An 18 years old male patient, with history of RV overload preoperatively, undergoes surgical closure of secundum ASD. After anesthesia induction in the OR, he has multiple runs of VT and so had to be put on emergency cardiopulmonary bypass. The surgery otherwise is uneventful. The defect is closed primarily without the use of any patch.. postoperatively he has low cardiac output , renal and hepatic failure and poor blood gases. ECHO shows global dysfunction and an EF 25%.Ck-MB is 246 U/L, and CPK is 4407 U/L and is on heavy ionotropic support. his condition gets worse only after extubation. what went wrong with this patient? i hope my seniors can guide me on this. thank you.
Was the shunt bidirectional. How much were preoperative pa pressure?
Dear Sir Ankush! the shunt was left to right and the properative PASP was 29 mmHg
Was the pump time too prolonged.The anaesthetist will have the answer.
A very uncommon situation as disfunction was severe after an unenventfull closure of ASD. Is this pte with pulmonary hypertension (he should be on cardiac cath for better diagnosis) and coronary ischemia some how as a patogenic cause? (myocardial cyntilography could be helpfull or NMR).
Diagnosis should be done along with therapeutic measures as vasodilators and betablockers.
Sir Edmar Atik, coronary ischemia because of air embolism seems an explaination to this but there were no compatible changes in the ECG. the Ck-MB and CPK were sky high only on the fourth day.. again not in favor of ischemia.
Very uncomon LV or RV dysfuncion in post-op of closure ASD.Ventricular tachcardia after anethesia induction could be the first cause of thiese complications
I centum agree with @ Joao, Ventricular Tachycardia could be the cause for the heart failure. Lack of coordinated atrial contraction in the setting of extreme heart rate in VT could cause acute cardiac failure from low cardiac output.
hi Imran
The case highlighted could represent the net result of intraoperative events including the intraoperative vts and bypass related event.
I would like to know what has been the trend after surgery is the ef improving or worsening. Rv dysfunction may manifest after the shunt gets cut off by closure of the ASD. Also LV dysfunction with high LVEds may not manifest if there is a ASD as there is egress of the blood through ASD. At this stage you need to follow the trend support RV . Lasix infusion and wait on it.
Dear Sir Neeraj Awasthy! the preoperative TEE says the LV size and function is normal but dilated RV. PASP preop was 29 mmHg. the moment the pt is extubated, the blood gases went worse.
The patient may have extra intracardiac anomaly such as partial pulmoary venous return anomaly especially if the mixt venous saturation is high, another TEE examination would be helpfull. Otherwise the VT induced heart failure is the probable reason.
The phisiolpahology of an ASD of more about 2:1 QP/QS is that : the LV that developed along the years to accept only small amount of blood (the big part of blood was shunting at the atrial level..) suddenly has to accept, after the closure, much more blood than before. Not all LV are able to do it (eg. olds, hypertensive, diabetics..and in general all patients having a diastolic dysfuncion... but also youngs if the shunt was so high to prevent a good anatomical development of the LV itself). Because of this sudden flow overload of the LV, the patient can experience a sudden failure of the LV with pulmonary oedema and reduced EF just after the closure of the defect. The way of treating of course is to redude preload and afterload pharmacologically in the first hours after the closure. Anyway a good echocardiographic study of the patient before the intervention, relating on several parameters like diastolic function, size of the LV, systolic function and so on, can give to the Heart Team an idea whether or not that LV will suffer hard or not when getting this sudden blood overload because of the closure of tye ASD.
The patient had the abnormality for 18 years. The left to right shunt may have overloaded the right side of the heart for many years. Right ventricular hypertrophy is not uncommon for theses patients. It may also be important to know what his preoperative Pulmonary artery pressures were. If they were very high then, right heart failure is not surprising. The low cardiac output from the right side would ultimately reduce the cardiac output from the left side.
I think that you have to reduce the preload and afterload to allow the RV to remodel and wait for an improvement. Measure your pulmonary artery pressures and see if they are very elevated. If so this has to be reduced
I have two remarks on this case:
The first one is that the first manifestation was VTs before bypass and this could be due to a coronary air embolism from infusion line. With mechanical ventilation the atrial shunt may be right to left.
The second is that you close the defect without patch, therefore the defect was small and probably the shunt was not very important. This patient was unlikely to have severe pulmonary hypertension.
An unexpected global dysfunction and especially with initial ventricular ectopic beats, tachycardia or fibrillation is a sign of coronary hypo perfusion.
VT is a result of acute coronary ischemia and likely from coronary air. Global air could result in minimal or no ECG changes. Would expect this to resolve during the pump run. However, the period of time required to get on pump could have resulted in some degree of global insult to the heart. Agree that there is likely another issue here as well and obstruction of the coronary sinus could result in this picture although another batch of air without proper deairing should have resulted in more arrhythmias. RV dysfunction is not unexpected after ASD closure with someone who has severe RV overload and possibly pulmonary hypertension. Was there a left sided SVC so that the heart had inadequate myocardial protection?
Roger L Royster, thank you for the comment.there was no left sided SVC in this patient.
Probably coronary issue secondary to ?air.. Or something gone wrong with myocardial preservation. Remember, ASD patients have early electrical and geometric changes as described by Santoro et al., which may be good substrate for sustained arrhythmia and its after effects.
Two or even three effects might be to consider:
ASD created left to right shunting (RV overload), thus precapillary pulmonary hypertension most likely lead to remodelling of pulmonary vessels (chronic).
Prior RV overload shifts to LV, causing higher wall tension and microstructural dilation.
Accelerated heart rate, wall tension and structural dialtion lead to less perfusion of coronary vessels.
All of these mechanisms should be well compensatable by a healthy heart...in this case they could have added up to the state this young patient was in.
Sad but interesting!
Mix of Coronary Air embolism,and chronic RV OVERLOAD and RV interdependence induced Lv dysfunction.of course you must rule out surgical CS obstruction.
Don't rely on inotropes and lasix not enough,POST OP ECMO support required
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