Heart Failure

                        

Heart Failure

Heart failure is defined as a state in which the heart cannot deliver an adequate cardiac output to meet the metabolic needs of the body

Pathophysiology.

Heart is a pump with an output proportional to its filling volume and inversely proportional to the resistance against which it pumps. As the ventricular end-diastolic volume increases force of contraction increases till a maximum is reached when it starts failing.

cardiac output = heart rate x stroke volume.

determinants of stroke volume are the

            afterload (pressure work),

            preload (volume work),

            contractility (myocardial function).

Abnormalities of heart rate can also affect cardiac output, producing bradyarrhythmias or tachyarrhythmias

anemia or hypoxemia also lead to a decrease in oxygen transport à CCF

sometimes the cardiac output is normal or increased, because of decreased oxygen content (secondary to anemia) or increased oxygen demands (secondary to hyperventilation, hyperthyroidism, or hypermetabolism), = high-output failure, results in the development of signs and symptoms of heart failure - there is no abnormality in myocardial function and the cardiac output is greater than normal.

It is also seen in large systemic arteriovenous fistulas.

compensatory mechanism = increase in sympathetic tone,à increased adrenal secretion àincreased heart rate and myocardial contractilityàhypermetabolism, increased afterload, arrhythmogenesis, increased myocardial oxygen requirements,

Clinical manifestations

history

            Cyanosis - “a deep coloring”

            feeding less per feeding, becomes dyspneic while sucking, sweat profusely. Physical activity decreased

signs and symptoms of heart failure are

effort intolerance,

anorexia,

abdominal pain,

cough.

Dyspnea is a reflection of pulmonary congestion.

Elevation of systemic venous pressure may be gauged by clinical assessment of the jugular venous pressure and liver enlargement.

Orthopnea and basilar rales may be present;

edema is in dependent portions of the body, or anasarca

Cardiomegaly is noted.

A gallop rhythm is common

other auscultatory findings are specific to the basic cardiac lesion.

In infants,

tachypnea,

feeding difficulties,

poor weight gain,

excessive perspiration,

irritability,

weak cry,

noisy, labored respirations

intercostal and subcostal retractions

flaring of the alae nasi.

The signs of cardiac pulmonary congestion = bronchiolitis and so difficult to differentiate

wheezing

Pneumonitis with or without atelectasis - especially of the right middle and lower lobes; it is due to bronchial compression by the enlarged heart.

Hepatomegaly usually occurs,

cardiomegaly is present.

gallop rhythm can be recognized.

auscultatory signs are those of underlying cardiac lesion.

jugular venous pressure in infants may be difficult to see because of the shortness of the neck

Edema may be generalized, usually involving the eyelids as well as the sacrum, and less often the legs and feet.

Laboratory diagnosis

X ray chest

            cardiac enlargement.

            pulmonary vascularity depending on the cause of the heart failure.

pulmonary edema in severe heart failure.

Electrocardiography-

Chamber hypertrophy --, left or right ventricular ischemic changes may correlate well with clinical - Low-voltage QRS - with ST-T wave abnormalities - myocardial inflammatory disease , pericarditis.

rhythm disorders

Echocardiographic

assessing ventricular function.

fractional shortening, - - the difference between end-systolic and end-diastolic diameters divided by the end-diastolic diameter.

            normal fractional shortening is between 28 and 40%,

            normal ejection fraction (which measures volume) of 55–65% measured by angiography.

long pre-ejection time with a short ejection time denotes myocardial failure.

Doppler studies -calculate cardiac output.

Arterial oxygen levels decreased when ventilation-perfusion inequalities occur secondary to pulmonary edema.

When heart failure is severe, respiratory or metabolic acidosis, or both, may be present.

hyponatremia caused by renal water retention. -diuretic treatment can decrease serum sodium levels further.

Treatment.

The underlying cause of cardiac failure must be removed

congenital cardiac anomaly amenable to surgery,

medical treatment is indicated to prepare the patient for operation

cardiomyopathy, medical management provides temporary relief from symptoms

General Measures.

Strict bed rest in extreme cases, - rest and sleep adequately.

sleeping in a semi-upright position

severe pulmonary edema, positive-pressure ventilation - b-Adrenergic agonists, such as dopamine, epinephrine, and dobutamine, along with afterload-reducing agents (e.g., nitroprusside, captopril), may be required

Diet.

Increasing daily calories

Ineffective sucking because of extreme fatigue, rapid respirations, and generalized weakness.

nasogastric feedings

gastroesophageal reflux

continuous drip nasogastric feedings at night, Nissen's fundoplication

malnutrition - factor in the decision to undertake earlier surgical intervention in patients who have an operable congenital heart lesion.

