Congestive Heart Failure

Chapter 31:  Congestive Heart Failure

Return to Section Table of Contents

Return to Site Table of Contents

Page Back

Clinical Manifestations and Physical Findings in Congestive Heart Failure

Acute pulmonary edema: severe form of cardiac asthma

Figure and description adapted from "Robbins: The Pathological Basis of Disease" Fifth Edition, p. 96

Figure and description from "Imaging Diseases of the Chest" , p. 388, by Peter Armstrong, Alan G. Wilson, and Paul Dee, Yearbook Medical Publishers, Inc. 1990.

  • Subcutaneous edema of the legs is an important and common manifestation of congestive heart failure.
  • This type of edema is termed "dependent" since it is influenced by gravity.
  •  If finger pressure over edematous subcutaneous tissue squeezes out fluid and produces depression, the edema is referred to as "pitting".
  • Loop diuretics such as furosemide, bumetanide, torsemide, and ethacrynic acid are effective in reducing peripheral edema in CHF.
  • Figure and description adapted from "Robbins: The Pathological Basis of Disease" Fifth Edition, p. 96

 

Cardiac Cachexia. Serious weight loss and cachexia may occur in chronic, severe congestive heart failure due to:
increased circulating tumor necrosis factor increased metabolic rate need to support the increased effort of breathing anorexia, nausea, vomiting due to digitalis intoxication, congestive
hepatomegaly, and abdominal fullness impairment of intestinal absorption due to intestinal venous congestion protein-losing enteropathy (rare)

 

Congestive Heart Failure
The fundamental abnormality in heart failure is embodied in:
  1. depression of the myocardial force-velocity relationship and
  2. length-active tension curves that result in impairment of myocardial contractility.

(see Figure, right)

  •  When a normal heart transitions from the resting state (1) to exercise (2) a significant increase in ventricular performance occurs.

  • By contrast in the failing heart, the exercise-induced increases in ventricular performance are minimal (3' to 3).

 

 
  1. With disease progression increases in left ventricular preload causes pulmonary capillary pressure to increase
  2. This increase produces pulmonary congestion and dyspnea
  3. Systemic compensatory responses to heart failure include fluid retention and increased in left ventricular afterload.(see Figure, right)

Figures from "Harrison's Principles of Internal Medicine", Thirteenth Edition, pages 995 and 996.

 

Factors Influencing Cardiac performance and Output

 

Ventricular end-diastolic volume (preload)

Atrial contraction

Inotropic state (myocardial contractility)

Factors that influence the inotropic state affect ventricular performance at a given ventricular end-diastolic volume. These factors change the concentration of Ca2+ at the myofilaments and include in part:

Drugs that improve ventricular performance include:
cardiac glycosides dopamine (Intropin)/dobutamine (Dobutrex) caffeine
isoproterenol (Isuprel) theophylline calcium
Drugs that decrease ventricular performance:
procainamide (Procan SR, Pronestyl-SR) disopyramide (Norpace) certain calcium channel blockers
alcohol barbiturates local and general anesthetics

Ventricular afterload

La Place's law 
  • "Imagine blood flowing through a blood vessel which has a certain radius and a certain wall thickness. The blood vessel wall is stretched as a result of the difference between the blood pressure inside the vessel and the surrounding pressure outside the vessel. 

  • La Place's law describes the relationship between the transmural pressure difference and the tension, radius, and thickness of the vessel wall.  

  • Obviously, the higher the pressure difference the more tension there will be. On the other hand, the thicker the wall the less tension there is. Also, the larger the radius the more tension there is. These three rules culminate into one equation:
    T = ( P * R ) / M

P = (T * M)/R

  • Where T is the tension in the walls, P is the pressure difference across the wall, R is the radius of the cylinder, and M is the thickness of the wall. 

  • An example of LaPlace Law is Dilated cardiomyopathy. 

    • In this condition heart becomes greatly distended and the radius (R) of ventricle increases. 

    • Therefore to create the same pressure (P) during ejection of the blood much larger wall tension (T) has be developed by the cardiac muscle. 

