Cardiovascular

After initial tachycardia, progressive bradycardia develops. The pulse usually decreases by 50% at 28° C. If an observed tachycardia is inconsistent with a patient’s temperature, associated conditions such as hypoglycemia, drug ingestion, and hypovolemia should be considered.

The bradycardia of hypothermia results from decreased spontaneous depolarization of the pacemaker cells. As a result, the bradydysrhythmia is refractory to atropine. The electrocardiographic features of hypothermia are unique.12,13 Initially described by Tomaszewski in 1938, the Osborn (J) wave is seen at the junction of the QRS complex and ST segment (Fig. 140-2). J waves are potentially diagnostic but not prognostic. They may appear at any temperature below 32° C. The size of the J wave is not related to arterial pH but does increase with temperature depression.

J waves are normally upright in the aVL, aVF, and left precordial leads.¹⁴ The J deflection may be a result of hypothermic ion flux alterations, with delayed depolarization or early repolarization of the left ventricular wall. It can also be seen during local cardiac ischemia and with sepsis or CNS lesions, hypercalcemia, and the Brugada syndrome.

Some J waveform abnormalities simulate a myocardial injury current. Hypothermic electrocardiographic changes are not easily recognized by computer programs. Reliance on computer interpretations can result in mistaken thrombolysis, which would be expected to exacerbate preexistent coagulopathies.¹⁵

All atrial and ventricular dysrhythmias are common in moderate or severe hypothermia. Reentrant dysrhythmias result from decreased conduction velocity with increased myocardial conduction time and a decreased absolute refractory period. Because the conduction system is more sensitive to the cold than the myocardium is, cardiac cycle prolongation occurs. Fluctuations of available oxygen, pH, electrolytes, and nutrients also alter conduction. As hypothermia worsens, the PR interval, then the QRS interval, and finally (and most characteristically) the QTc interval become prolonged. In the absence of obvious shivering, thermal muscle tone may obscure P waves or produce artifacts.

Atrial fibrillation is common when the core temperature is below 32° C. Other rhythms are sinus, atrial, or junctional. Atrial fibrillation usually converts spontaneously during rewarming, but mesenteric embolization is a hazard.

The development of ventricular fibrillation (VF) or asystole in hypothermia is multifactorial. Putative explanations include tissue hypoxia, physical jostling, electrophysiologic or acid-base disturbances, and autonomic dysfunction. Asystole and VF can occur spontaneously when the core temperature falls below 25° C.16,17 Hypothermia causes a decrease in transmembrane resting potential, which in turn decreases the threshold for ventricular dysrhythmias. VF can also result from an independent focus or a reentrant phenomenon. When the heart is cold, a large dispersion of repolarization exists, which facilitates the development of a conduction delay. The action potential is also prolonged.

The term core temperature afterdrop refers to a further decline in an individual’s core temperature after removal from the cold. The two processes that contribute to afterdrop are simple temperature equilibration across a gradient and circulatory changes. Countercurrent cooling of the blood, which is perfusing cold tissues, results in a temperature decline until the gradient is eliminated.¹⁸

Active external rewarming of the extremities obliterates peripheral vasoconstriction and reverses arteriovenous shunting. This was most vividly demonstrated by Hayward, who measured his own esophageal, rectal, tympanic, and cardiac temperatures (by use of a flotation tip catheter) after cooling in 10° C water on three different days.¹⁹ Warm bath immersion rewarming caused a 30% fall in mean arterial pressure coupled with a 50% decline in peripheral vascular resistance.

Core temperature afterdrop is a clinically relevant consideration in the treatment of patients with a large temperature gradient between the core and the periphery. This is common in patients who are dehydrated after chronic exposure. Major afterdrop can also occur in severely hypothermic patients if frostbitten extremities are thawed before thermal stabilization of the core.

Central Nervous System

Hypothermia progressively depresses the CNS. Significant alteration of the brain’s electrical activity begins below 33.5° C. The electroencephalogram silences at 19 to 20° C.

Cerebral autoregulation is maintained with an increase in vascular resistance until 25° C. In cases of severe hypothermia, there is a disproportionately higher redistribution of blood flow to the brain. Like the heart, the brain has a critical period of tolerance to hypothermia. There are temperature-dependent neural enzyme systems that are unable to function at temperatures that are well tolerated by the kidney.

