CPR: WHEN TO START, WHEN TO STOP ?

Fluid Management in Children with Heart FailurePediatric Critical Care Working GroupMedan, 17 May 2013OutlineDefine pediatric heart failure (HF)Hemodynamic and pathophysiologyClinical manifestationsFluid strategy in management of pediatric HFIntroductionCardiac failure is a clinical syndrome where the heart is unable to provide the output required to meet the metabolic demands of the body.The causes and mechanisms are significantly different between adults and children. In adults, usually failure of the left ventricle, with the most common causes is coronary artery disease. 3In children, usually due to congenital malformations, such as lefttoright shunts. The function of the right and the left ventricles will be affected highoutput cardiac failure. Other significant causes is cardiomyopathy, which lead to low output cardiac failure. 4Blood PressureCardiac OutputSystemic Vascular ResistanceStroke VolumeHeart RatePreloadAfterloadContractilityHemodynamic and PathophysiologyDO2CaO2HbOxygenation5

Tissue edemaImpaired oxygenation and metabolite diffusion Distorted tissue architectureObstruction of capillary blood flow & lymphatic drainageDisturbed cell-cell interaction progressive organ dysfunctionConsequences of fluid overload

Flow across the cardiac shunt depends on:size of the defect.pressure difference.Blood will always flow from the high-pressure chamber to the low-pressure chamber. The larger the pressure difference the more blood will be shunted across the defect.In newborns:the pulmonary vascular resistance and the right heart pressures are high low-pressure gradient minimal flow across the defect. Cardiac pathophysiology in cardiac shuntsMurmurs heard are generated by turbulent blood flow across a valve mid-diastolic rumble.The heart chamber volume loaded and dilateContractility is well preserved until end-stage diseaseToo little SV reaches the systemic circulation poor perfusion stimulation of the neuroendocrine response: discharge of the sympathetic nervous system activation of the renal renin angiotensin system

Cardiac pathophysiology in cardiac shunts cardiac output (Q=HRxSV)maintain blood pressure (BP=SVxHRxR)fluid retentionCardiac pathophysiology in cardiac shunts

PDALA, LV enlargementIncreased pulmonary flowContinuous murmur due to flow during systole and diastole

ASDRA, RV enlargementIncreased pulmonary flowRelative PS murmur

Large VSDRV, LA, LV enlargementIncreased pulmonary flowRelative PS and MS murmur

AVSDRA, RV, LA, LV enlargementIncreased pulmonary flowRelative PS and MS murmurCardiac pathophysiology in cardiac shuntsShunt size is often expressed as a Qp:Qs ratio.Normal Qp:Qs is 1:1 equal flow to the lungs and the systemicA Qp:Qs >1.5:1 1.5 times more blood flowing through the lungs compared with the systemic circulation.Large cardiac shunts (Qp:Qs >1.5) are at risk to develop PHT Work of breathing Oxygen demandHypoxiaV/Q MismatchDilated vessels & heart chambersExternal bronchi compressionResistanceAir trapping Hydrostatic pressureCapillary leakPulmonary oedema ComplianceAtelectasisPeribronchial oedema Pulmonary flowFlow diagram of pulmonary pathological changes in large cardiac shunt lesionsPulmonary vasoconstrictionLocal inflammationStructural changesPHT RV afterloadRV failurePulmonary pathophysiology in cardiac shuntsTachycardia.Venous congestion:Right-sided: hepatomegaly, ascites, abdominal pain, pleural effusion, edema, jugular venous distention.Left-sided: tachypnea, retractions, nasal flaring or grunting, rales, pulmonary edema.Low cardiac output:Fatigue or low energy, pallor, cool extremities, and altered consciousnessSigns and symptomsCongestive heart failure:normal cardiac output: compensated inadequate cardiac output: decompensatedEjection fraction is not a pure measure of systolic contractility but is a measure of ventricular function which also depends on:Diastolic compliancePreloadAfterload.

16To balance the lung and systemic circulation. to limit lung flooding to limit systemic underperfusion. The mainstay of cardiac shunt treatment is diuresis.Once pulmonary over-circulation is recognised clinically/radiographically, diuretics should be startedMonitor Na +, K +, Mg 2+ and Ca 2+ (myocardial function is dependent on optimal electrolyte levels)Spironolactone is often added to counteract K+ lossesThiazides are used in neonates (less renal Ca 2+ loss)ManagementAssessment of fluid balanceInfants presenting with an intercurrent illness and poor perfusion should first receive a 5 - 10ml/kg crystalloid bolusPerfusion should be reassessed immediately after the fluid bolusInotropic supportIf perfusion remains poor after a fluid challenge, start dobutamine infusionToo high inotropic doses have been shown to cause myocardial damage in infants. The key is gentle inotropic support

General careOptimise the haemoglobin (Hb) to ensure adequate oxygen-carrying capacity to the peripheral tissues.

Bedside hemodynamic profiles in acute heart failure determined by the absence or presence of congestion (wet vs dry) and adequacy of perfusion (warm vs cold).

VasodilatorDiuretic

InotropeVasodilator

Body volume and fluid composition must be consideredin conjunction with all the inputs and outputs from the body

Other(5%)(15%)

Components of fluid balance calculation and fluid distribution in the body

Distribution of FluidsICFISFIVFDextrose 5%

RL, NaCl 0.9%

ColloidBloodPlasmaPlasma expanderCapillary wall (endothelial cells):Freely permeable to water and small molecules but not for protein such as albuminTBW devided into 2 compartments:

1. Intracellular fluid 40%2. Extracellular fluid 20%- Interstitial fluid 15%- Intravascular fluid 5%

Infants presenting with respiratory distress should be assessed for CHD as part of the differential diagnosisThe heart and lungs cannot be seen as separate entities in cardiac shunt lesionsThe main medical treatment for large cardiac shunt lesions is aimed at active pulmonary diuresisBlood flow should be balanced between the pulmonary and systemic circulationsGentle inotropic support should be used when perfusion is poorAttention should be given to nutritional support to all children with cardiac shunts

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