Koolaid for ROSC

[FL_Medic]

This is the article from Newsweek, for more info & research check out WakeEMS.com or google the topic.

Byline: Jerry Adler

Consider someone who has just died of a heart attack. His organs are intact, he hasn’t lost blood. All that’s happened is his heart has stopped beating–the definition of “clinical death”–and his brain has shut down to conserve oxygen. But what has actually died?

As recently as 1993, when Dr. Sherwin Nuland wrote the best seller “How We Die,” the conventional answer was that it was his cells that had died. The patient couldn’t be revived because the tissues of his brain and heart had suffered irreversible damage from lack of oxygen. This process was understood to begin after just four or five minutes. If the patient doesn’t receive cardiopulmonary resuscitation within that time, and if his heart can’t be restarted soon thereafter, he is unlikely to recover. That dogma went unquestioned until researchers actually looked at oxygen-starved heart cells under a microscope. What they saw amazed them, according to Dr. Lance Becker, an authority on emergency medicine at the University of Pennsylvania. “After one hour,” he says, “we couldn’t see evidence the cells had died. We thought we’d done something wrong.” In fact, cells cut off from their blood supply died only hours later.

But if the cells are still alive, why can’t doctors revive someone who has been dead for an hour? Because once the cells have been without oxygen for more than five minutes, they die when their oxygen supply is resumed . It was that “astounding” discovery, Becker says, that led him to his post as the director of Penn’s Center for Resuscitation Science, a newly created research institute operating on one of medicine’s newest frontiers: treating the dead.

Biologists are still grappling with the implications of this new view of cell death–not passive extinguishment, like a candle flickering out when you cover it with a glass, but an active biochemical event triggered by “reperfusion,” the resumption of oxygen supply. The research takes them deep into the machinery of the cell, to the tiny membrane-enclosed structures known as mitochondria where cellular fuel is oxidized to provide energy. Mitochondria control the process known as apoptosis, the programmed death of abnormal cells that is the body’s primary defense against cancer. “It looks to us,” says Becker, “as if the cellular surveillance mechanism cannot tell the difference between a cancer cell and a cell being reperfused with oxygen. Something throws the switch that makes the cell die.”

With this realization came another: that standard emergency-room procedure has it exactly backward. When someone collapses on the street of cardiac arrest, if he’s lucky he will receive immediate CPR, maintaining circulation until he can be revived in the hospital. But the rest will have gone 10 or 15 minutes or more without a heartbeat by the time they reach the emergency department. And then what happens? “We give them oxygen,” Becker says. “We jolt the heart with the paddles, we pump in epinephrine to force it to beat, so it’s taking up more oxygen.” Blood-starved heart muscle is suddenly flooded with oxygen, precisely the situation that leads to cell death. Instead, Becker says, we should aim to reduce oxygen uptake, slow metabolism and adjust the blood chemistry for gradual and safe reperfusion.

Researchers are still working out how best to do this. A study at four hospitals, published last year by the University of California, showed a remarkable rate of success in treating sudden cardiac arrest with an approach that involved, among other things, a “cardioplegic” blood infusion to keep the heart in a state of suspended animation. Patients were put on a heart-lung bypass machine to maintain circulation to the brain until the heart could be safely restarted. The study involved just 34 patients, but 80 percent of them were discharged from the hospital alive. In one study of traditional methods, the figure was about 15 percent.

Becker also endorses hypothermia–lowering body temperature from 37 to 33 degrees Celsius–which appears to slow the chemical reactions touched off by reperfusion. He has developed an injectable slurry of salt and ice to cool the blood quickly that he hopes to make part of the standard emergency-response kit. “In an emergency department, you work like mad for half an hour on someone whose heart stopped, and finally someone says, ‘I don’t think we’re going to get this guy back,’ and then you just stop,” Becker says. The body on the cart is dead, but its trillions of cells are all still alive. Becker wants to resolve that paradox in favor of life.

