Hemodynamic Changes and Intravascular Hydration State in Heat Stroke
1989; King Faisal Specialist Hospital and Research Centre; Volume: 9; Issue: 4 Linguagem: Inglês
10.5144/0256-4947.1989.378
ISSN0975-4466
AutoresSaad S. Al-Harthi, M.S.Sharaf El-Deane, Jawaid Akhtar, Mansour M. Al-Nozha,
Tópico(s)Thermal Regulation in Medicine
ResumoOriginal ArticlesHemodynamic Changes and Intravascular Hydration State in Heat Stroke Saad S. Al-Harthi, MD, Facharzt M. S. Sharaf El-Deane, MD, FACC Jawaid Akhtar, and MD, MRCP, MRCPI Mansour M. Al-NozhaFRCP, FRCPI Saad S. Al-Harthi Address reprint requests and correspondence to Dr. Al-Harthi: Department of Medicine (38), College of Medicine, King Saud University, P.O. Box 2925, Riyadh 11461, Saudi Arabia. From the Division of Cardiology, Department of Medicine, College of Medicine, King Saud University, Riyadh , M. S. Sharaf El-Deane From the Division of Cardiology, Department of Medicine, College of Medicine, King Saud University, Riyadh , Jawaid Akhtar From the Division of Cardiology, Department of Medicine, College of Medicine, King Saud University, Riyadh , and Mansour M. Al-Nozha From the Division of Cardiology, Department of Medicine, College of Medicine, King Saud University, Riyadh Published Online::1 Jul 1989https://doi.org/10.5144/0256-4947.1989.378SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutAbstractAcute and serial hemodynamic measurements in 13 pilgrims (average age, 55.2 ± SD 9.3 years) suffering from heat stroke (average rectal temperature, 41.3 ± 1.0°C) revealed a hyperdynamic circulation pattern and a low total peripheral resistance. Five patients had pulmonary edema with an average cardiac index of 5.29 ± SD 0.56 L/min/m2, which was slightly higher than the average cardiac index in the group of eight patients without pulmonary edema, 4.76 ± SD 0.6 L/min/m2. This higher cardiac index was believed to be due to iatrogenic fluid overload which was hard to accommodate intravascularly with the cooling process raising the peripheral vascular resistance, decreasing the venous capacitance, and redistributing the blood from the dilated circulatory bed in the skin to the central circulation. Our data highlight the fact that there is no major intravascular dehydration in heat stroke. The treatment of choice is cooling. The entire process of "supporting the cardiovascular system" should take into consideration avoidance of fluid overload by rapid intravenous fluid administration. Gradual hydration, allowing time for intracellular compartment repletion after cooling, is more appropriate.SS Al-Harthi, MSS El-Deane, J Akhtar, MM Al-Nozha, Hemodynamic Changes and Intravascular Hydration State in Heat Stroke. 1989; 9(4): 378-383IntroductionHeat stroke is a major health problem during pilgrimage to Makkah (Hajj) in Saudi Arabia. High ambient temperature (up to 48°C), overcrowding, strenuous exercise performing the rituals, and lack of adequate acclimatization are the main contributing factors to heat stroke. Between 1500 and 2000 cases are reported every year during the pilgrimage season. Heat stroke is a medical emergency with a high mortality.1,2 Serious complications include acute circulatory failure, adult respiratory distress syndrome, disseminated intravascular coagulopathy, and renal failure. Early recognition and prompt appropriate treatment are expected to reduce the high mortality.1–3 Dry hot skin suggesting total body fluid depletion coupled with hypotension in heat stroke left many physicians, short of any hemodynamic study support, with the prevailing belief that victims of heat stroke were suffering from marked intravascular fluid depletion. Such a belief encouraged doctors, in an attempt to support the cardiovascular system, to infuse rapidly large amounts of intravenous fluids1,4 (3000 mL or more) in victims of heat stroke on arrival at heat stroke centers. Such a supportive measure has been associated with 35% to 65% incidence of bronchospasm and respiratory distress,4 which is attributed to aspiration and/or to adult respiratory distress syndrome without adequate hemodynamic assessment to determine cases of pulmonary edema secondary to fluid overload.A prospective study was designed and conducted in heat stroke centers in Makkah and Mina (holy places for muslim pilgrims from all over the world) in summer 1986. The purpose of the study was to investigate the acute hemodynamic parameters in the early phases of heat stroke and during the cooling process to throw some