Congestive heart failure pathophysiology

pathophysiology of Congestive heart failure

1. PATHOPHYSIOLOGY OF PATHOPHYSIOLOGY OF
CONGESTIVE HEART CONGESTIVE HEART
FAILUREFAILURE

2. INTRODUCTION:
Blood goes out of the heart when the heart muscle contracts (called
systole) and comes into the heart when the muscle relaxes (called
diastole).
Heart failure is a disorder in which the heart pumps blood
inadequately, leading to reduced blood flow which further weaken the
heart.
It can result from any structural or functional cardiac disorder that
impairs ability of ventricle to fill with or eject blood.
Most people have no symptoms at first - shortness of breath and fatigue
develop gradually over days to months.
It can occur in any age, even in young children. But more common
among older people.
About 5,00,000 new cases occur each year. Worldwide, about 23
million people are affected.

3. Heart failure is called CCF/CHF because blood may build up in the tissues
causing congestion in those tissues.
Accumulation of blood coming into the left side of the heart causes
congestion in the lungs, making breathing difficult.
Accumulation of blood coming into the right side of the heart causes
congestion and fluid accumulation in other parts of the body, such as the legs.
Heart failure ® ¯ CO ® ¯ kidney perfusion ® stim. Of RAA system

4. Types of heart failure:

6. ETIOLOGY:

7. SYMPTOMS:

8. PATHOPHYSIOLOGY:
 Heart failure is caused by any condition which reduces the efficiency of the
myocardium or heart muscle, through damage or overloading of the ventricle,
leads to reduced force of contraction.
 In a healthy heart, increased filling of the ventricle results in increased force
of contraction (by the Frank–Starling law of the heart) and thus a rise in
cardiac output.
 In heart failure this mechanism fails because heart muscle contraction
becomes less efficient, due to reduced ability to cross-link actin and myosin
filaments in over-stretched heart muscle.
 Decreased Systolic volume is caused by reduced contractility.
 Decreased diastolic volume results from impaired ventricular filling.
Cardiac output (CO) = Heart Rate (HR) x Stroke
Vol.(SV)

9.  As the heart works harder to meet normal metabolic demands, the amount
cardiac output can increase in times of oxygen demand (e.g. exercise) is
reduced. This is failed during heart failure.
 Sympathetic activity may also cause potentially fatal arrhythmias.
 Hypertrophy (Enlargement) of the myocardium occur which result in
increased stiffness and decreased ability to relax during diastole.
 The increase in ventricular volume also causes a reduction in stroke volume
due to mechanical and contractile inefficiency.
 This increases the risk of cardiac arrest (specifically due to ventricular
dysrhythmias) and reduces blood supply to the rest of the body.
 This destimulates baroreceptors in the carotid sinus and aortic arch which
link to the nucleus tractus solitarii (center in the brain increases sympathetic
activity, releasing catecholamines into the blood stream).

12.  Reduced perfusion of muscle causes atrophy of the muscle fibres.
 This can result in weakness, increased fatigueability and decreased peak
strength – all contributing to exercise intolerance.
 As a result, arm and leg muscles may tire more quickly and the kidneys
may not function normally.
 The kidneys filter fluid and waste products from the blood into the urine,
but when the heart cannot pump adequately, the kidneys malfunction and
cannot remove excess fluid from the blood.
 As a result, the amount of fluid in the bloodstream increases, and the
workload of the failing heart increases, creating a vicious circle.
 Thus, heart failure becomes even worse.

13. The increased peripheral resistance and greater blood volume place load on
the heart and accelerates the process of damage to the myocardium.
 Vasoconstriction and fluid retention produce an increased hydrostatic
pressure in the capillaries.
 This results in edema in the tissue.
 In lungs – this is called cardiogenic pulmonary edema.
 This reduces capacity for ventilation, causes stiffening of the lungs and
reduces the efficiency of gas exchange by increasing the distance between the
air and the blood causes dyspnea.

16. DIAGNOSIS
ECG
Echocardiography
Chest X-rays
Blood tests - electrolytes (sodium, potassium), measures of renal
function, liver function tests, thyroid function tests, a complete blood
count, elevated BNP.
Angiography

17. TRAETMENT:
Immediate treatments - Vasodilators + diuretics such as
furosemide with ventilation.
First-line therapy – Digoxin, ACE inhibitors, Diuretics,
Beta-blockers, AT receptor blockers, Vasodilators,
Parenteral iron if anaemia is found
Immunosuppressive drugs to prevent rejection