What does your institution use for cerebral protection during DHCA? I'm mainly interested in any barbiturate that you give or not give. What about propofol? How do you dose it?
DHCA and barbiturates
- Thread starter DrN2O
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We don't use barbiturates, propofol or anything else aside from packing the head in ice and innominate artery cannulation for antegrade cerebral perfusion.
Years ago, I saw an attending give a 1.5 mg/kg of lidocaine just before arrest to reduce neuronal activity, but I have not done it myself.
Years ago, I saw an attending give a 1.5 mg/kg of lidocaine just before arrest to reduce neuronal activity, but I have not done it myself.
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I hand the perfusionist about 3 mg/kg propofol and ask him to push it 15-30 sec before circ arrest.
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This is one of the few times I actually use the BIS. I do titrate a propofol gtt to a BIS of 0 prior to and during antegrade perfusion. We cool to 28. It's probably overkill, but whatever, doesn't hurt and may help.
I think using barbiturates is unnecessary, propofol accomplishes the same thing with less side effect IMO.
I have played with lido prior to DHCA also. I'll dig up the papers later if I have time. If I recall non-diabetics benefited from it somewhat. Then again, the techniques and patients in those studies were probably different from my population and surgical techniques.
As we all know, the most important thing is for the surgeon to be as fast as possible. The rest is just window dressing.
I think using barbiturates is unnecessary, propofol accomplishes the same thing with less side effect IMO.
I have played with lido prior to DHCA also. I'll dig up the papers later if I have time. If I recall non-diabetics benefited from it somewhat. Then again, the techniques and patients in those studies were probably different from my population and surgical techniques.
As we all know, the most important thing is for the surgeon to be as fast as possible. The rest is just window dressing.
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In the few cases I did during residency we used barbiturates once. I got them for the second case and the attending told me not to bother. In all cases the BIS went to 0 and remained there during DHCA.
We also gave propranolol at the request of the surgeon. His rationale was to decrease myocardial oxygen consumption and reduce incidence of fibrillation. I don't know if this is standard or not. It was where I trained, because it was one surgeon who did most of the DHCA cases.
To second what Hawaiian said, hypothermia and surrounding the head with ice + fast surgeon is what matters the most -- that's what I was taught.
We also gave propranolol at the request of the surgeon. His rationale was to decrease myocardial oxygen consumption and reduce incidence of fibrillation. I don't know if this is standard or not. It was where I trained, because it was one surgeon who did most of the DHCA cases.
To second what Hawaiian said, hypothermia and surrounding the head with ice + fast surgeon is what matters the most -- that's what I was taught.
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No pharmacologic agent has been shown to decrease neurologic deficits after DHCA. Both antegrade and retrograde cerebral perfusion improve outcomes. Hypothermia is the only effective way of reducing both the neurophysiologic ("housekeeping") and function (neuronal activity) oxygen demand. We typically do antegrade cerebral perfusion via axillary cannulation and a clamp on the brachiocephalic. We also use continuous EEG monitoring and will circ arrest after 15 min of electrocerebral inactivity. Ice isn't placed on the head (that doesn't make a difference because the skull is in insulator). The alternative is for the surgeon to place an additional cannula in the SVC and the perfusionist gives retrograde cerebral perfusion. The theoretical advantage to that is that there may be fewer emboli sent to the brain.
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For our PTE's perfusion gives 200mg propofol just prior to circ arrest (I think technically it's supposed to be 2.5mg/kg but it seems like they always just give the 20cc's). We cool to 18 and have a "polar shoulder" wrap around the head. 20 minutes of circ arrest on each side with a 10 minute reperfusion period between arrests. No anterograde or retrograde perfusion to the head of any kind. We confirm flat EEG prior to arrest as well. I think the propofol is really just a formality as the hypothermia is really what's providing the neuro protection as proman said. There is an old paper somewhere that shows you can also decrease housekeeping functions with lidocaine but it requires obscene doses (like 20mg/kg, I think they did it in dogs).
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Do you think it would make sense to include the azygos vein in the retrorgade flow so as to send some cold blood to protect the spinal cord as well? This would mean low SVC cannulation.
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At normothermia, brain injury occurs after around 4 min of circulatory arrest. Cerebral metabolism decreases by 6–7% for every 1°C decrease in temperature from 37°C; therefore, brain cooling results in a reduction in oxygen requirements. Circulatory arrest is typically undertaken at 18–20°C and a range of safe periods for DHCA have been reported at this temperature. Most patients tolerate 30 min of DHCA without significant neurological dysfunction, but when this is extended to longer than 40 min, there is a marked increase in the incidence of brain injury. Above 60 min, the majority of patients will suffer irreversible brain injury, although there are still a small number of patients who can tolerate this. Longer periods of DHCA are tolerated in neonates and infants compared with adults. It should be borne in mind that neurological injury may occur as a result of prolonged CPB and rewarming (
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In a recent survey of members of the Association of Cardiothoracic Anaesthetists, 83% reported using some form of pharmacological cerebral protection during DHCA in adult thoracic aortic surgery.4 Drugs used for this purpose included thiopental (59%), propofol (29%), and others (48%), most commonly corticosteroids.4 Thiopental and propofol have both been investigated at doses sufficient to cause burst suppression. Propofol does not appear to be associated with cardiac depression or delayed emergence from anaesthesia.5 Although the use of thiopental is associated with dose-dependent myocardial depression and delayed emergence, it does not adversely impact on the ability to separate from CPB. There is no evidence that either drug improves neurological outcome in adults.
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So you don't use any sedatives/ anesthetics at all? You just induce the hypothermia with them awake and they become unconscious from the cold itself?
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I take it you're a non-medical person digging up this old thread while looking into DHCA.
No, they are already under a general anesthetic when deep hypothermia is initiated. He just doesn't give additional drug to lead to burst suppression, relying instead on hypothermia to reduce the brain's requirement for oxygen, and selective perfusion of the brain to maintain some delivery of oxygen during the period of decreased demand.
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Oh I see, and once they has burst suppression from the hypothermia then cerebral perfusion was initiated with an ecmo machine?
I read that during instances of induced hypothermia (where the individual might not be sedated or unconscious as in this case) that shivering stops once the body researches a certain temperature threshold. What temperature is that at and why does shivering stop?
