Heart Failure Non-Drug Therapy

Heart Failure Therapy

• Non-Drug Therapy: Lifestyle modifications are essential for managing heart failure.
  • Rest is crucial to reduce strain on the heart.
  • Dietary adjustments include restriction of sodium and fat intake.
  • Stress management is important; avoid smoking and alcohol consumption.
  • Weight reduction can alleviate symptoms.
  • Control risk factors, including surgical correction of valvular diseases and treatment of hyperthyroidism and hypertension.
  • Avoid drugs that can elevate blood pressure, such as sympathomimetics and sodium-containing medications.

Drug Therapy

• Positive Inotropic Drugs: Enhance heart muscle contraction.
  • Cardiac glycosides: Digoxin is the most commonly used.
  • Dopamine and dobutamine are for short-term use only; stimulate the heart.
  • Phosphodiesterase inhibitors: Inamrinone and milrinone are examples.
• Additional Medications:
  • Diuretics help reduce fluid overload.
  • ACE inhibitors (ACEIs) lower blood pressure and reduce workload on the heart.
  • Vasodilators, such as nitrates and hydralazine, improve blood flow.
  • Beta-blockers and spironolactone also play a role in managing heart failure.

Cardiac Glycosides - Digoxin

• Derived from the foxglove plant; contains a lactone ring and steroid moiety attached to sugar molecules.
• Increases intracellular sodium, thereby preventing calcium expulsion and enhancing contractility.
• Autonomic Effects:
  • Increases vagal activity and decreases sympathetic activity, improving tissue oxygenation.

Pharmacological Effects

• Increases Contractility and Cardiac Output (COP):
  • Enhances renal blood flow and diuresis, reducing fluid retention through reduced RAAS activity.
  • Alleviates lung congestion.
• Decreases Heart Rate:
  • Caused by increased vagal tone and inhibition of the AV conduction system, potentially leading to bradycardia.
• Conducting Velocity:
  • Intra-atrial conduction increases; A-V conduction decreases due to vagal effects.
• Excitability and Automaticity:
  • Can lead to ectopic foci and various arrhythmias.

Clinical Considerations

• Cardiac Conditions:
  • In cases of acute myocardial infarction or cardiomyopathy, digoxin may worsen the situation.
  • Digitalis should be avoided in renal or hepatic disease.
• Drug Interactions:
  • Antacids, cholestyramine, and metoclopramide can affect digoxin absorption and bioavailability.
  • Quinidine increases digoxin levels and can lead to toxicity.
  • Loop diuretics may cause hypokalemia, enhancing digoxin's effects and toxicity risk.

Dosage and Administration

• Digoxin Digitalization:
  • Initial dosing involves 0.25 mg per day for five days, with the goal of achieving steady-state concentration after one week.
  • In emergencies, rapid loading at 0.5 mg twice daily for two days may be required.
• Maintenance Dose:
  • Continue with one tablet (0.25 mg) daily, five days a week.

Digitalis Toxicity

• Predisposing Factors:
  • Hypokalemia increases digoxin binding and effect; hypomagnesemia also raises toxicity risk.
  • Renal impairment poses additional risk for toxicity.

Toxicity Manifestations

• Cardiac Symptoms:
  • Bradycardia, various degrees of heart block, and any type of arrhythmia.
• Extracardiac Symptoms:
  • Fatigue, anorexia, gastrointestinal disturbances (diarrhea, nausea, vomiting).
  • Central Nervous System effects: headache, delirium, hallucinations, and vision changes (e.g., yellow vision).
  • Additional symptoms may include skin rash and gynecomastia.

Management of Digitalis Toxicity

• Discontinue digitalis administration immediately.
• Correct hypokalemia via oral or IV potassium.
• Administer antiarrhythmic drugs such as:
  • Lidocaine for ventricular arrhythmias.
  • Phenytoin for ventricular arrhythmias complicated with heart block.
  • Atropine for bradycardia or heart block.

Heart Failure Therapy

• Non-drug therapy includes lifestyle modifications: rest, dietary sodium and fat restriction, stress avoidance, smoking cessation, and alcohol elimination.
• Weight reduction is crucial, along with controlling risk factors, such as surgical correction for valvular diseases and managing hyperthyroidism and hypertension.
• Avoid sympathomimetics and sodium-containing drugs due to potential increases in blood pressure.

