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CONGESTIVE CARDIAC FAILURE WITH VOLUME OVERLOAD.

Definition:

Congestive cardiac failure(CCF) is a clinical syndrome that is characterized by the inability of the heart to pump enough blood to the body to meet its need, to dispose off venous return adequately or a combination of the two (1).

Cause:

The cause of CCF may be due to three broad groups of disorders

a) Congenital heart disease

b) Acquired Heart Disease

c) Myocardial Insufficiency due to a variety of Causes.

A) Congenital Heart Disease

It the most common cause of CCF in the Pediatric Age group. Mostly it is due volume or pressure overload. The time of onset of CCF in pediatric age group varies with the type of defect. Below is given a small list of causes of CCF with age at presentation.

a) CCF in first hours of life

i) Asphyxia neonatorum

ii) Anemia

iii) Tachyarrhythmia, Bradyarrhythmia

iv) Metabolic abnormalities

v) Tricuspid Insufficiency

vi) Critical PS

vii) Pulmonary Atresia with Intact septum

viii) Pulmonary hypertension

ix) Cardiomyopathy

b) CCF in the first week of life

i) Hypoplastic left heart syndrome

ii) Transposition of great Arteries

iii) Coarctation

iv) Interrupted Aortic Arch

v) TAPVC with obstruction

vi) Cor Triatriatum

vii) Severe Ebstein’s

viii) PDA (in preterms)

ix) AV malformation

x) Iatrogenic

c) CCF in the First month of life

i) Coarctation of Aorta

ii) VSD

iii) Transposition

iv) PDA

v) DORV

vi) Truncus Arteriosus

d) CCF in 1st to 6th month

i) VSD

ii) Truncus Arteriosus

iii) PDA

iv) Severe AS

v) AV Canal defect

vi) TAPVC without obstruction

vii) Anomalous left coronary artery from pulmonary artery

viii) Tachyarrhythmia

ix) Myocarditis

x) Glycogen storage disease

e) Older than 1 year

i) Tachyarrhythmia, Brady arrhythmia

ii) Myocarditis

iii) Endocarditis

iv) Anemia, Polycythemia

v) Severe Hypertension

vi) ASD

vii) Post op congenital heart disease

Though the list for CCF in the pediatric age group is long the ibid mentioned categories are the commonest in the different age groups.

B) CCF in Acquired heart disease

i) Infective Endocarditis

ii) Rheumatic fever

iii) Collagen Vascular disease

iv) Other systemic diseases like sepsis, Kawasaki, thyroid disorders, Acute or Chronic renal disease, Neuromuscular disease

v) Congenitally acquired syndrome like Marfans, Hurler’s , Noonan’s Syndrome respectively

vi) Pulmonary hypertension due to Chronic lung disease or Primary pulmonary hypertension.

Mechanism of Congestive Cardiac failure

The various mechanisms leading to CCF are based on a number of factors that determine cardiac output like, preload, afterload, cardiac filling and contractility. There are other factors too that are responsible for CCF like salt and water retention (aldosterone), reflex vasoconstriction (α- adrenergic), redistribution of blood flow to CNS and Heart, and increased catecholamine release.

a) Increased preload- This refers to increased return to the heart due to any cause. This will lead compensatory mechanism in the heart in the form of ventricular dilatation which initially increases ejection fraction, cardiac output and velocity by Frank Starling mechanism. This is usually seen in lesions with large left to right shunts, valvular insufficiency, anemia, iatrogenic causes, and renal failure.

b) Increased Afterload: - The compensatory mechanism is ventricular hypertrophy to increase contractile mass. The age of onset of lesion is related to the severity of lesion. Obstructive lesions come in this category.

c) Cardiac filling: - Fast heart rates lead to reduced diastolic filling and coronary perfusion (which takes place in diastole). In case of very slow heart rates then the cardiac output is compromised. If not corrected then long standing tachyarrhythmia or Brady arrhythmia lead to cardiomyopathic changes.

d) Contractility: - This is based on the health of myocardium. This may be compromised in ischemia, metabolic derangements, sepsis, cardiomyopathy, and myocarditis.

Clinical Manifestation

The diagnosis of congestive cardiac failure relies on a number of clinical findings which almost always include history and chest x-rays. One important point should always be noted that besides clinical finding , the presence of cardiomegaly on chest x-ray is a near pre requisite for the presence of congestive cardiac failure. No single test is specific for congestive cardiac failure.

