CPR and Therapeutic Hypothermia Forum
Welcome to the CRS forum. The following are questions that we have received through our website. We are always happy to answer any questions you may have about CPR, therapeutic hypothermia, and cardiac arrests. Please note that the responses posted on this page are only opinions from our medical professionals. We do our best to answer these important questions, but we are dealing with a complex field and nothing below can be considered an absolute certainty. Thank you for your questions!
In addition, we have created the Penn Hypothermia Discussion Forum providing an opportunity for clinicians and medical professionals to discuss hypothermia implementation success stories and challenges. To request information or become a member of this forum, please email Audrey Blewer at audrey.blewer@uphs.upenn.edu.
Top FAQs:
-Cold fluid via central line & temperature issues
-Neuroprognostication
-Temperature monitoring options
-Coagulopathy issues and Lab values
March 25, 2011
Q: Do you initiate/complete for all causes of arrest, including respiratory that leads to cardiac?
A: Yes; if comatose after arrest, of any type, we treat (with caveat of above).
-David Gaieski, MD
Q: Will you initiate/complete TH on patients who have a baseline CPC of 3 or 4, if known?
A: In general, no. This is a complicated question because it is pretty clear that TH confers a survival as well as a neurological benefit. However, none of the studies or implementation studies/databases included patients w/ the baseline CPC you are describing and so it is impossible to know if the survival benefit is experienced by that patient population as well.
-David Gaieski, MD
March 22, 2011
Q: Have you read any research that specifically addresses outcomes in regard to time it took to reach target temperature? I'd like to find some data to support cooling SOONER rather than LATER after ROSC. Why is 6-8 hours after ROSC the cutoff? Worse outcomes?
A: There are very little data on this… 6-8 hours is mentioned only because that was the average time to target temp in the randomized trials from 2002 (the HACA and Bernard trials). Based on a number of animal studies, we think cooling earlier is better, but no clinical studies have conclusively shown this.
-Benjamin Abella, MD
February 2, 2011
Q: I am teaching staff and one of my colleagues questioned why a hemorrhagic bleed would be contraindicated. I explained that hypothermia increases the incidence of coagulopathies, however he brought up a good point, if we are treating post arrest, the chance of an MI is there, therefore they will go to the cath lab.... were anticoagulation is started. So what do you do and how can I explain that?
A: Good questions – while true that TH may increase the risk and/or severity of bleeding (i.e., cooling causes coagulopathy) – the extent of this increased risk is small. Therefore it’s a question of balancing risks and benefits. If someone has clinically dangerous bleeding (big GI bleed or brain bleed, for example), something that could worsen this would be high risk. If someone is on heparin, Coumadin, or going to the cath lab, without actual clinical bleeding, the risk is small, so its much more comfortable for us to proceed with TH.
It’s kind of analogous to the treatment of elevated INR. If someone’s INR is found to be very high, you might just give vitamin K if there is no actual bleeding (low risk for bad outcomes). But if an INR is very high AND they are coughing up blood (high risk for bad outcomes), you wouldn’t rest with just vitamin K, you would also give FFP and/or other clotting factors.
-Benjamin Abella, MD MPhil
December 14, 2010
Q: I understand that hypothermia causes decreased cardiac output, but how much?
A: Cardiac output decreases 25-40% depending upon exact target temperature and is mostly relatted to bradycardia; this is usually more than balanced (in regard to oxygen delivery) by decreased metabolism (and decreased oxygen consumption) so that the oxygen delivery/consumption profile is improved.
Q: What effect does a temperature of 33 degrees ALONE have of ejection fraction?
A: Mostly related to bradycardia. See previous comment above.
Q: Combined with a stunned myocardium, 1 day post MI, is there any value to this ECHO?
A: Yes, there is a value to the ECHO as it is telling you what the patient's EF and wall motion are @ that time; most of the stunning from arrest is reversible; the injury from MI leading to arrest is dependent upon how quickly reperfused, how much was penumbra vs. necrosis, and effects of TH on myocardial recovery; Data suggest good outcomes can be attained in this exact patient population if IABB, inotropes, and aggressive post-cath care is used in conjunction with TH.
Q: How long after the patient has been rewarmed would we be seeing "real" LV function data on ECHO?
A: The change in EF related to TH itself will go away as the patient is rewarmed and heart rate increases; the myocardial stunning of post-arrest period usually resolves by hour 40 or so; the injury from MI is dependent upon how much necrosis occurred.
-Dave Gaieski, MD
November 29, 2010
Q: How does TH affect lab values?
