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Cardiovascular Alterations in Heat Stroke

1993; Elsevier BV; Volume: 103; Issue: 4 Linguagem: Inglês

10.1378/chest.103.4.987

1931-3543

Zakauddin Vera, Carroll E. Cross,

Thermal Regulation in Medicine

Heat stroke (HS) constitutes a medical emergency and is associated with a significant mortality.1Austin MG Berry JW Observations on one hundred cases of heat stroke.JAMA. 1956; 161: 1525-1529Crossref PubMed Scopus (114) Google Scholar It has been categorized into the "exertional" and "classic" varieties. Exertional HS occurs in generally healthy persons during physical activity in hot, humid climates. It is associated with sweating, central nervous system (CNS) dysfunction, and rectal temperatures of 41°C and higher. Rhabdomyolysis, disseminated intravascular coagulation (DIC), and lactic acidosis are common complications. Classic HS occurs in the older individual, often with intercurrent illness and medication use and after exposure to high ambient temperature for extended periods. Hyperpyrexia, hot dry skin and altered mental status (eg, confusion, stupor, coma) are hallmark features.1Austin MG Berry JW Observations on one hundred cases of heat stroke.JAMA. 1956; 161: 1525-1529Crossref PubMed Scopus (114) Google Scholar Rhabdomyolysis, DIC, and lactic acidosis are rarely seen in the classic syndrome. In this issue of Chest, Dahmash et al (see page 1210) present right heart catheterization data on ten patients who developed HS during the Hadj pilgrimage in Mecca, Saudi Arabia. As the authors state, the temperatures during the hot summer days in Mecca may reach as high as 50°C, with humidity of 50 percent or higher. About the weather in Mecca it has been said that "the heat is stifling in winter, and almost insupportable, even by Arabs, in summer."2de Gaury G The rulers of Mecca. Dorset Press, New York1991: 17-51Google Scholar Some 1 million to 2.5 million Muslims from all over the world, many in advanced years of life, perform the Hadj every year. This pilgrimage lasts several days, during which time the pilgrims are exposed to the elements. Services include circumambulating the Kaabah, the house of worship built by Abraham and his son Ishmael, and hastening between the hills of Safa and Marwah, where Hagar, carrying her infant son Ishmael, had wandered the desert in search of water.2de Gaury G The rulers of Mecca. Dorset Press, New York1991: 17-51Google Scholar, 3Haneef S What everyone should know about Islam and Muslims. Library of Islam, Des Plaines, Il1985: 51-59Google Scholar Because the Islamic calendar is lunar, the year is some 11 days shorter compared to the Gregorian calendar. Thus, the Hadj season may fall during the height of summer for several years in a row, during which time hundreds of pilgrims suffer HS. In the United States, HS is generally considered in association with boot camps, sports (particularly football), and heat waves.4Knochel JP Heat stroke and related heat disorders.Dis Mon. 1989; 306: 304-377Google Scholar This problem came into national focus during the 1990–1991 Persian Gulf crisis. When exercise or environmental heat stress result in increased body temperature, activation of CNS hypothalamic reflexes results in increased cardiac output, cutaneous vasodilation, increased cutaneous blood flow, and splanchnic vasoconstriction.5Rowell LB Human cardiovascular adjustments to exercise and thermal stress.Physiol Rev. 1974; 54: 75-159Crossref PubMed Scopus (1197) Google Scholar, 6Rowell LB Kraning KK Kennedy JW Evans TO Central circulatory responses to work in dry heat before and after acclimation.J Appl Physiol. 1967; 22: 509-518PubMed Google Scholar Thus, efficient heat dissipation requires a functional thermoregulatory center and normally responsive cardiocirculatory and dermal systems. In individuals acclimated to exercise under conditions of heat, cardiovascular adaptation includes increased plasma volume,5Rowell LB Human cardiovascular adjustments to exercise and thermal stress.Physiol Rev. 1974; 54: 75-159Crossref PubMed Scopus (1197) Google Scholar increased stroke volume, and decreased heart rate (HR).6Rowell LB Kraning KK Kennedy JW Evans TO Central circulatory responses to work in dry heat before and after acclimation.J Appl Physiol. 1967; 22: 509-518PubMed Google Scholar Heat stroke is caused by excessive body heat storage when high ambient temperature prevents heat dissipation by radiation or convection and sweat evaporation is limited by humidity. Although the fundamental initiating pathophysiology of HS is not fully understood, intense hyperthermia with varying degrees of heat-induced tissue injury, neurohumoral factors, mediator releases, and CNS mechanisms (integrated complex afferent and efferent hypothalamic reflexes involving thermoregulatory, cardiovascular, and pulmonary mechanisms) probably all contribute.4Knochel JP Heat stroke and related heat disorders.Dis Mon. 1989; 306: 304-377Google Scholar, 7Bouchama A Parhar RS El-Yazigi A Sheth K Al-Sedairy S Endotoxemia and release of tumor necrosis factor and interleukin la in acute heatstroke.J Appl Physiol. 1991; 70: 2640-2644PubMed Google Scholar Excluding preexisting coronary or other structural heart disease and the influence of cardiodepressant drugs, a central question is whether circulatory shock and collapse in HS are due to myocardial dysfunction, volume depletion, peripheral vascular failure, or a combination of those factors. Are other factors involved? And what molecular and cellular mechanisms and transducing neurohumoral pathways are involved? Using right heart catheterization, Sprung8Sprung CL Hemodynamic alterations of heat stroke in the elderly.Chest. 