Download Guidelines for Postoperative Care of Tetralogy of Fallot Hala Agha, MD

Guidelines for Postoperative Care
of Tetralogy of Fallot
Hala Agha, MD
Professor of Pediatrics & Pediatric Cardiology
Children Hospital, Cairo University
Tetralogy of Fallot
TOF represents approximately 10% of cases of
congenital heart disease.
Tetralogy of Fallot
1. RV outflow tract obstruction, usually
infundibular and/or valvular pulmonic
stenosis
2. VSD, usually large, subaortic,
perimembranous, and nonrestrictive
3. Right ventricular hypertrophy, usually
concentric
4. Rightward deviation of the origin of
the aorta, over-riding the VSD
Natural history of TOF
Natural history is determined mainly by the
degree of RVOT obstruction.
Surgical treatment of TOF

Palliative surgery
Blalock-Taussig shunt to
secure pulmonary blood
flow

Total surgical correction
The goals of total repair OF TOF
– To close the ventricular
septal defect
– To open the RV outflow
obstruction, and
– To repair any pulmonary
artery stenosis
Conditions which may complicate the
postoperative care of the child with TOF are
the following:

Right ventricular dysfunction

Residual VSD

Residual RV outflow tract obstruction

Arrhythmias
Right ventricular dysfunction
This may occur by the cumulative effects of:
1-Right ventriculotomy
2-Inadequate myocardial protection
3-Residual RVOTO ( infundibular, valvular stenosis, hypoplasia or stenosis of distal pulmonary
arteries)
4-Pulmonary regurge caused by placement of transannular patch. Sudden reperfusion of the
lungs and the use of by pass may produce pulmonary edema on the basis of altered
pulmonary capillary permeability. Other contributing factors to respiratory failure include
residual VSD, presence of large collaterals ( manage with diuretics).
5-Residual VSD.
Suspect RV dysfunction in TOF repair:

Hypotension

Raised CVP

Large liver

RV function is described as restrictive since
the problem is predominantly poor RV
compliance.
Restrictive Physiology of RV

Restrictive physiology of RV after TOF repair is defined by the need to maintain CVP to
maintain cardiac output.

CVP causes 3rd space accumulated in the pleural and peritoneal cavities as well as
peripheral edema.

Because of low CO, 3rd space is not easily removed by diuretic and may interfere with
mechanical ventilation and organ function.

Clinically is diagnosed by low CO, slower postoperative recovery & persistent pleural
effusion.
Restrictive Physiology of RV

Classic Echo finding shows forward
flow of blood across pulmonary valve
with atrial systole. Typically recovers
in 3-5days.

Restrictive physiology of RV may
predict a more favorable long term
outcome specially in patients with
significant pulmonary regurge.
Clinical assessment of cardiac output
PHYSICAL
EXAMINATION
Low cardiac output
Adequate cardiac
output
PERIPHERAL PERFUSION
Poor capillary refill
Good capillary refill (<3 secs)
CORE-PERHIPERAL TEMP.GRADIENT
>3 C
<3 C
PULSES
Impalpable or weak peripheral pulses
Full peripheral pulses
URINE OUTPUT
< 1 ml/kg/hr
>1 ml/kg/hr
MENTAL STATUS
Combative, disorientated
Co-operative
ARTERIAL PRESSUREWAVEFORM
Dichrotic notch soon after peak
Dichrotic notch occurs later
BASE DEFICIT
Base excess > -5 mmol/L
Base excess < -5 mmol/L
LACTATE
>4 mmol/L
<2mmol/L
BLOOD PRESSURE
Refer to age – related
normal
ranges
Treatment of RV dysfunction

Manage with volume and optimize RV filling and RA pressures of-15mmHg to
18mmHg may be necessary to ensure left sided filling and adequate systemic output.

Inotropic support with dopamine, dobutamine or milrinone .

-Maintain AV synchrony. Increase heart rate either pharmacologic or with pacing
wires are usually required to improve cardiac output .

Ventilator maneuvers to reduce pulmonary vascular resistance and may reduce the
afterload on the RV .
-Particularly in infants, opening an atrial communication may be beneficial
Treatment recommendations for phosphodiesterase
inhibitors (milrinone) in TOF:

It is recommended that milrinone be considered for any patient following
TOF repair to prevent the occurrence of low cardiac output due to
restrictive right ventricular physiology after TOF repair.

It is recommended that milrinone be started for any patient with a right
atrial pressure >15 mm Hg or with signs or symptoms of low cardiac
output.

The recommended loading dose of milrinone is 50 mcg/kg over 30 to 60
minutes followed by an infusion at 0.375 to 0.75 mcg/kg/min.
Mode of action of Milrinone

Milrinone is classed as an INODILATOR
(inotrope with vasodilator properties).