Drug Therapy

• Positive inotropic agents:
  • Cardiac glycosides (e.g., Digoxin).
  • Dopamine and Dobutamine are for short-term use only.
  • Phosphodiesterase inhibitors (Inamrinone, Milrinone).
• Other important drug classes include diuretics, ACE inhibitors, vasodilators (nitrates, hydralazine), beta-blockers, and spironolactone.

Cardiac Glycosides

• Derived from natural plant sources (e.g., Foxglove).
• Contain a lactone ring and a steroid moiety linked to sugar molecules.
• Digoxin is the most common glycoside used.
• Caution in patients with pulmonary hypertension or acute myocardial infarction, as digitalis may worsen their condition.
• Contraindicated in renal disease (use caution with Digoxin) and in hepatic disease (avoid Digitoxin).
• Can lead to fatal arrhythmias if used prior to cardioversion.

Drug Interactions

• Antacids and cholestyramine can reduce digoxin bioavailability.
• Metoclopramide increases gut motility, decreasing digoxin absorption; Atropine has the opposite effect.
• Quinidine can increase serum digoxin levels by decreasing renal clearance.
• Diuretics (loop or thiazide) may cause hypokalemia, increasing the risk of digoxin toxicity.

Dosage and Administration

• Initial dosage: 0.25 mg/day for 5 days to achieve therapeutic levels.
• Rapid loading method involves a higher initial dose (0.5 mg) twice daily for two days if in an emergency.
• Maintenance dose: 0.25 mg/day, five days a week.
• Monitor plasma potassium levels continuously during therapy.

Digitalis Toxicity

• Predisposing factors include hypokalemia, renal impairment, and hypomagnesemia.
• Cardiac manifestations include bradycardia, heart block, and various arrhythmias.
• Extracardiac symptoms: fatigue, anorexia, gastrointestinal symptoms (diarrhea, nausea), CNS effects (headache, delirium), and vision changes (chromatopsia).
• Management includes stopping digitalis, correcting hypokalemia, and administering antiarrhythmic drugs (Lidocaine, Phenytoin, Atropine), as well as specific digoxin antibodies (Digibind).

Other Positive Inotropic Drugs

• PDE inhibitors (Inamrinone, Milrinone) increase cAMP levels, leading to enhanced myocardial contractility and vasodilation.
• Used only intravenously for short-term treatment of heart failure; long-term use is not recommended due to toxicity risks.
• Adverse effects: thrombocytopenia, cardiac arrhythmias, and liver enzyme elevation (hepatotoxicity), with Milrinone being less toxic than Inamrinone.

Mechanisms of Action

• Increased intracellular sodium (Na+) inhibits calcium (Ca2+) expulsion from the cell via the Na+/Ca2+ exchanger.
• Autonomic effects include:
  • Increased vagal activity through direct and indirect mechanisms.
  • Decreased sympathetic activity due to relief of hypoxia and improved tissue oxygenation.

Pharmacological Effects

• Positive inotropic effect increases contractility and cardiac output (COP).
  • Enhances renal blood flow (RBF), leading to diuresis and decreased renin-angiotensin-aldosterone system (RAAS) activity, reducing fluid retention.
  • Alleviates lung congestion.
• Decreased heart rate (bradycardia) results from:
  • Increased vagal tone and reduced sympathetic activity.
  • Direct inhibition of the atrioventricular (AV) conducting system.
• Conductance enhancements occur:
  • Increased intra-atrial conduction due to vagal stimulation.
  • Decreased A-V conduction stemming from direct and vagal effects.
• Increased excitability and automaticity may lead to ectopic foci and various arrhythmias.

ECG Changes

• Prolonged PR interval.
• Shortened QT interval.
• ST segment depression and T-wave inversion.

Hemodynamic Effects

• Normalization of arterial and venous pressures due to improved hemodynamics.

Therapeutic Indications

• Digoxin is indicated for chronic congestive heart failure (CHF) associated with atrial flutter or fibrillation (AF), balancing contractility enhancement and AV conduction reduction.
• Other agents like verapamil or beta-blockers are preferred for AF alone.
• Diuretics and ACE inhibitors are recommended for CHF without AF.

Contraindications

• Absolute contraindications:
  • Heart block, as digitalis worsens AV conduction.
  • Hypertrophic obstructive cardiomyopathy (HOCM), due to increased outflow tract resistance.
  • Wolff-Parkinson-White (WPW) syndrome, as it can exacerbate arrhythmias.
  • Paroxysmal ventricular tachycardia due to increased excitability from digitalis.
• Relative contraindications:
  • Bradycardia conditions, which may worsen with digoxin addition.
  • Systemic hypertension that strains the left ventricle; must be corrected prior to use.
  • Chronic lung disease causing pulmonary hypertension increases right ventricle strain.
  • Certain cardiac diseases like acute myocardial infarction amplify infarct size and arrhythmia risk.
  • Renal or hepatic diseases; digoxin is contraindicated in renal failure, and digoxin should be avoided in hepatic failure.

