Question

Discuss tha pathophysiology of Left side heart failure

Answer 1

ANSWER:  Left-sided heart failure occurs when the left ventricle, the heart’s main pumping power source, is gradually weakened. When this occurs, the heart is unable to pump oxygen-rich blood from the lungs to the heart’s left atrium, into the left ventricle and on through the body and the heart has to work harder.

• Heart failure with reduced ejection fraction (HFrEF), also called systolic failure: The left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation.
• Heart failure with preserved ejection fraction (HFpEF), also called diastolic failure (or diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can't properly fill with blood during the resting period between each beat.

CAUSES:  

• Coronary artery disease

• Heart attack in the past (also known as acute myocardial infarction, or AMI)

• High blood pressure

• Damaged heart valve

• Diabetes

• Obesity

• Cigarette smoking

• Alcohol abuse

PATHOPHYSIOLOGY:

• In heart failure, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion
• This condition can result from abnormalities of systolic or diastolic function or, commonly, both.
• However, in some patients, marked restriction to LV filling can cause inappropriately low LV end-diastolic volume and thus cause low CO and systemic symptoms. 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, or constrictive pericarditis
• In heart failure that involves left ventricular dysfunction, CO decreases and pulmonary venous pressure increases. When pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins (about 24 mm Hg), fluid extravasates from the capillaries into the interstitial space and alveoli, reducing pulmonary compliance and increasing the work of breathing
• Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema) significantly alters ventilation-perfusion (V/Q) relationships: Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation (PaO2) and causing dyspnea.

• However, dyspnea may occur before V/Q abnormalities, probably because of elevated pulmonary venous pressure and increased work of breathing; the precise mechanism is unclear.

• In severe or chronic LV failure, pleural effusions characteristically develop, further aggravating dyspnea. Minute ventilation increases; thus, PaCO2 decreases and blood pH increases (respiratory alkalosis). Marked interstitial edema of the small airways may interfere with ventilation, elevating PaCO2—a sign of impending respiratory failure.