Renal System

Simple exposure to cold induces a diuresis regardless of an individual’s state of hydration. Hypothermia depresses renal blood flow, reducing it by 50% at 27 to 30° C. The kidneys then excrete a large amount of dilute urine, termed cold diuresis. Cold diuresis is essentially glomerular filtrate, which does not clear nitrogenous waste products. Severe hypothermia causes an initial relative central hypervolemia as a consequence of peripheral vasoconstriction. Cold diuresis may act as a volume regulator to diminish the vasoconstriction-induced capacitance vessel overload. Cold-water immersion can further increase urinary output by 3.5 times. Ethanol doubles that increase.²⁰

Respiratory System

Hypothermia initially stimulates respiration. This is followed by a progressive decrease in the respiratory minute volume. Carbon dioxide production decreases 50% with an 8° C fall in temperature. The normal stimuli for respiratory control are altered in severe hypothermia, and carbon dioxide retention with respiratory acidosis can occur. Hypercapnia increases core temperature cooling during snow burial.²¹

Numerous other pathophysiologic factors adversely affect the respiratory system. These include viscous bronchorrhea, decreased ciliary motility, and noncardiogenic pulmonary edema.

Decreased Heat Production

Decreased thermogenesis is often secondary to an endocrinologic failure, such as hypopituitarism, hypoadrenalism, or myxedema. Myxedema coma is several times more common in women; up to 80% of these persons are hypothermic. Hypothyroidism is often occult in this setting. There is usually no available history of lassitude, dry skin, arthralgias, or cold intolerance.

Hypoglycemia with central neuroglycopenia also predisposes to hypothermia. Another cause of decreased heat production is malnutrition, which causes a decrease in subcutaneous fat. Severe malnutrition, as with marasmus, contributes to heat loss. Kwashiorkor is less commonly associated with hypothermia because of the insulating effect of the hypoproteinemic edema.¹¹

The young and the old are commonly at risk. The neonate has a large surface area–to–mass ratio, a relatively deficient subcutaneous tissue layer, and an inefficient shivering mechanism. Neonates lack behavioral defense mechanisms.

Acute neonatal hypothermia is common after emergency deliveries or resuscitations. Many neonates are lethargic, fail to thrive, and have a weak cry. Half have deceptively rosy cheeks. Late-onset hypothermia, which occurs after 72 hours of life, is commonly a result of septicemia. Hypothermia can occur in the shaken baby syndrome and may be a factor in some cases of apparent sudden infant death syndrome.

Homeostatic capability progressively decreases with aging. Thermal perception is altered and elderly people manipulate the indoor ambient temperature less precisely. Most elderly patients are capable of normal thermoregulation but are prone to conditions, including immobility and systemic diseases, that interfere with heat production and conservation. Inability to sense cold, abnormal adaptive behavioral responses, and decreased peripheral blood flow reflect geriatric autonomic dysfunction.²²

Increased Heat Loss

Patients with erythrodermas, including psoriasis, exfoliative dermatitis, ichthyosis, eczema, and burns, can have increased peripheral blood flow. Iatrogenic causes of heat loss include exposure during resuscitations, massive cold or room temperature infusions, overcooling of patients with heat stroke, and overzealous burn treatment.

Ethanol is metabolized at a slower rate in hypothermic individuals and interacts with every putative thermoregulatory neurotransmitter. It may directly suppress the activity of the posterior hypothalamus and the mammillary bodies. Cutaneous heat loss increases through vasodilation, and shivering thermogenesis is decreased.²³

Ethanol is the most common cause of excessive heat loss in urban settings.7,16 Intoxicated persons often lack protective adaptive behavior to avoid the cold. “Paradoxical undressing,” which is the removal of clothing in response to a cold stress, is common.²⁴ Aging is associated with an increased sensitivity to the hypothermic actions of ethanol. Hypothermic alcoholic ketoacidosis also occurs. Hypothermia is common in patients with Wernicke’s encephalopathy. Hypothermia can mask the usual clinical triad of ophthalmoplegia, confusion, and truncal ataxia. Intravenous thiamine can be both diagnostic and therapeutic.

Impaired Thermoregulation

Thermoregulation can be impaired centrally, peripherally, or metabolically. Skull fractures, particularly basilar fractures, and chronic subdural hematomas are implicated in central impairment. Other causes include cerebrovascular accidents, neoplasms, anorexia nervosa, and Hodgkin’s and Parkinson’s diseases. The final common pathway in these disorders may be centrally mediated vasodilation. Cerebellar lesions produce choreiform, less efficient shivering.