Drug Interactions

• Antacids and cholestyramine reduce digoxin bioavailability.
• Metoclopramide increases gut motility, reducing digoxin absorption.
• Atropine increases digoxin absorption by decreasing gut motility.
• Quinidine may increase digoxin serum levels by reducing renal clearance and displacing it from plasma proteins.
• Diuretics may cause hypokalemia or hypomagnesemia, raising digitalis toxicity risk.

Dosage and Administration

• Initial digitalization involves administering 0.25 mg tablet daily, increasing dosage for rapid loading in emergencies.
• Steady-state concentration achieved after one week.
• Maintenance dose: 0.25 mg daily, five days a week.
• Continuous monitoring of serum potassium levels is essential during digoxin therapy.
• Specific digoxin antibodies (Fab fragments) can bind digoxin to promote renal clearance in cases of toxicity.

Other Positive Inotropic Drugs

• Phosphodiesterase (PDE) inhibitors such as inamrinone and milrinone increase cAMP and calcium influx, enhancing myocardial contractility and possessing vasodilatory properties.
• Designed for short-term CHF management when digitalis is ineffective; not safe for long-term use due to adverse effects like thrombocytopenia, arrhythmia, and liver enzyme increase. Milrinone has lower toxicity compared to inamrinone.

Non-Drug Therapy for Heart Failure

• Implement lifestyle modifications: rest, dietary sodium and fat restriction, stress avoidance, and cessation of smoking and alcohol.
• Weight reduction and management of risk factors are essential.
• Surgical correction for valvular diseases and treatment of hyperthyroidism or hypertension may be needed.
• Avoid medications that raise blood pressure, e.g., sympathomimetics and sodium-containing drugs.

Drug Therapy for Heart Failure

• Positive inotropic drugs improve heart contractility:
  • Cardiac glycosides (e.g., Digoxin).
  • Short-term use of dopamine and dobutamine.
  • Phosphodiesterase inhibitors: inamrinone and milrinone.
• Diuretics help manage fluid retention.
• ACE inhibitors are used to lower blood pressure and reduce heart workload.
• Vasodilators such as nitrates and hydralazine improve blood flow.

Cardiac Glycosides

• Derived from natural plant sources like the foxglove plant.
• Composed of a lactone ring, steroid moiety, and sugar molecules.
• Digoxin is the most commonly used cardiac glycoside.
• Increases intracellular sodium, resulting in calcium retention in cells.

Autonomic Effects of Cardiac Glycosides

• Enhances vagal activity and decreases sympathetic activity.
• Improves tissue oxygenation, alleviating hypoxia effects.

Pharmacological Effects

• Increases cardiac output and renal blood flow, leading to diuresis and reduced fluid retention.
• Relieves lung congestion by decreasing heart rate via increased vagal tone.
• Can lead to bradycardia due to vagal stimulation and inhibition of AV conduction.
• Increased excitability may lead to ectopic foci and arrhythmias.

ECG Changes with Digoxin

• Prolongation of PR interval.
• Shortening of QT interval.
• ST segment depression and T wave inversion.
• Normalization of arterial and venous pressures due to improved hemodynamics.

Therapeutic Indications for Digoxin

• Indicated for chronic congestive heart failure (CHF) with atrial fibrillation (AF).
• Preferred treatments for AF without heart failure include verapamil or beta-blockers.
• In CHF without AF, diuretics and ACE inhibitors are favored.

Contraindications for Digoxin Use

• Absolute contraindications include heart block (worsens conduction), hypertrophic obstructive cardiomyopathy (HOCM), Wolff-Parkinson-White syndrome, and paroxysmal ventricular tachycardia.
• Relative contraindications involve bradycardia conditions and systemic hypertension.

Dosage and Administration

• Initial digitalization starts at 0.25 mg daily for five days.
• Rapid loading method uses 0.5 mg twice daily for two days in emergencies.
• Maintenance dose is 0.25 mg daily for five days a week.

Precautions While Using Digoxin

• Avoid intravenous administration without confirming the absence of prior digoxin in the last 14 days to prevent toxicity.
• Continuous monitoring of potassium levels is crucial.

