Balancing the heart & lungs final

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Balancing the Heart & Lungs in Cardiac Shunt Lesions Beyra Rossouw Intensive Care Unit Red Cross War Memorial Children’s Hospital Red Cross War Memorial Children’s Hospital University of Cape Town

Transcript of Balancing the heart & lungs final

Page 1: Balancing the heart & lungs final

Balancing the Heart & Lungs in Cardiac Shunt Lesions

Beyra RossouwIntensive Care Unit

Red Cross War Memorial Children’s Hospital Red Cross War Memorial Children’s Hospital University of Cape Town

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Scope of talk

• Cardiac symptoms of cardiac shunts

• Pathophysiology of lung disease

• Treatment principles

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LA & LV ENLARGEMENT

VSD Flow across VSD depends on:

•VSD size

•Pulmonary pressures

RIGHT ATRIUM

LEFT ATRIUM

ENLARGEMENT

↑Pulmonary vascular

resistanceSmall: PSMMedium: PSM & MDMLarge: ESM & MDM & loud P2

RIGHT VENTRICLE

LEFT VENTRICLE

Adapted from pediatric cardiology 5th edition, M Park

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LA & LV ENLARGEMENT

LATE VSD

RV HYPERTROPHY

RIGHT ATRIUM

LEFT

ATRIUM

RIGHT

VENTRICLE

LEFT

VENTRICLE

↑↑↑↑ ↑↑↑↑ PULMONARY VASCULAR

RESISTANCE

HYPERTROPHY

CYANOSIS

Eisenmenger

RV heave

Very loud P2

Murmurs softer

VENTRICLE VENTRICLE

Adapted from pediatric cardiology 5th edition M Park

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VSD pathophysiology

Reduced stroke volume to systemic circulation

Exposed to systemicpressures

Systemic circulationPulmonary circulation

Exposed to excess flow

Neuro -humeral compensation Q= SV X HR

Volume loading of left heart

Myocardial contractility failure

Pulmonary hypertension

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ASD

RV

RA ENLARGEMENT

RV ENLARGEMENT

Fixed split S2PS murmurTS murmur

Adapted from pediatric cardiology 5th edition, M Park

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LA & LV ENLARGEMENT

AVSD Flow across VSD depends on:

•AVSD size

•Pulmonary pressures

RIGHT ATRIUM

LEFT ATRIUM

RA & RV

ENLARGEMENT ENLARGEMENT

↑Pulmonary vascular

resistance

RIGHT VENTRICLE

LEFT VENTRICLE

ESM & MDM & loud P2

ENLARGEMENT

Adapted from pediatric cardiology 5th edition, M Park

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PDA

LV

LA ENLARGEMENT

Flow across PDA depends on:

•PDA size

•Pulmonary pressures

RA LA

RV LVLV ENLARGEMENT

Continuous murmur

Lungs

↑Pulmonary vascular

resistance

RV LV

Adapted from pediatric cardiology 5th edition, M Park

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“Cardiac failure”a misnomer in shunt lesions

Myocardial contraction function preserved till end stage BUT ………

A large % of stoke volume is pumped away

through shunt to RV

instead of aorta

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Cardiac failure symptoms

• Neuro- endocrine compensation for low cardiac output– ↑Sympathetic discharge

• Tachycardia • Vasoconstriction • Sweaty• Sweaty

– ↑ Renin-angiotensin: • Na & H2O retention • Vasoconstriction

• Chamber dilatation• Flooding the lungs

– Increase flow

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Respiratory effect of cardiac shunts

• Pulmonary edema

• ↑ Airway resistance

• V/Q mismatching• V/Q mismatching

• Atelectasis

• Pulmonary hypertension↑Work of breathing

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Pulmonary edema↑ Hydrostatic pressure & ↓lymphatic clearance

• ↑Pulmonary arterial flow – Left to right shunts

• Pulmonary capillary leak– LRTI, sepsis, shock– LRTI, sepsis, shock

• Pulmonary vein congestion – ↑ Left heart pressure

• L heart obstructions

• LV failure

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Alveolar capillaries

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Consequence of pulmonary edema↑Work of breathing

• Interstitial edema– ↓ Lung compliance

– Compress small airways

Alveolar edema

Bronchus

Vessels

• Alveolar edema– Hypoxia

– Atelectasis

– ↓Lung compliance

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Effect of edema on airway resistance

Normal infant

Normal adult

1 mm Edema

4 mm

8 mm

Resistance: ↑16xCross sectional area:↓ 75%

Resistance: ↑3xCross sectional area:↓ 44%adult

Resistance = 1radius 4

Cross sectional area:↓ 44%

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Atelectasis• Pulmonary edema

