Congestive Heart Failure

 Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Heart failure does not mean that the heart has stopped or is about to stop working. It means that the heart is not able to pump blood the way that it should. The heart can ’t fill with enough blood or pump with enough force, or both.

Pathophysiology

Systolic HF decreases the amount of blood ejected from the ventricle, which stimulates the sympathetic nervous system to release epinephrine and norepinephrine. The purpose of this initial response is to support the failing myocardium. The sympathetic stimulation and the decrease in renal perfusion by the failing heart cause the release of renin by the kidney

Renin promotes the formation of angiotensin I. 

Angiotensin-converting enzyme (ACE) in the lumen of blood vessels converts angiotensin I to angiotensin II, a vasoconstrictor that also causes the release of aldosterone.

Aldosterone promotes sodium and fluid retention and stimulates the thirst center. Aldosterone causes additional detrimental effects to the myocardium and exacerbates myocardial fibrosis. All of this alteration causes increasing preload and afterload which increase workload on the heart

Diastolic HF develops because of continued increased workload on the heart, which responds by increasing the number and size of myocardial cells. These responses cause resistance to ventricular filling, which increases ventricular filling pressures despite a normal or reduced blood volume. Less blood in the ventricles causes decreased CO. The low CO and high ventricular filling pressures cause the same neurohormonal responses as described for systolic HF.

Angiotensin II 

constricts the walls of arterioles closing down capillary beds; 

stimulates the proximal tubules in the kidney to reabsorb sodium ions; 

stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim still more sodium and thus water. 

 increases the strength of the heartbeat; 

 stimulates the pituitary to release the vasopressin.

Classification of HF

• Class I: no limitation in any activities (ADLs); there are no symptoms (fatigue, dyspnea or chest pain) from ordinary activities. 
• Class II: slight, mild limitation of activity (ADLs); the patient is comfortable at rest but increased physical activities will cause symptoms. 
• Class III: marked limitation of any activity; the patient is comfortable only at rest.
•  Class IV: symptoms of cardiac insufficiency occur at rest.

Causes of HF

narrowed arteries that supply blood to the heart muscle — coronary artery disease. 

• past heart attack, or myocardial infarction, with scar tissue that interferes with the heart muscle's normal work. 
• high blood pressure. 
• heart valve disease due to past rheumatic fever or other causes. 
•  primary disease of the heart muscle itself, called cardiomyopathy. 
•  heart defects present at birth — congenital heart defects. 
• infection of the heart valves and/or heart muscle itself — endocarditis and/or myocarditis

Signs and sysmptoms

Generally 

• Pale, cyanotic skin (with decreased perfusion to extremities) 
• Dependent edema (with increased venous pressure) 
• Deceased activity tolerance 

Cardiovascular 

• Apical impulse, enlarged and left lateral displacement (with cardiac enlargement)
• Third heart sound (S3) 
• Murmurs (with valvular dysfunction) Tachycardia 
• Increased jugular venous distention (JVD)

Cerebrovascular 

• Lightheadness, Dizziness, Confusion 

Gastrointestinal 

• Nausea and anorexia & abdominal pain. 
• Enlarged liver, Ascites, 

Renal 

• Decreased urinary frequency during the day 
• Nocturia 

Respiratory 

• Dyspnea on exertion, Orthopnea 
• Paroxysmal nocturnal dyspnea 
• Bilateral crackles that do not clear with cough

Right side HF

Right-sided heart failure causes the blood entering the heart from the body to back up in the veins causing swelling of the legs, feet , and stomach.

Left side HF

Left-sided heart failure causes fluid to back up and accumulate in the lungs. This leads to the patient symptoms of shortness of breath, inability to sleep and waking up in the middle of the night gasping for breath, inability to exercise without shortness of breath, inability to catch your breath while at rest, and for severe cases coughing and gurgling with frothy sputum

Medical management

The basic objectives in treating patients with HF are the following:

Eliminate or reduce any etiologic contributory factors, especially those that may be reversible, such as atrial fibrillation or excessive alcohol ingestion. 

 Reduce the workload on the heart by reducing afterload and preload.

ex:

• Angiotensin-Converting Enzyme Inhibitors. 
• Angiotensin II Receptor Blockers (ARBs). 
• Beta-Blockers.
• Diuretics
• Digitalis
• Vasodilators