1979; 75: 362-366Crossref PubMed Scopus (33) Google Scholar studied seven elderly individuals with classic HS. All were hypotensive. Two patients had increased cardiac index (CI), increased right atrial pressure (RAP), normal pulmonary capillary wedge pressure (PCWP), and decreased systemic vascular resistance (SVR). Five patients had decreased CI, decreased RAP, normal PCWP, and increased SVR. Sprung concluded that circulatory failure appeared to be secondary to peripheral pooling of blood or hypovolemia. O'Donnell and Clowes9O'Donnell Jr, TF Clowes Jr, GHA The circulatory abnormalities of heat stroke.N Engl J Med. 1972; 287: 734-737Crossref PubMed Scopus (103) Google Scholar studied eight marine recruits suffering from exertional HS. There was a hyperdynamic circulatory pattern in seven with increased mean CI (6.45 L/min/m2), HR (120 beats/min), and central venous pressure (CVP) (11 cm H2O) and low SVR. One patient with a rectal temperature of 43.4°C was in shock with a hypodynamic response (CI, 1.7/L/min/m2; mean arterial pressure, 37 mm Hg; HR, 140 beats/min; CVP, 18 cm H2O). The authors concluded that in HS, owing either to direct thermal injury to the myocardium or to increased pulmonary vascular resistance, the heart may not meet the elevated circulatory demand. The hypothesis of myocardial injury is supported by a pathologic study of victims of HS.10Malamud NW Haymaker W Custer RP Heat stroke: a clinicopathological study of 125 fatal cases.Milit Surg. 1946; 99: 397-499PubMed Google Scholar The findings included right-sided cardiac dilatation, subendocardial hemorrhage in the left ventricle, and severe degeneration of cardiac muscle in patients who died within 24 h. Zahger et al11Zahger D Moses A Weiss AT Evidence of prolonged myocardial dysfunction in heat stroke.Chest. 1989; 95: 1089-1091Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar described two cases of exertional HS in whom a radionuclide ventriculogram demonstrated dilatation and diffuse hypoldnesis of the right ventricle which persisted for several weeks, suggesting myocardial damage. A mechanism for ventricular dysfunction in HS has been proposed by Gathiran et al.12Gathiran P Wells M Raidoo D Brock-Utne J Gaffin SL Portal and systemic arterial plasma lipopolysaccharide concentration in heat-stressed primates.Circ Shock. 1988; 25: 223-230Google Scholar They found that in monkeys, elevation of core temperatures to 40°C was associated with increased portal and systemic arterial lipopolysaccharide (endotoxin) concentration. Lipopolysaccharide not removed by the liver enters the systemic circulation and at a sufficient concentration can cause vascular collapse, shock, and death. An elevated plasma lipopolysaccharide concentration is known to cause pulmonary and systemic edema and cardiac dysfunction.13Suffredini A Fromm R Parker M Brenner M Kovacs J Wesley R et al.The cardiovascular response of normal humans to the administration of endotoxin.N Engl J Med. 1989; 321: 280-287Crossref PubMed Scopus (812) Google Scholar These findings12Gathiran P Wells M Raidoo D Brock-Utne J Gaffin SL Portal and systemic arterial plasma lipopolysaccharide concentration in heat-stressed primates.Circ Shock. 1988; 25: 223-230Google Scholar, 13Suffredini A Fromm R Parker M Brenner M Kovacs J Wesley R et al.The cardiovascular response of normal humans to the administration of endotoxin.N Engl J Med. 1989; 321: 280-287Crossref PubMed Scopus (812) Google Scholar are supported by studies in HS victims during the 1989 Hadj.7Bouchama A Parhar RS El-Yazigi A Sheth K Al-Sedairy S Endotoxemia and release of tumor necrosis factor and interleukin la in acute heatstroke.J Appl Physiol. 1991; 70: 2640-2644PubMed Google Scholar The hemodynamic data of Dahmash et al are of interest since few studies in the literature have included data concerning cardiovascular and pulmonary hemodynamic function in early presentations of classic HS. The hyperdynamic circulatory profiles (increased cardiac output, low SVR, and low to normal BP) have been described previously. The normal PCWP and SVR appear to exclude any substantial left or right ventricular systolic (and perhaps diastolic) dysfunction, although the data do not contain information on cardiac chamber size, diatolic volume, and ejection fraction. The suggestion is that in relatively "uncomplicated" forms of classic HS treated expeditiously with cooling before severe tissue damage has occurred (and with no coexisting cardiopulmonary disease, no significant tissue injury or rhabdomyolysis, and no DIC), the hyperdynamic cardiovascular profile is not accompanied by significant abnormalities in pulmonary hemodynamics or in cardiac function. Whether more severe forms of HS mimic much of the pathophysiology of sepsis syndromes, implicating roles for endotoxin12Gathiran P Wells M Raidoo D Brock-Utne J Gaffin SL Portal and systemic arterial plasma lipopolysaccharide concentration in heat-stressed primates.Circ Shock. 1988; 25: 223-230Google Scholar, 13Suffredini A Fromm R Parker M Brenner M Kovacs J Wesley R et al.The cardiovascular response of normal humans to the administration of endotoxin.N Engl J Med. 1989; 321: 280-287Crossref PubMed Scopus (812) Google Scholar and a complex array of inflammatory immune mediator systems,7Bouchama A Parhar RS El-Yazigi A Sheth K Al-Sedairy S Endotoxemia and release of tumor necrosis factor and interleukin la in acute heatstroke.J Appl Physiol. 1991; 70: 2640-2644PubMed Google Scholar remains to be fully elucidated.