– Destroy surfactant

• External airway compression– Dilated PA’s, LA, PDA– Bronchomalacia– Bronchomalacia

• Recurrent LRTI– Secretions

• Hepatomegaly & ascitis– Splint diaphragm

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O2

Venous Arterial

Sats

Sats 80%Sats 70%Sats 100%

V/Q mismatch

Sats70%

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Pulmonary hypertension

• ↑ Pulmonary flow & pressure

• Hypoxic vasoconstriction

• Recurrent LRTI → ↑inflammation in pulmonary vesselspulmonary vessels

S. Haworth Progress in Pediatric Cardiology 12(2001)

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Pulmonary hypertension

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IVS flattening in Pulmonary hypertension

D- shape LV Crescent shape LV

Normal

LVRV

D- shape LV Crescent shape LV

•LV D- shape in diastole = volume loaded RV•LV D- shape in systole & diastole = pressure loaded RV

LV LVRV RV

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Aspiration / GORD

• Feeding difficulty

• Aerophogia

• Esophagus compression

• Syndromes, VACTREL• Syndromes, VACTREL

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Poor growth & muscle mass

• ↓ Caloric intake

• ↑Caloric demand– ↑Work of breathing

Maintain cardiac output– Maintain cardiac output

• ↑Muscle fatigue

• ↓ Secretion clearing

• Poor cough →hypoxic

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Treatment

Goal: Optimize O2 Delivery to tissues

↓↓↓↓O2 Demand↑O2 Delivery

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Oxygen Delivery to Tissues

Ventilation

Gas exchange

O2 Delivery

Alveoli

O2 Delivery

O2 extraction

ATPCell

LVRV

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Treating the lungs

• Lasix for the lungs– Improve lung compliance– Watch elects

• Exclude / prevent aspirationExclude / prevent aspiration

• CPAP/ PEEP – Recruit atelectasis– ↓Alveolar edema– ↓Oxygen demand– ↓LV afterload

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Aims of ventilation• Adjust goals

– Sats in low 90’s

– Use Ph & PaCo2 to manipulate PVR

• Do not damage lungs– Maintain normal lung volumes– Maintain normal lung volumes

– Tidal volumes 6-8ml/kg, PEEP to recruit

• Pulmonary hypertensive – Comfortable, avoid hypoxia & stress

– Keep Mg+ high

Ventilate to manipulate pulmonary blood flow

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Overinflated lungs & capillary compression

Pulmonary vascular resistance vs lung volumes

Hypoxic vasoconstriction

West , Pulmonary pathophysiology: the essentials. 6th edition

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Oxygen damage: FiO2 > 0.6

• O2 toxicity →free radicals – Cell injury & DNA damage

• Worsen V/Q mismatch– ↓Hypoxic pulmonary vasoconstriction– ↓Hypoxic pulmonary vasoconstriction

• Pulmonary vasodilator

↓PVR:→ ↑L to R shunt

– ↑flooding lungs

– steel blood from systemic circulation

• Nitrogen wash out→ atelectasis

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Treating the heartOptimize O2 Delivery to tissues

• Hb: > 10-12g/dl

• ↑Stroke volume – Afterload reduction

• Myocardial contraction• Myocardial contraction– Optimize K+, Ca 2+, Mg+ & Glucose

– Low dose inotropes if ↑ lactate

• Do not ↑ myocardial O2 demand– Limit tachycardia,

– Keep comfortable

↑ Contraction will ↑ L to R shunt

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NORADRENALINE

ADRENALINE

αADRENALINE

β1 & β2

Inotropes ↑Stroke volume, ↑ HRVasoconstriction

ADRENALINE

DOPAMINE

DOBUTAMINE

NORADRENALINE

DOPAMINE

Pediatric Cardiac Intensive Care . Chang & Wernovsky

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Optimize nutrition

• Optimize caloric intake, vitamins & trace elements

• Do not restrict volume of fluids unless ventilatedventilated

• NGT fed if very tachypnea

• NJ fed if GORD suspected

• Educate parents

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General treatment

• Immunizations

• Dental care & education

• Surgery for large shunts– VSD ideal before 18 months– VSD ideal before 18 months

– AVSD ideal before 6 months

– Primum ASD at 2-4jr

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Take home message• In high pulmonary flow

– Diurese the flooded lungs– Maintain normal lung volumes– Limit lung damage

• In low cardiac output state• In low cardiac output state– Decrease cardiac work

• ↓ respiratory effort• ↓ afterload

• Attention to nutrition• Infection prevention

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