Moderate alcohol dose and chronic obstructive pulmonary disease: not a cause of hypoventilation.

Six patients with chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second, 1.01 +/- 0.08 L [mean +/- SEM] ) were given either 1 mL of 100% alcohol per kilogram of body weight in an aqueous solution or a similar volume of water in a crossover design on consecutive days. All subjects became intoxicated and the peak alcohol concentration was 137 +/- 11 mg/dL, 40 minutes after ingestion. No significant difference was found in either PaO2 or PaCO2 between the alcohol and control period. A significant decrease in arterial pH occurred following alcohol (P less than .05), and represented a mild metabolic acidosis. Alcohol ingestion resulted in an increase in oxygen consumption (P less than .05) and carbon dioxide production (P less than .05) but no change in respiratory rate. It appears that small to moderate amounts of alcohol will not cause marked changes in oxygen tension or alveolar hypoventilation in patients with severe COPD who do not have marked hypercapnia. Nevertheless, other effects of alcohol on the cardiopulmonary system and the concomitant use of sedatives have to be considered before condoning the use of alcohol.

Hypomagnesemia is a frequent finding in the emergency department in patients with chest pain.

STUDY OBJECTIVE: To evaluate the frequency of low blood levels of total and ultrafilterable magnesium (total and ultrafilterable hypomagnesemia) in patients with chest pain in the emergency department, and to determine if hypomagnesemia is associated with other clinically important diagnostic and outcome variables in cardiac care. SETTING: An emergency department of a university teaching hospital. DESIGN: Prospective study of extracellular magnesium homeostasis in patients with chest pain in the emergency department and a cohort of patients without chest pain with a clinical indication for blood sampling. PATIENTS: During a 4-month period, 147 patients presenting to the emergency department were studied: 67 patients (mean +/- SD age, 61.4 +/- 13 years) with a chief complaint of chest pain (study group) and 80 patients (55.6 +/- 19 years) with other diagnoses (control group). RESULTS: Total and ultrafilterable hypomagnesemia occurred more frequently in patients with chest pain (20/67 [30%] and 9/67 [13%]) than in the control group (12/80 [15%] and 3/80 [4%]). Patients with a chief complaint of chest pain who were receiving diuretic medications were hypomagnesemic more frequently (9/16 [56%]) than patients not receiving diuretics (12/51 [23%]). In patients with chest pain admitted to the hospital with a diagnosis of "rule out" myocardial infarction, the frequency of hypokalemia was greater among hypomagnesemic patients (6/14 [43%]) than normomagnesemic patients (3/31 [10%]). A similar frequency of hypomagnesemia was noted in patients with a final diagnosis of myocardial infarction (4/15 [27%]) when compared with other patients admitted with chest pain (10/31 [32%]) in whom myocardial infarction was excluded. No association was noted among hypomagnesemia and length of hospital stay or the occurrence of hypotension or dysrhythmias. CONCLUSIONS: Total and ultrafilterable hypomagnesemia are frequent occurrences in patients with and without chest pain in the emergency department. Diuretic use is associated with hypomagnesemia in patients presenting with chest pain in the emergency department. These results support the concept that hypomagnesemia is common in patients with chest pain in the emergency department and is associated with hypokalemia but is not predictive of whether the patient with chest pain has had an acute myocardial infarction.

Local dental anesthesia with epinephrine. Minimal effects on the sympathetic nervous system or on hemodynamic variables.

To define the hemodynamic effects of local dental anesthesia, we measured the mean arterial pressure (MAP), heart rate, and plasma catecholamine responses for 60 minutes following an inferior alveolar nerve block with epinephrine-and nonepinephrine-containing lidocaine hydrochloride anesthesia in 14 men using a randomized double-blind crossover trial. Lidocaine alone caused no significant change in MAP or heart rate and only slight, transient changes in plasma catecholamine concentrations when compared with baseline values. Lidocaine with epinephrine caused significant, sustained (60 minutes) increases in plasma epinephrine concentrations (mean +/- SEM, 27 +/- 4 to 94 +/- 13 pg/mL) and a slight, but transient (two-minute) increase in heart rate from 68 +/- 3 to 70 +/- 3 beats per minute. Lidocaine with epinephrine caused no significant change in MAP. There is no significant hemodynamic response to lidocaine dental anesthesia (with or without epinephrine) in healthy young men.

