreased renal elimination.

a. Cholestyramine and Neomycin

b. Phenobarbital

c. Loop and Thiazide Diuretics

d. CCBs

e. Quinidine

f. None

f. All

Beta1 agonist

a. Taken parenterally for Acute Heart Failure

b. Increase adenylate cyclase

c. Increase cAMP levels

d. a and b

e. b and c

f. All

e. None

Phosphodiesterase 3 (PDE3) Inhibitors except:

a. Taken parenterally fro Acute Heart Failure

b. Include Bipyridines such as Inamrinone and Milrinone

c. Used in patients who do not respond to digitalis; most effective in individuals with elevated left ventricular filling pressure

d. Prevent degradation of cAMP sustaining PDE3 levels

e. None

c. PDE3 inhibitors

Used in patients who do not respond to digitalis; most effective in individuals with elevated left ventricular filling pressure.

a. Beta1 agonist

b. Cardiac glycosides

c. PDE3 inhibitors

d. ACEis and ARBs

e. Diuretics

c. Both

Beta Agonists & Phosphodiesterase 3 inhibitors cAMP induction mechanisms.

a. (+) Inotropy: Stronger force of contraction in the heart

b. (+) Chronotropy: Faster pump of the heart

c. Both

d. None

a. Adenylate cyclase

Synthesis of cAMP is via

a. Adenylate cyclase

b. Phosphodiesterase 3

c. Both

d. None

f. All

Unloader medications:

a. 1st line agents, must be used in combination always

b. Antihypertensives

c. 100% Contraindicated with CCBs

d. a and b

e. b and c

f. All

a. CCBs

Unloader medications are 100% contraindicated with

a. CCBs

b. PDE3 inhibitors

c. Cardiac glycosides

d. Beta blockers

a. ACEis and ARBs

Lower both afterload and preload.

a. ACEis and ARBs

b. Diuretics

c. Vasodilators

d. Beta Blockers

b. Diuretics

Lower preload

a. ACEis and ARBs

b. Diuretics

c. Vasodilators

d. Beta Blockers

c. Vasodilators

Lower preload at lower dose, lower afterload when combined with hydralazine.

a. ACEis and ARBs

b. Diuretics

c. Vasodilators

d. Beta Blockers

d. Beta Blockers

Generally contraindicated with CHF.

a. ACEis and ARBs

b. Diuretics

c. Vasodilators

d. Beta Blockers

BMCN

Bisoprolol

Metoprolol succinate

Carvedilol

Nebivolol

Beta blockers not contraindicated with CHF

a. Pulmonary edema (left-sided HF) vs. Peripheral edema (right-sided HF)

Organ site of fluid accumulation distinguishing left-sided from right-sided heart failure.

a. Pulmonary edema (left-sided HF) vs. Peripheral edema (right-sided HF)

b. Cerebral edema (left-sided HF) vs. Hepatic edema (right-sided HF)

c. Renal edema (left-sided HF) vs. Pulmonary edema (right-sided HF)

d. Ascites (left-sided HF) vs. Anasarca (right-sided HF)

a. Hypokalemia, Hypomagnesemia, Hypercalcemia

Electrolyte imbalances that significantly increase the risk of Digoxin-induced Ventricular Tachycardia toxicity.

a. Hypokalemia, Hypomagnesemia, Hypercalcemia

b. Hyperkalemia, Hypermagnesemia, Hypocalcemia

c. Hyponatremia, Hyperkalemia, Hypophosphatemia

d. Hypernatremia, Hypocalcemia, Hyperkalemia

a. Quinidine and Cimetidine

Drug-drug interaction leading to increased Digoxin toxicity due to reduced renal clearance.

a. Quinidine and Cimetidine

b. Rifampicin and St. John's Wort

c. Antacids and Cholestyramine

d. Spironolactone and Amiloride

c. Lidocaine

Management interventions for Digoxin-induced Ventricular Tachycardia toxicity.

a. Atropine

b. Epinephrine

c. Lidocaine

d. Amiodarone

b. ACEi/ARBs

Foundational base treatment components among antihypertensive unloader drugs for CHF.

a. Direct renin inhibitors

b. ACE inhibitors (ACEIs) / Angiotensin Receptor Blockers (ARBs)

c. Alpha-1 adrenergic receptor antagonists

d. Central alpha-2 agonists

c. Loop diuretics, Thiazide diuretics, and Spironolactone

Diuretic classes utilized as unloader agents in chronic heart failure management.

a. Potassium-retaining ENaC blockers

b. Carbonic anhydrase inhibitors and Osmotic diuretics

c. Loop diuretics, Thiazide diuretics, and Spironolactone

d. Vasopressin receptor antagonists

Hydralazine + Isosorbide Dinitrate (ISDN)

Vasodilator combination therapy specifically indicated for African-American patients with heart failure.

d. Nesiritide

Recombinant Brain Natriuretic Peptide (BNP) analogue that increases cGMP to promote natriuresis and vasodilation.

a. Sacubitril

b. Bosentan

c. Tezosentan

d. Nesiritide

c. Bosentan & Tezosentan

Dual Endothelin receptor antagonist vasodilators used in cardiovascular management.

a. Nitroprusside & Nitroglycerin

b. Hydralazine & Minoxidil

c. Bosentan & Tezosentan

d. Sildenafil & Tadalafil

a. SGLT2 Inhibitors (e.g., Dapagliflozin, Empagliflozin, Canagliflozin, Luseogliflozin)

Antidiabetic drug class approved for reducing mortality/hospitalizations in CHF and T2DM.

a. SGLT2 Inhibitors (e.g., Dapagliflozin, Empagliflozin, Canagliflozin, Luseogliflozin)

b. DPP-4 Inhibitors (e.g., Sitagliptin, Linagliptin)

c. GLP-1 Receptor Agonists (e.g., Liraglutide, Semaglutide)

d. Sulfonylureas (e.g., Glimepiride, Gliclazide)