Predisposing Factors for Digoxin Toxicity

• Hypokalemia increases binding and effects of digoxin.
• Presence of renal impairment enhances toxicity risk.

Manifestations of Digoxin Toxicity

• Cardiac symptoms: bradycardia, various arrhythmias, and atrial tachycardia.
• Extracardiac symptoms: fatigue, anorexia, gastrointestinal disturbances, and central nervous system effects (e.g., headache, hallucinations).
• Visual disturbances include yellow vision and diplopia.

Management of Digoxin Toxicity

• Discontinue digoxin immediately.
• Correct hypokalemia with potassium supplements.
• Antiarrhythmic drugs may be necessary (e.g., Lidocaine, Phenytoin) in case of ventricular arrhythmias.
• Atropine may be administered for bradycardia or heart block.

Therapy of Heart Failure

• Non-drug therapy focuses on lifestyle modifications which include:

  • Rest and adequate sleep
  • Dietary sodium and fat restriction
  • Stress management, smoking cessation, and avoidance of alcohol
  • Weight reduction to improve heart health
  • Control of risk factors such as surgical correction of valvular diseases and treatment of conditions like hyperthyroidism and hypertension
  • Avoidance of drugs that can increase blood pressure, including sympathomimetics and sodium-containing drugs

• Drug therapy options for heart failure:

  • Positive inotropic drugs:
    • Cardiac glycosides (e.g., Digoxin)
    • Dopamine and Dobutamine (short-term use)
    • Phosphodiesterase inhibitors (Inamrinone and Milrinone)
  • Diuretics to reduce fluid overload
  • ACE inhibitors for blood pressure control
  • Vasodilators such as nitrates and hydralazine
  • Other medications include beta-blockers and spironolactone

Cardiac Glycosides

• Sourced from natural plant derivatives like the Foxglove plant
• Structure includes a lactone ring attached to a steroid (aglycone) and sugar molecules
• Digoxin is the most commonly used cardiac glycoside

Pharmacokinetics of Digoxin

• Distributes widely in body tissues and accumulates in cardiac tissue
• Concentration of Digoxin in the heart is twice that in skeletal muscle and at least 15 times that in plasma
• Renal elimination necessitates dose adjustments based on creatinine clearance

Mechanism of Action

• Positive inotropic effect achieved by increasing intracellular calcium levels
• Blocks Na+/K+ ATPase, leading to sodium and calcium accumulation within cells
• This mechanism enhances calcium release from the sarcoplasmic reticulum and displaces calcium from binding sites
• Important to manage pulmonary hypertension before using digitalis, as it can strain the right ventricle

Clinical Considerations

• In acute myocardial infarction (MI), digitalis can worsen infarct size and arrhythmias
• Caution in patients with renal impairment and hepatic diseases
• Risk of fatal arrhythmia if used shortly before cardioversion

Drug Interactions with Digoxin

• Antacids (e.g., Kaolin) bind Digoxin, reducing bioavailability
• Cholestyramine affects absorption
• Metoclopramide increases gut motility, decreasing Digoxin absorption
• Quinidine decreases renal clearance and displaces Digoxin from proteins

Digitalis Toxicity

• Predisposing factors include hypokalemia, anemia, and renal impairment
• Cardiac manifestations: bradycardia, variable heart block, and arrhythmias
• Extracardiac symptoms: fatigue, anorexia, gastrointestinal issues (diarrhea, nausea), CNS effects (headache, delirium), visual disturbances (yellow vision), and skin reactions (rash, gynecomastia)

Management of Digitalis Toxicity

• Discontinue Digoxin
• Correct hypokalemia through potassium supplementation
• Use antiarrhythmic medications (Lidocaine, Phenytoin, Atropine)
• Specific antidote includes digoxin-specific antibodies (Digibind)

Other Positive Inotropic Drugs

• Phosphodiesterase (PDE) Inhibitors:
  • Inamrinone and Milrinone increase intracellular cAMP, enhancing myocardial contractility
  • Exhibit vasodilatory properties and are used intravenously for short-term treatment in CHF
  • Long-term use is not recommended due to associated toxicity
  • Adverse effects may include thrombocytopenia and hepatotoxicity, with Milrinone being less toxic than Inamrinone

This quiz focuses on lifestyle modifications for managing heart failure without medication. It covers important factors such as diet, stress management, and risk control strategies. Test your knowledge on how these lifestyle changes can effectively contribute to heart health.