CARDIAC FAILURE

DR MRS ODOCHI EWURUM

FWACP, FMCPaed
INTRODUCTION
Heart failure is a clinical state that occurs when the
heart cannot deliver adequate cardiac output to meet
the metabolic needs of the body despite adequate
atrial filling.

There are various situations in health or disease that

may impose a volume or pressure overload thereby
increasing the normal demands of the heart.
INTRODUCTION
In such circumstances the body is able to maintain or
increase the cardiac output appropriately by putting
into place a complex interplay of physiologic adaptive
or compensatory mechanismns such as;
 Increase in heart rate
 Dilatation/hypertrophy of the heart and chambers
 Salt and water retention
AETIOLOGY
Causes of heart failure can be cardiac or non cardiac.
Cardiac causes include;
1) Acyanotic congenital heart diseases such as ASD,
ASD, PDA, AS, PS,MS, AI, MI etc
2) Cyanotic congenital heart diseases such as TGA,
TAPVD, TA.
3) Acquired heart diseases such as cardiomyopathy,
EMF, RHD, infective endocarditis etc.
AETIOLOGY
Non cardiac causes include;
1) Hematologic: Anaemia, Polycythemia
2) Respiratory disorders: Acute lower respiratory tract
infection, Chronic lung dx.
3) Metabolic abnormalities: hypoxia, hypoglycemia,
metabolic acidosis
4) Renal disorders: AGN, Chronic renal failure
AETIOLOGY
5) CNS disorders: Coma, Intracranial space occupying
lession, cerebral malaria.
6) Miscellaneous: septicemia, over transfusion of blood
or intravenous fluids.
PATHOPHYSIOLOGY
The heart can be viewed as a pump with an output
proportional to its filling volume and inversely
proportional to the resistance against which it pumps.

As ventricular end-diastolic volume increases, a

healthy heart increases cardiac output until a
maximum is reached and cardiac output can no longer
be augmented (the Frank-Starling principle).
PATHOPHYSIOLOGY
Frank Starling’s law states that the stroke volume of
the left ventricle will increase as the left ventricular
volume increases due to the myocyte stretch causing a
more forceful systolic contraction if all other factors
remain constant. Thus, the more the ventricular
muscles are stretched, the more forcefully they
contract.
PATHOPHYSIOLOGY
• Heart failure results from injury to the myocardium
from a variety of causes as listed in the aetiology
documented above that would affect the delivery of
cardiact output.
• Cardiac muscle with compromised intrinsic
contractility requires a greater degree of dilatation to
produce increased stroke volume and does not achieve
the same maximal cardiac output as normal
myocardium does.
PATHOPHYSIOLOGY
• Cardiac output can be calculated as the product of
heart rate and stroke volume.
• The primary determinants of stroke volume are the
preload (volume work), afterload (pressure work) and
contractility (intrinsic myocardial function).
• Abnormalities in heart rate can also compromise
cardiac output and produce both bradyarrhythmias
and tachyarrhythmias; the latter shorten the diastolic
time interval for ventricular filling.
PATHOPHYSIOLOGY
In some cases of heart failure, cardiac output is
normal or increased, yet because of decreased
systemic oxygen content (secondary to anemia) or
increased oxygen demands (secondary to
hyperventilation, hyperthyroidism, or
hypermetabolism), an inadequate amount of oxygen is
delivered to meet the body's needs.
PATHOPHYSIOLOGY
This condition, which is a high-output failure, results
in the development of signs and symptoms of heart
failure when there is no basic abnormality in
myocardial function and cardiac output is greater than
normal.
It is also seen with large systemic arteriovenous
fistulas. These conditions reduce peripheral vascular
resistance and cardiac afterload and increase
myocardial contractility.
PATHOPHYSIOLOGY
LEFT VENTRICULAR HEART FAILURE
 This is due to left ventricular dysfunction
 Cardiac output decreases and pulmonary venous
pressure increases.
 When pulmonary capillary pressure exceeds the
oncortic pressure of plasma proteins(about 24mmhg),
fluid extravasates from the capillaries into the
interstitial space and alveoli.
 This leads to a reduction in pulmonary compliance
and increase in the work of breathing.
PATHOPHYSIOLOGY
-The lymphatic drainage increases but cannot
compensate for the increase in pulmonary fluid.
-Marked fluid accumulation in the alveoli causes
pulmonary edema which significantly alters the
ventilation-perfusion(V/Q). In severe cases, pleural
effusion developes.
-Therefore, deoxygenated pulmonary arterial blood
passes through poorly ventilated alveoli, decreasing
the systemic arterial oxygenation(Pao2) and causing
dyspnea.
PATHOPHYSIOLOGY
RIGHT VENTRICULAR HEART FAILURE
 Involves right ventricular dysfunction.
 Systemic venous pressure increases, causing fluid
extravasation and consequent edema.
 The edema is primarily in the dependent areas( feet
and ankles of ambulatory patients) and abdominal
Viscera.
PATHOPHYSIOLOGY
There are multiple systemic compensatory
mechanisms used by the body to adapt to chronic
heart failure. They include:
(1)Mediation at the molecular/cellular level;
This involves up- or down regulation of various
metabolic pathway components leading to changes in
efficiency of oxygen and other substrate utilization.
PATHOPHYSIOLOGY
(2) Mediation by neurohormones;
(i)The renin-angiotensin system: Its activation, leads to
the elevation of blood volume and arterial tone by
increasing sodium reabsorption, water retention and
vascular tone. Increased angiotensin can result in net
vasoconstriction and increase afterload.
PATHOPHYSIOLOGY
(ii) Sympathoadrenal axis: One of the principal
mechanisms for increasing cardiac output is an
increase in sympathetic tone secondary to increased
adrenal secretion of circulating epinephrine and
increased neural release of norepinephrine.
PATHOPHYSIOLOGY
-these hormones act on cardiac β-adrenergic receptors to
increase the heart rate and myocardial contractility leading
to increase in cardiac output.
-Because of localized vasoconstriction, mediated by these
hormones' action on peripheral arterial α-adrenergic
receptors, blood flow may be redistributed from the
cutaneous, visceral, and renal beds to the brain and the
heart to increase cardiac output.
CLINICAL MANIFESTATIONS
SYMPTOMS
 Feeding difficulties such as less volume per feeding,
dyspnea while sucking.
 poor weight gain.
 profuse perspiration.
 Fatigue.
 effort intolerance.
 Anorexia.
 Irritability, weak cry.
CLINICAL MANIFESTATION
-Abdominal pain
-Reduced urinary output
-dyspnea
-cough
-tachypnea
-noisy, labored respirations with intercostal and
subcostal retractions, as well as flaring of the alae nasi.
CLINICAL MANIFESTATION
 SIGNS
-Tachycardia
-Tachypnea cardinal

