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Oxygen Supply Sufficient To Sustain Heart During Hypothermia

Physiological keys to heart attack during rewarming still a mystery

BETHESDA, MD. (July 18, 2006) – Researchers from Norway may have ruled out insufficient oxygen supply to the heart as the critical variable in whether a mammal’s heart survives while in a hypothermic state.

Writing in the July issue of the American Journal of Physiology-Heart and Circulatory Physiology, researchers found no significant difference in the amount of oxygen available to the heart between rats exposed to one hour of severe hypothermia and rats exposed to five hours. However, the rats in the five-hour group were more likely to experience fatal heart failure during rewarming.

The issue is important because the rewarming of victims of severe hypothermia almost always causes heart failure of varying severity, but little is known about why that happens, said Torkjel Tveita, the study’s senior researcher. Tveita is an anesthesiologist who treats victims of hypothermia, including fishermen who have fallen into the frigid Norwegian waters, and cross-country skiers marooned in bad weather.

“We still do not know the pathophysiological mechanism of hypothermia, which is necessary to developing the best way to rewarm hypothermia victims,” Tveita explained. This study -- which examined the effect hypothermia had on the heart, not on other vital organs such as the brain -- is a step in that direction.

Timofei V. Kondratiev, Kristina Flemming, Eivind S.P. Myhre, Mikhail A. Sovershaev and Tveita did the study “Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?” The study is published by The American Physiological Society. The researchers are from the University of Tromsø (Norway) and University Hospital of North Norway.

“Due to the limited amount of oxygen the body needs when hypothermic, I want to stress the importance of starting and continuing cardiopulmonary resuscitation (CPR) efforts with all victims of hypothermia,” Tveita said. Doctors typically cease CPR efforts in a normothermic patient after 30 minutes. But CPR should continue on hypothermic patients until after they have returned to normal temperature, Tveita advised.

Body shuts down

As the body cools, the metabolism slows, reducing the need for oxygen. Limited blood circulation is directed to vital organs, including the brain, heart and kidneys, but not to non-vital organs such as the muscles, skin and periphery.

When hypothermia victims arrive in the emergency room, they are unresponsive and may have only one or two respirations per minute, compared to the 10-15 per minute that is normal. Doctors often cannot even detect a peripheral pulse to determine whether the heart is beating, Tveita said. In fact, victims of hypothermia may appear to be dead, even when they are not.

Understanding the body’s physiological response to hypothermia became a popular research topic 40 years ago, when doctors wanted to use hypothermia during heart surgery. In fact, doctors did learn to use hypothermia to reduce oxygen consumption, to induce cardiac standstill and to restart the heart by rewarming, Tveita noted.

But research on hypothermia dropped off markedly after the surgical application was established. However, deaths from accidental hypothermia continue, and not just in the coldest climes. Tveita recalled the recent case of a person in a warmer climate who became hypothermic after being swept out to sea on a cold current.

Rats serve as model

“In this study, we wanted to find out if there are problems with low blood pressure, low pulse, low cardiac output (the volume of blood the heart can pump per minute), or with oxygen transport to the cells,” Tveita said. In particular, the research team wanted to know if insufficient circulation leads to inadequate oxygen supply to the heart cells, which in turn leads to heart failure.

The researchers divided anesthetized rats into three groups: two hypothermic groups and a control group. They exposed one hypothermic group to 15°C (59°F) for one hour before rewarming. They exposed the second group to 15°C, but for five hours. The control group was kept at normal temperature, 37°C (98.6°F). The researchers followed the hemodynamic changes during hypothermia and rewarming and later examined the rats’ heart cells.

When core body temperature was lowered to 15°C, both hypothermic groups experienced a similar reduction in circulating blood volume. And both showed that the physiological mechanisms that help transport oxygen and help unload oxygen from hemoglobin were working. “As a consequence, oxygen supply was not a limiting factor for survival in the present experiments,” the authors wrote.

The rats in the one-hour group spontaneously normalized their blood pressure, cardiac output and heart rate after they were rewarmed, Tveita noted. However, the rats in the five-hour group, which were significantly more likely to experience heart failure during rewarming, experienced substantial lowering of cardiac output and other cardiac functions.

 “We conclude that the heart failure we see after rewarming is not due to a lack of oxygen supply or oxygen transportation because unloading of oxygen at the cell level from hemoglobin is functioning,” Tveita stated. Thus, it appears that the problem comes as a result of the lower cardiac output, he added.

 “Thus, efforts aimed at elevating cardiac output in this phase seem advisable in order to optimize oxygen supply, reperfuse (restore blood flow to) vascular beds (minute blood vessels) and prevent rewarming shock formation,” the authors wrote

Source and funding

“Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?” by Timofei V. Kondratiev, Kristina Flemming, and Mikhail A. Sovershaev, University of Tromsø, Norway; Eivind S.P. Myhre, Sørlandet Hospital, Kristiansand; and Torkjel Tveita, University of Tromsø and University Hospital of North Norway, appears in the July issue of the American Journal of Physiology-Heart and Circulatory Physiology published by the American Physiological Society.

The study was supported by a grant from the Laerdal Foundation for Acute Medicine.

Editor’s note: The media may obtain a copy of Kondratiev et al. by contacting Christine Guilfoy, The American Physiological Society, (301) 634-7253 or cguilfoy@the-aps.org.

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The American Physiological Society was founded in 1887 to foster basic and applied bioscience. The Bethesda, Maryland-based society has 10,500 members and publishes 14 peer-reviewed journals containing almost 4,000 articles annually.

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APS  provides a wide range of research, educational and career support and programming to further the contributions of physiology to understanding the mechanisms of diseased and healthy states. In 2004, APS received the Presidential Award for Excellence in Science, Mathematics and Engineering Mentoring (PAESMEM).

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