Abstract
Over two million pilgrims perform annual rituals in Makkah region, which when coincides with summer months, exposes them to outdoor temperatures exceeding 45 °C and humidity approaching 80%. Accordingly, heat illnesses are common including explicit heat strokes and heat exhaustion. No previous studies elaborated on electrocardiographic changes among this unique cohort.
Objective
To compare electrocardiographic changes in three groups exposed to high outdoor temperatures, namely, patients with heat stroke compared to patients with heat exhaustion and a control group exposed to the same outdoor temperatures without clinical manifestations.
Subjects and methods
Through case control design, two case groups of patients were selected. The first group (G1) was 34 patients admitted to the cooling units with clinical picture of heat stroke and the second group (G2) comprised 28 patients admitted with heat exhaustion. The control group (G3) included 31 patients selected from relatives of patients and outdoor workers. The outcome for comparison was 12-lead electrocardiographic changes done for all selected individuals. For (G1), the ECG was done while they were prepared for cooling or immediately when cooling was started.
Results
In G1, 18 were females and 16 males with ages of 20–76 years (59 ± 11 years). Their heart rates ranged from 64 to 160 beats per minute (mean 120 ± 24 per minute). Only 5/34 ECGs were completely normal. Sinus tachycardia was present in 27/34 patients (79%), with ischemic changes in 9/34 ECGs.
In G2, 24 were males and four females with ages of 25–80 (mean 47 ± 15 years), the heart rate ranged from 64 to 170 per minute (mean 97 ± 16 per minute). Seven out of 28 ECGs were normal (25%) while 21/28 had some abnormalities. None had ischemic changes.
Control group (G3), was five females and 26 males ages 18–80 years (mean 38 ± 15 years), 22/31 had normal ECGs (71%). All had normal sinus rhythm, 56–98 beats per minute (74 ± 11). Nine patients had some electrocardiographic abnormalities but none had ischemic changes.
Conclusion
We conclude that electrocardiographic abnormalities occur with a high frequency in patients with heat stroke and heat exhaustion, with sinus tachycardia and ischemic changes occurring more frequently in patients with heat stroke.
Keywords: Heat stroke, Heat exhaustion, Electrocardiography, Pilgrims
Pilgrimage season in Makkah involves more than two million pilgrims every year. Muslims from all over the world gather in the holy areas for the performance of Hajj rituals. This may occur during the summer season in which outdoor temperatures exceed 45 °C. Exposure to high outdoor temperatures can result in heat exhaustion or heat stroke in many pilgrims, especially those who are not acclimatized.
Several reports have described electrocardiographic changes in patients with heat stroke [1–4], but none of them have described the changes occurring in the acute phase of heat stroke and compared them with other patients exposed to heat but without the full-blown picture of heat stroke.
Materials and methods
The study was conducted in Makkah region, Saudi Arabia, during Hajj season which was coinciding with summer months. Through a case control design, two groups were selected to represent cases.
The first group (G1) was patients admitted to the cooling units immediately from triage with a clinical diagnosis of heat stroke. We managed to study 34 patients before cooling or immediately on starting cooling out of 50 patients admitted with heat stroke to eight cooling units, over a period of 5–6 h. In the remaining 16 patients, ECG was not done since cooling was already started for more than 30 min. All of these patients have history of prolonged exposure to heat, have core rectal temperatures exceeding 41 °C, and have disturbed level of consciousness ranging from confusion and disorientation to coma with loss of bowel and bladder control. The 12-lead ECG was performed immediately upon admission to the cooling units and before the active cooling was in progress.
The second group (G2) constituted 28 patients admitted with heat exhaustion for oral or intravenous volume repletion. These patients had prolonged exposure to heat, with symptoms of fatigue, lethargy and drowsiness. They were all conscious and with rectal temperatures of <40 °C. They all have clinical evidence of some degree of volume depletion evidenced by low JVP, postural drop in blood pressure, and increase in heart rate.
The third group (G3) consisted of 31 controls, who were selected from patients admitted with other diagnoses or relatives of patients admitted, in addition to outdoor workers in the area of the hospital, all exposed to the same outdoor temperatures. This group could not be matched regarding age to G1 and G2 because of the short time of the study. The study and its goal were explained to the above two groups.
A 12-lead electrocardiogram was done for all individuals in the three groups using commercially available HP4700 Pagewriter, and the data collected were entered into a computer program (Statsoft Statistica) for statistical analysis, including clinical and demographic data and detailed electrocardiographic analysis. ECGs are interpreted by two cardiologists blinded to the diagnosis.
Because of the need of the pilgrims to complete the rituals within a limited time frame, a follow-up ECG could not be obtained for all of the patients. Patients in G2 and G3 left as soon as they felt better, and patients in G1 were transferred to other hospitals within 12 h. The study protocol was approved by the Medical Research Council in King Faisal Specialist Hospital & Research Centre and the consent was waived for patients with clinical diagnosis of heat stroke.
