Congestive Heart Failure

Sushila Dhaon

Definition

Congestive heart failure (CCF) is a clinical syndrome in which the heart is unable to pump enough blood to the body:

1. to meet the metabolic needs of the body (Systolic failure)
2. to dispose of its venous return adequately (Diastolic failure)
3. or combination of the both

Manifestation Of Congestive Heart Failure

Symptoms

1. Poor weight gain.
2. Difficulty in feeding, due to easy fatiguability.
3. Irritability, excessive perspiration and restlessness.
4. Persistent cough and wheezing, shortness of breath.
5. Puffiness of face.
6. Pedal oedema.

Signs

1. Tachycardia.
2. Tachypnoea.
3. Rales in chest.
4. Cardic enlargement.
5. Gallop ryhthm.
6. Hepatomegaly.
7. Facial oedema.
8. Jugular venous enlargement.
9. Pedal oedema.

Causes Of Congestive Cardiac Failure

The commonest cause of CCF in infants is congenital heart disease whereas in older children, it is rheumatic fever and rheumatic heart disease. The causes of congestive heart failure according to the age of onset are:

1. Fetal
   1. Severe anemia
   2. Hemolysis
   3. Fetal Maternal Transfusion
      1. Hypoplastic Anemia
      2. Supra Ventricular Tachy cardia (SVT)
      3. Ventricular tachy cardia (VT)
      4. Complete heart block.

2. Premature Neonate
   1. Fluid overload
   2. PDA
   3. VSD
   4. Corpulmonale (Broncho pulmonary dysplasia)
   5. Hypertension

3. Full Term Neonate
   1. Asphyxia cardiomyopathy
   2. Arterio venous malformation
   3. Left sided obstructive lesion (COA, HLHS) (Coarc tation of Aorta, Hypoplastic left heart syodrome)
   4. Large mixing cardiac defects e.g. single ventricle, truncus arteriosus
   5. Viral myocarditis

4. Infant/Toddler
   1. L-R cardiac shunts (VSD)
   2. Haemangioma(AV malformation)
   3. Anomalous left coronary artery
   4. Metabolic cardiomyopathy
   5. Acute hypertension due to acute glomerulonophritis
   6. SVT
   7. Kawasaki disease

5. Child/Adolescent
   1. Acute Rheumatic Carditis
   2. Acute hypertension (glomerulo nephritis)
   3. Viral myocarditis
   4. Thyrotoxicosis
   5. Hemochromatosis, hemosiderosis
   6. Sickle cell anemia
   7. Infective endo carditis
   8. Corpulmonale (cystic fibrosis)
   9. Cardiomyopathy (hypertrophic, dilated)

   Management

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   Before planning out the treatment, a few baseline investigations have to be done to monitor the patient:

   Investigations

   1. X-ray Chest: Shows cardiomegaly Absence of cardiomegaly almost rules out the diagnosis of congestive heart failure. Pulmonary vascularity is variable, depending on the etiology of heart failure. Infants and children with left to right shunts show exaggeration of pulmonary vascular bed while patients with cardio-myopathy will show normal pulmonary vascular bed, in the early course of disease. Fluffy perihilar pulmonary markings suggest venous congestion and acute pulmonary oedema, which are suggestive of severe degrees of congestive heart failure.
   2. Electrocardiography It is helpful in assessing the etiology of heart failure but does not establish the diagnosis of congestive heart failure. It is the best investigation when arrythmia is the cause of heart failure.
   3. Echocardiography We can directly visualise the anatomic deformity on the two dimensional echo-cardiography. It is also helpful in assessing the ventricular function. It is also useful in monitoring efficiency of therapy especially in cardiomyopathy and also to assess the flow by Doppler.
   4. Arterial Oxygen Levels It may be decreased when severe respiratory/metabolic acidosis is present or when pulmonary oedema secondary to congestive heart failure is present.
   5. Serum Electrolytes Infants with congestive heart failure show hyponatremia and hypokalemia due to renal water retention and sodium and potassium loss. Total body sodium may actually be increased. Chronic diuretic treatment can decrease serum sodium and potassium levels even further.

   Treatment

   1. General measures
   2. Drug therapy
   3. Surgical treatment

   General measures
   Aim is to reduce the cardiac work.

