Chapter 19

Heart Failure

• General Definition: Heart failure is a broad term describing various cardiac dysfunctions leading to inadequate tissue perfusion.

• Patient Presentation: A patient may complain of shortness of breath during activity.

• Core Problem: The heart's inability to maintain sufficient cardiac output to meet the metabolic demands of tissues and organs.

• Results:

  • Congestion of blood flow in systemic or pulmonary venous circulation.
  • Inability to increase cardiac output to meet the demands of activity or increased tissue metabolism.

• Incidence: Increasing, and it's the most common reason for hospitalization in individuals over 65.

• Etiology and Pathogenesis:

  • HF is a potential consequence of most cardiac disorders.
  • Most common cause is myocardial ischemia, followed by hypertension and dilated cardiomyopathy.
  • Results from impaired ability of myocardial fibers to contract (systolic failure), relax (diastolic failure), or both.
  • Involves issues with the heart's muscle, valves, electrical conduction, and blood supply.

• Left vs. Right Heart Failure:

  • Left ventricular failure is the most common.
  • Often leads to right ventricular failure.

• Right Heart Failure: Can result from increased left ventricular filling pressure reflected into the pulmonary circulation (pulmonary hypertension).

• Symptoms and Signs of Heart Failure:

  • Decreased Forward Flow:
    • Fatigue.
    • Weakness.
    • Shortness of breath.
  • Backup of Flow:
    • Increased JVP (Jugular Venous Pressure).
    • Edema.
    • Ascites.
  • Pulmonary Congestion:
    • Shortness of breath.
    • Orthopnea.
    • Paroxysmal Nocturnal Dyspnea.
  • Increased Right Heart Work.

• Additional Symptoms:

  • Coughing.
  • Pleural effusion (excess fluid around lungs).
  • Swelling in the abdomen (ascites).
  • Tiredness.
  • Swelling in ankles and legs.
  • Pulmonary edema (excess fluid in lungs).

• Preload: BP in the left ventricle after filling and before ventricles contract. Originates from the venous system.

• Afterload: BP in the systemic system that the heart must work against. Created by the arteries.

• Compensatory Mechanisms and Remodeling: Initially helpful in restoring cardiac output but detrimental long-term.

  • Current management of HF is directed toward reducing the harmful consequences of these compensatory responses.

1. Sympathetic Nervous System Activation:
   • Result of baroreceptor reflex stimulation detecting a fall in pressure.
   • CNS increases sympathetic nerve activity to the heart, resulting in venoconstriction.
   • Juxtaglomerular cells release renin, activating the RAAS cascade, increasing sodium and water retention.
2. Increased Preload:
   • Consequence of reduced EF (Ejection Fraction) with an increase in residual ESV (End-Systolic Volume).
   • Decreased CO (Cardiac Output) to the kidney reduces glomerular filtration, leading to fluid conservation.
   • RAAS cascade activation results in elevated blood volume.
3. Myocardial Hypertrophy and Remodeling:
   • Results from chronic elevation of myocardial wall tension.
   • High systolic pressure in the ventricle needed to overcome high afterload leads to hypertrophy.
   • Neurohormonal factors have a hypertrophic effect on the heart.
   • Angiotensin II is involved in remodeling.

• Left-Sided Heart Failure:

  • Backward effects: Accumulation of blood within the pulmonary circulation, causing pulmonary congestion and edema.
  • Forward effects: Insufficient CO, diminishing oxygen and nutrient delivery to peripheral tissues and organs.

• Right-Sided Heart Failure:

  • Pulmonary disorders increase pulmonary vascular resistance, leading to high afterload, right ventricular hypertrophy, and eventually right ventricular failure.
  • Backward effects: Congestion in the systemic venous system.
  • Forward effects: Low output to the left ventricle, leading to low CO.

• Signs of Right Heart Failure: Elevated JVP, edema (swelling) in the leg, ankle, and foot.

• Left-Sided HF vs. Right-Sided HF:

  • Left-Sided HF:
    • Backward Effects: Dyspnea on exertion, orthopnea, cough, paroxysmal nocturnal dyspnea, cyanosis, basilar crackles.
    • Forward Effects: Fatigue, oliguria, increased heart rate, faint pulses, restlessness, confusion, anxiety.
  • Right-Sided HF:
    • Backward Effects: Hepatomegaly, ascites, splenomegaly, anorexia, subcutaneous edema, jugular vein distention.
    • Forward Effects: Fatigue, oliguria, increased heart rate, faint pulses, restlessness, confusion, anxiety.

• Biventricular Heart Failure:

  • Most often the result of primary left-sided HF progressing to right-sided HF.
  • Reduced CO.
  • Pulmonary congestion (due to left-sided HF).
  • Systemic venous congestion (due to right-sided HF).

• Class and Stage of Heart Failure:

  • FACES: Fatigue, activity limitation, congestion, edema, shortness of breath.
  • Diagnostic assessment includes x-ray and echocardiography.
  • B-type natriuretic peptide level is assessed.
  • Severity of symptoms is used to identify the class/stage of HF.

• Treatment of Heart Failure:

  • Increase forward flow (cardiac output).
  • Decrease backup of flow (reduce the heart’s workload).
  • Aimed at improving CO while minimizing congestive symptoms and cardiac workload.
  • Obtained by manipulating preload, afterload, and contractility.

• Treatment Strategies:

  • Increase the force of ventricular contraction using inotropes.
  • Decrease the rate of contraction (using beta blockers) to increase filling time, which subsequently increases the force of ventricular contraction.
    • Enhances cardiac output and forward flow while decreasing backup of flow and the heart's workload.
  • Decrease preload: Dilate veins, reduce intravascular volume using nitrates and diuretics.
  • Decrease afterload: Dilate arteries using ACE inhibitors and hydralazine.

• Specific Treatments:

  • Preload: Reduces intravascular volume with diuretics and ACE inhibitors.
  • Afterload: β-blockers.
  • Contractility: Digitalis or other cardiac glycosides.
  • Pacemakers may be used to help synchronize ventricular contraction.

Cardiac Dysrhythmias

• Definition: Disturbance of the heart rhythm.

• Range: From occasional “missed” or rapid beats to severe disturbances that affect the pumping ability of the heart.

• Electrical Activity: Uncoordinated.

• Three Major Types:

  • Abnormal rates of sinus rhythm.
  • Abnormal sites (ectopic) of impulse initiation.
  • Disturbances in conduction pathways.

• Significance:

  • Indicate an underlying pathophysiologic disorder.
  • May impair normal CO.

• Treatment:

  • Indicated when dysrhythmias produce significant symptoms or are expected to progress to a more serious level.
  • Antiarrhythmic drugs are used (may be proarrhythmic).
  • Measures to improve CO (pacemakers and drugs to increase contractility).
  • Ablation procedures.