POTENTIAL COMPLICATIONS
Cardiac effects
1. The J wave seen on this electrocardiogram is related to body temperature. It results from a voltage gradient between the
epicardium and endocardium that, in turn, produces a prominent epicardial action potential notch.
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Common electrocardiographic changes seen with hypothermia include sinus bradycardia, an increased Q-T interval, and the J,
or Osborn, wave (Figure 1).13,14 In people, sinus bradycardia and decreased T wave voltage are seen at 95 F (35 C), and with progressed hypothermia there
is prolongation of the P-R and Q-T intervals and QRS complex. In dogs and cats, the J wave is typically seen at temperatures
from 86 to 93.2 F (30 to 34 C), and there is usually atrial fibrillation or ventricular irritability that terminates as ventricular
fibrillation at temperatures below this rate.13,15-17
The prominence of the J wave is related to body temperature, and its genesis is related to dysfunction of the intramyocardial
M cells.18 This dysfunction results from a voltage gradient between the epicardium and endocardium that, in turn, produces a prominent
epicardial action potential notch.18 This abnormal deflection is more or less present and prominent in each electrocardiographic plane, and the wave occurs as
a convex elevation at the junction of the QRS complex and the S-T segment.19
The responsiveness of alpha-1 adrenergic receptors decreases in dogs and cats with decreased core temperatures. Initially,
alpha-1 receptor catecholamine binding increases, but with prolonged and progressive hypothermia, there is decreased receptor
affinity. Reduced receptor binding results in a diminished contractile response and, ultimately, vasodilation of the cutaneous
veins.20 Previous studies have demonstrated hypersensitivity in beta-1 receptors during hypothermia; additionally, alpha-1 adrenoceptor-mediated
vasoconstriction was attenuated while alpha-2 adrenoceptor response was unaffected.21,22 Both alpha and beta adrenoceptors are desensitized in people with hypothermia associated with cardiopulmonary bypass.23 Hypothermia around 95 F (35 C) is associated with markedly decreased left ventricular contractility and leads to reduced
cardiac output and impaired diastolic relaxation in neonatal pigs.24,25 Cardiac function in dogs with experimentally induced hypothermia is characterized by an initial period of increased ventricular
contractility followed by decreased contractility at temperatures less than 68 F (20 C).26 Ventricular fibrillation was documented in 50% of the dogs with temperatures below 74 F (23.3 C).26
Pulmonary effects
Severe hypothermia causes a reduction in both respiratory rate and tidal volume because of decreased cellular metabolism and
lowered carbon dioxide production, thus diminishing the stimulation of ventilation.27-29 Patients with subnormal body temperatures also have a blunted response to carbon dioxide, but the degree of oxygen use concurrently
decreases, leaving the respiratory quotient unaffected.30 The shifting of the oxygen-hemoglobin dissociation curve to the left, blood sludging, and a decline in alveolar ventilation
may lead to hypoxia, pulmonary edema, acute respiratory distress syndrome, or pneumonia.31-33 Patients that experience near-drowning initially hyperventilate secondary to the mammalian dive reflex, potentially resulting
in an alkalosis that may exacerbate a left shift of the oxygen-hemoglobin dissociation curve. Severely hypothermic patients
may hypoventilate, possibly contributing to the development of acidosis.
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