    • Thus dilated heart requires more energy to pump the same amount of  blood as compared to the heart of normal size."

  • library.thinkquest.org/C003758/Function/laplacelaw.htm

Exercise

  1. With exercise, venous return is significantly increased and results in enhanced ventricular filling and preload.

  2. Increases in cardiac adrenergic activity and increases in circulating levels of catecholamines increase heart rate and enhance the myocardial contractility.

    • These factors result in significantly augmented cardiac output.

  3.  Arterial pressure does not increase substantially since vasodilatation in exercising muscles offset the increase in cardiac output.

Myocardial Adaptation including Neurohumoral Adjustments

Adaptive mechanism to assist the failure heart

Congestive Heart Failure: Causes

  • Tachyarrhythmias decrease filling time and as a result decrease cardiac output.

    • Since increased heart rate increases myocardial oxygen demand, cardiac ischemia may be induced which may lead to reduced contractility.

 
  • A-V dissociation results in loss of the atrial contribution to ventricular filling.

    •  Therefore end-diastolic volume is reduced with an attendant reduction in cardiac output.

  • Abnormal intraventricular conduction may cause a reduced synchronicity of contraction with a reduction in myocardial performance.

    • Optimal output requires coordinated impulse propagation and contraction

 

 

  • Severe bradycardia in the absence of increased stroke volume can seriously reduce cardiac output and thus precipitate CHF. 

    • Increased stroke volume may not be possible if the patient has significant heart disease.

 

*Isselbacher et al. (eds): "Harrison's Principles of Internal Medicine"New York, McGraw-Hill Inc, 1994, p. 999.

Receptor polymorphism

Wild type Structure non-wild type phenotype structure

arginine 16 (Arg16)

glycine 16 (Gly16)

agonist promoted down-regulation enhanced

glutamine 27 (Gln27)

glutamate 27 (Glu27)

agonist-promoted down-regulation absent

Valine 34 (Val34)

Methionine 34 (Met34)

no difference compared to wild type

Threonine 164

Isoleucine 164

uncoupled from stimulatory G protein

Beta2 adrenergic receptor polymorphism: Heart from Patient on the left exhibited the Ile164 substitution which causes uncoupling of the second messenger G protein system from the beta2 adrenergic receptor.This picture  is from the research laboratory of Professor Stephen B. Liggett  University of Cincinnati College of Medicine http://receptors.med.uc.edu/FOverview.html

This diagram and related work is from the research laboratory of Professor Stephen B. Liggett  University of Cincinnati College of Medicine http://receptors.med.uc.edu/FOverview.html

Comparative pathophysiology: diastolic vs. systolic heart failure

From: 1Weinberger, H., Diagnosis and Treatment of Diastolic Heart Failure, Hospital Practice http://www.hosppract.com/issues/1999/03/weinb.htm

From: 1Weinberger, H., Diagnosis and Treatment of Diastolic Heart Failure, Hospital Practice http://www.hosppract.com/issues/1999/03/weinb.htm, as adapted from Zile MR: Diastolic dysfunction: Detection, consequences, and treatment. Part I: Definition and determinants of diastolic function. Mod Concepts Cardiovasc Dis 58:67, 1989 

 1Normally, most of the left ventricular filling occurs during the second phase (rapid filling); however, with impaired filling such as might occur with reduced ventricular compliance, less filling occurs during the second phase in more during the atrial contracting phase.

From: 1Weinberger, H., Diagnosis and Treatment of Diastolic Heart Failure, Hospital Practice http://www.hosppract.com/issues/1999/03/weinb.htm, Note on the left figure, increased pulmonary capillary wedge pressure was taken as an indication of increased left ventricular filling pressure.  In the right figure, there is a decrease in left ventricular end diastolic volume associated with those patients with diastolic dysfunction.  By contrast, control individuals exhibited an increase in left ventricular end diastolic volume accompanying increased workload associated with exercise.

General References

Return to Section Table of Contents

Return to Site Table of Contents

Page Back

 

 

Google