A: The main effect of TH on lab values is on blood gases. Need to know whether your lab corrects values or not to the body temperature. In other words, most blood gas analyzers warm blood to 37 degrees C before running; some labs report the values @ 37 degrees C, others @ the patient's temp @ time labs were drawn. That is what you need to know to manage the patient clinically.
Can approximate as follows:
for every 1 degree
C below 37 degrees C, for PO2, substract 5 mmHg; for PCO2, substract 2 mmHg; for
pH, add 0.012.
-Dave Gaieski, MD
November 19, 2010
Q: What is the danger of infusing large quantities of cold IV fluids via a SC, IJ or PICC? My understanding is potential arrythmias.
A: This is a theoretical concern, that is why we recommend chilled saline via peripheral IVs, preferably in the antecubetal location. Adequate peripheral access (2 minimum) should be obtained in the peri-arrest period and these can be used for induction of TH while central venous access is obtained.
-David Gaieski, MD
November 16, 2010
Q: Is any time delay recommended to see what the neuro assessment is prior to sedating and cooling?
A: The way we do this at our institution, if there is a question regarding neurological status of a patient right after the arrest and sedation was given, sometimes, we will wait an hour, let the medications wear off and then decide if they are waking up. And by waking up I mean following commands appropriately. The patient has to be able to give a thumbs up or squeeze your hands appropriately for us to decide not to cool. Just moving extremities or "reaching of the ET tube" is not, for our determination, following commands appropriately. In our protocol we go with a Glasgow Motor Score of <6, which is not following commands, since a GMS of 6 is "following commands". I would recommend using GMS over the full GCS.
We always error on the side of cooling, since there are very little risks and very big benefits. We reason that we only have one chance to save the brain and if we decide not to cool because they some what look like they might be following commands or opening their eyes, there is no going back and we have lost our chance.
As always, these things are a case by case basis. If they arrested in the field and they are already paralyzed and sedated, we may just cool regardless.
-Marion Leary BSN, RN
Q: I heard recently that a rectal temperature is contraindicated in a pt post MI. Can you explain to me why that is?
A: The general concern about rectal temperatures post-MI is that it might stimulate the vagus nerve and cause bradyarrhythmias. There aren't a lot of data to support this. Some institutions have successfully used rectal temp probes in post-arrest patients (without reported increases in bradyarrhythmias), though we don't feel this temp modality is as accurate as esophageal or bladder.
-David Gaieski, MD
October 06, 2010
Q: Can you tell me your experience with temperature monitoring - rectal probe, bladder probe etc.?
A: We use the temperature probe foley at Penn. If the patient is not producing enough urine (4cc/hr) we will put in an espophgeal probe. We try to stay away from rectal probes as there is a temperature lag that could be dangerous when initiating cooling. There was a Case Study published in 2009 that showed a significant delay between esophageal temperature (core temp) versus rectal probe. The patient was given saline boluses and the esophageal probe showed a temperature of 33.5 at 19 minutes while the rectal probe had the patient temperature at 35.5 at 19 min. The concern is that you could over-cool a patient and get into a dangerous range (30 degree C or lower) where ventricular rhythms could occur. There is also a lag with bladder temperature as well, but it is more evident with the rectal probe.
-Marion Leary BSN, RN
August 10, 2010
Q: What does the evidence say about neurological assessment after a cardiac arrest patient is brought back to a normothermic level? Are there studdies available on how long we need to wait and be patient to see if the patient will make further progress?
A: In terms of neurological prognostication after cardiac arrest, currently the standard guidelines are to not neuro prognosticate until at least 72 hours post ROSC, by that time the patient should be re-warmed. Although the guidelines say 72 hours we have seen in our patients a range anywhere from 2 day post ROSC up to 14 days or more, with the average being 3-5 days. There was a Consensus statement put out by the International committee on Resuscitation, for which the AHA is a part of, which explains why older neurologic prognostication tests are not reliable and it also goes into more detail about prognostication in this population. There are new International/AHA guidelines coming out at the end of this year, so things may change even more, we will just have to wait and see.
-Marion Leary BSN, RN
Q: We have only recently (in the last year) developed our order set and protocol for therapeutic hypothermia in cardiac arrest. In our first 14 patients, we have had trouble getting to our goal temperature very quickly. I think much of this is a learning curve. I've seen that some facilities have a "Code Ice" team that is paged with any cardiac arrest patient to help facilitate the process. I'm thinking of initiating that here. I see from your website that you have a "Resuscitation Team", and I was wondering about that ... is this different from your code blue team? What are their responsibilities?
