Study Notes on Cardiac Glycosides, Antianginals, and Antidysrhythmics

Chapter 40: Cardiac Glycosides, Antianginals, and Antidysrhythmics

Heart Failure Characteristics

  • Definition: Heart failure (HF) is a condition characterized by the inability of the heart muscle to pump blood effectively.

    • Acute heart failure:

    • Heart muscle weakens and enlarges.

    • Loses ability to pump blood adequately.

    • Compensatory mechanisms fail.

    • Results in congestion in both lungs and peripheral systems.

  • Pathophysiology:

    • Preload: The volume of blood in the ventricles at the end of diastole.

    • Afterload: The resistance the heart must overcome to eject blood.

    • Right-sided heart failure: Blood backs up in the periphery.

    • Left-sided heart failure: Blood backs up in the lungs.

ACC/AHA Stages of Heart Failure

  • Stage A: At high risk for heart failure but without structural heart disease or symptoms of HF.

  • Stage B: Structural heart disease present but without signs or symptoms of HF.

  • Stage C: Structural heart disease with prior or current symptoms of HF.

  • Stage D: Refractory heart failure requiring specialized interventions.

Heart Failure Nonpharmacologic Treatment

  • Lifestyle Modifications:

    • Limit salt and saturated fat intake, and manage fluid intake.

    • Limit or avoid alcohol; cessation of smoking.

    • Encourage mild exercise and weight loss.

  • Laboratory Tests:

    • Atrial natriuretic peptide (ANP): Normal range 20 to 77 pg/mL; 20 to 77 ng/L (SI units).

    • Brain natriuretic peptide (BNP):

    • Desired value: less than 100 pg/mL.

    • Positive value: greater than 100 pg/mL.

Cardiac Glycosides

Digitalis Preparations (Digoxin)

  • Action:

    • Positive inotropic effect:

    • Increases myocardial contractility.

    • Increases stroke volume.

    • Decreases preload.

    • Increases blood flow.

    • Negative chronotropic effect: Decreases heart rate.

    • Negative dromotropic effect: Decreases conduction of heart cells.

Side Effects/Adverse Effects of Digoxin

  • Bradycardia and cardiac dysrhythmias.

  • Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea.

  • Neurological effects: Headache, dizziness.

  • Visual disturbances: Blurred or yellow vision.

  • Cognitive effects: Confusion, weakness.

Digitalis Toxicity

Causes

  • Overdose or accumulation of digoxin in the body.

Antidote

  • Digoxin immune fab:

    • Action: Binds with digoxin to form complex molecules that are excreted in urine.

Side Effects of Antidote

  • Headache and bradycardia.

  • Visual disturbances: Blurred vision, visual illusions.

  • Cognitive effects: Confusion, delirium.

  • Gastrointestinal symptoms: Anorexia, nausea, vomiting.

Drug Interactions with Digoxin Immune Fab

  • Diuretics: Risk of hypokalemia.

  • Cortisone: Can cause sodium retention.

  • Antacids: May decrease the absorption of digitalis.

Clinical Judgment: Digoxin

Concepts and Cues

  • Perfusion: Critical in evaluating the effectiveness of digoxin therapy.

    • Obtain a baseline pulse rate.

    • Assess for signs of digitalis toxicity.

Prioritization of Hypotheses

  • Consider ischemia or decreased tissue perfusion as primary concerns.

Solutions/Patient Education

  • Teach patients to check their pulse rate daily before taking digoxin.

Actions to Implement

  • Verify the apical pulse rate prior to administering digoxin.

  • Assess for peripheral and pulmonary edema.

  • Monitor serum digoxin levels and serum potassium levels.

  • Advise patients to report any side effects experienced.

Outcomes Evaluation

  • Determine the effectiveness of education and monitoring through patient compliance and symptom tracking.

Phosphodiesterase Inhibitors

Milrinone Lactate

  • Action:

    • Inhibits the enzyme phosphodiesterase.

    • Promotes positive inotropic effects increasing stroke volume and cardiac output, as well as causing vasodilation.

