case scenarios atrial switch univentricular repair dr.yasser salem

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Case scenarios Atrial switch Univentricular repair Dr.Yasser Salem

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Case scenariosAtrial switch

Univentricular repair

Dr.Yasser Salem

The case of Dr. Marwa Khyry

Atrial switch ??

Atrio-ventriculo-arterial sequence

Atrio-ventriculo-arterial sequence

• Concordance

Normal sequence AV & VA

• Discordance

Reversed sequence AV & VA

Corrected TGA = AV discordance + VA discordance

Atrial switch

Corrected TGA = AV discordance + VA discordance

Corrected TGA = AV discordance + VA discordance

Atrial switch

Senning operationMustard operation

Anatomic consideration:

• RV facing systemic pressure

• Pulmonary hypertension may be present

• Baffle may leak or obstruct flow

• Suture line near the SA node

Atrial switchFunctional consideration:

Mysterious RV

Mysterious RV

CO

AFTERLOAD (MEAN PRESSURE)

RV LV

Positive inotropes

45 mmHg 150 mmHg

Mysterious RV

Ventricular interdependence

PVA

SVA

PVA

SVA

Atrial interdependence

Ventricular interdependence

• RV facing systemic pressure

• Pulmonary hypertension may be present

• Baffle may leak or obstruct flow

• Suture line near the SA node

Atrial switch

Functional consideration:

• Evaluation of RV function

• Evaluation of pulmonary pressure

• Evaluation of baffle status

• Evaluation of arrhythmias and pacemaker

Preoperative assesment:

Single ventricle physiology

Mixing lesions

• Defects with mixing of oxygenated and deoxygenated blood

• Partial desaturation lead to compensatory in red cell mass and increase 2,3 DPG with increase in blood viscosity.

Single ventricle physiology

• The driving force for Qp is SVC pressure

• Qp must pass through two separate and highly regulated vascular beds: cerebral and pulmonary vasculature

• Removes the left-to-right shunt and thus the volume load from the single ventricle

Single ventricle physiology

Single ventricle physiology

SVC Pressure

• Acute rise in SVC pressure

• Selection of patients with low PVR minimizes the risk from elevated SVC pressure

• Failure to maintain low SVC pressure lead to problems maintaining adequate SaO2

• Small veno-venous collateral vessel contribute to arterial desaturation

Single ventricle physiology

PSVC = PPA – PPV x

QPA : QSA

QPB : QSB

+ PLA

Single ventricle physiology

PSVC = PPA – PPV x

QPA : QSA

QPB : QSB

+ PLA

PSVC PLA- = PPA – PPV

xQPA : QSA

QPB : QSB

PSVC PLA-

=PPA – PPV

QPA : QSA

QPB : QSB

Minimize SVC Pressure

• Minimize use of positive pressure, including PEEP, following surgery

• Allow the end-expiratory lung volume to approximate FRC

• Minimal mean airway pressure and early extubation in patient with healthy lungs– Negative-pressure ventilation associated with increased Qp

• Higher airway pressure to maintain FRC in pneumonia or ARDS

• Aprotinin and modified ultrafiltration: transpulmonary pressure gradient, less pleural drainage, improved SaO2

Vascular Resistance

• Qp largely dependent on resistance of 2 highly but differentially regulated vascular beds

• Cerebral and pulmonary vasculatures– Opposite responses to changes in CO2, acid-base status,

and O2

– Qp dependent on venous return through SVC (largely cerebral blood flow)

– Hyperventilation following bidirectional cavopulmonary anastomosis impair cerebral blood flow and decrease SaO2

– Inhaled NO may be the best treatment for high PVR and low SaO2 after bidirectional cavopulmonary anastomosis

Volume Unloading

• The right-to-left shunt is eliminated and all Qp is effective pulmonary flow

• An acute increase in wall thickness and decrease in cavity dimension has been associated with improved tricuspid valve function

• Preload and afterload are both decreased• Change in ventricular geometry may increase

risk for systemic outflow obstruction in some

Single ventricle physiology

• Backward effect– Systemic venous congestion– Need for higher SVC pressure to drive flow in

the shunt

• Forward effect– Non pulsatile pulmonary flow– Left atrial filling totally dependant on pulmonary

flow– Systemic hypotension

Single ventricle physiology

• Pitfalls– Saturation is not sytemic pressure dependent

– Saturation is pulmonary pressure dependent

– All circulatory and ventilatory support should bedirected to:

• Lower PVR• Higher SVR• Higher Rt filling pressure(within limits)

Single ventricle physiology

• Pitfalls

(within limits)

↓PVR↑SVR↑CVP