A: Thanks for the email. Our resuscitation team is different than our hospital code team. We (the resuscitation team) do not respond to codes in the hospital for the purpose of “coding” the patient, but will follow up after every code to assist with hypothermia eligibility if the patients get their pulse back and then if the patient is eligible for cooling we will assist the team in getting the protocol started and will follow the patient throughout their course of hypothermia care. We are available to the treating team 24/7 with any and all hypothermia and post-resuscitation questions. We may be a little different as one of our physicians is actually credentialed to leave notes in the chart as an actual resuscitation consult, although that may not be necessary for what your needs are, which sound like assisting the teams in initiating hypothermia more quickly.
I think that starting that type of service is definitely a good way to get hypothermia started more quickly, and it is always helpful to have a hypothermia champion within any given hospital, but it is also very time intensive depending on how you set it up.
-Marion Leary, RN, BSN
August 6, 2010
Q: At our small community hospitals our
ED docs are concerned about inserting
alines. Without residents and a "cool
team" on call, who inserts the aline is still undetermined. We will have to call the on call surgeon to come in and insert the aline.
My concern is that the patients will be at goal when they arrive in the ICU, or even in the ED after EMS starts the process. I know getting a radial aline will be very difficult, how about a femoral aline, have you had trouble with that when the patients are cooled?
A:We would not delay implementation of therapeutic hypothermia because of questions of who is going to place the arterial line. If the patient is at goal on arrival to the ICU, the benefits of that probably far outweigh the increased difficulty of placing a radial a-line in a patient vasoconstricted from therapeutic hypothermia. You have to work within the resources of your system and if the emergency physicians are not going to place a-lines but will start hypothermia then those constraints can be worked within to set up a successful program.
You are correct in saying that a radial arterial line may be more difficult to obtain in these patients but experienced providers such as the on call surgeon you are consulting should be able to achieve placement of radial a-line in a number of patients (especially if they are using ultrasound to assist them). Femoral a-lines are a completely reasonable alternative and remain easier to place properly in hypothermic patients because of the size of the femoral artery. Our standard approach is not to delay induction of therapeutic hypothermia to attempt a-line access; to make a few attempts at a radial a-line, then proceed with femoral access if necessary, with or without ultrasound guidance.
Hope this is helpful.
-David F. Gaieski, MD
February 2, 2010
Q: Has your facility done any research on the survival of morbidly obese patients who suffer cardiac arrest? Some specific concerns:
Are we able to deliver enough joules?
How effective is manual CPR for obese patients vs average wt. patients?
Are there mechanical devices available to provide compressions for obese patients?
Is special airway equipment available for the obese patient?
A: We have not specifically examined outcome differences in morbidly obese patients who suffer cardiac arrest versus patients with normal BMI. This is an important question, however, and one I am interested in examining. I am just finishing up a paper on BMI in severe sepsis and septic shock, which shows no differences in outcomes (but differences in sources of infection) in the morbidly obese versus non-obese.
We have noted challenges in reaching target temperature in therapeutic hypothermia in morbidly obese patients but have not yet systematically studied the topic. We have successfully treated a >150 kg post-arrest patient using therapeutic hypothermia and our post-arrest algorithm. The patient was discharged to home in pre-arrest condition with normal mental status.
The issue of quality of CPR (QCPR) in the morbidly obese is an important issue.
We are currently trialing the Lucas mechanical compression device in our ED and it will fit many obese patients but there is a limit in the AP diameter it can accept and we were unable to use it on one patient who was approximately 300 pounds.
Regarding your other questions, I am attaching an abstract from Dana Edelson, at University of Chicago, and some of my colleagues at CRS, which addresss many of the QCPR issues.
Regarding airway management--the most important issue with intubating the morbidly obese is positioning, not specialized equipment; placing the patient on a ramp of folded towels or a commercially available ramp, which helps achieve proper head positioning, is the most important single intervention that can be performed; if a morbidly obese person is positioned properly and remains unintubatable, an algorithm for rescue airway management should be in place at the institution - we typically use a CMAC as a video-assisted rescue device if the patient is able to be ventilated and a King airway or LMA if the situation is more tenuous.
-David Gaieski, MD
Abstract link: Click here for the abstract
December 14, 2009
Q: Thrombocytopenia is considered a contraindication for TH - is there a platelet level you would consider as an absolute contraindication in the absence of bleeding? AND if hypothermia was initiated post arrest , at what platelet count would you consider stopping the protocol and rewarming?
