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.