-Tender Hepatomegaly usually occurs Signs

-Cardiomegaly invariably occurs
-Splenomegaly occurs sometimes
-Edema may occur on dependent areas such as the eyelids
as well as the sacrum and less often the legs and feet or
anasarca may be present.
CLINICAL MANIFESTATIONS
SIGNS
-Raised jugular venous pressure in older children
-Crepitations or rhonchi
-Pallor
- Orthopnea
-A gallop rhythm is common.
-When ventricular dilatation is advanced, the
holosystolic murmur of mitral or tricuspid valve
regurgitation may be heard.
CLINICAL MANIFESTATION
PATHOPHYSIOLOGICAL BASIS OF THE CLINICAL
MANIFESTATION OF CARDIAC FAILURE
 Pulmonary venous congestion: gives rise to tachypnea,
dyspnea, crepitations and rhonchi.
 Systemic venous congestion: result to raised JVP,
Edema and hepatomegaly.
 Increased sympathetic adrenergic activity triggered by
reduced cardiac output: is the cause of pallor,
tachycardia, sweating, cold extremities and poor
pulses.
CLINICAL MANIFESTATION
PATHOPHYSIOLOGICAL BASIS OF THE CLINICAL
MANIFESTATIONS OF CARDIAC FAILURE CONTD.
 Fluid retention: causes abnormal weight gain,
reduced urinary output, pulmonary/systemic venous
congestion.
INVESTIGATION
These are carried out for the following reasons;
- To confirm the diagnosis.
 To ascertain the cause.
 Determine the severity.
 Monitor the response to treatment.
INVESTIGATION
-They include;
Chest x-ray
ECG
2D-Echo
Arterial blood gas analysis
 Serum electrolyte levels
 Serum BNP.
INVESTIGATION
(1) Chest X-ray: May reveal;
 Cardiac enlargement.
 Variable pulmonary vascularity depending on the
cause.
 Fluffy perihilar pulmonary markings suggestive of
venous congestion.
 Acute pulmonary edema.
INVESTIGATION
(2) Electrocardiography;
- Identify cardiac chamber enlargement.
- Used to evaluate rhythm disorders as a cause of cardiac
failure.
(3) Echocardiography;
- Useful in assessing ventricular function.
- Doppler studies are used to estimate cardiac output.
INVESTIGATION
(4) Arterial blood gas analysis;
- Arterial oxygen levels may be decreased when
ventilation-perfusion inequalities occur secondary to
pulmonary edema.
 Respiratory or metabolic acidosis, or both, may be
present when heart failure is severe.
INVESTIGATION
(5) Serum electrolyte levels;
- Infants with heart failure often display hyponatremia
as a result of renal water retention.
INVESTIGATION
(6) Serum B-type natriuretic peptide (BNP) is a cardiac
neurohormone released in response to increased
ventricular wall tension. It may be elevated in children
with;
(a) heart failure due to systolic dysfunction
(cardiomyopathy)
(b) heart failure due to volume overload (left-to-right
shunts such as ventricular septal defect).
TREATMENT
The principles of treatment is aimed at;
(1) Reducing the work load on the heart.
(2) Improving myocardial perfomance.
(3) Correcting the underlying causes.
GENERAL MEASURES;
- Bed rest to reduce the demand on the heart.
- Nurse patient in semi-upright (cardiac) position for
comfort.
- Increase the daily caloric intake.
TREATMENT
Nasogastric tube feeding is required in severely ill
infants who may lack sufficient strength for effective
sucking because of extreme fatigue, rapid respirations,
and generalized weakness.
Competitive and strenuous sports activities are usually
contraindicated.
TREATMENT
SPECIFIC MEASURES
(1) Diuretics: These agents interfere with reabsorption
of water and sodium by the kidneys, which results in
a reduction in circulating blood volume and thereby
reduces pulmonary fluid overload and ventricular
filling pressure.
Common examples are frusemide, spironolactone
and chlorthiazide.
TREATMENT
(a)Furosemide inhibits the reabsorption of sodium
and chloride in the distal tubules and the loop of
Henle. Dose is 1-2mg/kg in two divided doses.