Angiotensin-converting enzyme activity. A potential marker of tissue hypothyroidism in critical illness.

We measured serum angiotensin-converting enzyme (ACE) activity radiometrically as a possible indicator of reduced thyroid function in 57 euthyroid controls, 27 patients in a noncardiac intensive care unit (13 with medical and 14 with surgical disorders), and 29 patients having coronary artery bypass grafting. In the last group, blood was obtained preoperatively and one day and one month after surgery (group 1; n = 18) or preoperatively and six hours and one day after surgery (group 2; n = 11). Patients in group 1 had significant reductions in levels of serum thyroxine (T4), triiodothyronine (T3), and thyrotropin response to protirelin one day postoperatively. The ACE activity fell significantly. Patients in group 2 had low levels of T4, T3, thyrotropin, and ACE six hours postoperatively. All these levels remained low the next day, and free T4 and free T3 levels were also reduced; the reverse T3 level became elevated. Changes in ACE significantly paralleled changes in T3. The 27 patients without coronary artery bypass grafting also had significant reductions in serum T4, T3, and ACE levels. Dilution studies and dialysis of serum with low ACE activity failed to demonstrate an inhibitor to explain the reduced enzyme function.

Diagnostic dosages of protirelin (TRH) elevate BP by noncatecholamine mechanisms.

While performing thyroid function tests, we noticed that protirelin (TRH) raised BP, and, therefore, we investigated the effect of diagnostic dosages of protirelin (500 micrograms) on plasma catecholamine levels and cardiovascular function in eight patients one day before, one day after, and four weeks following heart surgery. Mean arterial pressure (MAP), heart rate (HR), plasma norepinephrine (NE), epinephrine (EPI), dopamine (DA), thyroid hormone (triiodothyronine [T3], thyroxine), and thyrotropin (TSH) levels were measured before and after the intravenous injection of protirelin. Protirelin increased MAP transiently from 88 +/- 2 to 103 +/- 3 mm Hg (before surgery), 86 +/- 4 to 102 +/- 4 mm Hg (one day after surgery), and 86 +/- 4 to 104 +/- 5 mm Hg (four weeks after surgery). There were no notable changes in HR or plasma NE, EPI, or DA levels. The T3 and TSH response to protirelin was normal on all three study days. Protirelin raised MAP by an effect on systemic vascular resistance (SVR) rather than an increase in cardiac output. We conclude the following: (1) diagnostic dosages of protirelin transiently elevate MAP and SVR by a noncatecholamine mechanism, (2) clinicians who perform protirelin tests should be aware of protirelin's transient pressor effects.

Lack of effectiveness of magnesium in chronic stable asthma. A prospective, randomized, double-blind, placebo-controlled, crossover trial in normal subjects and in patients with chronic stable asthma.

BACKGROUND: Magnesium sulfate has been helpful in the treatment of acute exacerbations of asthma. We hypothesized that magnesium would also be an effective bronchodilator in patients with chronic stable asthma. METHODS: We performed a prospective, randomized, double-blind, placebo-controlled, crossover trial in 15 patients with chronic, stable asthma and 10 nonasthmatics. On study day 1, spirometry and albuterol challenge were used to confirm the presence of asthma according to American Thoracic Society criteria. On study day 2, subjects received intravenous magnesium sulfate (2 g) or placebo (saline). On study day 3, subjects were crossed over to receive the other drug. Spirometry was performed before, during, and after drug or placebo administration. Circulating ionized magnesium concentrations were determined before and after intravenous magnesium or placebo administration. RESULTS: Magnesium infusion caused no statistically significant changes in forced expiratory volume in 1 second (mean +/- SEM, 1.92 +/- 0.13 L before, 1.98 +/- 0.12 L during, and 2.01 +/- 0.14 L after magnesium administration), forced vital capacity (mean +/- SEM, 3.44 +/- 0.25 L before, 3.60 +/- 0.26 L during, and 3.59 +/- 0.25 L after magnesium administration), or maximum forced expiratory flow rate (mean +/- SEM, 5.42 +/- 0.44 L/second before, 5.46 +/- 0.46 L/second during, and 5.57 +/- 0.49 L/second after magnesium administration). Placebo caused no changes in these three physiologic variables. CONCLUSION: Magnesium is not effective as a bronchodilator in chronic, stable asthmatics or in normal non-asthmatic adults.

