Sunteți pe pagina 1din 32

Fluid Management

in Children with Heart Failure

Pediatric Critical Care Working Group

Medan, 17 May 2013

Outline
Define pediatric heart failure (HF)
Hemodynamic and pathophysiology
Clinical manifestations
Fluid strategy in management of pediatric HF

Introduction
Cardiac 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.

In children,
usually due to congenital malformations, such as left
toright 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.

Hemodynamic and Pathophysiology


Oxygenation

Hb

Contractility

CaO2
Stroke
Volume

DO2
Cardiac
Output

Blood
Pressure

Afterload
Heart
Rate

Systemic
Vascular
Resistance

Preload

Consequences of fluid overload


Tissue edema
Impaired oxygenation and metabolite diffusion
Distorted tissue architecture
Obstruction of capillary blood flow & lymphatic drainage
Disturbed cell-cell interaction progressive organ
dysfunction

Cardiac pathophysiology in cardiac shunts


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 shunts

Murmurs heard are generated by turbulent blood flow


across a valve mid-diastolic rumble.
The heart chamber volume loaded and dilate
Contractility is well preserved until end-stage disease
Too little SV reaches the systemic circulation
poor perfusion
stimulation of the neuroendocrine response:
o discharge of the sympathetic nervous system
o activation of the renal renin angiotensin system

Cardiac pathophysiology in cardiac shunts

cardiac output (Q=HRxSV)


maintain blood pressure (BP=SVxHRxR)
fluid retention

Cardiac pathophysiology in cardiac shunts

ASD
RA, RV
enlargement
Increased
pulmonary flow
Relative PS
murmur

AVSD
RA, RV, LA, LV
enlargement
Increased
pulmonary flow
Relative PS and
MS murmur

Large VSD
RV, LA, LV
enlargement
Increased
pulmonary flow
Relative PS and
MS murmur

PDA
LA, LV
enlargement
Increased
pulmonary flow
Continuous
murmur due to
flow during
systole and
diastole

Shunt size is often expressed as a Qp:Qs ratio.


Normal Qp:Qs is 1:1
equal flow to the lungs and the systemic
A 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

Pulmonary
pathophysiology
in cardiac shunts

Pulmonary flow

Hydrostatic pressure

Dilated vessels &


heart chambers

Capillary leak
Pulmonary oedema

External bronchi
compression

Compliance

Resistance

Atelectasis

Air trapping

Local
inflammation

Work of breathing

Pulmonary
vasoconstriction

Oxygen demand
Hypoxia

Structural changes
PHT

Peribronchial
oedema

RV afterload
RV failure

V/Q Mismatch

Flow diagram of pulmonary pathological changes


in large cardiac shunt lesions

Signs and symptoms


Tachycardia.
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 consciousness

Congestive heart failure:


normal cardiac output: compensated
inadequate cardiac output: decompensated
Ejection fraction is not a pure measure of systolic
contractility but is a measure of ventricular function
which also depends on:
Diastolic compliance
Preload
Afterload.

Management
To 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 started
Monitor Na +, K +, Mg 2+ and Ca 2+ (myocardial
function is dependent on optimal electrolyte levels)
Spironolactone is often added to counteract K+ losses
Thiazides are used in neonates (less renal Ca 2+ loss)

Assessment of fluid balance


Infants presenting with an intercurrent illness and
poor perfusion should first receive a 5 - 10 ml/kg
crystalloid bolus
Perfusion should be reassessed immediately after the
fluid bolus
Inotropic support
If perfusion remains poor after a fluid challenge, start
dobutamine infusion
Too high inotropic doses have been shown to cause
myocardial damage in infants. The key is gentle
inotropic support

General care
Optimise 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).

Vasodilator
Diuretic

Vasodilator

Inotrope

Other

(5%)

(15%)

Body volume and fluid composition must be considered


in conjunction with all the inputs and outputs from the body

Components of fluid balance calculation and fluid distribution in the body

Distribution of Fluids
TBW devided into 2 compartments:
1. Intracellular fluid 40%
2. Extracellular fluid 20%
- Interstitial fluid 15%
- Intravascular fluid 5%

ICF

ISF

IVF

Dextrose 5%
RL, NaCl 0.9%
Colloid
-Blood
-Plasma
-Plasma expander

Capillary wall (endothelial cells):


Freely permeable to water and small
molecules but not for protein such as albumin

Conclusions
Infants presenting with respiratory distress should be
assessed for CHD as part of the differential diagnosis
The heart and lungs cannot be seen as separate entities
in cardiac shunt lesions
The main medical treatment for large cardiac shunt
lesions is aimed at active pulmonary diuresis
Blood flow should be balanced between the pulmonary
and systemic circulations
Gentle inotropic support should be used when perfusion
is poor
Attention should be given to nutritional support to all
children with cardiac shunts

Thank you