It appears to selectively inhibit
Phosphodiesterase enzyme 3 (PDE 3),
which results in an increase in intracellular
c-AMP and alteration in intracellular and
extracellular calcium transport and relax
arterial and venous smooth muscle.

Milrinone may have synergistic activity
with catecholamines.
Guidelines on the use of Milrinone
Indications for use:

Congestive Heart Failure

Low cardiac output states following cardiac surgery

Patient’s refractory to escalating doses of catecholamines.

Prophylaxis in patients at high risk of developing low cardiac output
syndrome (LCOS) following cardiac surgery e.g. Arterial switch, TOF
Milrinone
Parameters to monitor

Blood Pressure

Heart Rate

Platelet counts

Renal function

Peripheral perfusion
Side effects
Increased heart rate, risk of arrhythymias, thrombocytopenia,
Hypotension, insomnia, nausea and vomiting, diarrhoea.
Residual VSD

In the operating room, if the post-repair pulmonary
artery saturation is normal and TEE is performed, the
likelihood of undetected residual ventricular septal
defect (VSD) is very low.

The sutures securing the VSD patch may tear and an
unimportant left-to-right shunt may not be tolerated
well in a patient with poorly compliant ventricles
and/or pulmonary regurgitation.
Residual VSD

A hemodynamically significant leak will
result in elevated heart rate, left atrial
equal to or exceeding RA pressure, and PA
saturation (>80%). Findings such as
these warrant investigation with
echocardiography and early reoperation is
required.
RV outflow tract (RVOT)
obstruction

Post-repair right ventricular pressure may be satisfactory when measured
in the operating room, but RVOT obstruction may become more apparent
later.

Moderate amounts of residual RVOTO are often well tolerated in the early
postoperative period but it is associated with development of ventricular
dysrhythmias later.

A patient who has suboptimal postoperative recovery, with high RV/LV
pressure ratio, may need to return to the operating room. If a transannular
patch was not performed initially, it should be considered.
Arrhythmias

Complete heart block

Right bundle branch block

Junctional ectopic tachycardia (JET)

Ventricular Arrhythmias
A-Complete heart block

It is often transient.

3-5% patients.

A permanent pacemaker system may be
required if CHB persists more than 2weeks.
B- Right bundle branch block

RBBB can be expected on the postoperative ECG in all patients
who have undergone a right ventriculotomy.

Peripheral conduction across the infundibulum is slowed. Rarely
does this represent injury to the His-Purkinje system.

The presence of left anterior hemiblock may lead to complete
heart block. AV pacing should be used in these patients .
C - Junctional ectopic tachycardia
(JET)

JET is a potentially serious rhythm
which usually occurs in the early
postoperative period.

ECG reveals AV dissociation with a
rate as high as 200-230/min.

The very rapid ventricular rate and
lack of atrial contribution to filling
can produce hemodynamic
compromise and cardiac output may
be seriously affected .
JET Management

Hypovolemia, anaemia and metabolic abnormality (hypokalemia,
hypocalcemia, hypomagnesemia) should be corrected.

Induction of hypothermia or at least correction of fever, suppresses
automaticity and may slow JET. This entails use of cooling blankets, ice
bags, cold gastric lavage, sedation with fentanyl, and muscle relaxation
with vecuronium. A decrease in core temperature to 34 degree will reduce
HR to 150-160/min (provided there is no metabolic acidosis.

Reduction in catecholamines ,

Atrial pacing to restore AV synchrony; such as overdrive atrial pacing to
induce 2:1 or paired ventricular pacing may be effective.
JET Management

Medications :
1-Digitalization may lower the rate.
2-Amiodarone: (oral or IV) to lower the ventricular response and convert
JET to normal sinus rhythm.
3-Procainamide: type IA antiarrhythmic agents
4-- Others agents: propafenone (IV), propanolol and verapamil. They
may slow the rate or induce 2nd degree A-V block which slows the
ventricular response.

In extreme cases when JET is refractory, emergent cryoablation for the His
bundle.
D- Ventricular Arrhythmias

Ventricular arrhythmias may lead to late sudden
death.

This is usually the result of reentrant ventricular
tachycardia arising from the site of ventriculotomy
scar.

Patients with ventricular ectopy and residual RVOTO
are at the greatest risk for VT.
Sum-up

Don’t extubate the patient with heomdynamic instability and
low CO.

Do echocardiography within the 1rst day of postop to assess
RV compliance and restrictive physiology pattern, residual
shunt, RVOTO.

Volume augmentation and maintain high CVP in patient with
poor RV function.

Early decision to add milrinone once sign of low CO was
evident.
Thank You