Hormonal responses to graded surgical stress.

We tested the hypothesis that selected hormonal responses to surgery reflect the degree of surgical stress. Plasma norepinephrine, epinephrine, thromboxane B2, cortisol, serum angiotensin converting enzyme, thyroxine, triiodothyronine, free thyroxine, and free triiodothyronine levels were measured preoperatively, and then one hour, 24 hours, and five days postoperatively in three groups of patients. The groups were as follows: group 1, "minimal" stress, eg, inguinal hernia repair (n = 10); group 2, "moderate" stress, eg, cholecystectomy (n = 12); and group 3, "severe" stress, eg, subtotal colectomy (n = 9). Patients in group 1 showed no significant surgery-induced changes in hormonal values. The stress-induced changes in patients in groups 2 and 3 were seen at one and occasionally 24 hours; however, by five days postoperatively, circulating hormone values had returned to preoperative levels. Increases in plasma cortisol, norepinephrine, and epinephrine, and decreases in serum angiotensin converting enzyme levels characterized the surgery-induced hormonal changes. Conclusions are as follows: hormonal responses do reflect the degree of surgical stress; the hormonal changes are transient, lasting no longer than 24 hours in patients after uncomplicated surgery; hormonal responses to minimal surgical stress are negligible.

"Bovine ketosis" in a nondiabetic postpartum woman.

A 19-yr-old woman developed ketoacidosis 7 wk after the delivery of her first child. Despite breast feeding, she had been on a weight reduction diet resulting in a loss of 12 kg/body wt. With the development of a urinary tract infection, the patient became dehydrated and was found to be in ketoacidosis (arterial pH was 7.25 and PaCO2 was 17 mm Hg). The patient did not use alcohol and was nondiabetic. Therapy with adequate calories, intravenous fluids, and an appropriate antimicrobial agent resulted in prompt normalization of the laboratory abnormalities and resolution of the patient's symptoms. The hypothesis is advanced that the postpartum status of the patient put her at particular risk for development of ketoacidosis and that this may represent the first reported episode of "bovine ketosis" in a human.

Free fatty acids alter calcium binding: a cause for misinterpretation of serum calcium values and hypocalcemia in critical illness.

FFAs are bound with calcium on the albumin molecule. We hypothesized that changes in circulating FFA levels during critical illness altered calcium-albumin binding. We found that serum from both normal subjects and critically ill patients contained an ether-extractable factor which lowered ionized calcium concentrations and increased albumin-calcium binding. This factor was found in higher concentrations in serum from ill patients. Oleic acid and palmitic acid increased albumin-calcium binding from 2-28% in a dose-dependent manner when added in vitro to calcium-albumin solutions. Scatchard analysis demonstrated that 0.1 mM oleic acid increased the number of calcium-binding sites on the albumin molecule (from three to five sites per molecule) without altering binding affinity. A similar effect was found when we performed Scatchard analyses of ether extracts in serum from three critically ill patients (number of calcium-binding sites increased from three to six). We also found that lipid infusions (during parenteral nutrition) lowered mean serum ionized calcium values in six critically ill patients [4.6 +/- 0.2 (+/- SEM) to 4.1 +/- 0.2 mg/dL; P less than 0.05]. These data support the concept that FFAs increase calcium binding to the albumin molecule. Alterations in FFA concentrations during critical illness may contribute to the poor correlation between corrected total serum calcium and ionized calcium concentrations in critically ill patients. In addition, acute elevations in circulating FFA concentrations may contribute to hypocalcemia in patients with defects in bone calcium mobilization.

Evidence of extraocular muscle restriction in autoimmune thyroid disease.

