Cardiac systolic and diastolic function during whole body heat stress

Abstract

During a whole body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and/or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole body heat stress. Echocardiographic indexes of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of approximately 1.0 degrees C via passive heat stress. Despite previous reports of heat stress-induced decreases in ventricular filling pressures and central blood volume, no changes in indexes of diastolic function were identified during heating [i.e., unchanged early diastolic mitral annular tissue velocity (E'), mitral inflow during the early diastolic phase (E), the E/E' ratio, and isovolumetric relaxation time]. Heat stress increased late diastolic septal (P = 0.03) and lateral (P = 0.01) mitral annular tissue velocities (A'), mitral inflow velocity during atrial contraction (P < 0.001), and the relative contribution of atrial contraction to left ventricular filling during diastole (P = 0.01), all indicative of improved atrial systolic function. Furthermore, indexes of ventricular systolic function were increased by heat stress [i.e., increased septal (P = 0.001) and lateral (P = 0.01) mitral annular systolic velocities and isovolumic acceleration at the septal (P = 0.03) and lateral (P < 0.001) mitral annulus]. These data are suggestive of improved atrial and ventricular systolic function by the heat stress. Together these data support previous findings, which used the less precise measure of ejection fraction, that heat stress improves indexes of systolic function, while diastolic function is maintained.

Fig. 1.

Early and late diastolic septal and lateral mitral annular velocities. Individual (left) and group averaged (right) echocardiographic measurements of early diastolic septal mitral annular velocity (A), early diastolic lateral mitral annular velocity (B), late diastolic septal mitral annular velocity (C), and late diastolic lateral mitral annular velocity (D) during normothermic (NT) and whole body heat stress (WBH) conditions. Early diastolic septal annular and lateral annular velocities were unchanged, whereas late diastolic septal annular and lateral annular velocities were increased during heat stress relative to normothermia. The significant increase in late diastolic tissue velocities is indicative of increased left atrial systolic function. Group data are means ± SD.

Fig. 2.

Mitral inflow velocities during different phases of diastolic filling. Individual (left) and group averaged (right) echocardiographic measurements of mitral inflow velocity during early diastolic filling (E wave; A), mitral inflow velocity during atrial contraction (A wave; B), the ratio of E/A (C), and the contribution of atrial contraction to diastolic filling (D) during NT and WBH conditions. Heat stress increased A velocity but not E velocity, which resulted in an increased relative contribution of atrial filling during diastole and a decrease in the E/A ratio. The significant increase in A velocity suggests that heat stress augments atrial systolic function. Moreover, heat stress increases the dependence on atrial booster to maintain left ventricular filling in the face of reduced ventricular filling pressures. Group data are means ± SD.

Fig. 3.

Relationship between early diastolic inflow velocity and early diastolic tissue velocity (E/E′) at the septal and lateral wall. Individual (left) and group averaged (right) calculations of the E/E′ ratio at the septal (A) and the lateral (B) wall during NT and WBH conditions. The E/E′ ratio at both the septal and lateral walls were unchanged during heat stress relative to normothermia.

Fig. 4.

Isovolumetric relaxation time. Individual (left) and group averaged (right) isovolumetric relaxation times during NT and WBH conditions. The isovolumetric relaxation time was unchanged during heat stress relative to normothermia. Group data are means ± SD.

Fig. 5.

Peak septal and lateral mitral annular systolic velocities (S′). Individual (left) and group averaged (right) echocardiographic measurements of peak septal mitral annular systolic velocity (A) and peak lateral mitral annular systolic velocity (B) during NT and WBH conditions. Septal annular and lateral annular systolic velocities were increased during heat stress relative to normothermia, thereby indicating an increase in cardiac systolic function. Group data are means ± SD.

Fig. 6.

Isovolumic acceleration of the septal and lateral mitral annulus. Individual (left) and group averaged (right) calculations of isovolumic acceleration at the septal mitral annulus (A) and the lateral mitral annulus (B) during NT and WBH conditions. Isovolumic acceleration was significantly increased at both locations during heat stress relative to normothermia, which is indicative of increased cardiac systolic function. Group data are means ± SD.