   1. Cardiac chair or propped up position at 45 degrees to relieve cardio repiratory distress.
   2. Humidified oxygen therapy
   3. Sedation is indicated only in acute left venticular failure Morphine sulphate (0.1 to 0.2 mg/kg oral or IM every 8 hr. or as and when necessary).
   4. High calorie salt restricted diet Salt restriction is not indicated in infants. In older children salt restriction (<.5gms/day) and avoiding salty snacks pickles & table salts are recommended.
   5. Daily weight measurement is essential in hospitalised patients to see the progress of therapy.
   6. Predisposing factors such as fever anemia and infection are eliminated.
   7. Underlying causes such as hypertension, arrythmias and thyrotoxicosis are treated.

   Drug Therapy
   

   1. Inotropic agents
   2. Diuretics
   3. After load reducing agents
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   1. Inotropic Agents
      Improve the cardiac output by augmenting myocardial contractility.
      1. Digoxin is the most commonly used digitalis preparation in pediatric patients. It is available for oral and parentral administration. It has a rapid onset of action and is eliminated quickly. Oral digoxin is available in 0.25 mg tablets and as lanoxin elixer (1ml is 0.05 mg). For parentral use lanoxin and parentral digoxin (0.5 mg/2 ml) are available. It decreases the heart rate and increases myocardial contractility. The strength and velocity of myocardial contraction is increased due to direct action on the myocardium whether it is normal or failing. The total digitalising dose and maintenance dosage of digoxin by oral and IV routes is shown in
         table 1.

         DRUG	DOSAGE
         Digoxin Digitalization PO (in 3 divided doses)	Premature 0.02 to 0.25 mg/kg Neonate (<1month) 0.05 to 0.04 mg/kg Infant or child 0.04 to 0.05 mg/kg Adolescent or adult 1.0 to 1.5 mg in divided doses
         Digitalization IV	75% of per oral Dose Maintainance
         Timing of the doses variable depending upon Clinical

         The dosage may be higher in treating SVT in which goal of treatment is to delay AV conduction.

         How to Digitalize
         Loading doses of the total digitalising dose are given in 12 to 18 hours and are followed by maintenance doses. This results in pharmacokinetic steady state in 3 to 5 days. An intravenous route is preferred over the oral route; particularly in infants in severe heart failure. An intramuscular route is not recommended because absorption of the drug from the injection site is unreliable. In an infant with mild heart failure the maintenance dose may be administered orally without loading doses, which results in a steady state in 5-8 days.

         Step by Step Method of Digitalisation
         

         1. Obtain a baseline ECG (Rhythm and PR interval) and baseline levels of S. Electrolytes (changes in ECG rhythm & PR interval are important signs of digitalis toxicity). Hypokalemia and hypo calcemia predispose to digitalis toxicity.
         2. Calculate the total digitalising dose
         3. Give one half of the total digitalising dose immediately followed by one fourth and final one fourth of the total digitalising dose at 6-8 hours intervals.
         4. Select the maintenance dose 12 hours after the final total digitalising dose. Obtain an ECG before starting the maintenance dose.

         Monitoring for Digitalis Toxicity
         

         1. Clinical Manifestation
         2. ECG
         3. S.Electrolytes
         4. Serum Digoxin Levels
         1. Clinical Manifestation
            Nausea and vomitting are less frequent in pediatric patients. On examination brady cardia and irregular heart beats are more common and can be confirmed on ECG.
         2. ECG
            Digitalis toxicity is best detected by monitoring with ECG during first 3-5 days after digitalization.

            In general the digitalis effect is confined to ventricular repolarisation, whereas toxicity involves disturbances in the formation and conduction of the impulse. One should assume that any arrythmia or conduction disturbance occurring with digitalis is caused by digitalis unless proved otherwise. ECG changes associated with digitalis.

            1. Effects
               
               1. Slowing of heart rate.
               2. Prolonged P-R interval - 1' heart block.
               3. Sagging ST segment and diminished amplitude of T wave.
               4. Shortening of QTC, the earliest sign of digitalis effect.