[Just Plain Ruff]

Oh boy, now if we can only put a heart lung bypass machine on every ambulance as well as a cryogenic chamber on each pumper then we can beat back mr. Death with a stick.

[FL_Medic]

Oh boy, now if we can only put a heart lung bypass machine on every ambulance as well as a cryogenic chamber on each pumper then we can beat back mr. Death with a stick.

Sureley you have a better response than that. This procedure was performed on a 20 y/o [M] asystolic upon arrival, near-drowning. The patient was unresponsive for a week in the ICU, and as the doc was talking to the family about the horrible prognosis the pt called out "mom". I understand your statement in regards to the 90 y/o guy we are prolonging for a couple years, but for the young patient's with medical arrest...

[VentMedic]

Medicine recycles itself. Old practices becomes new again. Hypothermia and Cardiopulmonary Bypass were both popular in the ED in the 1980s. Both still stayed around primarily in Neo/Pedi, but re-emerged to the adult mainstream about 5 years ago.

We do one or both in the Neo/Pedi inside the hospital.

We do initiate hypothermia protocols in the ED for some adult cardiac arrests, case by case. Some doctors want to see it initiated for all, but there are other factors to consider.

There have been discussions again about initiating hypothermia protocols on the amubulances, but many do not carry paralytics to control the shivering. I do remember the early 1980s when we were packing ice around the heads of near-drowning victims. No easy task in Florida. Unfortunately in Florida, we have no body of water to chill a person and get the results as they have in Michigan or Minnesota.

[FL_Medic]

Yea, Wake county EMS doesn't even RSI any other patients, they added the meds specifically for this procedure.

[Just Plain Ruff]

Ok, show me anywhere in what you posted that said anything about a 20 year old male patient?

I was responding to the article you posted. If you are going to bring in more information please post that too.

[Just Plain Ruff]

Sureley you have a better response than that. This procedure was performed on a 20 y/o [M] asystolic upon arrival, near-drowning. The patient was unresponsive for a week in the ICU, and as the doc was talking to the family about the horrible prognosis the pt called out "mom". I understand your statement in regards to the 90 y/o guy we are prolonging for a couple years, but for the young patient's with medical arrest...

Just curious where did you get this information? I didn't see it referenced in the article you posted, I could not find it in the Wakeems.com site and I didn't bother to google it.

Please post where you got this information. You called my response into question and I'm doing the same to you.

[FL_Medic]

Here is some more research & text.

Summary

Purpose

We reported previously that therapeutic hypothermia with extracorporeal lung and heart assist (ECLHA) improved neurological outcome after 15 min cardiac arrest (CA) in dogs, although 45 min was needed to achieve hypothermia. We now investigate whether rapidly induced hypothermia with ECLHA (RHE) would result in a better outcome than slowly induced hypothermia with ECLHA (SHE) in dogs.

Methods

Fifteen mongrel female dogs were divided into two groups: an RHE (n = 7) and an SHE (n = 8) group. Normothermic ventricular fibrillation was induced for 15 min and the animals were resuscitated by ECLHA. Rapid hypothermia was induced with a heat exchanger added to the ECLHA circuit in the RHE group, and by immersing the drainage tube of the ECLHA circuit in an ice water bath in the SHE group. Hypothermia (33 °C) was maintained for 20 h. The dogs were weaned from ECLHA at 24 h after resuscitation and treated for 96 h; neurological deficit scores (NDS) were measured throughout this period.

Results

It took 1.6 ± 0.8 min to reach 33 °C in the RHE group and 49.5 ± 12.1 min to reach 33 °C in the SHE group. There was no difference in survival rate between the two groups. The NDS at 96 h in the RHE group was better than that in the SHE group (26% (range: 10–28%) versus 32% (26–37%); p < 0.05) although there was no significant difference in NDS between the two groups until 72 h.

Conclusion

Rapid hypothermic induction might be an important factor to improve neurological outcomes in prolonged CA models.