Results
While males and females were almost equally represented in G1, there was preponderance of males in both G2 (85.7%) and G3 (83.9%). As shown in Table 1 the patients in G1 and G2 were significantly older than those in G3, and their mean body surface area was significantly higher than that in G3.
Table 1.
Characteristics of the study groups.
| Characteristics | Heat stroke group G1 (n = 34) | Heat exhaustion group G2 (n = 28) | Controls G3 (n = 31) |
|---|---|---|---|
| Gender | |||
| Males | 16(47%) | 24(85.7%) | 26(83.9%) |
| Females | 18(53%) | 4(14.3%) | 5(16.1%) |
| Mean age (yrs) | 59 ± 11⁎ | 47 ± 15⁎ | 38 ± 15 |
| Mean body surface area (m2) | 1.9 ± 0.2⁎ | 1.8 ± 0.1⁎ | 1.7 ± 0.1 |
P value <0.005 comparing each group to control.
As denoted in the study design and selection criteria for each group, Table 2 shows that the mean core temperature accounted for 41.7 ± 0.9 among G1, and 38.7 ± 1.0 among G2 which were significantly higher than that in G3 (37.1 ± 0.6). All participants in the control group (G3) showed normal sinus rhythm (mean ± SD:74 ± 11; range 56–98 beats per minute) compared to each of the other two groups where the mean heart rate was significantly higher in G1 (mean ± SD: 120 ± 24; range 64–160 beats per minute) with frank sinus tachycardia in 27/34 patients (79%), and in G2 (mean ± SD: 97 ± 16; range 64–170 beats per minute). On the same line, while the control group had within normal mean blood pressure (BP) (92 ± 16), G1 showed a significantly lower mean BP (76 ± 25) while it was significantly higher among G2 (102 ± 18).
Table 2.
Recorded vital signs of the study groups.
| Vital signs | Heat stroke group G1 (n = 34) | Heat exhaustion group G2 (n = 28) | Controls G3 (n = 31) |
|---|---|---|---|
| Mean core temp. (°C) | 41.7 ± 0.9⁎ | 38.7 ± 1.0⁎ | 37.1 ± 0.6 |
| Mean HR (beats/min) | 120 ± 24⁎ | 97 ± 16⁎ | 74 ± 11 |
| Mean (mean BP) (mmHg) | 76 ± 25⁎ | 102 ± 18⁎ | 92 ± 16 |
P value <0.005 comparing each group to control.
Regarding electrocardiographic (ECG) changes, as shown in Table 3, only 5/34 of G1 showed normal ECG in all parameters, ischemic ECG changes (more than 2 mm horizontal or downsloping ST depression) were present in 9/34 patients (Fig. 1). This was significantly different from the other two groups which had no ischemic changes (P < 0.001). There were more conduction abnormalities in G1 in the form of incomplete Right Bundle Branch Block (RBBB) compared to G3 (P = 0.02) but this did not reach statistical significance comparing G2 to G3 (P = 0.4).
Table 3.
Recorded electrocardiographic changes for the study groups.
| Vital signs | Heat stroke group G1 (n = 34) | Heat exhaustion group G2 (n = 28) | Controls G3 (n = 31) |
|---|---|---|---|
| Mean PR interval (ms) | 158 ± 22 | 152 ± 22 | 159 ± 22 |
| Mean QT interval (ms) | 314 ± 43⁎ | 326 ± 30⁎ | 364 ± 28 |
| Pathological Q-waves | 0 | 2 | 0 |
| Conduction abnormalities | |||
| IRBBB | 8⁎ | 4⁎ | 1 |
| RBBB | 1 | 0 | 0 |
| LAHB | 1 | 2 | 1 |
| Bifascicular block | 3 | 0 | 0 |
| Non-specific ST-T changes | 9⁎ | 5⁎ | 2 |
| Ischemic ST-T changes | 9⁎ | 0 | 0 |
P value <0.05 comparing each group to control, IRBBB (Incomplete Right Bundle Branch Block), RBBB (Right Bundle Branch Block), LAHB (Left Anterior Hemi-Block).
Figure 1.
ECG in heat stroke post cooling.
The QT interval was significantly shorter in both G1 (314 ms) and G2 (326 ms) compared to G3 (364 ms) with P value in both <0.0001. This is related to the faster heart rates in G1 and G2.
Echocardiographic studies were done on all patients that showed ischemic ST-T changes during the cooling period and none of which showed regional wall motion abnormalities. Four out of these nine patients had left ventricular hypertrophy while one had moderate aortic regurgitation with left ventricular dilatation and hypertrophy. The other four patients had no echocardiographic abnormalities to explain the ST-T changes seen on ECG.
