Questions
- 1.
How is hypothermia defined and graded?
- 2.
What mechanisms lead to hypothermia in surgical patients under general anesthesia?
- 3.
Explain the physiologic responses to hypothermia.
- 4.
Describe the physiologic consequences of hypothermia.
- 5.
Are there any benefits to mild intraoperative hypothermia?
- 6.
Where are the commonly used temperature monitoring sites?
- 7.
- 8.
Is hypothermia prevention warranted for patients receiving central neuraxial blockade?
A 71-year-old man underwent subtotal colectomy complicated by hypothermia. He was brought to the postanesthesia care unit (PACU) with a temperature of 31.9° C.
2
What mechanisms lead to hypothermia in surgical patients under general anesthesia?
The first phase of hypothermia is due to redistribution. Core temperature decreases by 0.5°–1.5° C during the first hour after induction of general anesthesia if warming measures are not instituted on entry to the operating room. During this time, heat is redistributed from the core to the periphery. The second phase is due to heat loss in excess of heat production and lasts 2–3 hours. Heat production decreases by approximately 20% after induction of general anesthesia. Core temperature plateaus after 3–4 hours because of peripheral vasoconstriction that is triggered by a core temperature of 33°–35° C. However, peripheral temperature continues to decrease.
There are four mechanisms of heat loss, as follows:
- •
Radiation is the movement or transfer of heat from a warm object to a colder one that is not in direct contact and accounts for approximately 60% of heat loss.
- •
Evaporation is heat lost as body fluids leave the liquid (water) state and enter the gaseous phase and typically accounts for 15%–20% of heat loss (e.g., respiratory tract, open abdomen, or thorax).
- •
Convection is the movement or transfer of heat from the patient to the passing cooler air and typically accounts for 15%–20% of heat loss.
- •
Conduction is the movement or transfer of heat from the patient to an adjacent object and typically accounts for ≤5% of heat loss (e.g., the operating table).
In other settings, hypothermia can result from loss of central thermoregulation (e.g., stroke, head trauma, spinal cord injury), drugs (e.g., alcohol or barbiturate overdose), or metabolic derangement (e.g., hypoglycemia, hypothyroidism, sepsis, burns, hepatic failure).
3
Explain the physiologic responses to hypothermia.
There are three physiologic responses to hypothermia.
Vasoconstriction
Vasoconstriction is the result of sympathetic stimulation. Volatile agents reduce the threshold for vasoconstriction by 2°–4° C. The vasoconstrictive threshold is also reduced by approximately 1° C in elderly patients, who are at higher risk for hypothermia.
Shivering thermogenesis
Shivering thermogenesis is an involuntary oscillatory muscular activity that augments the basal metabolic rate by a factor of two to four times. The threshold for shivering is usually about 1° C less than the vasoconstriction threshold. Shivering is a “last resort” response and is metabolically much less efficient than vasoconstriction. The shivering threshold is decreased by potent inhalation anesthetics even more than the vasoconstriction threshold. Two types of patterns are seen, as follows:
- •
A tonic pattern resembles normal shivering at four to eight cycles per minute and has a waxing and waning component.
- •
A phasic pattern resembles clonus with a 5- to 7-Hz burst pattern seen most specifically in the postanesthesia period. This pattern is often secondary to volatile anesthetic administration and probably results from anesthetic-induced disinhibition of normal descending control over spinal reflexes .
Shivering in the postoperative period can increase oxygen consumption by 300%–500% contributing to a potentially significant oxygen/demand mismatch that can lead to myocardial ischemia in susceptible patients. It can also increase the serum potassium level.
Nonshivering thermogenesis
Nonshivering thermogenesis is the mechanism of heat production in infants that is not associated with muscle activity. This mechanism may double the metabolic heat production in infants, but it does not play a significant role in adults. (See Chapter 64 for a detailed explanation of nonshivering thermogenesis.)
4
Describe the physiologic consequences of hypothermia.
The physiologic consequences of hypothermia are summarized in Table 79-1 . Electrocardiogram (ECG) changes include sinus bradycardia, widened P–R interval, widened QRS, and prolonged Q–T interval. The Osborn wave is characteristic for hypothermia ( Figure 79-1 ). This wave is a deflection at the J point (the junction between the QRS complex and the ST segment) in the same direction as that of the QRS complex, with a height proportional to the degree of hypothermia. It is frequently mistaken for genuine ST segment elevation.
| Parameter | Change | Implication |
|---|---|---|
| Oxygen and CO 2 solubility | Increased | pH increases by 0.015 per 1° C decrease |
| Volatile anesthetics solubility | Increased | May contribute to prolonged emergence from general anesthesia with potent inhalation anesthetics |
| MAC | Decreased | Delayed awakening |
| Postoperative confusion | ||
| Cardiac output | Decreased | Blood flow decreases in the following order: muscle, kidneys and gut, brain and heart |
| Speed of induction | Unchanged | No change seen because both MAC and cardiac output are decreased |
| Oxygen consumption and CO 2 production | Decreased | Decreased by 7%–9% per 1° C decrease |
| PaCO 2 | Decreased | Decreased by 1.5% per 1° C decrease (i.e., PaCO 2 equals temperature [° C]) |
| Plasma catecholamines | Increased | Hypertension |
| Tachycardia | ||
| Hyperglycemia | ||
| Plasma insulin | Decreased | Hyperglycemia from activation of glycogenolysis and gluconeogenesis |
| Hemoglobin affinity for oxygen | Increased | Increased by 6% per 1° C decrease (left shift in oxyhemoglobin dissociation curve) |
| Hypoxic ventilatory drive | Depressed | Hypercarbia driven ventilation |
| Bronchomotor tone | Decreased | Increased anatomic dead space |
| Hypoxic pulmonary vasoconstriction | Decreased | Worsening of ventilation/perfusion mismatch |
| Threshold for ventricular fibrillation | Decreased | Risk of ventricular fibrillation becomes significant at <32° C |
| Systemic vascular resistance | Increased | May contribute to left ventricular failure |
| Pulmonary vascular resistance | Increased | May contribute to right ventricular failure |
| Hepatic blood flow | Decreased | Proportional to decrease in cardiac output |
| Renal blood flow | Decreased | Decreases proportionately more than cardiac output |
| Diluting and concentrating capacity; tubular transport of sodium, chloride, water, and potassium | Decreased | “Cold diuresis” can lead to hypovolemia and hemoconcentration |
| Blood viscosity | Increased | Increased by 2%–3% per 1° C decrease |
| Coagulation | Impaired | Decreased circulating factors |
| Platelets sequestered in portal circulation | ||
| Platelet function | Impaired | Perioperative bleeding may contribute to increased transfusion requirements |
| Urinary nitrogen excretion | Increased | Remains high for several days postoperatively |
| Drug metabolism | Decreased | Effect of most intravenous pharmacologic agents requiring end-organ metabolism (e.g., vecuronium, propofol) is prolonged |
| Immune function | Impaired | Reduced monocyte HLA-DR surface expression |
| Delayed clearance of TNF-α | ||
| Increased IL-10 release |
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