Body - Cooling Therapy Launches to Save Lives in Wake County

10/4/2006

Wake County will launch a new induced hypothermia therapy, to increase survival rates of cardiac arrest patients. Working together, Wake County EMS, WakeMed and Rex Healthcare will make Wake County only the third place in the nation to undertake this procedure, which requires inducement of hypothermia in the field and continued temperature-dropping therapy in two designated hospitals: WakeMed and Rex Hospital.

Picture: Tony Gurley, Chairman Wake County Board of Commissioners, introduces the hypothermia therapy while Brent Myers, Medical Director Wake County EMS System, watches.

Hypothermia is a well-known cause of death, but doctors and paramedics in Wake County are eager to take advantage of the incredible benefits of controlled cooling of the human body, or induced hypothermia, for cardiac arrest patients. A news briefing to announce and explain this exciting procedure will be held at the Wake County Emergency Medical Services (EMS) Training Facility on Wednesday, October 4, at 2:30 p.m. This is located in the Wake County Commons Building on Carya Drive, off Poole Road in Raleigh. Emergency medical physicians and staff will be available for interviews, and equipment used in Induced Hypothermia Therapy will be available for photos.

Wake County, WakeMed and Rex Healthcare are announcing that a community effort to coordinate field to hospital use of Induced Hypothermia Therapy will be launched in Wake County on Thursday, October 5, 2006. The Wake EMS System has worked with Rex Healthcare and WakeMed Health and Hospitals to implement this change in the standard of care that is consistent with recommendations from the American Heart Association. Based on studies in Denmark and Australia, this new treatment protocol could save the lives of an additional 10 people annually.

Some patients who regain a pulse after cardiac arrest suffer injuries from resumed blood flow to the brain too quickly, often resulting in brain death. Multiple studies have demonstrated improved neurological outcomes for patients who are cooled for the first 24 hours after they have return of pulse.

Wake County is already one of the best places in the nation to live if you suffer a cardiac arrest - your chances of survival are three times the national average, according to local EMS experts.

“Emergency response is well-coordinated here,” said Wake County EMS Medical Director Dr. Brent Myers. “Our emergency medical dispatchers in the 9-1-1 centers provide CPR instructions over the phone, our fire fighter first responders provide rapid defibrillation and excellent CPR, and our paramedics employ evidence-based, sophisticated advanced life support.” With induced hypothermia, Wake County’s potential outcomes will be even better.

powerpoint presentation on why it isn't popular yet:

www.uic.edu/com/ferne/slides/icep0404/hypothermia.pps

the protocol:

http://www.med.upenn.edu/resuscitation/hyp...miaProtocol.pdf

another abstract:

The effect of mild hypothermia and induced hypertension on long term survival rate and neurological outcome after asphyxial cardiac arrest in rats.

Hachimi-Idrissi S, Corne L, Huyghens L.

Department of Critical Care Medicine and Cerebral Resuscitation Research Group, Vrije Universiteit Brussel, Laarbeeklaan, 101, B-1090 Brussels, Belgium. ndphiis@az.vub.ac.be

STUDY OBJECTIVE: we studied the long-term effect of a combined treatment with resuscitative mild hypothermia and induced hypertension on survival rate and neurological outcome after asphyxial cardiac arrest (CA) in rats. METHODS: 36 male Wistar rats, were randomised into three groups: Group I (n=10): anaesthetised with halothane and N(2)O/O(2) (70/30%) had vessel cannulation but no asphyxial CA; mechanical ventilation was continued to 1 h. Group II (n=13): under the same anaesthetic conditions and vessel cannulation, was subjected to asphyxial CA of 8 min, reversed by brief external heart massage and followed by mechanical ventilation to 1 h post restoration of spontaneous circulation (ROSC). Group III (n=13): received the same insult and resuscitation as described in group II, but in contrast to the previous group, a combination treatment of hypothermia (34 degrees C) and induced hypertension was started immediately after ROSC and maintained for 60 min ROSC. Survival rate and neurological deficit (ND) scores were determined before arrest, at 2 and 24 h, and each 24-h up to 4 weeks after ROSC. RESULTS: Baseline variables were the same in the three groups. Comparison of the asphyxial CA groups (groups II and III), showed an increased, although not statistically significant, survival rate at 72 h after ROSC in group III, and it became highly significant at 4 weeks after ROSC. The ND scores were the same in both asphyxial CA groups (groups II and III). CONCLUSIONS: Resuscitative mild hypothermia and induced hypertension after asphyxial CA in rats is associated with a better survival rate. This beneficial effect persisted for 4 weeks after ROSC.

