Deep Hypothermic Circulatory Arrest (DHCA), is a concept discussed here in this forum, as well as a significant perfusion event when it comes to the horizon.
Obviously an issue for aortic dissections, transections, or congenital malformations that require a surgical approach and repair that can only be accomplished by intermittent or momentary cessation of blood flow to the head (brain).
There are so many theories and approaches associated with DHCA- and they lie beyond the scope of this post- however I was having an interesting discussion with a colleague of mine who as of late has employed nitroglycerine as a vaso-dilatory strategy effecting very rapid cooling for patients requiring cerebral protection ASAP- as well as global cooling at the microvascular level.
It made sense to me, as long as mean arterial pressure drops don’t represent a caveat to adequate tissue perfusion, but the point that was intriguing, was the speed @ which he was able to achieve sub-20 degree (Celsius) global temperatures for a run of 4 patients, all of which recovered absent any discernible neurological deficit.
So my question to you is this: Have you employed this technique- or would you consider it? What is your opinion regarding the theory?
Please offer any opinions or suggestions in the comments section?
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What Happens When the Brain Cools Down ?
“Hypothermia is the most efficient measure to prevent or reduce ischemic damage to the central nervous system when blood circulation is reduced. The central nervous system has a high metabolic rate and limited energy stores, which make it extremely vulnerable to ischemia. Because the central nervous system is the organ that is most sensitive to ischemia, attention has been mainly centered on neurologic outcome when perfusion was reduced, with the indirect assumption that, if the brain or the spinal cord could tolerate undamaged the reduced perfusion, the other organs would too.”
Consequences of circulatory arrest in relation to temperature and duration of cerebral ischemia. The light color depicts the periods of safe circulatory arrest. The dark color depicts the periods of obligatory harmful circulatory arrest. The transitional area depicts the periods where the risk and extent of brain damage are dependent on the conduct of surgery and pharmacological intervention. The light gray area is compatible with reversible deficits, while the dark gray area is associated with irreversible injuries.
Autoregulation vs Global Pooling
preserves autoregulation of brain perfusion and optimizes cellular enzyme activity. Because of blood alkalemia,the curve of oxyhemoglobin dissociation is shifted toward the right, corresponding to an increased affinity of oxygen for hemoglobin.
With the further shift of oxyhemoglobin to the right due to hypothermia, the availability of oxygen carried by the hemoglobin molecule becomes tremendously reduced.
At deep temperature reductions, oxygen diluted in blood represents the major source of oxygen to tissues.
The pH-stat strategy
results in a powerful and sustained dilatation of the cerebral vessels because of the high level of carbon dioxide. Autoregulation of brain perfusion is lost and cerebral blood flow greatly increased.
The time for temperature equilibration between blood and brain is shortened, resulting in a quick and homogenous cooling of the brain.
Hypercapnia shifts the oxyhemoglobin-dissociation curve toward the left and results in an increased availability of oxygen to tissues.
Is there a Need for Speed ?
Oxygen availability is reduced during hypothermia because of the shift to the right of the oxyhemoglobin curve. The parallel decrease in metabolic rate is likely to preserve an appropriate balance between availability and requirement of oxygen.
During rapid cooling, however, the affinity of oxygen to hemoglobin rises sharply during the period that the tissue temperature is not equilibrated with that of blood.
This effect, combined with the dilution of blood by the priming volume of cardiopulmonary bypass, may temporarily create a state of insufficient oxygen availability.
Studies in animals confirm that expedited cooling associated with excessive hemodilution resulted in an uncompensated consumption of energetic molecules and in the development o fcellular acidosis before institution of circulatory arrest.
In one study, it was demonstrated that an increased concentration of hemoglobin was able to compensate for the decreased oxygen availability related to hypothermia.
Intracellular acidosis was not present with a hematocrit of 30%, mild with a hematocritof 20%, and severe with a hematocrit of 10%.40,41
Using microscopy, these investigators further established that the cerebral capillary flow was maintained despite increased blood viscosity (which is associated with high hematocrit values).41,42
These findings support the consensus that cooling should be performed slowly and with an adequate hematocrit.
Rewarming & Bringing Them Back
- Providing a favorable hematologic environment,
- ensuring optimal hemodynamic conditions,
- and avoiding cerebral hyperactivity should set the best conditions for optimal recovery of the energy-depleted brain.
- It is, therefore, important to restart perfusion slowly after circulatory arrest.
- An initial period of “cold blood–low-pressure reperfusion” washes out accumulated metabolites, buffers free radicals, and provides substrates for regeneration of high-energy molecules before the resumption of cerebral electrical activity.
- A sufficient hematocrit during this reperfusion period is theoretically attractive because of its buffer, redox, and free radical scavenging capacity.43
- Glycemia should be monitored closely and hyperglycemia treated aggressively. Hyperglycemia, stimulated by the release of endogenous catecholamines, increases intracellular acidosis and can prevent or delay the restitution of metabolic homeostasis.43
- During rewarming, cerebral vascular resistance and energetic metabolism are impaired in proportion to the severity of ischemia.44,45
- Cerebral perfusion is reduced, glucose is in part diverted to the less efficient anaerobic pathway, and oxygen coupling with the oxidative phosphorylation is disturbed.21
- During this time, an abnormally high extraction of oxygen and glucose is necessary to sustain the cerebral metabolic rate.45
- Jugular venous oxygen saturation is often below 40% during this recovering period.45
- Cerebral autoregulation may become unable to compensate for another reduction in oxygen delivery, which could occur with postoperative events like acute hypotension,hypoxemia, or anemia.
Integrated Cerebral Protection
Probably the safest approach to a patient requiring a long period of circulatory arrest resides in the integration of complementary methods of perfusion and monitoring.50
Retrograde perfusion of the aorta through the femoral artery should be avoided in the presence of a thoracic aortic aneurysm in order to reduce the risk of particulate dislodgment with embolization in the brain and myocardium.
Antegrade perfusion of the aorta is performed with cannulation of the ascending aorta or right subclavianartery. The body is cooled to 18°C.
Electroencephalogram and venous jugular saturation are monitored to ensure adequater eduction of cerebral metabolism.
Circulatory arrest is established only after electro-cerebral silence is obtained and jugular venous saturation is superior to 95%.
During the 10 to 20 minutes preceding circulatory arrest, the temperature of the perfusate can be lowered to 13°C to further reduce brain temperature and metabolism.
The arch arteries are connected to a graft (either with the use of a patch of aortic wall or separately), and antegrade perfusion of the brain is resumed before more extensive resection and repair of the aorta is performed.
When the risk of particle embolization to the brain is substantial (old age, severe atherosclerosis of the aorta, arch aneurysm with thrombotic material), a short period of retrograde cerebral perfusion can be performed to wash out the arch arteries before antegrade perfusion is definitively reestablished.50