Published
Therapeutic hypothermia for cardiac arrest survivors has been shown to improve neurologically intact survival. Precise temperature control is important to evaluate because unintentional overcooling below the consensus target range of 32–34°C may place the patient at risk for serious complications ie: arrhythmias. Hypothermia itself causes cardiac arrhythmia as well as the electrolyte imbalances that accompany hypothermia like K+, Mg and Photos. All which cause arrhythmias when low. Add this to an already irritated myocardium and it spells arrhythmia. Flip flopping the patient can also irritate the myocardium further stressing the myocardium and precipitate arrhythmia. Does every facility not turn? Maybe not. I am however surprised that they don't paralize to minimize rigors which increase acidosis and lactic acid futher producting an arrythmia prone enviorment.
So in this arrythmia prone enviorment leaving the patient unstimulated may have it's benefits. I hope this helps
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Oh MomRN, don't get me started on the central access problem in our ICU. Most patients don't have central lines. "Decreased risk of infection!". Give me a break. I agree with what you said. It's very stressful trying to find a vein on an emedetous, clamped down pt, with a AV fistula in one arm. We have loads of pts with IVs in legs/feet.
At my facility when a patient is put on "hypothermic protocol," we almost always put the patient on some kind of paralysis. Usually an atracrium drip to titrate using the train of four. The rationale for paralyzing the patient is to prevent them from shivering and increasing oxygen demand for the tissues, which would be the exact opposite thing to do in this scenario. Especially since many hypothermia patient's are on high FiO2s and PEEPs on the ventilator. When the patient's muscles are contracting, the body will resort to lactic acid metabolism due to the lack of excess oxygen for use in the body. This allows lactate to build up which will make the patient even more acidic, as if this was not already a problem since the patient was most likely a full arrest and had NO oxygen supply for some time. Not to mention that when a patient is cooled to 33 degrees, all the vessels are going to vasoconstrict like no other. Most often, patient's on hypothermia are VERY unstable and on multiple pressors so we always have atleast one central access, and an arterial line for appropriate blood pressure monitoring and pressor titration. (Atleast that I have seen so far.)
In addition, we do serial chemistrys every 4 to 6 hours depending on the physician to monitor electrolytes, especially potassium because cooling the body and rewarming causes a potassium shift into the cells and then back into the bloodstream respectively. I have never seen a hypothermia patient not have atleast a central line. That seems very crazy and scary to me! That would drive me insane, haha. The last patient I had who was cooled was on multiple drips: fentanyl, versed, atracrium, levophed, neosynephrine, vasopressin, sodium bicarb, and insulin.
In order to monitor that the patient is adequately sedated, we recheck the train of four q 4 hours to verify that the patient has 1 to 2 twitches, showing adequate paralysis.
May I just ask at the risk of sounding completely daft, how does paralyzing prevent increases in lactic acid formation? Thank you in advance :-)[/quote']Of course you may......
Because it stops the movement of the muscles involved with the rigors caused by the hypothermia. Lactic acid is indeed due, in part, to constant muscle contraction. Lactic acid is created when the muscle burns sugars (in whatever form) without the presence of oxygen, anaerobic metabolism. So you have a lot of lactic acid building up. Normally it gets squeezed out by normal muscle movement and lymphatic fluid, into the lymphatic ducts, where it is processed and eliminated from the body. Which does not happen in this critical population therefore causing metabolic acidosis which can lead to arrhythmias.
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maloneys
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I used to work for a trauma hospital, and we often had neurotraumas that we kept hypothermic. Assuming they were stable enough, we turned q2h. Now I work in a diff. peripheral hosp. We accepted a post arrest pt and we're cooling her. Nurses say not to turn hypothermic pts as it can cause fatal cardiac arrythmias. Pt is stable. No drip, except Versed. Does this make sense??