light on the actual intravascular hydration state and to estimate the average safe intravenous fluid requirement needed to obtain adequate cardiovascular support.PATIENTS AND METHODSPatients were studied upon arrival to the heat stroke center in Mina and Makkah. Inclusion criteria were (1) rectal temperature of 40°C or more; (2) hot dry skin; and (3) central nervous system disturbance (e.g., delirium, semicoma, or coma). All patients fulfilling these criteria and having available the Swan-Ganz insertion team upon arrival to the cooling room were studied regardless of their clinical status. Thirteen patients were studied randomly. Along with cooling initiation, a No. 8 French Cordis subclavian introducer was inserted, and a No. 7 French Swan-Ganz thermodilution catheter was advanced, guided with pressure tracing monitor. Right atrial pressure, right ventricular pressures, pulmonary arterial pressures, and pulmonary capillary wedge pressure (PCWP) were measured. Cardiac output was calculated using thermodilution technique and a thermodilution computer. Pulmonary pressure and PCWP measurements and cardiac output assessment along with systemic blood pressure and heart rate were obtained as frequently as the field management circumstances allowed. Central blood temperature was recorded along with rectal temperature throughout the whole cooling process, and systemic vascular resistance and systemic vascular resistance index, as well as total pulmonary vascular resistance and total pulmonary vascular resistance index were calculated5 for each recording. Mean time between the diagnosis and hemodynamic study was 15 minutes (range, 10 to 20 minutes). The thermodilution catheter along with the Cordis introducer were removed when the patient's hemodynamic status was thought to be essentially back to normal or when there was a malfunction in the catheter device (one patient). The statistical method used was the Student t test. The standard least-squares correlation coefficients were evaluated and tested for significance.RESULTSGroup 1 comprised eight patients who recovered completely with no pulmonary edema or complications. Their average age was 58.3 ±SD 4.3 years. Group 2 comprised five patients (38%) who had acute respiratory distress with bronchospasm with no evidence of aspiration. Their average age was 63.8 ± SD 8.5 years. (There was no statistical difference in age between the two groups.) All five patients had pulmonary edema, as evidenced both clinically and radiologically, which was confirmed by pulmonary capillary wedge pressure measurement, but they did not qualify for being actual cases of adult respiratory distress syndrome. Two patients in the pulmonary edema group were treated with intravenous sodium nitroprusside drip, and the other three patients were treated with intravenous furosemide (Lasix). One patient from group 2 who was treated with intravenous furosemide never woke from his coma, and he developed disseminated intravascular coagulopathy and renal failure and died after transfer to a referral hospital in Jeddah.It was estimated that eight patients without pulmonary edema received 400 to 1200 mL of normal saline in the first 4 hours of management, while the five patients in the pulmonary edema group received 1200 to 1800 mL of normal saline in the first 4 hours of management, most within the first hour. The amount of fluid given to an individual patient depended on the physician. Sometimes the patients arrived in the heat stroke center with an intravenous line already in place.Average rectal temperature on arrival was similar in both groups, 42.56°C ± SD 0.78°C in group 1 versus 41.96 ± SD 0.73°C in group 2, showing no statistical difference.There was a direct correlation between the cardiac index and the rectal temperature. In group 1, the r value was .59 (P < 0.01), and in group 2, the r value was .89 (P < 0.001). The cardiac index was only slightly higher for the rectal temperature in group 2 (Figure 1). The systemic vascular resistance index correlated inversely with rectal temperature. In group 1, the r value was .67 (P < 0.005), and in group 2, the r value was .44 (P < 0.02) (Figure 2). The systemic vascular resistance index rose during and after cooling; the rise was completed in 2 to 4 hours in most patients in group 1 and 3 to 6 hours in group 2 (Figure 3).Figure 1. Correlation between cardiac index (C.I.) and rectal temperature.Download FigureFigure 2. Systemic vascular resistance index (SVRI) correlation