-There is the potential for significant loss of potassium

during the administration of frusemide thus dietary
potassium supplementation may be required to
maintain normal serum potassium levels.
TREATMENT
-Chronic administration of frusemide may cause
contraction of the extracellular fluid compartment and
result in “contraction alkalosis.

(b)Spironolactone is an inhibitor of aldosterone and

enhances potassium retention. The dose is 2–3
mg/kg/24 hr, usually given orally in two to three
divided doses
TREATMENT
(c )Chlorothiazide affects the reabsorption of
electrolytes in the renal tubules only. The usual dose is
20–40 mg/kg/24 hr in two divided doses. Less potent
than frusemide.

(2) Afterload reducing agents and ACE inhibitors:

-This group of drugs reduces ventricular afterload by
decreasing peripheral vascular resistance and thereby
improving myocardial performance.
TREATMENT
-Some of these agents also decrease systemic venous
tone, which significantly reduces preload.
Examples include;
(i)nitroprusside
(ii)prazosin
(iii)nitroglycerin
(iv)Hydralazine.
TREATMENT
(3) ACE inhibitors may have additional beneficial
effects on cardiac remodeling independent of their
influence on afterload.
Examples include;
(a)Captopril: This produces arterial dilatation by
blocking the production of angiotensin II, thereby
resulting in significant afterload reduction.
Venodilation and consequent preload reduction have
also been reported.
TREATMENT
In addition, captopril interferes with aldosterone
production and therefore also helps control salt and
water retention. The oral dose is 0.3–6 mg/kg/24 hr
given in two to three divided doses.
(b)Enalapril is a longer acting ACE inhibitor that can
be taken once or twice daily. Dose is 0.08–0.5
mg/kg/dose q12–24h.
TREATMENT
(3) α and β-adrenergic agonist
These drugs are usually administered in an intensive
care setting, where the dose can be carefully titrated to
hemodynamic response.
(a)Dopamine : is a predominantly β-adrenergic receptor
agonist. The dose is 2–10 μg/kg/min.
-Has α-adrenergic effects at higher doses.
TREATMENT
-Has less chronotropic and arrhythmogenic effect
than the pure β-agonist.
-It results in selective renal vasodilation because of its
interaction with renal dopamine receptors.
(b) Dobutamine, a derivative of dopamine, is useful in
treating low cardiac output. It causes direct inotropic
effects with a moderate reduction in peripheral
vascular resistance. The usual dose is 2–20 μg/kg/min.
TREATMENT
(c)Isoproterenol is a pure β-adrenergic agonist that has a
marked chronotropic effect; it is most effective in
patients with slow heart rates. The dose is 0.01–0.5
μg/kg/min.
(d)Epinephrine is a mixed α- and β-adrenergic receptor
agonist that is usually reserved for patients with
cardiogenic shock and low arterial blood pressure. The
dose is 0.1–1.0 μg/kg/min.
TREATMENT
(4) Phosphodiesterase Inhibitors: These drugs works by
inhibition of phosphodiesterase, which prevents the
degradation of intracellular cyclic adenosine
monophosphate. Examples are milrinone and
amrinone.
(a)Milrinone has both positive inotropic effects and
significant peripheral vasodilatory effects on the heart.
TREATMENT
-Has generally been used as an adjunct to dopamine or
dobutamine therapy in the intensive care unit.
-It is given by intravenous infusion at 0.25–1 μg/kg/min.
- useful in treating patients with low cardiac output who
are refractory to standard therapy and has been shown
to be highly effective in managing low-output state in
children after open heart surgery.
TREATMENT
(5) Digoxin therapy: It increases myocardial
performance by;
(i) Increasing the force of contraction
(ii) Slowing the heart rate
(iii) Decreasing the conduction through the AV node.