A: The exact risk of bleeding during therapeutic hypothermia (TH) is not known. TH has been used safely with thrombolytics and anticoagulants although this has not been carefully investigated. None of the large studies involving TH for cardiac arrest, stroke, or intracranial hemorrhage have reported large increases in bleeding. At 35 deg C, a mild decrease in platelet counts and qualitative dysfunction of platelets is seen, while at temp < 33 deg C, clotting factors will begin to be affected. That being said we do not have an absolute platelet count as a contraindication in our protocol. The only contraindications we have in terms of bleeding are if there is an intracranial bleed, bleeding due to significant trauma, or clinically relevant bleeding from other sources (GI bleed, dialysis graft bleeding etc). You can also consider prophylactically transfusing platelets (if it is not contraindicated for the patient) for counts < 20K with no bleeding, and < 50K with active bleeding. These are just our protocol recommendations, they have not been validated by scientific studies. I can not give you an absolute platelet count that I would not cool or stop cooling when present as It really depends on whether the patient is actively bleeding as well as many other patient specific factors. The risk of spontaneous bleeding from thrombocytopenia is classically noted at 20K so you may want to use this number, but again we may choose to cool someone with a platelet count below 20K if the specific situation calls for it. Bottom line is that in patients who are coagulopathic, the risk of bleeding should always be weighed against the benefits of cooling on a case by case basis.
November 9, 2009
Q: We have had several TH patients who were also Code Mi patients. Cardiologists have had questions regarding
TH and these patients, specifically whether spasm is more easily
induced or if medications such as bilvalirudin and thrombolytics
interact with TH. Are there any resources or studies on
this specific patient population? I have had little
luck with a literature search - what do you see in clinical
practice?
A: You ask an excellent question - alas, there are very little data published on the specifics of PCI/cath and cooling. The only data that DO exist suggest that morbidity and mortality of combining therapeutic hypothermia (TH) and cath is not worse than cath itself (so that, in aggregate, TH doesn't make things worse) - but no data are published on specific issues with drug metabolism, coronary flow, etc. I can say that we have performed cath on a number of patients while cooled and things seem about the same with regard to medication use, etc. We definitely need more research in this area.
-Benjamin S Abella, MD
July 27, 2009
Q: I can find references that say that overshooting the target temperature (too cold) is harmful and that rapid rewarming can create instability. Is there literature that addresses potential harm of mild fluctuation in temperature during the treatment period of 24 hours?
One of the selling points used by many of the equipment vendors is the claim that their equipment is superior at maintaining the temperature exactly at 33 degrees a high percentage of the time. Is there evidence to indicate that this is most beneficial or that failure to provide this is potentially harmful? Is time frame from initiation until reaching target temperature a higher priority in achieving the best outcomes or is steady maintenance a higher priority? Have protocols that use only iced IV fluids and conventional cooling blankets with less precise temperature maintenance been associated wtih worse outcomes?
A: As you have pointed out there are references for overshooting the target temperature (including my colleague Raina Merchant's paper from 2006) and for the potential risks of rapid rewarming. There is less available on the clinical relevance of variations from the target temperature during maintenance phase related to different devices. Hoedemaekers and colleagues published a paper in Critical Care looking at the speed of cooling and degree of variation with different devices but this didn't address clinical outcomes/relevance (Hoedemaekers CW, et al. Crit Care. 2007; 11(4): R91). It is highly unlikely that 0.3 degrees C variation versus 0.6 degrees C variation is clinically relevant. There currently is no evidence that such tight control is clinically relevant--that doesn't mean data won't emerge at any point.
A large French study comparing surface cooling to endovascular cooling has been completed and is being prepared for press. I don't know the results but one of the questions they will likely address is the precision of maintenance of target temperature. Joe Ornato in Richmond has discussed improvement in their outcomes after they switched from surface to endovascular cooling and attributes some of the improvement to the speed of cooling but this is not a randomized controlled trial.
As you have pointed out many of these details are "selling points" of different devices and focusing too much on those points is, to some extent, missing the forest for the trees. The important point is cooling and high quality ICU care. The recent publication by Friberg and colleagues (Neilson et al, "Outcome, Timing, and Adverse Events in Therapeutic Hypothermia After Out-of-Hospital Cardiac Arrrest," Acta Anesthesiol Scand 2009; 53: 926-936) doesn't discuss variation from goal temperature but does suggest NO relationship between time to target temperature and outcome (median time from arrest to goal temperature [< 34 degrees C] was 260 minutes, IQR 178-400 minutes). I always try to keep in mind that the two landmark studies (NEJM, 2002; 346) used fairly primitive cooling equipment (Bernard-->ice packs; HACA-->forced cold air blankets that were ineffective enough that 70% of the patients required supplemental ice packs) to achieve the statistically significant improvements in neurologic outcomes (Bernard and HACA) and mortality (HACA) that are the foundation for current therapy.