with rectal temperature.Download FigureFigure 3. Systemic vascular resistance index (SVRI) and its correlation to time.Download FigureThe average cardiac index was 4.76 ± SD 0.6 L/min/m2 in group 1. This was slightly higher in group 2, 5.29 ± SD 5.6 L/min/m2. The high cardiac index went down in 2 to 3 hours in group 1, and this decrease took slightly longer (3 to 4 hours) in group 2 (Figure 4). The average PCWP on inserting the Swan-Ganz catheter in group 1 was 9.0 ± SD 1.4 mm Hg, while in group 2, it was 12.2 ± SD 6.0 mm Hg (no statistically significant difference). The PCWP did not change significantly in group 1 throughout management while it increased sharply in group 2 early after cooling was started. The nitroprusside appeared to act more promptly in decreasing the PCWP than furosemide (Figure 5).Figure 4. Correlation of vascular cardiac index (C. I.) to time.Download FigureFigure 5. Pulmonary capillary wedge (PCW) pressure and its correlation to time.Download FigureThe total pulmonary vascular resistance index did not change significantly during and after cooling in group 1, while it went to high levels in group 2 and responded well to treatment (Figure 6).Figure 6. Total pulmonary vascular resistance index and its correlation to time.Download FigureDISCUSSIONOur data illustrate the fact that high cardiac output in heat stroke is a direct response to the increase in tissue oxygen demand reflected by high rectal temperature. All of our patients showed a high cardiac output response and hyperdynamic circulation and not low cardiac output, as has been reported rarely.6 The systemic vascular resistance appears to correlate inversely with the rectal temperature in group 1, the patients without pulmonary edema; such a correlation was expectedly attenuated in group 2, the patients with pulmonary edema, due to fluid overload and the pharmacologic therapeutic interventions altering the systemic vascular resistance natural response.These data lead us to believe that the decrease of systemic vascular resistance in heat stroke causes the hypotension observed in most patients when first seen rather than hypotension being due to intravascular dehydration which appears to be mild. This is evidenced by the fairly good PCWP values on arrival even in patients without pulmonary edema, the group which was not overloaded with fluid early on. Infusing intravenous fluids aggressively seems only to increase the cardiac index a little at the expense of raising the PCWP significantly, producing a state of pulmonary edema. The slightly higher PCWP values on arrival in the pulmonary edema group, which did not reach statistical significance, are probably related to the early and more vigorous intravenous hydration that they received prior to completing the insertion procedure of the Swan-Ganz catheter. The continuation of such an aggressive hydration resulted in a significant rise of PCWP. This rise was early, coinciding with an early but a more gradual rise in systemic vascular resistance. Early increase in vascular tone during cooling translates on the venous side as a limitation in venous capacitance. Such a limitation does not allow the accommodation of rapidly infused intravenous fluids at a time when cooling is also redistributing the blood from the skin-dilated circulatory bed to the central circulation, making it more likely to express the state of fluid overload as acute pulmonary edema.The cardiac index in group 2 was slightly higher, making it unlikely that the pulmonary edema was due to myocardial failure. The response to sodium nitroprusside drip was prompt, increasing venous capacitance, allowing time for exchange between the excess intravascular fluid and the depleted intracellular compartment to occur. The afterload reducing effect of nitroprusside did not increase the cardiac index at all, attesting to the absence of heart failure as the heart was already working at full capacity. The thermal challenge to the myocardium was similar in the two groups and cannot explain any difference.We do understand the limitation of our study which involves a small number of patients. Still the study underscores the potential risks of rapid intravenous fluid administration during treatment of heat stroke victims. We cannot rule out completely the existence of myocardial depression in heat stroke, but our unpublished data of systolic function in heat stroke patients by two-dimensional echocardiography in 20 patients suggest that a significant