Heart Failure Quiz

Heart Failure (HF)

• Inability of ventricles to pump enough blood for the body's needs
• Weakening of the heart muscle due to aging or disease.

Diseases Associated with Heart Failure

• Coronary artery disease (CAD)
• Mitral stenosis
• Myocardial infarction (MI)
• Chronic hypertension (HTN)
• Diabetes mellitus
• No cure, only prevention and slowing of progression

Left-Sided Heart Failure

• Blood accumulates in the left ventricle
• Left ventricle thickens and enlarges (hypertrophy)
• Cardiac remodeling
• Blood backs up into the lungs
• Cough and shortness of breath result

Right-Sided Heart Failure

• Blood backs up into veins
• Causes peripheral edema and organ engorgement
• Less common than left-sided HF

Pathophysiology of Heart Failure

• Failing heart: decreased cardiac output
• Diminished renal blood flow
• Vasoconstriction: increased blood pressure
• Activation of renin-angiotensin-aldosterone system
• Retention of sodium and water
• Increased plasma volume
• Increased cardiac workload
• Myocardial dysfunction: worsening heart failure
• Pulmonary and peripheral edema

Preload

• Affects cardiac output
• Degree myocardial fibers are stretched prior to contraction
• Frank-Starling law: More stretched fibers, more forceful contraction
• Drugs that increase preload contractility increase cardiac output (Positive inotropic agents)

Afterload

• Affects cardiac output
• Pressure in aorta that must be overcome before blood is ejected from the left ventricle
• Lowering blood pressure creates less afterload, resulting in less workload for the heart

Pharmacologic Management of Heart Failure

• Mechanisms:
  • Slowing the heart rate
  • Increasing contractility
  • Reducing myocardial workload

Drugs for Heart Failure

• Treat symptoms:
  • Slow heart rate
  • Increase contractility
  • Reduce heart workload

Stages for Treating Heart Failure

• (1 of 2)*

• Stage A: High risk of developing HF without structural heart disease or symptoms. Lifestyle modifications, treat comorbid conditions such as HTN, dyslipidemia, and diabetes.

• Stage B: Structural evidence of heart disease but no symptoms(NYHA Class I). Continue prior lifestyle modifications, and treat with ACE inhibitor or ARB. Beta blockers may be added.

• (2 of 2)*

• Stage C: Structural evidence with symptoms such as fatigue, fluid retention, or dyspnea (NYHA Class II and III). Continue lifestyle modifications, ACE inhibitor or ARB or Entresto. Add beta blocker, isosorbide dinitrate with hydralazine, digoxin, or an aldosterone antagonist if necessary.

• Stage D: Symptoms at rest or during minimal exertion despite optimal medical therapy (NYHA Class IV). Continue lifestyle modifications, and may include ivabradine, IV diuretics, dopamine, dobutamine, IV nitroglycerin, nitroprusside, nesiritide, or phosphodiesterase inhibitors.

ACE Inhibitors (1 of 2)

• Reduce afterload
• Drugs of choice for heart failure
• Enhance sodium and water excretion
• Lower peripheral resistance and reduce blood volume
• Increase cardiac output

ACE Inhibitors (2 of 2)

• Prototype drug: lisinopril (Prinivil, Zestril)
• Mechanism of action: inhibit ACE enzyme and decrease aldosterone secretion
• Primary use: decrease blood pressure and reduce blood volume, dilate veins
• Adverse effects: first-dose hypotension, cough, hyperkalemia, renal failure

Angiotensin II Receptor Blockers (ARBs)

• Actions very similar to ACE inhibitors
• Usually used for patients who can't tolerate ACE inhibitor adverse effects

Diuretics

• Increase urine flow
• Reduce blood volume and cardiac workload
• Reduce edema and pulmonary congestion
• Prescribed in combination with other drugs

Cardiac Glycosides (1 of 2)

• Increase force of heartbeat, slow heart rate
• Improve cardiac output
• Second-line treatment for HF
• Narrow therapeutic range.

Cardiac Glycosides (2 of 2)

• Prototype drug: digoxin (Lanoxin)
• Mechanism of action: cause more forceful heartbeat, slower heart rate
• Primary use: increase contractility or strength of myocardial contraction
• Adverse effects: neutropenia, dysrhythmias, digitalis toxicity

Beta-Adrenergic Blockers (1 of 3)

• Slow heart rate and reduce blood pressure
• Inotropic effect
• Reduce workload of heart

Beta-Adrenergic Blockers (2 of 3)

• Prototype drug: metoprolol (Lopressor, Troprol XL)
• Mechanism of action: block cardiac action of the sympathetic nervous system to slow heart rate and BP, reducing workload of heart

Beta-Adrenergic Blockers (3 of 3)

• Primary use: reduce symptoms of heart failure and slow progression of disease
• Adverse effects: fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block

Direct Vasodilators

• Minor role in HF treatment
• Lower blood pressure
• Relax blood vessels

Phosphodiesterase Inhibitors (1 of 2)

• Block enzyme phosphodiesterase
• Increase calcium for myocardial contraction
• Cause positive inotropic response and vasodilation
• Increase contractility and decrease afterload
• Short-term therapy only

Phosphodiesterase Inhibitors (2 of 2)

• Prototype drug: milrinone (Primacor)
• Mechanism of action: block enzyme phosphodiesterase in cardiac and smooth muscle, increasing myocardial contraction force and cardiac output
• Primary use: as short-term therapy for heart failure
• Adverse effects: hypokalemia, hypotension, ventricular dysrhythmias

Mechanisms of Action of Drugs Used for Heart Failure

• (Diagram)*
• Shows how various drugs (adrenergic blockers, vasodilators, phosphodiesterase inhibitors, ACE inhibitors, angiotensin receptor blockers, cardiac glycosides, and diuretics) influence various systems in the body to improve heart function in heart failure.

Patient Teaching (1 of 5)

• Therapeutic response time: weeks or months
• Sodium and potassium restrictions
• Don't use with other medications, herbals, or vitamins

Patient Teaching (2 of 5)

• Monitor sodium intake
• Report weight loss
• Report fatigue and muscle cramps
• Change position slowly

Patient Teaching (3 of 5)

• Monitor blood pressure/pulse
• Report pulse below 50
• Report signs/symptoms of worsening heart failure
• Do not stop taking abruptly

Patient Teaching (4 of 5)

• Monitor therapeutic levels with laboratory tests
• Know signs/symptoms of toxicity
• Monitor pulse rate
• Report weight gain
• Eat foods high in potassium

Patient Teaching (5 of 5)

• Report irregular or rapid heart rate
• Report fever of 101 degrees F or higher or increase in chest pain
• If given IV, report fever of 101 degrees F or higher or pain/swelling at infusion site