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Definition: 

 

A clinical syndrome that develops when the heart cannot maintain an adequate cardiac output, or can do so only at the expense of an elevated filling pressure.

Epidemiology:

• The prevalence of heart failure in the United States is more than 5.8 million and more than 23 million cases worldwide.

• The main cause of heart failure is Ischemic Heart Diseases.

Classification and types:
Acute vs. chronic:

1. Acute HF:

• Can be reversible.

• Usually progresses into chronic HF.

      2.    Chronic HF:

• More common.

• Compensatory changes.

Left sided vs. Right sided:

1. Left sided HF:

• Most common causes: ischemic heart disease, HTN, mitral or aortic valve disease, or primary disease of the myocardium

     2.    Right sided HF:

• Most common cause in general is left sided HF.

• Another important cause is severe pulmonary HTN (Cor Pulmonale.)

Systolic vs. Diastolic:

1. Systolic HF (decreased ejection fraction EF):

• Ventricle contracts poorly and empties inadequately, leading initially to increased diastolic volume and pressure and decreased EF.

     2.     Diastolic HF (preserved EF):

• Ventricular filling is impaired, resulting in reduced ventricular end-diastolic volume, increased end-diastolic pressure, or both. 

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Risk factors:

• Age >65 Y/O.

• Gender (M>F).

• Race (more common in African Americans).

• Obesity & increased weight.

 

Pathophysiology:
Neuro-humoral adaptation:

• Sympathetic nervous system activation:

  1. Increase the release and decrease uptake of norepinephrine.

  2. Catecholamines help in maintaining the cardiac output during exercise especially in early HF.

• Renin-angiotensin- aldosterone system:

  1. Activation of the RAAS is dependent on low cardiac output, and low renal perfusion.

  2. RAAS activation  → fluid retention → increases the ventricular preload.

  3. Angiotensin II actions:

                           A. Increase the Na+ reabsorption in the proximal tubules (due to aldosterone).
                           B. Systemic and renal vasoconstriction.
                           C. Acts directly on the myocytes to promote the pathological remodeling in HF.
Systolic dysfunction with decreased EF:

• The ventricle contracts poorly and empties inadequately, leading initially to increased diastolic volume and pressure and decreased EF.

• Predominant systolic dysfunction is common in HF due to MI, myocarditis, and dilated cardiomyopathy. 

Diastolic dysfunction with preserved EF:

• Ventricular filling is impaired, resulting in reduced ventricular end-diastolic volume, increased end-diastolic pressure, or both.

• Contractility and hence EF remain normal; EF may even increase as the poorly filled LV empties more completely to maintain CO.

• Elevated left atrial pressures can cause pulmonary hypertension and pulmonary congestion.

• Diastolic dysfunction usually results from impaired ventricular relaxation (an active process), increased ventricular stiffness, valvular disease, Acute MI, or constrictive pericarditis.

• Diastolic dysfunction is common among the elderly due to increased resistance to filling.

Left ventricular failure (LVF):

• Cardiac output deceases and pulmonary venous pressure increase.

• Marked pulmonary edema, which alters the V/Q relationship leading to significant dyspnea.

• In severe LVF, pleural effusion might develop exacerbating the dyspnea.

Right ventricular failure: 

• Back flow of the blood leading to increase of the systemic venous pressure.

• Leading to fluid extravasation and edema primarily in ankles & feet in ambulatory patients, sacral area in bedridden patients, and abdominal viscera (hepatomegaly and ascites).

• Moderate hepatic dysfunction with increased of total bilirubin.

 

Causes:
Main causes: 

• IHD 40%.

• Dilated cardiomyopathy 34%.

• HTN 20%. 

Others:

• Other causes of cardiomyopathy.

• Valvular heart disease (mitral and aortic).

• Congenital heart disease.

• Chaga’s disease (myocarditis).

• Pericardial diseases. 

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Symptoms & Signs:
Symptoms: they might overlap.