Discussion
In this study, the electrocardiographic changes occurring in patients exposed to prolonged high outdoor temperatures were not specific to patients with heat stroke. They can occur roughly with the same frequency in patients with heat exhaustion and some of the patients exposed to heat without heat stroke or heat exhaustion. The higher frequency of tachycardia can be explained by the higher core temperatures in patients with heat stroke and heat exhaustion compared to the control group (heart rate increase by 10 beats/min for each 1 °C rise in core temperature). In a study by El-Sherif, it was shown that an increase in ambient temperature from 22 ± 1 to 40 ± 1 °C, keeping a relative humidity of 65 ± 5% for 2 h in six healthy subjects and three cardiac groups of 18 patients increased a normal subject’s respiratory rate by 35%, oxygen consumption by 35% and heart rate increased by 34% [5]. The higher heart rate and mean age in patients with heat stroke can explain the higher frequency of ST-T changes in this age group with more prevalence of hypertension, ischemic, and valvular heart diseases. Some of these were documented by echocardiography as mentioned and medical history was available on a limited number of comatosed patients when relatives were available or when patient recovered. In addition, cardiovascular changes occurring in heat stroke include hyperdynamic (high cardiac output state) although a hypodynamic or hypovolemic state may also be encountered. The pulse is usually rapid and full with wide pulse pressure and a CVP of 17 cm water or more is common [6–9]. In a study conducted by Dahmash using invasive monitoring in 10 patients with heat stroke, all patients studied were tachycardic with hypotension in 9/10 patients with a mean arterial pressure of 62 mmHg. Cardiac index was decreased in 1/10, normal in 5/10 patients and increased in 4/10 patients. Pulmonary capillary wedge pressure was normal in 6/10 patients, elevated in 3/10 and low in 1/10. Systemic vascular resistance was decreased in 8/10 patients and normal in 2/10 patients [10].
Shibolet et al. [1] reported that the only ECG abnormality among 36 cases was sinus tachycardia. Other ECG abnormalities have been reported in patients with heat stroke, the majority of which are ST segment and T wave abnormalities. In our study, ECG changes (more than 2 mm horizontal or downsloping ST depression) were present in 9/34 patients which were significantly different from the other two groups which had no ischemic changes (P < 0.001). Almost similar findings were reported among pilgrims in 1993 [11], and in Japan [12]. It is difficult to attribute these ST-T changes to electrolyte imbalance. Moreover, these EGG changes did not correlate well when serum potassium and other electrolyte imbalances were considered to be the causative factor [13]. The prognosis and consequent changes of the coronary or cardiovascular status of the patients could not have been assessed because the follow-up of these patients is almost impossible as they are highly mobile population during the Hajj pilgrimage. Nevertheless, it is likely that patients with heat stroke may have developed ST-T changes at least partly secondary to myocardial ischemia brought on by the increase in oxygen demand due to high fever, tachycardia, and a significantly high cardiac output state, or hypotension [14,15]. Therefore, it was stressed that when interpreting ST-T elevation in the ECG of a heat stroke patient, caution should be used so as to not misdiagnose it as an acute myocardial infarction [12]. One might question the significance of these ST-T changes in the absence of hard criteria (stress EGG, stress thallium, and coronary angiography), but as in the reported cases with acute myocardial infarction, the circumstantial evidence and EGG changes are highly suggestive of myocardial ischemia [11].
Conduction abnormalities with IRBB and IVCD with prolonged QT intervals have been reported in heat stroke cases [2–4]. The higher incidence of non-specific intraventricular conduction delay, especially incomplete RBBB detected among G1 in our study was similar to what was found in Spain [16], that may be related to electrolyte imbalance [17] characterizing heat stroke, true change in the conduction rate of the ramifications of the right bundle branch that could be attributed to the possible role of heat shock proteins in ion channels trafficking to cell membrane that has been recently described [16], or it may be secondary to increased pressure in the right side of the heart.
Conclusion
In this study, most of the ECG changes described were non-specific to the heat stroke group. The significant increase in heart rate is attributed to the higher core temperature in the heat stroke and heat exhaustion groups. The relative bradycardia in some patients could be related to increased intracranial pressure. The shorter QT interval in G1 and G2 can be explained by the significantly higher rate in those two groups. Some of the ST-T changes in G1, as discussed, were explained by the echocardiographic findings of underlying cardiovascular abnormalities.
A larger scale study involving multiple centers comparing these groups during the period of pilgrimage, preferably with follow-up ECG before discharge and detailed studies of patients who show significant electrocardiographic changes, may help identify patients with cardiac abnormalities explaining the above difference in the three groups.
Acknowledgement
Special thanks to Dr. Hend Al-Mansour, Ms. Dina Zawawi, and the research team of KFSH and RC, in addition to the medical team in Mena Hospital, who helped to conduct this study.
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