I) History

a) Infants- in this category of patients a recent onset poor feeding, tachypnea that worsens during feeding, poor weight gain and cold sweat point out to the possible cause being congestive cardiac failure.

b) Older children- Shortness of breath which is more with activities, easy fatigability, puffy eyelids and lips, swollen feet are clinical pointers of congestive cardiac failure.

II) Physical examination

These are classified on the basis of pathophysiology:

1) Compensatory responses to impaired cardiac function.(contractility)

a) Tachycardia, gallop rhythm, and in severe cases weak and thready pulses.

b) Cardiomegaly- on chest x-ray is almost always present.

c) Signs resulting from increased sympathetic discharges, viz; growth failure, perspiration and cold wet skin.

2) Pulmonary venous congestion- this is usually the manifestation of left sided failure and results in:

a) tachypnea

b) dyspnea on exertion(poor feeding in small infants)

c) Orthopnea

d) Wheeze+ pulmonary crackles

e) Occasionally hemoptysis

3) Systemic Venous congestion (Right sided Failure)

a) Hepatomegaly- common but not always indicative of heart failure. Absence of hepatomegaly does not rule out congestive cardiac failure.

b) Puffy eyelids and puffy lids due to aldosterone induced sodium retention and hence water

c) Distended neck veins and ankle edema may be seen in older children and adults and not in infants.

d) Splenomegaly- its presence usually indicates infection and rarely congestive cardiac failure.

III) Investigations

A) X-ray studies

- Cardiomegaly is important and is best detected by a chest X-ray film.

- The absence of cardiomegaly rules out Congestive cardiac failure.

- Cardiomegaly may also be present without congestive cardiac failure.

B) Electrocardiogram

- It is not helpful in diagnosing congestive cardiac failure

- Usually helps us determine the type of defect.

- In older children and adults it helps in defining chamber enlargement.

C) Echocardiogram

- It is the gold standard in the diagnosis of congestive cardiac failure now a days.

- It also tells us about impaired left ventricular function(↓ Fractional shortening or ↓ ejection Fraction)

- Serial echocardiograms help in knowing about the efficacy of therapy.

MANAGEMENT

The basic guidelines in management consist of:

a) Elimination of underlying causes- e.g., surgical repair of congenital heart disease.

b) Elimination of predisposing or precipitating factors (infection, anemia, arrhythmia, fever).

c) Control of heart failure.

General Measures

A) Respiratory distress needs to be relieved and for this one can use a cardiac chair or infant seat.

B) Oxygen administration- 40%-50% FiO2 to infants with respiratory distress. (If not relieved then ventilator should be kept ready).

C) Sedation will be required to quieten irritable infants. The choice of sedative depends on the medical care giver. We usually use Inj Morphine in low doses of 0.1mg/kg – 0.2 mg/kg subcutaneously. We can also use Phenobarbital at doses of 2-3mg/kg/dose.

D) Fluids- usually 2/3- 3/4th of daily maintenance is started and if feasible may be given as feed by nasogastric tube. In older children we use IV fluids initially then move on to oral once better. It should be a policy to use enteral nutrition where feasible (avoid this in cases of congestive cardiac failure due to critical aortic stenosis any other left sided obstructive lesion where gut perfusion is compromised). Salt restriction is not required in infants but may be restricted in older children and adults.

E) Daily weight check is important and in patients a progressive daily weight loss indicates good response to diuretic cover.

F) All predisposing factors like anemia, fever, infection and tachyarrhythmia should be eliminated. It is important to remind here that Hematocrit should preferably be kept over 35 %(> 35%).

G) Underlying causes like hypertension, thyrotoxicosis, or congenital heart disease should be treated.

DRUG THERAPY

In children we use three major classes of drug in the treatment of congestive cardiac failure:

A) Inotropes

B) Diuretics

C) Afterload reducing agents

PRINCIPLES INVOLVED IN DRUG THERAPY

1) Digoxin and diuretics are used in noncritically ill children. If the condition does not improve with this then we add oral vasodilators like ACE inhibitors or oral nitrates.

2) We use Inotropes in critically ill children where rapid stabilization is must and also as bridge to surgery.

3) We use dopamine in all obstructive lesions in congestive cardiac failure,viz Coarctation of aorta, TOF, Obstructed total anomalous pulmonary venous return(TAPVC) , arch interruption, Post PA bands. Use of inodilators here may lead to sudden collapse and shock. If BP still low despite dopamine then add epinephrine.