-David Gaieski, MD
June 18, 2009
Q: In a patient with cardiomyopathy EF 15%, and severe pulmonary hypertension RSVP in 60's, who arrests in hospital, what are your thoughts about post-arrest cooling potentially exacerbating pulmonary HTN and myocardial oxygen demand in a pt vulnerable to re-arresting? -Baltimore, MD
A: The use of hypothermia is definitely not without risks for complex patients such as this - alas, no clear data exist to answer your question, but I suspect one could still cool such a patient but with extreme caution.
What we often do, as a matter of practicality, is to cool more "gently" (only to 34 C) in such patients, under the assumption that this mild degree of cooling, while still supported by clinical data and AHA guidelines, might provoke less untoward hemodynamic effect.
-Benjamin S. Abella, MD
April 21, 2009
Q: Have you used Therapeutic Hypothermia in patients with non-cardiac etiologies for arrest? Specifically, we are looking at whether to cool overdose patients, and also we had a young man attempt suicide by hanging. We used TH in both, but ran into logistic issues when MICU critical care attendings balked at taking care on TH patients, as literature generally supports use only in cardiac arrest.
A: Yes, we use hypothermia on most etiologies of arrest – and this seems to be the practice of many other hospitals that use hypothermia. There are growing data from various case series reports that other arrest rhythms and causes of arrest benefit from hypothermia as well. However, we don’t use hypothermia for non-arrest situations (if your near-hanging or OD patients didn’t actually arrest from their problems, we wouldn’t have cooled them).
-Benjamin S. Abella, MD
February 12, 2009
Q: If an athlete gets hot while playing outside with temp of 102 and he is immersed in a tub filled with ice, is there any danger of V.fib or other risk to the patient?
A: I am not aware of any risk of VF or other serious health risks to the rapid sudden cooling of a healthy person with hyperthermia, unless the patient was overcooled to a core body temperature of less than 30 C, when VF becomes a risk.
-Benjamin S. Abella, MD
February 9, 2009
Q: It seems to me that the primary damage mechanism as described by the article is oxidation by free radicals. Have you considered other methods of limiting the supply of oxygen? I am not a medical professional, but my image of a person being resuscitated involves chest compressions, electric shocks if necessary, and an oxygen mask. What would happen if instead of giving the patient extra oxygen, you gave them a limited supply of oxygen, intentionally keep the o2 level provided to the patent low through using a N2 rich blend of breathing air. You could monitor the oxygen levels in the blood and gradually bring them back up so that you don’t cause cell death. Keeping the oxygen levels low might be less traumatic to the patient than intentionally causing
hypothermia.
A: We have been considering a clinical trial of this, although there are some complex issues to figure out (how to easily manage the O2 “ramp up”, what the comparison group should be in a trial, etc). Stay tuned!
-Benjamin S. Abella, MD
February 2, 2009
Q: I just read the article about you, Benjamin Abella and your research on hypothermia in Popular Science (Carnett, J.B. "Cold Relief" Popular Science 274(2) Pg. 54-59). Very interesting, but I was struck by how hard it was to get someone cold quickly. I just watched a TED talk by Peter Ward on mass extinctions and how breathing hydrogen sulfide can help lower body temperature. I don't know much about animal physiology, but perhaps breathing hydrogen sulfide while being on an "IV slushee" would make a person become colder faster.
A: It turns out that this is a gas of great current interest, it also appears to have cell-protective properties in small quantities. A number of laboratory experiments in simulated cardiac arrest are underway using this fascinating molecule … stay tuned! Not quite ready for human testing, I suspect. It’s a tricky gas, and can be toxic at higher doses.
-Benjamin S. Abella, MD
January 13, 2009
Q: Could a Thermosuit spinoff, a 'Neck Vest' that both braces the neck and supercools it immediately, be used in cases where someone gets the same type of SCI, (Spinal Cord Injury) that crippled actor Chris Reeve, which happens a lot in sports arenas and car wrecks, to use cold temperatures in the area of their SCIs so that they DON'T get paralysed later on?
A: This is indeed an area of active investigation at a number of research centers around the country, especially the Miami Project to Cure Paralysis, a research group at the University of Miami. Many investigators believe that hypothermia, such as via a neck cuff as you describe, may hold great promise to prevent paraplegia or other injury from spinal cord trauma.
-Benjamin S. Abella, MD