HEART FAILURE
A condition where heart can’t deliver adequate COP that meet metabolic demand of the body .Cardiac work under different stress conditions :-
• Cardiac muscle compromise• pre-load
• after load
• premature heart
Heart failure
Heart failure
Body demands NBody demands
COPCOP N
A condition results in development of signs and symptoms of heart failure when there is no basic abnormality in myocardial function and the cardiac output is greater than normal .
Can be seen in anemia , hyperthyroidism , hypermetabolism.A-V fistulas
High output heart failure• Fetal
• PrematureCauses of HF
Severe anemia
SVT
VT
Complete HB
Fluid overload
PDA
VSD
HPT
Corpulmonale (BPD)
• Full term
• Infant – toddlerAsphyxial cardiomypathy
AV-malformation
Lt –sided obstructive lesions (COA, Lt heart syndrome )
Large mixing disease (single ventricle , TA )
VSD
Acute HPT ( HUS )
Anomoulus Lt coronary artery
Metabolic CM
Viral myocarditis
Kawasaki disease
SVT
• Childhood -Adolescence
Renal failure
Acute HPT (GN)Viral myocarditis
Thyrotoxicosis
Infective endocarditis
Cardiomyopathy
Corpulmonale ( cystic fibrosis )
SCA
Chemotherapy
Age dependant
According to severityClinical features
Severe : symptoms at rest
Less severe : symptoms even to mild activity but comfortable when quite
Less less severe : just vigorous exercise causes symptomsInfant
Tachypnea
Feeding difficulty
Poor weight gain
Excessive perspiration
Irritability
Weak cry
Noisy , labored breathing
Flaring of alae nasi
Intercostal and subcostal recession
Cardiomegaly invariably present
According to age
Hepatomegaly common
Gallop rythemJugular venous pressure difficult
Edema usually generalized ( eyelids , sacrum , and less often legs and feet)
Fatigue
Effort intoleranceCough
Dyspnea
Abdominal pain
systemic venous pressure hepatomegaly , jugular pressure
Orthopnea & basilar ralves variable
Edema usually in dependant parts
Cardiomegaly invariable
Gallop rhythem common
Dilated heart hologystolic murmur of MR , TR
Older children
• CXR : cardiac enlargement , pulmonary vascular pattern fluffy perihilar pulmonary marking suggestive venous congestion and acute pul. edema kerly b line
• ECG : ventricular hypertrophy , assess the cause , low voltage QRS , ST-T changes , evaluate rhythm disorder .
• ECHO ;ven. function ,shorting fraction(the difference between end-systolic and end diastolic diameter divided by the end diastolic diameter normaly between 28 and 40%
• Measure ejection fraction normaly(55%-65%)
• DOPPLER ECHO to calculate COP.
Diagnosis
• Oximeter decrease arterial O2 levels resparitory or metabolic acidosis or bothmay be present .
• 6-Hyponatremia renal water retention .
• 7- β-natriuretric peptide(cardic neurohormone) which increased in response to increased ventricular wall tension.
1-general measures:rest,o2,Na and fluid restriction
2-diurtics3-inotropic agents :digitalis dopamine ,dobutamine
4-afterload reduction hydralazine,nitoprusside,captopril,enalapril
5-other measures:transplantion,extracorporal membrane oxygenation,carvedilol(b-blocking agent)
treatment
General measures :
• child rest often , sleep adequately.• Exercise and sports contraindicated .
• When respond to treatment movement restriction modified .
Treatment
Diet :
• HF FTT because of metabolic requirement and caloric intake .
• caloric intake per ounze of infant formula, many infant not tolerate 24 cal/oz formula because of diarrhea .
• If severe and can’t suck N/G feeding is necessary.
• Low – Na formula not recommended so the best Na-low formula is human breast milk small fruqent feeding .
• In older children no added salt diet is recommended .
reabsorption of Na + H2O blood volume , pulmonary edema , ventricular filling pressure .
Lasix : most commonly usedInitial dose 1-2 mg/kg /dose i.v.
Chronic dose 1-4 mg/kg/day ÷ 1-4 times/day orally.
Aldactone inhibit aldosterone K retention need for K supplement ( 2-3 mg/kg/day ÷ 2 or 3 times).