A good abstract:

Induced hypothermia after cardiopulmonary resuscitation: possible adverse effects

Download PDF | SIGNA VITAE 2007; 2(1): 15 - 17

Rudlof Milanovic

Department of Surgery,

University Hospital Dubrava Zagreb

Sanja Husedzinovic, Nikola Bradic

Department of anesthesiology, reanimatology and intensive care medicine,

University Hospital Dubrava, Zagreb

Gojko Susak Avenue No 6

10000 Zagreb, Croatia

Phone: +385 1 290 3197

Fax: + 385 1 290 3440

E-mail: nbradic@kbd.hr

Abstract

The last several years have seen an increased interest in the use of induced hypothermia after witnessed cardiopulmonary resuscitation (CPR). The main reason for its use is protection of the brain and hence, better neurological outcome in these patients. Therefore, induced hypothermia after CPR has become a part of standard recommendations in the 2005 Resuscitation Guidelines. At the same time, hypothermia can have many adverse effects. In the event of pre-hospital and/or in-hospital induction of hypothermia, without adequate monitoring and controlled cooling, hypothermia can cause serious complications, without beneficial effects on the brain. This article explains the most frequent adverse effects of hypothermia and possible hazardous outcomes for patients.

Key words: cardiopulmonary resuscitation, hypothermia, hemodynamics

Introduction

Interest in hypothermia for neuroprotection began in the 1980s. For some surgical procedures, primary cardiac and neurosurgical, hypothermia can be used for conservation of brain tissue and decreasing cerebral metabolic oxygen rate (CMRO2). States of strongly controlled and deep hypothermia are usually achieved using cardiopulmonary bypass devices and neuroprotective agents combined with brain monitoring.

The last several years have seen an increased interest in the use of induced hypothermia after witnessed cardiopulmonary resuscitation (CPR). The main reason for its use is to protect the brain against irreversible hypoxic damage and hence, to achieve better neurological outcomes in these patients. For these reasons, induced hypothermia after CPR has became a part of the 2005 Guidelines for Resuscitation (1).

Clinical purpose

By definition, hypothermia is a body temperature less than 36 oC and it is divided into three stages: mild hypothermia, when the body temperature is between 35 oC-32 oC, moderate hypothermia when the body temperature is between 32 oC and 30 oC, and deep hypothermia when the body temperature is less than 30 oC. Methods for decreasing core temperature have varied. In animal studies, cardiopulmonary bypass, cold aortic flush, external cooling and peritoneal cooling are some examples of the methods that have been used. Clinical studies have been performed using external cooling with icepacks, forced cooled air or a cooling helmet device or by using a rapid (30 min) intravenous infusion of a large volume (30 ml/kg) of lactated Ringer's solution, cooled at 4 oC. The main problem with all of these methods is the slow decrease in core temperature. The measured drop in temperature was between 0.3 oC/h for forced cooled air (2), 0.9 oC/h for icepacks (3), and the highest decrease in core temperature (1.7 oC) was reached with fluid administration (3). All of the above mentioned methods do not provide a quick and safe means of decreasing core temperature. In pre-hospital and/or in-hospital induction of hypothermia, without adequate monitoring and controlled cooling, hypothermia can cause serious complications, without beneficial effects on the brain.

