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Chapter 19: Heart Failure and Dysrhythmias

Overview of Heart Failure

  • Definition: Inability of the heart to maintain sufficient cardiac output to meet the metabolic demands of tissues and organs.

  • Consequences: Results in congestion in systemic or pulmonary circulation and inability to increase cardiac output with increased demand.

  • Statistics: Increasing incidence with more common hospitalization in individuals over 65; five-year survival rate is about 50% even with treatment.

Etiology and Pathogenesis

  • Common Causes:

    • Myocardial ischemia.

    • Hypertension.

    • Dilated cardiomyopathy.

  • Mechanism: Impaired myocardial fiber contraction, relaxation, or both.

Types of Dysfunction

Systolic Dysfunction

  • Description: Impaired contractility leading to a low ejection fraction.

  • Characteristics:

    • Evidenced by reduced inotropy during ventricular systole.

    • Loss of cardiac muscle cells and reduced ATP production.

Diastolic Dysfunction

  • Causes: Associated with ischemic heart disease and hypertension.

  • Affected Populations: Elderly, women, and those without a history of myocardial infarction.

  • Characteristics:

    • Noncompliant ventricle failing to fill effectively.

    • Low cardiac output, edema formation, normal ejection fraction.

Compensatory Mechanisms and Remodeling

  • Importance: Helpful in restoring cardiac output toward normal but detrimental long-term.

  • Responses:

    • SNS activation.

    • Increased preload.

    • Myocardial hypertrophy.

  • Note: Cardiac muscle can regenerate if stem cells are present.

Sympathetic Nervous System Activation

  • Trigger: Baroreceptor reflex due to pressure drop.

  • Responses:

    • Increased CNS activity leading to venoconstriction, increasing venous return and cardiac output.

    • Renin release from juxtaglomerular cells, activating RAAS, resulting in sodium and water retention.

Increased Preload

  • Mechanism:

    • Reduced ejection fraction leads to elevated residual end-systolic volume (ESV).

    • Decreased cardiac output to the kidney reduces glomerular filtration.

    • RAAS activation increases blood volume.

  • Frank-Starling Mechanism: Changes in preload affect muscle contraction efficiency.

Myocardial Hypertrophy and Remodeling

  • Cause: Chronic elevation of myocardial wall tension.

  • Consequences: High systolic pressure required to overcome afterload leading to hypertrophy.

  • Involvement: Neurohormonal factors like angiotensin II contribute to remodeling.

Clinical Manifestations

  • Left Ventricular Failure: Most common type; can lead to right ventricular failure.

    • Forward Effects: Insufficient pumping leads to poor cardiac output.

    • Backward Effects: Congestion of blood behind the pumping chamber.

Left-Sided Heart Failure

  • Backward Effects: Pulmonary circulation congestion, edema, and diminished oxygen delivery.

  • Forward Effects: Insufficient cardiac output impacting tissues and organs.

Right-Sided Heart Failure

  • Mechanism: Often from pulmonary disorders increasing vascular resistance leading to right ventricular failure.

    • Backward Effects: Congestion in systemic venous system.

    • Forward Effects: Low output to left ventricle causing low cardiac output.

Biventricular Heart Failure

  • Cause: Primary left-sided failure progressing to right-sided failure.

  • Symptoms: Reduced cardiac output, pulmonary congestion, and systemic venous congestion.

Class and Stage of Heart Failure

  • Assessment: FACES criteria (fatigue, activity limitation, congestion, edema, shortness of breath).

  • Diagnosis: X-Ray and echocardiography, B-type natriuretic peptide levels indicating fluid overload and try to decrease blood volume and pressure.

Treatment of Heart Failure

  • Goals: Improve cardiac output, minimize congestive symptoms, decrease workload.

  • Strategies:

    • Preload Management: Diuretics and ACE inhibitors to reduce intravascular volume.

    • Afterload Management: Beta-blockers.

    • Contractility Management: Use of cardiac glycosides, digitalis, and possible use of pacemakers.

Dysrhythmias Overview

  • Definition: Abnormality in the cardiac rhythm affecting impulse generation or conduction.

  • Significance: Indicative of underlying pathophysiology and may impair normal cardiac output.

Mechanisms of Dysrhythmias

  • Types of Mechanisms:

    • Abnormal automaticity.

    • Triggered activity from depolarization.

    • Reentrant circuits.

Automaticity

  • Definition: Spontaneous generation of action potentials.

  • Causes: Failure to repolarize, sodium or calcium influx at rest.

Triggered Activity

  • Occurrence: Impulse generated during or just after repolarization due to membrane potential changes.

Reentry Mechanism

  • Impact: Associated with most tachydysrhythmias; occurs when the impulse continues to depolarize after the main impulse.

  • Predisposing Conditions: Myocardial ischemia or electrolyte abnormalities.

ECG Analysis

  • Function: Measures waveform amplitude, duration, and heart rate to evaluate dysrhythmias.

Types of Cardiac Dysrhythmias

Normal Sinus Rhythm

  • Characteristics: 60-100 beats/min, regular rhythm, normal PR and QRS intervals.

Sinus Tachycardia

  • Description: Fast heart rate (>100 beats/min); often compensatory.

    • Treatment: Correct underlying causes.

Sinus Bradycardia

  • Description: Slow heart rate (<60 beats/min); normal in some trained individuals.

    • Treatment: Address low cardiac output.

Atrial Dysrhythmias

  • Definition: Originate in the atria not involving the SA node, including premature atrial contractions.

  • Atrial Flutter and Fibrillation: Flutter shows rapid atrial rate; fibrillation is disorganized and irregular.

Ventricular Dysrhythmias

  • Types: Premature ventricular complexes and tachycardia (3+ complexes >100 beats/min).

  • Characteristics: Vital signs and CO may be compromised; may require quick intervention.

Conduction Disturbances

  • Types: Include delay, blocks, and abnormal pathways:

    • Atrioventricular Blocks:

      • First-degree: prolonged conduction through AV node (long PR interval).

      • Second-degree: Progressive prolonged PR intervals (Type I) or fixed number of P waves (Type II).

      • Third-degree: Complete block requiring pacemaker.

Accessory Pathways

  • Example: Wolff-Parkinson-White syndrome causing tachycardia from congenital extra conduction pathways.

Intraventricular Conduction Defects

  • Type: Bundle branch block affecting right and left ventricle conduction through conducting pathways.

Treatment of Dysrhythmias

  • Indication: For symptoms or progression risk; antiarrhythmic drugs utilized.

  • Interventions: Pacemakers, drugs to enhance contractility, and ablation procedures.