“no added salt” diets

Digitalis.

digitalis glycoside - half-life of 36 hr - daily

absorbed well by the gastrointestinal tract

Absorption is greater with the elixir than with tablets.

effect can be seen as early as 30 min after administration,

intravenously, the initial effect is seen in 15–30 min, and the peak effect occurs at 1–4 hr. The drug crosses the placenta, and therefore the fetus with heart failure (secondary to arrhythmia) can be treated by administering digoxin to the mother.

Digoxin is eliminated by the kidney,

Rapid digitalization -recommended schedule - one half of the total digitalizing dose immediately and the succeeding two one-quarter doses at 12-hr intervals later.

The electrocardiogram must be closely monitored and rhythm strips obtained

Digoxin should be discontinued if a new rhythm disturbance is noted.

serum electrolyte levels should be measured

Hypokalemia and hypercalcemia exacerbate digitalis toxicity.

normal daily dose of digoxin for older children (>5 yr of age) calculated by body weight should not exceed the usual adult dose of 0.2–0.5 mg/24 hr.

Measurement of a serum

1) when a standard dose of digoxin is not having beneficial therapeutic effects,

2) when an unknown amount of digoxin has been administered or ingested accidentally, 3) when renal function is impaired or if drug interactions are possible (e.g., quinidine),

4) when there is a question regarding compliance,

5) when a toxic response

normal blood level in an infant is 2–4 ng/mL and in older children 1–2 ng/mL.

Nausea and vomiting are less frequent in pediatric patients.

Hypokalemia, hypomagnesemia, hypercalcemia, cardiac inflammation due to myocarditis, and prematurity may all potentiate digitalis toxicity.

A cardiac arrhythmia that develops in a child who is taking digitalis also may be related to the primary cardiac disease rather than to the drug.

Any form of arrhythmia occurring after the institution of digitalis therapy must be considered to be drug-related until proved otherwise.

Diuretics.

They interfere with reabsorption of water and sodium by the kidneys,

results in the reduction of circulating blood volume and thereby reduces pulmonary fluid overload and ventricular filling pressures.

Furosemide - inhibits the reabsorption of sodium and chloride in the distal tubules and the loop of Henle. - given intravenous or intramuscular furosemide - dose of 1–2 mg/kg.

Chronic furosemide therapy - dose of 1–4 mg/kg/24 hr given

monitoring of electrolytes -loss of potassium.

Potassium chloride supplementation is required

Spironolactone is an inhibitor of aldosterone and enhances potassium retention.

It is usually given orally in two to three divided doses of 2–3 mg/kg/24 hr.

Combinations of spironolactone and chlorothiazide are commonly used for convenience and because they eliminate the need for potassium supplementation

Chlorothiazide = diuresis in children with less severe chronic heart failure.

affects the reabsorption of electrolytes in the renal tubules only.

The usual dose is 20–40 mg/kg/24 hr in divided doses. Potassium supplementation is required

Afterload-Reducing Agents.

reduces ventricular afterload by decreasing peripheral vascular resistance

decrease systemic venous tone, reducing preload.

Afterload reducers are useful in children with heart failure due to cardiomyopathy and in severe mitral or aortic insufficiency, heart failure secondary to left-to-right shunts. - not used in the presence of stenotic lesions of the left ventricular outflow tract.

Afterload-reducing agents are most often used with digoxin and diuretics.

Nitroprusside –

intensive care setting - short time -Peripheral arterial vasodilation and afterload reduction -Blood pressure must be monitored because sudden hypotension can occur. - circulating cyanide are produced,

Captopril angiotensin-converting enzyme inhibitor - produces arterial dilatation - blocking the production of angiotensin II, resulting in afterload reduction. decreases aldosterone production and helps control salt and water retention. The oral dose is 0.3–6 mg/kg/24 hr given in two to three divided doses. The adverse reactions to captopril - hypotension - syncope, weakness, and dizziness,

 maculopapular pruritic rash

Neutropenia, renal toxicity,

chronic cough also occur.

Enalapril is a longer acting angiotensin-converting enzyme inhibitor.

Hydralazine is a direct arteriolar smooth muscle relaxant

headache, palpitations, nausea, and vomiting. systemic lupus erythematosus

Adrenergic Agonists.

Dopamine - renal vasodilation- useful in compromised kidney function

Dobutamine, - low cardiac output.

Dobutamine used as an adjunct to dopamine therapy

Isoproterenol,

Phosphodiesterase Inhibitors.

Milrinone - inhibition of phosphodiesterase,

preventing the degradation of intracellular cyclic adenosine monophosphate.

side effect is hypotension

Amrinone, - phosphodiesterase inhibitor, thrombocytopenia;

Chronic Treatment with b-Blockers.

dilatated cardiomyopathy - b-adrenergic blocking agents, introduced gradually improves exercise tolerance, decreasing hospitalizations, and reducing overall mortality.

metoprolol, a b1 -receptor selective antagonist,

carvedilol, an agent with both a- and b-receptor blocking as well as free radical scavenging effects.