Patients with Graves' disease lacking eye symptoms frequently have abnormal intraocular pressure (IOP) increases on upward gaze (greater than or equal to 3 mm Hg) indicative of apparent subclinical ophthalmopathy. Because of the close relationship between Graves' disease (GD) and Hashimoto's thyroiditis (HT), we examined 30 patients with a history of HT as well as 26 patients with a history of GD, 4 patients with a history of subacute thyroiditis, 1 patient with a history of silent thyroiditis, and 25 normal subjects for the presence of IOP abnormalities at 15 degrees and 25 degrees upgaze. While all of the patients were asymptomatic, had no exophthalmos, and were euthyroid at the time of the exam, Hertel exophthalmometer readings (mean +/- SD) for the patients with GD were significantly higher (P less than 0.005) than those for either the HT patients or normal subjects (17.1 +/- 2.4 vs. 14.5 +/- 2.3 vs. 14.4 +/- 4.2 mm, respectively). At 15 degrees upgaze, IOP abnormalities occurred in 25% and 13% of patients with GD and HT, respectively. At 25 degrees upgaze, these figures rose to 54% for the GD patients and 37% in HT patients. Only 1 of 25 normal subjects had elevated IOP changes on upgaze, as did the 1 patient with silent thyroiditis, but the patients with subacute thyroiditis did not. These data suggest the frequent presence of extraocular muscle restriction in patients with a history of HT as well as in patients with a history of GD. Maximal detection of these IOP abnormalities requires that patients be examined at 25 degrees upgaze. These data support the belief that the autoimmune bases of both GD and HT are closely linked, at least as manifested by eye muscle involvement.

Age-dependence of hypertensive-normotensive differences in plasma norepinephrine.

We compared venous plasma norepinephrine (NE) concentrations in 191 resting, supine patients with essential hypertension and 129 normotensive controls. Among normotensives, plasma NE increased significantly with age, but among hypertensives, no age-related increase occurred, due to relatively high NE values among young hypertensives. When patients and controls less than 40 years old were considered, hypertensives showed significantly higher plasma NE than the controls (317 vs 245 pg/ml, t = 3.15, p less than 0.01); but above the age of 40 years, no significant hypertensive-normotensive difference was obtained. These results, predicted by recent literature reviews, help to resolve the persistent controversy about sympathetic neural activity in essential hypertension, since such activity appears to be abnormal mainly in young patients. The data are consistent with increased sympathetic nervous system activity in the early stages of essential hypertension.

Phenylpropanolamine increases plasma caffeine levels.

The effects of the widely consumed drugs caffeine and phenylpropanolamine are mediated through activation of the central and sympathetic nervous systems. Severe, life-threatening, and occasionally fatal hypertensive reactions have been reported after their combined use. This study examined the possible pharmacokinetic interaction of phenylpropanolamine and caffeine. Sixteen normal subjects received combinations of caffeine, phenylpropanolamine, and placebo. In subjects receiving 400 mg caffeine plus 75 mg phenylpropanolamine, the mean (+/- SEM) peak plasma caffeine concentration of 8.0 +/- 2.2 micrograms/ml was significantly greater than after 400 mg caffeine alone (2.1 +/- 0.3 micrograms/ml; t[24] = 2.4; p less than 0.01). Physical side effects were more frequent after the phenylpropanolamine-caffeine combination than after either drug alone or after placebo. Greater increases in both systolic and diastolic blood pressures occurred after the combination than after either drug alone. Because caffeine levels can be increased greatly when certain other drugs are coconsumed, these data indicate that phenylpropanolamine may enhance absorption or inhibit elimination of caffeine and may explain increased side effects reported after their combined use.

The effect of propranolol on catecholamine clearance.

Normal subjects given propranolol increased their plasma t1/2 for infused isoproterenol from 2.68 to 6.25 minutes. Propranolol increased plasma norepinephrine (NE) levels only slightly. Propranolol increased the t1/2 of isoproterenol but not that of NE in men with autonomic nervous system degeneration. This suggests that propranolol acts on nonneuronal uptake-2 processes, rather than on uptake-1 mechanisms. alpha-Blockers slow uptake-1 and beta-blockers slow uptake-2 processes. When 27 subjects exercised, those who attained the highest plasma levels of the alpha- and beta-receptor agonist NE also had the briefest apparent t1/2 for NE. Adrenergic receptor blocking drugs slow catecholamine clearance. NE may stimulate its own clearance.

The effects of phenylpropanolamine on human sympathetic nervous system function.