Adverse effects of hypothermia on the heart and hemodynamics

The adverse effects of hypothermia mainly disturb heart function and function of the vascular system. It is known that more than 80% of all cardiac arrests are caused by presumed cardiac disease, of which more than 60% of adult deaths result from coronary heart disease (4). According to these data, cardiac and hemodynamic disturbances are augmented by hypothermia. Firstly, after return of spontaneous circulation (ROSC), following ventricular fibrillation, the myocardium shows huge electrical and mechanical instability. This instability may cause refibrillation within a short time after ROSC. Refibrillation is especially dangerous if cooling starts immediately after ROSC and if performed by emergency medical personnel, as reported by Nolan et al (5), and Bernard et al (3). In comparison with normothermic myocardium, the fibrillating hypothermic myocardium is characterized by increased contraction amplitude (6), decreased contraction velocity (6) and a decreased median fibrillation frequency (7). These characteristics of the fibrillating hypothermic heart may contribute to a reduced efficiency of electrical counter shock therapy, as observed in both experimental animals and humans (8-10). Electrophysiological changes associated with ischemia are similar to those induced by hypothermia (11). As mentioned earlier, most cardiac arrests are a consequence of myocardial ischemia. Thus ischemia may potentiate the arrhythmogenic potential of hypothermia (11). Improving myocardial perfusion by increasing coronary perfusion pressure (CPP) may reverse some of the electrophysiological changes and improve the outcome of CPR. This increase in CPP was associated with a significant improvement in defibrillation success (12). To improve CPP it is necessary to involve vasoactive drugs. In a state of post CPR instability, these agents can also provoke malignant arrhythmias. These agents increase myocardial oxygen consumption, what in a state of compromised coronary circulation, can worsen myocardial ischemia and enlarge the infarction zone. On the other hand, it is known that receptors for inotropes and vasoactive drugs become unresponsive during hypothermia and that the action of these drugs shifts from the heart to the vasculature producing an undesirable increase in peripheral vascular resistance.

In one of the first studies about induced hypothermia, Bernard et al (3) had significantly higher values of systemic vascular resistance and lower values of cardiac index in a group of patients with hypothermia throughout the whole 24 hour period of treatment compared with patients in normothermia. This unfavourable effect was not commented on and outcome, according to their cardiac function after induced hypothermia, was not evaluated. Furthermore, in the same study, patients with induced hypothermia received much more epinephrine infusions.

In a newer study by Kliegel et al (13), was instilled 2000 mL of ice-cold infusions cooled to 4 oC via an endovascular catheter. The only hemodynamic monitoring was invasive arterial pressure monitoring. Except for 3 patients, all other patients had a cardiac event due to acute coronary syndrome (ACS). Unfortunately, there is no data on central venous pressures (CVP) and/or changes in pulmonary artery pressures during the cooling process with high doses of infusions. During ACS, especially with acute left ventricular myocardial infarction, the main problem is decreasing left ventricular compliance and diastolic dysfunction. These patients are very vulnerable to volume overload and rapidly develop pulmonary edema, which happened in this study in 7% of patients. There is no evidence in this study as to the reasons for pulmonary edema in these patients.

Adverse effects of hypothermia on other organs and organ systems

There are many adverse effects of hypothermia on the functioning of organs and organ systems. Firstly, hypothermia impairs immune function and leads to nosocomial pneumonia. Secondly, hypothermic patients with a core temperature 1.5 oC - 2.0 oC below normal (35.5 oC- 35.0 oC) have an approximately 19% rate of infection as opposed to a 6% rate of infection in normothermic patients. These findings may be a result of the fact that hypothermia increases a patients' vulnerability caused by vasoconstriction and impaired immunity. In a large European study (2) the incidence of sepsis was almost twofold higher in the group of patients randomised to hypothermia than in normothermic patients (7% vs. 13%).

