Therapy for Congestive Heart Failure

Pertinent Characteristics of CHF

Myocardial disease leads to poor contractility

Poor contractility Decreases Stroke Volume

Primary "Lesions"

• Cardiomyopathy - primary degeneration of cardiac muscle
  

  

  
  
  
• Mitral Insufficiency
  

  

  Reflexes

  provoked by decreased blood pressure or oxygenation (Secondary to decreased ouput. Either primary mechanism)

  JG apparatus triggers Renin-Angiotensin-Aldosterone

  

  Baroreceptor triggers increased Sympathetic Tone

  • Increases Heart Rate (cardiac output)
    Controlled by β-1 receptors in the myocardium
  • Increases Vascular Resistance (further reduces Stroke Volume)
    Controlled by α receptors in the arteries and arterioles
  • Increases Venous Return (preload)
    Subtle effect by α receptors in veins (not many receptors, not much muscle)

   

  Clinical Signs of Congestive Heart Failure

  Compensation becomes "Reflex Excess"

  Congestion

  pulmonary edema, pleural effusions, ascites (because) preload is increased and stroke volume is decreased

  Low Output

  weakness, syncope, exercise intolerance (because) stroke volume is decreased and afterload is increased. afterload

  Specific Therapeutic Objectives

  Increase Contractility

  Increase Stroke Volume
  Decrease need for reflex "Increases"
  
  
  • Cardiac Glycosides
    
  • Sympathomimetic Amines
    
  • Non-glycoside inotropes
    
  • Xanthine bronchodilators
    
  
  

  Decrease Heart Rate

  Atrial fibrillation
  High sinus rate contributes to low output
  
  Direct negative chronotropic activity or
  Reduced sympathetic tone secondary to increase in contractility
  
  
  • Cardiac Glycosides (increased vagal tone)
    
  • ß-blockers
    
  
  

  Decrease Preload (end diastolic volume (or) filling pressure)

  Decrease blood volume (Decrease fluid retention)
  
  
  • Diuretics
    
  • "ACE"-Inhibitors
    
  
  Increase storage capacity (Decrease Venous Tone)
  
  
  • Nitrate vasidilators
    
  • "ACE"-Inhibitors
    
  
  

  Decrease Afterload - systemic vascular (arterial) resistance

  Decrease Arterial Tone
  Nitrates & related compounds (Direct smooth muscle)
  α-blockers (Decrease sympathetic response)
  Cardiac Glycosides (Decrease reflex IF increase contractility)
  "ACE" Inhibitors (Decrease Angiotensin II concentrations)
  

Topic Summary (Congestive Heart Failure)

1. Congestive heart failure is managed it is not cured.
   
   
2. The clinical effects of cardiovascular drugs are highly dependent on the pre-existing state of the cardiovascular system. Responses in diseased animals may be different from those in normal. Interactions between cardiovascular drugs are to be expected (and may be either desirable or undesirable). It is virtually impossible to predict the precise response of a patient to a given intervention.