Chlorthiazide occasionally used for less severe HF 20-40 mg/kg/day in dividing dose .
DiureticsHalf life = 36hr & 6 days if anuric .
Kidney eliminate digoxinRapid digitilization
Dosage according to age
Divide the dosage into 2 halves ( 1st given immediately & 2nd halves again divided into 2 halves which is given with 12 hr. apart.
Inhibits membrane Na,K-ATPase and increase intracellular Ca,improvees cardic contractility,increase myocardial oxygen consumption
digoxin
Premature =20 мg/kg
Full term = 20-30 мg/kg
Child + infant = 25-40 мg/kg
Maintainance
Start 12 hr after full digitalizationDose = 5-10 мg/kg /day divided into 2 doses .
ECG monitoring is required as baseline .
Baseline serum electrolyte is needed .• Factors increase digoxin toxicity :
• Hypokalemia• Hypercalcemia
• Hypomagnsemia
• Cardiac inflammation secondary to myocarditis.
• Renal failure .
• Hypothyroidism.
• Prematurity .
Extracardiac c/f : nausea , vomitting , diarrhea , feeding intolerance , blurred vision , yellow vision, vertigo, diplopia , photophobia.
Cardiac c/f :
BradycardiaP- R interval
Depression of AV conduction 2nd and 3rd degree heart block .
Toxicity
automaticity ……. Premature beatsParoxysmal SVT
VT
VF
Mx
Discontinue digoxin treatment
Draw blood for K, Ca , Mg , digoxin
ECG and monitor for arrhythmia .
If toxicity not severe + s.K normal discotinue and wait .
If low s.K add K
If ventricular irritability or tachycardia phenytoin or lidocaine
If ventricular extrasystole inderal
If slow heart rate atropin no response ventricular pacemakerFAB fragment of IgG digoxin AB (digiband ) . Each vial =40 mg = binds 0.6 mg of digoxin.
Dopamine;at low infusion rate dilate renal artery facilitating diuresis releases myocardial norepinephrine direct effect on B- receptorAt dose 2-10ug/kg/min
Dobutamine;B1 receptor agent often combined with dopamine
Epinephrine ;mixed alph and B-adrenergic receptor agonist use in cardiogenic shock and low arterial blood pressureInotropic agentes
Captopril/enalapril;inhibition of angiotensin-
converting enzyme ,reduces angiotensinII productionDose 0.3-6 mg /kg/day
S/E;hypotension,syncope weakness dizziness hyperkalemia maculopapular pruritic rash cough renal toxicity neutropenia
Nitroprusside;arterial and vvenous relaxation venodilation reduce preload.
Hydralazine;arteriolar vasodilator
Afterload reduction
One of the causes of tachyarrhythmia is SVT . These originate from an abnormal mechanism proximal to the bifurcation of the bundle of His.
Mainly caused by re-entry phenomenon through the AV node or through accessory conducting tissue pathways . The atria are exited through the aberrant retrograde entry causing circular movements of depolarization.
Supraventricular tachycardias
• Fetus : HF + Hydrops fetalis
• Infant : HF because of prolonged unrecognized tachycardia .• Heart rate :200-300 beats/min
• Irritable , restless, hepatomegaly, tachypnea ,fever , leuckocytosis.
• Children: abrupt onset and cessation
• Continue few min. to hrs.
• Ppt. by acute infection, sympathomemtic drugs , palpitation .
Clinical features
ECG
DiagnosisNarrow QRS complex.
P – wave visible in 50-60% of patients.
Heart rate 180-300 beats/min.
• Vagal stimulation : submersion of face in iced saline or place ice bag over face in infant. Or perform vagotonic maneuvers ( Valsalva , straining , breath holding , drinking ice water ,carotid sinus massage or firm abdominal pressure ).• Pharmacologic :
If stable i.v. bolus adenosine .
Verapamile contraindicated in children less than 1 year of age .
Treatment
If HF developed and urgent synchronized DC cardioversion 0.5-2 j / kg .
If convert to sinus rhythm keep him on maintenance ( either digoxin or propranolol )Other drugs for resistant cases
If still resistant radiofrequency ablation or surgical ablation .
treatment continue for minimum of 1 year then taper and monitor for recurrence .