- When administered orally, initial effect can be seen as

early as 30 min, peaks 2-6 hours and its half-life is 36
hours.
TREATMENT
-The drug crosses the placenta, and therefore a fetus
with heart failure (secondary to arrhythmia) can be
treated by administering digoxin to the mother.
-The kidney eliminates digoxin, so dosing must be
adjusted according to the patient's renal function.
-Its also excreted by the liver.
TREATMENT
DOSING OF DIGOXIN: Digoxin is given as follows;
-Calculate the total digitalizing dose as
0.04-0.06mg/kg/24hrs.
-Give half the total digitalizing dose immediately.
-Give the succeeding two one-quarter doses at 12 hr
intervals later.
- Maintenance digitalis therapy is started ≈12 hr after full
digitalization and it is one quarter of the total
digitalizing dose given in two divided doses at 12hourly
interval for children less than 10 years of age.
TREATMENT
-Thus maintenance dose is given as 1/8 of the TDD 12
hourly.
- Daily maintenance dose can be given to older children
greater than 10 years and adults.
- Closely monitor the heart rate of a patient on digoxin
and do not give if the heart rate is ≤ the lower limit of
normal for the age range of the child.
TREATMENT
 The margin of safety of digoxin is very small therefore
toxicity is a real risk.
 The serum drug levels of digoxin is routinely measured
in developed countries with facilities to do so.
 In developing countries, the clinical and ECG features
are used to monitor the levels of toxicity. Appropriate
blood level is ≈2–4 ng/mL in infants and 1–2 ng/mL in
older children.
TREATMENT
Symptoms of digoxin toxicity include;
-Malaise
-Nausea, Vomiting
-Anorexia, excessive salivation
-diahorrhea and yellow vision(in those who can
appreciate it).
Physical findings of digoxin toxicity include
bradycardia and arrhythmias
TREATMENT
ECG finding in digoxin toxicity include;
atrial ectopics
paroxysmal atrial tachycardia with AV –block
junctional rhythms
atrioventricular dissociation
complete heart block.
Ventricular ectopics (bigeminy) and paroxysmal
ventricular tachycardia occur less in children.
TREATMENT
Factors that potentiate digitalis toxicity include;
(i) hypokalemia
(ii)Hypomagnesemia
(iii)Hypercalcemia
(iv)cardiac inflammation secondary to myocarditis,
(v)prematurity.
TREATMENT
Treatment of toxicity:
Stop the drug,
↑ K+ intake,
Atropine for bradycardia,
propranolol or lignocaine for other arythmias.
TREATMENT
Normal effects of digoxin administration on ECG
include;
Sinus bradycardia
first and second degree heart block
sagging of ST segment
 diminished amplitude of T-wave.
TREATMENT
(6) Treatment of underlying conditions;
- Surgical correction of structural abnormalities in
congenital heart diseases, Rheumatic heart disease etc.
- Antibiotics for infective endocarditis,
bronchopneumonia and septicemia.
- Blood transfusion for treatment of anaemic heart
failure. Diuretic therapy is also used.
TREATMENT
 Digoxin is contraindicated in anaemic heart failure
because it increases the oxygen demands of tissues
including the myocardium which in this case is already
oxygen depleted due to anaemia.
.

THANKS FOR LISTENING

SUGGESTED READING
(1) Bernstein D. Heart Failure. In: Kleigman MR, Berham ER,
Jenson BH, Stanton FB, editors. Nelson’s Textbook of
Paediatrics.19th ed. Elsevier; 2011.
(2) Ogunkule O,Ekure E. Heart Failure in Childhood. In
Azubuike JC, Nkanginieme KEO. Paediatrics and Child
Health in a Tropical region.3rd ed. Owerri: African Educational
services; 2007.
(3) Jaiyesimi F. Cardiovascular diseases. In: Stanfield P, Brueton
M, Chan M, Parkin M, Waterston T, editors. Diseases of
Children in the Subtropics and Tropics. 4th ed. Educational
Low priced books.
(4) Internet.