left ventricular dysfunction does not occur.The only death occurred in one patient with fluid overload who remained unresponsive. It is not clear to us how many cases of brain edema in heat stroke are precipitated by acute fluid overload rather than by thermal injury to the brain; however, this potential hazard should be kept in mind.Our study also emphasizes the importance of using Swan-Ganz monitoring when broncho-spasm and dyspnea develop in heat stroke to avoid labeling these cases as "adult respiratory distress syndrome" by identifying a state of fluid overload which in our group of patients explained all cases of respiratory distress. Such differentiation is critical for management.CONCLUSIONSEfficient cooling of patients with heat stroke remains the treatment of choice.7–11 In light of our results, we believe that although victims of heat stroke may have an appreciable total body fluid deficit, it seems that this is mainly at the expense of the intracellular compartment accounting for signs of dehydration while the intravascular compartment manages to keep an adequate circulating volume and avoids significant depletion. The low blood pressure in heat stroke,12,13 in our experience, is due to low peripheral vascular resistance rather than to significant intravascular depletion or a low cardiac output.Rapid intravenous fluid administration while cooling patients with heat stroke to correct their hypotension before determining the effect of cooling on their blood pressure seems to be particularly hazardous, because this probably coincides with vasoconstriction and probably a decrease in venous capacitance along with redistribution of blood from the skin to the central circulation, making it even harder to accommodate excess fluid without resulting in pulmonary edema.In the routine treatment of heat stroke, we recommend administering not more than 1200 mL of normal saline in the first 4 hours of management. In most instances, 700 to 800 mL may be adequate, with later, more gradual repletion of the intracellular compartment with free water intravenously as 5% dextrose/water or orally when the patient is capable of taking fluids by mouth.The clinician has to individualize treatment in certain cases of obvious continuous volume loss by correcting for it. In cases where there is ambiguity, use of hemodynamic Swan-Ganz monitoring can guide fluid therapy.Carefully monitored intravenous administration of sodium nitroprusside proved to be safe and effective in treating pulmonary edema in heat stroke. This may particularly help skin perfusion and heat exchange in cases of skin vasoconstriction, and it may also prove particularly helpful in cases of poor tissue perfusion and lactic acidosis.13,14ARTICLE REFERENCES:1. Shibolet S, Lancaster MC, Danon Y. "Heat stroke: a review" . Aviat Space Environ Med. 1976; 47 (3): 280–301. Google Scholar2. Jones TS, Liang AP, Kilbourne EM, et al. 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New York: Grune and Stratton, 1979: 29–39. Google Scholar9. Weiner JS, Khogali M. "A physiological body-cooling unit for treatment of heat stroke" . Lancet. 1980; 1 (8167): 507–9. Google Scholar10. Khogali M, Weiner JS. "Heat stroke: report on 18 cases" . Lancet. 1980; 2 (8189): 276–8. Google Scholar11. Al-Harthi S, Yaqub B, Al-Nozha M, et al. "Management of heat stroke patients by rapid cooling comparing a conventional method with a body cooling unit" . Saudi Med J. 1986; 7: 369–76. Google Scholar12. Rowell LB, Brengelmann GL, Murray JA. "Cardiovascular responses to sustained high skin temperature in resting man" . J Appl Physiol. 1969; 27: 673–80. Google Scholar13. Costrini AM, Pitt HA, Gustafson AB, Uddin DE. "Cardiovascular and metabolic manifestations of heat stroke and severe heat exhaustion" . Am J Med. 1979; 66 (2): 296–302. Google Scholar14. Stadnyk AN, Glezos JD. "Drug-induced heat stroke" . Can Med Assoc J. 1983; 128 (8): 957–9. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 9, Issue 4July 1989 Metrics History Accepted5 November 1988Published online1 July 1989 ACKNOWLEDGMENTThe authors thank the administration, doctors, and nurses of Ajyad Makkah Heat Stroke Center, the staff of King Saud University Hajj Mission at Mina Al-Jesser Heat Stroke Center for their cooperation and help, Dr. Adrian Lambourne for statistical help, and Bennie Campos for secretarial assistance.InformationCopyright © 1989, Annals of Saudi MedicinePDF download
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