  • Caution:

    • Administer IV for no longer than 48 to 72 hours to avoid severe cardiac dysrhythmias.

    • Classified as a high-alert medication.

Other Agents Used to Treat Heart Failure

  • Vasodilators.

  • Angiotensin-converting enzyme (ACE) inhibitors.

  • Angiotensin II receptor antagonists (ARBs).

  • Diuretics: Includes thiazides, furosemide, spironolactone.

  • Select beta blockers.

  • Nesiritide.

  • Hydralazine/isosorbide dinitrate.

  • Vericiguat.

Angina Types

  • Classic (stable): Occurs with predictable stress or exertion.

  • Unstable (preinfarction): Occurs frequently with increasing severity, unpredictable with activity.

  • Variant (Prinzmetal or vasospastic): Occurs during periods of rest.

Antianginal Drugs

Nitrates

  • Action: Promote vasodilation, leading to decreased preload and afterload.

  • Side Effects/Adverse Reactions:

    • Headache, hypotension, flushing, dizziness, weakness, syncope.

  • Routes of Administration:

    • Sublingual, translingual, topical, aerosol spray (inhalation), IV, buccal, and oral extended-release capsules/tablets.

  • Caution: Patients should not abruptly discontinue the drug.

Beta Blockers

  • Action:

    • Block beta1 and beta2 receptor sites, inhibiting action of catecholamines (epinephrine and norepinephrine).

    • Decrease workload of the heart and oxygen demands.

  • Side Effects:

    • Bradycardia, hypotension, dizziness, depression, fatigue, erectile dysfunction, peripheral edema/vasoconstriction, bronchospasms.

  • Caution: Avoid abrupt discontinuation.

Calcium Channel Blockers

  • Action:

    • Relax coronary artery spasm and peripheral arterioles.

    • Decrease contractility, afterload, and resistance, reducing cardiac workload and oxygen demands.

  • Side Effects:

    • Dizziness, flushing, headache, hypotension, reflex tachycardia, peripheral edema, fatigue.

Clinical Judgment: Antianginal Drugs

Concepts and Cues

  • Perfusion: Recognizing cues for adequacy of treatment.

    • Obtain baseline vital signs for comparison.

Hypotheses Analysis

  • Consider decreased tissue perfusion or hypoxemia.

Solutions/Patient Education

  • Patients should report a decrease in anginal pain.

Action Steps

  • Monitor vital signs.

  • Position patient appropriately during first administration of nitrate.

  • Observe effects of IV nitroglycerin.

  • Administer SL nitroglycerin for chest pain

  • Advise patients against alcohol ingestion while taking nitroglycerin.

  • Teach pulse checking techniques.

Evaluate Outcomes

  • Assess for reduction in anginal symptoms and stabilization of vital signs.

Antidysrhythmic Drugs

Mechanisms of Drug Action

  • Class I: Sodium channel blockers

    • 1A: Slow conduction and prolong repolarization.

    • 1B: Slow conduction while shortening repolarization.

    • 1C: Prolong conduction with minimal effect on repolarization.

  • Class II: Beta-adrenergic blockers

    • Decrease conduction velocity, automaticity, and recovery time.

  • Class III: Prolong repolarization and action potential duration.

  • Class IV: Calcium channel blockers

    • Block calcium influx, slow conduction velocity, decrease myocardial contractility, and increase refractoriness in the AV node.

Clinical Judgment: Antidysrhythmics

Concepts and Cues

  • Perfusion: Recognizing cues for effective treatment.

    • Obtain baseline vital signs and ECG for comparison.

Hypothesis Prioritization

  • Focus on decreased tissue perfusion and dysrhythmia as primary concerns.

Solutions/Patient Education

  • Patients should expect to have normal sinus rhythm.

Actions to Implement

  • Monitor vital signs and ECG for abnormalities.

  • Encourage patients to report side effects or adverse reactions.

  • Advise patients to avoid alcohol, caffeine, and tobacco use.

Outcomes Evaluation

  • Assess heart rhythm and response to therapy.