4) Dobutamine or Afterload reducing agents(Amrinone, Milrinone, Sodium Nitroprusside, Nitroglycerine) are used in cases where there is Left ventricular dysfunction with no obstructive lesion (VSD with AR, Severe MR, Severe AR Large VSD, Large PDA).

5) Where feasible combine Afterload reducing agents with dobutamine as the effect is synergistic (4).

 

A) Inotropes

Table No.1 gives the list of Inotropes used in Congestive Cardiac Failure

Drug

Dose

mode of action

adverse effects

Comments

I Phosphodiesterase inhibitors

a) Amrinone

 

b) Milrinone

 

 

 

3-10 mcg/kg/min as infusion

0.25mcg/kg/min-1mcg/kg/min may go up to 1.4mcg/kg/min

 

 

 

Phosphodiesterase inhibitor, positive inotrope, inodilator

Phosphodiesterase inhibitor Acts as both a inodilator and lusitrophic agent

 

Arrhythmia, hypotension, thrombocytopenia and GI upset

Like Amrinone but with no thrombocytopenia.

 

Efficacy in newborns and small children questionable.

Start with loading dose of 50mcg/kg over 15-20 min. It has well documented use in neonates and children(young)

II) Dopamine

3-30mcg/kg/min

Renal vasodilator at low concentrations(questionable)

Β1 and β2 stimulator and mild α-agonist. Causes nor epinephrine release

Tacchyarrhythmia, increases pulmonary vascular resistance(not useful in PAH), nausea, vomiting

Drug effect may decrease secondary to catecholamine depletion

III) Dobutamine

5-20 mcg/kg/min

Β adrenergic agonist at low doses and α agonist at high doses. It is a peripheral vasodilator and improves gut perfusion.

Ventricular ectopy/ventricular arrhythmias. Can increase pulmonary capillary wedge pressure may increase pulmonary edema

Potent inotrope. Used as inodilator in postop cardiac surgical patients. Patients with high PAPO benefit from combination of this drug with milrinone

IV) Epinephrine

0.03-1 mcg/kg/min

It is a potent β agonist (β1>β2). Mild α agonist.

Tachycardia, arrhythmia, hyperglycemia, headache and restlessness.

Combined inotropic and chronotropic effect with BP maintenance.

V) Nor epinephrine

0.05-2 mcg/kg/min

β1>>β2 Mild α agonist

Hypertension and similar to epinephrine

To be used cautiously. Central line a must and prolonged use may lead to Gut ischemia. Used commonly in vasodilatory shock with hypotension

 

A) Diuretics

Table No 2 gives the list of common diuretics used in cardiac patients.

Drug

dose

mode of action

adverse effects

Comments

Loop diuretics

a) Furosemide(Lasix)

 

 

 

 

 

b) Ethacrynic Acid

0.5-2mg/kg/dose 8 to 6hrly

0.5-3mg/kg/dose per orally BID/TID

Infusion-0.1mg/kg/hr to 1.0 mg/kg/hr

 

0.5-2mg/kg/dose intravenously

2-3mg/k/dose per orally

Loop diuretic, blocks the Na+ Reabsorption in the Ascending limb of loop of Henle

 

 

 

Same as furosemide

Hypokalemia

Hyponatremia

Hypocalcemia

Alkalosis

Nephrocalcinosis

Hyperurecemia

Hypochloremic alkalosis

Hypokalemia, Alkalosis

Possible ototoxicity. Augmented response when used with captopril.

 

 

 

 

 

Possible ototoxicity

Thiazide diuretics

a) Chlorothiazide

 

 

 

 

b)Hydrochlorothiazide

20-40 mg/kg/day(max 2g) orally

 

 

2-4mg/k/day per orally BID(max 200mg/day)

Distal renal tubular inhibition

 

 

 

-do-

Hypokalemia, Hyperbilirubinemia

Hyperglycemia

 

 

-do-

Rare hypersensitivity reaction with rash pancytopenia. To be used with caution during co administration proarrhythmic drugs.

-do-

Potassium sparing and aldosterone antagonist

a) Spironolactone

 

1-3.5mg/kg/day divided BID-TID

 

Inhibits distal action of aldosterone and prevents Na Reabsorption

 

Hyperkalemia if used concurrently with ACE inhibitors

Hyponatremia,

hyperchloremic metabolic acidosis

vomiting ,diarrhoea

 

Mild diuretic usually used in combination with loop or thiazide diuretics.