The risk of infection can be augmented by poor glycemic control. An important side effect is insulin resistance and decreased insulin release. Other adverse effects in the gastrointestinal system are decreased gastrointestinal motility, raised serum amylase and liver enzymes which can produce metabolic acidosis as a result of increased lactate concentrations and increased production of free fatty acids, ketones and glycerol.

Intracellular movements of potassium, magnesium, and phosphate during hypothermia lead to lowered serum concentrations of these anions and may produce serious arrhythmias.

Hypothermia has several negative effects on the hematological system. Bleeding time is lengthened as a result of reduction in the number and function of platelets sequestered by the spleen and liver. The coagulation cascade may also be impaired, white cell count also decreases and their movement is also impaired.

Hypothermia produces significant altered actions of many drugs commonly used during the post-resuscitation period. The action of many agents used in CPR may be ineffective or occur with delayed action. Lidocaine has no documented beneficial effects during hypothermia. Clinical data suggest that amiodarone has an immediate antiarrhythmic effect, present already a few minutes after intravenous bolus administration (14,15), but in the state of hypothermia, amiodarone had no beneficial effects on the resuscibilty of the fibrillating hypothermic heart (12). In a state of hypothermia, non-depolarizing muscle relaxants with a predictable half-life, prolong their average duration of action more than double, with an unpredictable time of action.

Conclusion

The main reason why inducing hypothermia is now included in the new recommendations for CPR is to decrease the risk of hypoxic brain damage. Unfortunately, hypothermia may often cause very serious adverse effects or complications, which can be hazardous for the patient.

Many studies today, looking at induced hypothermia after CPR, are orientated exclusively on the neurological outcome of patients. In many of these studies there is no, or only very weak, evidence concerning functions and adverse effects of hypothermia on other organs or organ systems. Clinical follow-up of primary heart functioning after arrest is not well documented. Changes in hemodynamics during the first 24 hours after ACS may produce deleterious conditions for the patients, especially if relatively uncontrolled measures of cooling are used. Induction of core hypothermia using surface cooling blankets is a relatively slow process, especially when patients are vasoconstricted (16,17). On the other hand, the use of large amounts of ice-cold (4 oC) volume can decrease core temperature rapidly, but may be very hazardous in patients with unstable heart function and rhythm, and, finally, may cause depletion of platelets, leukocytes and impair coagulation function.

From all the studies, it is not clear in which real time it is best to perform induced hypothermia to achieve optimal neuroprotection. Data shows very different times from ROSC to applying hypothermia, regardless if it was started by emergency medical personnel on the field or by staff in the emergency departments/intensive care units.

In general, the use of induced hypothermia after CPR could be very dangerous if is not well controlled, especially if established in pre-hospital conditions. The final outcome, unfortunately, could be much more undesirable for the patient compared to the minimal improvement in neurological state.

A link to a PDF that briefly mentions it (#12)

http://www.emhealth.org/u_newsletter/June1306.pdf

There is more, but you have to dig. I will get all the human case studies I can find as well.

[FL_Medic]

Just curious where did you get this information? I didn't see it referenced in the article you posted, I could not find it in the Wakeems.com site and I didn't bother to google it.

Please post where you got this information. You called my response into question and I'm doing the same to you.

Dr Brent Myers was at Clin Con in Orlando last week. He showed us these case studies and I spoke with him after the conference. He has much more data, but hasn't published it yet because he needs more research to call it FACT. He is the medical director for Wake County EMS.

[VentMedic]

The simple Newsweek link is

http://www.msnbc.msn.com/id/18368186/site/newsweek/

I see you've done some serious research on the topic. Duke University was a leader in some of the data collection and articles published. I heard one of their physicians speak at an ATS meeting.

Intratracheal cooling will probably be the most practical for EMS if we can perfect a method. Liquid perfluorocarbons might not be the best for pre-hospital right now.

I haven't read through all of your protocols yet.

What are you using to chill the patient?