My son George collapsed with a cardiac arrest during a 100 meters athletic event at his school. He did not regain consciousness and still in the hospital. 
Basic life support was started only after the ambulance crew arrived and when it was started George was pulse less, cyanosed and had a breathing rate of 2 breadth per minutes. His heart was in a condition called Pulseless Electrical Activity (PEA) and ambulance crew could not shock the heart using the defibrillator.  The duration he was without basic life support (cardio pulmonary resuscitation-CPR) after the cardiac arrest is approximately 15 minutes.  Then CPR was done throughout the ambulance journey to hospital and also in the hospital. Doctors after a great effort restarted George’s heart at the hospital after 1 hour and 6 minutes from the time of his collapse. Then he was kept in Intensive care for neurological protection at a controlled body temperature of 93 degree Fahrenheit (34 deg centigrade) for 24 hours.  CT scan was done and no brain haemorrhage was found.  However the brain damage was so severe due to blood starvation to the brain. 30 hours later in the hospital doctors confirmed that none of his basic brain function is working to sustain life.
During this time sedative drug s are momentarily stopped and Electro Cardio Grams (EKG)are taken . These EKGs are showing a long Q-T interval. Therefore it is decided that the cause of his cardiac arrest at his school playing field is Long Q-T Syndrome(LQTS). Since then his genes were tested for KCNQ1, KCNH2, KCNE1 andKCNE2 genes. No pathogenic variants were identified. All other immediate family members have been tested and none of them have LQTS.

My main three concerns are

1.  As a result of the prolonged cardiac arrest George had, his brain was severely damaged. The next organ most prone to sustain damage due to oxygen starvation is his heart muscle.  In addition his body metabolism subjected to cascade events of instability.  With no active functions in his brain I believe George is not able to restore his fluid balance, electrical activity and normal body metabolism at all.  Are these surrounding circumstances showing a long Q-T interval in his EKG? In other words; was the sequence of events George underwent after his cardiac arrest are responsible for long Q-T interval in his EKG , now rather than a genetic condition?
    
2. Ambulance crew could not use the defibrillator.  George’s heart was in a condition called PEA when the ambulance crew arrived. LQTS related arrhythmias can be shocked using defibrillator.  Is this mean that George’s cardiac arrest was not triggered by LQTS?
    
3. He was tested for legal and illegal drugs and results were negative. There was no brain haemorrhage. Deep vein thrombosis was ruled out as he had a 12 hour long haul flight 2 weeks earlier and was complaining about a pain in right thigh. What other possibilities existed for his cardiac arrest at his school playing field during the athletic event?. What are the main tests that can be done when he is still alive to eliminate all other causes and only to say it is LQTS?

   Any advice about possible tests to verify that George had LQTS is greatly appreciated.