            2. Toxicity
               
               1. Paroxysmal Ventricular Contraction (PVC) common in children.
               2. The prolongation of PR interval may progress to second degree AV block Wenchebach's phenomenon.
               3. Supra ventricular arrythmias such as atrial or nodal ectopic beats and tachy cardias which are more common than ventricular tachy cardias in children.
               4. Profound sinus bradycardia or SA block (complete heart block),
            Dosage of Catecholamines

            Drug	Route & Dosage	Side effects
            Epinephrine	IV 0.1-1.0 ug/kg/min	Hypertension (Adrenaline) Arrythmia
            Isoproterenol	IV 0.1-0.5 ug/kg/min	Peripheral & Pulmonary vasodilatation
            Dobutamine	IV 5-8 ug/kg/min	Tachy-Cardia & vasodilatation & Arrythmias (Betareceptor agonist-short term infusion)
            Dopamine	IV 5-10 ug/kg/min	Vasodilation or hypotension Higher doses-Vaso-Constriction (not useful for control of CCF)

         3. Serum Electrolytes
            Serum potassium has to be monitored weekly in those patients who are on digoxin.
         4. Serum Digoxin Levels
            Therapeutic levels of serum digoxin levels for treating CHF are 0.8 to 2.0 mg/lit. Levels maintained during first 3 to 5 days of digitalisation are higher than those obtained when pharmacokinetic steady state is reached. Serum digoxin testing should be tested at least 6 weeks after the last dose or just before a scheduled dose. Serum digoxin levels are important in monitoring digoxin therapy in ideal circumstances.

            Elevated Serum digoxin levels are not in themselves diagnostic of toxicity but must be interpreted as an adjuvant to other clinical and electro cardiographic findings.

         Factors potentiating digitalis toxicity are:

         • Hypokalemia
         • Hypomagnesemia
         • Hypocalcemia
         • Cardiac inflammation due to myocarditis
         • Prematurity

         Cardiac arrhythmia in a child may be due to underlying, cardiac disease rather than the drug. Any form of arrhythmia occurring after institution of digitalis therapy must be considered as drug related until proven otherwise.

         General measures following diagnosis of digitalis toxicity

         1. Discontinuation of digitalis & diuretics unless absolutely indicated.
         2. ECG monitoring
         3. Potassium supplementation.
         4. Predisposing factors evaluated and eliminated

      2. Other Inotropic Agents
         These are sympathomimetic agents. These drugs combine inotropic effect with peripheral vaso dilatation. They have limited use.

         Indications

         1. in infants in severe CHF with distress
         2. with renal dysfunction e.g. CHF with COA
         3. post operative cardiac patients with heart failure.

      Rapidly acting catecholamines with a short duration of action are preferable to digoxin.

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      Diuretic Agents and Dosage

      Preparation	Route	Dosage
      Thiazide diureticsChlorothiazide	Oral	20-40 mg/kg/day
      Hydro chlorothiazide	Oral	2 to 4 mg/kg/day
      Loop diuretics	I.V.	1 mg/kg/dose
      Furosemide (Lasix)	Oral	2-3 mg/kg/dayIn 2-3 divided doses
      Ethacrynic acid(Edecrin)	IV, Oral	1 mg/kg/dose3 mg/kg/dayIn 2-3 divided doses
      Aldosterone AntagonistSpironolactone(Aldactone)	Oral	2-3 mg/kg/dayIn 2-3 divided doses

   2. Diuretics
      Patients with CHF improve rapidly after a dose of fast acting loop diuretics such as Ethacrynic acid or durosemide even before digitalisation .

      Side effects of diuretic therapy: Diuretic therapy alters the serum electrolyte balance and acid base equilibrium

      1. Hypokalemia: Commences with diuretics except with aldactone. It may increase the likelihood of digitalis toxicity.
      2. Hypochloremic Alkalosis: Chloride ion loss is greater than loss of sodium ions through the kidneys with a resultant increase in bicarbonate levels. Alkalosis also predisposes to digitalis toxicity. Careful monitoring of electrolytes is necessary with long term furosemide therapy because there may be significant loss of potassium. Potassium Chloride supplementation is required unless the potassium sparing diuretic spironolactone/dytide is given. When furosamide is given on alternate day, supplementation of potassium may be adequate to maintain normal serum potassium levels.

         Spironolactone is inhibitor of aldosterone and enhances potassium retention. Combination of Spironolactone and chlorthiazide is commonly used to eliminate the need for potassium supplementation.