Sulphonamide Diuretic

Metolazone

2.5-5mg/day

Properties are consistent with both loop and thiazide diuretics

Hypokalemia

Hyponatremia

Hyperglycemia

Hyperurecemia

GI upset

Contra indicated in patients allergic to sulpha drugs. Potent diuretic,Needs close mpnitoring of Potassium levels Indicated in diuretic resistant pulmonary edema.

 

B) Afterload reducing agents

Table No 3 gives a list of common Afterload reducers and Vasodilators

drug

dose

mode of action

adverse effects

comments

ACE inhibitors

a) Captopril

 

 

 

 

b) Enalapril

0.1mg/kg/dose as test dose followed by 0.2-0.5mg/kg/dose upto a max of 4mg/kg/day after 2 hrs of test dose.

 

0.08mg/kg/dose

It is a competitive inhibitor of Angiotensin converting enzyme, some aldosterone inhibition also seen

Same as captopril

First dose hypotension seen and may occur if volume depleted. Rash, taste impairment, GI upset, neutropenia, protenuria

Same as captopril lower incidence of renal toxicity

Avoid potassium sparing diuretics and potassium supplements.

 

 

Same as captopril.

Nitroglycerine

Used as infusion-1-5mcg/kg/min max 10 mcg/kg/min

It is a predominant venodilator and mediates action through changes in intracellular cGMP

Do not use if low preload, hypotension, tachycardia, nausea, vomiting, headache. Prolonged use leads to tachyphylaxis and hence after 48hrs needs 6 hrs of break in infusion. May lead to methemoglobinemia on prolonged use.

Post op low cardiac output with high filling pressures, Pulmonary hypertension, and systemic venous congestion.

Sodium Nitroprusside

0.5mcg/kg/min to 6mcg/kg/min infusion

It is a mixed vasodilator with predominant action of the arterioles.

Hypertension, cyanide toxicity(Met hemoglobin levels measured), head vomiting , tachypnea, tachycardia, change in consciousness

Light sensitive in solution and hence cover IV circuit while administration. Check thiocyanate levels intermittently. Avoid use in preterm neonates.

Hydralazine

0.1-0.5mg/kg IV or IM 0.25-1mg/kg PO 6hrly -8hrly max 7mg/k/day

Direct vasodilator

Hypotension, tachycardia, lupus syndrome, neutropenia, GI upset.

Useful in ventricular dysfunction and aortic and mitral insufficiency.

 

How to calculate inotrope dose

Different authors recommend different methods. We recommend a simple and quick method that is useful in critical situations.

For example we want to give 5mcg/k/min of dopamine to a 10kg child.

Then taking that all medications will be reconstituted in 50 ml syringes the formula is as follows:

Dose of InotropesX weight of childX 3(multiplying factor)/ amount of dopamine in mg in 50ml. = this will give us our infusion rate.

Hence for the example above

5x10x3/100mg=150/100=1.5 hence the if we constitute 100mg of dopamine in 50ml saline and want to run at 5 mcg/k/min then we infuse at 1.5ml/min.

FLOW DIAGRAM SHOWING THE MANAGEMENT OF CONGESTIVE CARDIAC FAILURE WITH VOLUME OVERLOAD

 

 

Hemodynamic support maintenance in infants and children in shock

 

 

References:

1) Park M. Congestive heart failure, Chapter 30 ,In: Park M Pediatric Cardiology for Practitioners 4th Edition 2002.Mosby.

2) Carcillo J, What is new in Pediatric Intensive care, Critical Care Medicine2006,Vol 34,No.9(supplement) pps183-s190.

3) Fisher D., Feltes T., Moore J., Marcus B., Johnson G., Management of Acute Congestive Heart Failure In : Garson A., Bricker J., Fisher D., and Neish S.(Eds), The Science and Practice of Pediatric Cardiology, 2nd edition Vol.1, 1999, Williams and Wilkins.

4) Chang A., Hanley F., Wernowsky G., Wessel D., (eds), Pediatric Cardiac Intensive Care, 1998, Williams and Wilkins.

5) Behrman,Kleigmen and Jenson (Eds), Nelson Textbook of Pediatrics 17th edition, 2004 Elsevier.