Phenylpropanolamine (PPA) is a sympathomimetic agent, very similar in structure to amphetamine. In the United States, it is present in over 130 medications, primarily anorectic agents and cough and cold remedies, many available without a prescription. The effects of PPA on blood pressure (BP) remain controversial and its mechanisms of action unknown. We studied acute (1 and 2 hours) and 2-week effects of a daily dose of 75 mg of sustained release PPA administered to 14 normal volunteers. Measurements of heart rate, BP, and plasma catecholamines (CA) were made with the subject in the supine and standing positions, and upon gripping a hand dynamometer for 5 minutes. Although systolic BP across all postures and sampling times was significantly higher when subjects were taking PPA in comparison to placebo (F = 5.95, p = 0.03), in no subject did the increase in BP reach hypertensive or clinically significant levels and no substantial changes in CA levels were found. Our study population was relatively young and normotensive; even such a small BP increase may pose greater problems for hypertensive, obese subjects likely to be users of diet aids. Strenuous isometric exercise did not cause any greater increase in BP or CA after subjects took PPA versus placebo. PPA blood levels 24 hours after the last of 14 daily doses were similar to levels 1 and 2 hours after an initial dose. We conclude from these data that recommended doses of PPA have only minimal sympathetic nervous system (SNS) and cardiovascular effects in young, healthy, normotensive populations at the times and dose studied.

Transient hypertension after two phenylpropanolamine diet aids and the effects of caffeine: a placebo-controlled follow-up study.

PURPOSE AND PATIENTS AND METHODS: Reports of severe adverse reactions following the ingestion of single (75 mg) or double doses of the sympathomimetic drug phenylpropanolamine (PPA), with and without caffeine, prompted us to undertake a study of the effects of five drug preparations (75 mg PPA, 150 mg PPA, 75 mg PPA plus 400 mg caffeine, 400 mg caffeine, and placebo) in 16 resting, normotensive subjects. The study was of a double-blind, randomized, crossover design. Each subject consented to take the five drug preparations on different study days, which were separated by at least 48 hours. RESULTS: Compared with blood pressure (BP) values obtained after placebo ingestion, significant BP increases occurred over several hours following 150 mg PPA and after 75 mg PPA plus 400 mg caffeine. Significant BP increases after ingestion of 75 mg PPA and after 400 mg caffeine were less frequent. The mean peak BP following 150 mg PPA was 173 +/- 9/103 +/- 4 mm Hg, compared with 148 +/- 4/97 +/- 3 mm Hg after the other three active preparations; after placebo, peak BP reached 137 +/- 8/85 +/- 5 mm Hg. CONCLUSION: These results indicate that 150 mg PPA (the amount in two diet aids) substantially elevates BP. Our findings may explain some of the recent case reports of nontraumatic intracranial hemorrhage in young, healthy persons ingesting PPA at recommended or minimally greater dosages. We suggest physicians inform patients who are likely consumers of PPA (i.e., those with allergies, those with eating disorders, overweight persons, women during the postpartum period) and patients at risk for stroke (i.e., the elderly and hypertensive patients) of the risks of taking more than the recommended amounts of PPA and of combining caffeine with PPA.

A double dose of phenylpropanolamine causes transient hypertension.

PURPOSE: Phenylpropanolamine is widely used and freely available without a doctor's prescription in drug and grocery stores; it is the active ingredient in most diet aids and many cold preparations. Several cases of multiple cerebral hemorrhages associated with transient hypertension have recently been attributed to phenylpropanolamine in dosages equal to or less than that contained in two diet aids (i.e., 150 mg). Some evidence also exists on the additive effects of the co-ingestion of phenylpropanolamine and caffeine. We therefore undertook a study to demonstrate that a significant health risk can be caused by a double dose of a typical over-the-counter (OTC) diet aid (i.e., 150 mg phenylpropanolamine) and also when 75 mg phenylpropanolamine is taken with caffeine. SUBJECTS AND METHODS: Five men and one woman, ranging in age from 20 to 30, participated in this study. The drug preparations were administered to each subject on different study days in a double-blind, randomized-crossover design. Identical capsules contained 75 mg sustained-release phenylpropanolamine, 400 mg of sustained-release caffeine, or placebo. Subjects ingested three capsules at the beginning of each study day. For 150 mg, two phenylpropanolamine-containing capsules and one placebo were taken; for 75 mg, one phenylpropanolamine capsule and two placebos; and for phenylpropanolamine plus caffeine, one 75 mg phenylpropanolamine capsule, one 400 mg caffeine capsule, and one placebo. Blood pressure and heart rate were monitored throughout the study. RESULTS: Although 75 mg of phenylpropanolamine did not cause clinically relevant hypertension in our subjects, 150 mg of phenylpropanolamine and 75 mg of phenylpropanolamine plus 400 mg caffeine did result in significant blood pressure increases into the hypertensive range. CONCLUSION: We believe that consumers often assume that double the recommended dosage of an OTC drug is safe and more effective. We suggest that requiring a physician's prescription or an additional, stronger warning label on phenylpropanolamine-containing products may prevent substantial mortality and morbidity.