      3. Afterload reducing agents

      Vasodilators

      Vasodilators reduce after load, increases the stroke volume without changing the contractility of the heart. Therefore the oxygen consumption of the myocardium is not increased. These agents are used with digitalis and diuretics.

      Indications of vasodilator therapy.

      1. Cardiomyopathy
         1. Dilated
         2. Adriamycin induced
      2. Hyper volumic states like some congenital heart diseases e.g. PDA, VSD, AV Canal with large left to right shunts, severe MR or AR.
      3. Systemic hypertension
      4. Post operative cardiac status

      After load reducing agents are divided in to three groups.

      1. Arteriolar vasodilators e.g. hydralazine These augment cardiac output by altering arteriolar bed with resulting reduction of the after load.
         Diuretic Agents and Dosage

         Drug	Route & Dosage	Comments
         Hydralazine	IV 1.5ug/min or 0.1 - 0.2 mg/kg/dose every 4 - 6 hours. (Max. 2mg/ kg 6hrs)	It may cause tachy cardia and it may be used with propranolol. May cause G.I. symptoms neutropenia and lupus like syndrome
         Nitro-prusside	IV 0.5-8ug/kg/min	May cause thio-cyanate toxicity e.g. nausta, fatigue, disorientation and hepatic dysfunction
         Nitro-glycerine	IV 0.5-2.0Ug/kg/min(Max 6mg/kg)	Start with a small dose and titrate, based on its effects.
         Captopril	New born 0.1-0.4 mg/kg/dose1-4 times/day Infant 0.5-6.0 mg/kg/day1-4 times/day Child 12.5 mg/dose1-2 times/day.	It may develop hypotension, dizziness, neutropenia, proteinurea The dose should be reduced in patients with impaired rental function.
         Enalapril	(0) 0.1mg/kg.	Pts. may develop hypotension, dizziness & syncope Once or twice a day.
         Prazosine(Minipress)	(0) 1st dose 5ug/kg increased to 25-150 ug/kg in four doses	Ortho static Hypo-tension

      2. Venodilators e.g. Nitroglycerine & iso sorbide-dinitrate. They act by dilating systemic veins and redistributing blood from the pulmonary to systemic circuit; with a resulting decrease in pulmonary symptoms.
      3. Balanced Vasodilators. They include angiotensin converting enzyme inhibitor (ACE inhibitors) e.g. captopril, enalapril. These agents are both arteriolar and venodilators.

      ACE Inhibitors

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      ACE inhibitors are substances which bind with the enzyme ACE and thus prevent the later from acting in its natural substrate ACE I to form the physiologically active ACE II.
      1. Present Status of ACE Inhibitors in CHF
         The benefit of these drugs as a part of triple drug therapy (along with digitalis & diuretics) is well established. But its role in a two drug regimen (with diuretics) is still not established, it may be preferable to digoxin in children.

         As a sole therapeutic agent, its role is not promising except when diastolic dys-function is predominant and diuretics & digoxin may cause some worsening effect.

      2. Contraindication: Regarding the use of ACE inhibitors in CHF:
         1. Impaired Renal Blood flow - renal artery stenosis & coarctation of aorta etc.
         2. Hypotension
         3. Aortic stenosis with CHF
      3. Side effects of ACE inhibitors
         1. Cough: It may be dry and severe enough to cause emesis. Enalapril has higher incidence of cough than captopril. Dose reduction was not effective in abating this symptom.
         2. Angioedema: Occurs within first few days of initiation of therapy.
         3. Hypotension: Therapy should be started with low dose
         4. Transient worsening of renal failure & hypercalcemia,
         5. Neutropenia, protein urea and impaired taste are some side effects associated with high dose captopril therapy.

      Drug Interaction

      Captropril has been reported to increase S.Digoxin by 25%, an effect not reported with Enalapril and Lisinopril.

      Hyperkalemia: When used with potassium sparing diuretics like spironolactone or when potassium supplement is used. These agents act on arteriolar and venous bed:

      Surgical Management

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      If medical treatment with previously mentioned regime does not improve CCF within a few weeks or months, one should perform either palliative or corrective cardiac surgery for the underlying cardiac defect.
      
      
      
      
      

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