In therapeutic or toxic doses, antidepressants, antimanic agents, antipsychotics, anxiolytics, and general anesthetics interfere with thermoregulation by impairing centrally mediated vasoconstriction. Overdosage of these medications and others (e.g., the organophosphates, heroin, glutethimide, and carbon monoxide) predisposes to hypothermia.²⁵

Peripheral thermoregulatory failure classically occurs in neurogenic shock after acute spinal cord transection. The interruption of the autonomic nervous system eliminates vasoconstrictive control. The patient effectively becomes poikilothermic and can rapidly become hypothermic. Neuropathies and diabetes are additional peripheral causes of heat loss. An abnormal plasma osmolality may explain hypothalamic interference in uremia, lactic acidosis, diabetic ketoacidosis, and hypoglycemia.²⁶

Acid-Base Balance

Blood gas analyzers warm blood to 37° C, which increases the partial pressure of dissolved gases. This results in an arterial blood gas report showing higher oxygen and carbon dioxide levels and a lower pH than the patient’s in vivo values.30–32 In fact, attempting to maintain a corrected pH at 7.4 and arterial partial pressure of carbon dioxide (PaCO₂) at 40 mm Hg during hypothermia depresses cerebral and coronary blood flow and cardiac output and increases the incidence of VF.³³ The ideal acid-base strategy is the ectothermic alpha-stat approach.¹⁰ Simply put, the goal is an uncorrected pH at 7.4 and PaCO₂ at 40 mm Hg.

Cold blood buffers poorly. In normothermia, when the PaCO₂ increases 10 mm Hg, the pH decreases 0.08 unit. At 28° C, the decrease in pH doubles. Because the neutral point of water at 37° C is a pH of 6.8, the normal 0.6-unit pH offset between blood and intracellular water should be maintained at all temperatures (Fig. 140-3).

Intracellular electrochemical neutrality ensures optimal enzymatic function at all temperatures.³¹ Relative alkalinity affords myocardial protection and improves the heart’s electrical stability.³³ Carbogen could prove valuable in the treatment of accidental hypothermia because it flattens and shifts the oxyhemoglobin dissociation curve to the right.

Hematologic Evaluation

A patient’s hematocrit can be deceptively high as the result of the decreased plasma volume. The hematocrit level increases 2% for every 1° C fall in temperature. A low-normal hematocrit level in a moderately to severely hypothermic patient should suggest acute or chronic blood loss.

A normal white blood cell count never excludes infection, especially if the patient is debilitated, alcoholic, myxedematous, or at either age extreme. Splenic, hepatic, and splanchnic sequestration in hypothermia decreases leukocyte and platelet counts.

Frequent evaluation of serum electrolytes during rewarming is essential. There are no safe predictors of their values or trends.¹⁶ Changes occur in membrane permeability and in the sodium-potassium pump. The patient’s preexisting physiologic status, the severity and chronicity of hypothermia, and the method of rewarming alter the serum electrolyte values.

The plasma potassium level is independent of the primary hypothermic process. Hyperkalemia is often associated with metabolic acidosis, rhabdomyolysis, or renal failure. An important caveat is that hypothermia enhances the cardiac toxicity of hyperkalemia and obscures the premonitory electrocardiographic changes associated with it.

Hypokalemia is most common with chronic hypothermia. It results from potassium’s entering muscle, not a kaliuresis. A discrepant decline in serum potassium level despite a decreasing serum pH is caused by intracellular pH fluxes greater than extracellular pH fluxes.

Conditions associated with hypokalemia include preexisting diabetic ketoacidosis, hypopituitarism, inappropriate secretion of antidiuretic hormone, previous diuretic therapy, and alcoholism. If the potassium level is less than 3 mEq/L, supplementation may be necessary during rewarming.

The blood urea nitrogen and creatinine levels are elevated with preexisting renal disease or decreased clearance. Because of hypothermic fluid shifts, the hematocrit and blood urea nitrogen levels are poor indicators of a patient’s actual fluid status.

The blood glucose level may also provide a subtle clue to the type of hypothermia. Acute hypothermia initially elevates blood glucose levels through catecholamine-induced glycogenolysis, diminished insulin release, and inhibition of cellular membrane glucose carrier systems. On the other hand, subacute and chronic hypothermia produce glycogen depletion, leading to hypoglycemia. Symptoms of hypoglycemia can be masked by hypothermia. A cold-induced renal glycosuria does not imply hyperglycemia or guarantee normoglycemia.²⁶

When hyperglycemia persists during rewarming, one should suspect hemorrhagic pancreatitis or diabetic ketoacidosis. Patients with diabetic ketoacidosis should be actively rewarmed past 30° C because insulin is ineffective below that temperature. Correction of hypoglycemia corrects the level of consciousness only to that of the corresponding level of hypothermia.

Severe hypothermia also causes serum enzyme elevation because of the ultrastructural cellular damage. Rhabdomyolysis is commonly associated with cold exposure.

Ischemic pancreatitis may result from the microcirculatory shock of hypothermia. The decreased pancreatic blood flow then activates proteolytic enzymes.⁷