Variables affecting outcome in critically ill patients.

Critical care medicine has evolved as a field of science and clinical care. Despite important contributions to our understanding of the molecular basis of critical illness, we still remain troubled by our lack of insight into why some patients have favorable outcomes from critical illness and others do not. This article explores the hypothesis that at least five important variables may alter the outcome of patients suffering from a variety of critical illnesses. These variables include the premorbid immune or genetic status of the patient, the patient's gender, the circulating cholesterol concentration, the patient's age, and various iatrogenic and nosocomial events. Insights into the importance of these five variables may provide opportunities for physicians and scientists to improve outcome in patients suffering from critical illness. Clearly, altering iatrogenic and nosocomial events is already within the realm of opportunity.

Hypomagnesemia in patients in postoperative intensive care.

In order to study the clinical consequences of postoperative hypomagnesemia, the serum magnesium (Mg) concentration was measured in samples of blood collected from 193 patients admitted to two postoperative ICUs. On admission to the ICU, 117 patients (61 percent) had hypomagnesemia (serum Mg less than 1.5 mEq/dl), 66 patients (34 percent) had normomagnesemia (1.5 to 2.0 mEq/dl), and ten patients (5 percent) had hypermagnesemia (greater than 2.0 mEq/dl). There were no correlations between the severity of illness score (r = 0.145) or the degree of hypoproteinemia (r = 0.01) and the postoperative serum Mg level. Patients with severe hypomagnesemia (serum Mg less than or equal to 1.0 mEq/dl) experienced hypokalemia more often (p less than 0.02) than the others in the study. Furthermore, those with severe hypomagnesemia had a higher mortality rate (7/17 or 41 percent) than the remainder of the population studied (22/176 or 13 percent) (p less than 0.02). Those with severe hypomagnesemia had received aminoglycosides more often (p less than 0.001) than those with normal serum Mg concentrations. The serum Mg level was not a sensitive (68 percent) or specific (37 percent) predictor of survival. Our conclusions were as follows: (1) hypomagnesemia is common in postoperative ICU patients; and (2) patients in the postoperative ICU who have severe hypomagnesemia have a higher mortality and more hypokalemia than similarly ill patients with normomagnesemia. Because of the association between aminoglycoside therapy and severe hypomagnesemia, we recommend measurement of this variable in those patients receiving aminoglycosides. Furthermore, Mg replacement therapy is recommended for those patients with serum Mg values of 1 mEq/dl or less.

Hypothyroidism and pleural effusions.

Serous effusions have been thought to be an unusual complication of hypothyroidism and most commonly have been associated with ascites, pericardial fluid and heart failure. Pleural fluid as an isolated finding in hypothyroidism is apparently rare and complete analysis of these hypothyroid-associated pleural effusions has not been described. To determine the frequency, chemical characteristics and clinical associations of hypothyroidism and pleural effusions, the medical records of 128 patients with hypothyroidism (defined by an increased serum TSH concentration) were reviewed. The majority of effusions in patients with hypothyroidism were due to other diseases. Effusions solely due to hypothyroidism appeared to be a real entity. These effusions were borderline between exudates and transudates and showed little evidence of inflammation.

Alterations in sympathetic nervous system activity with intraoperative hypothermia during coronary artery bypass surgery.

To determine how intraoperative hypothermia associated with coronary bypass surgery (CABS) alters sympathetic nervous system (SNS) activity, we prospectively studied 21 adult CABS patients and measured preoperative, intraoperative, and postoperative circulating catecholamine concentrations. Because thyroid hormone levels change rapidly following CABS, we also serially measured these hormone levels. The measured plasma concentrations for each of the above variables were corrected for hemodilution during CABS by using serum albumin changes as a reference. It was concluded that important alterations in SNS activity and thyroid hormone homeostasis occur in humans during CABS and deep hypothermia, and that changes in core temperature may contribute to these findings. We speculate that these hormonal changes may influence the response to adrenergic receptor therapy in hypothermic patients and may contribute to arrhythmias during rewarming and the immediate postoperative period.