Spectral analysis of heart rate variability in the sepsis syndrome

Abstract

Sympathetic and parasympathetic activity was evaluated on 39 occasions in 17 patients with the sepsis syndrome, by measurement of the variation in resting heart rate using frequency spectrum analysis. Heart rate was recorded by electrocardiography and respiratory rate by impedance plethysmography. The sepsis syndrome was established on the basis of established clinical and physiological criteria. Subjects were studied, whenever possible, during the period of sepsis and during recovery. Spectral density of the beat-to-beat heart rate was measured within the low frequency band 0.04 to 0.10 Hz (low frequency power, LFP) modulated by sympathetic and parasympathetic activity, and within a 0.12 Hz band width at the respiratory frequency mode (respiratory frequency power, RFP) modulated by parasympathetic activity. Results were expressed as the total variability (total area beneath the power spectrum), as the spectral components normalized to the total power (LFPn, RFPn) or as the ratio of LFP/RFP. During the sepsis syndrome, total heart rate variability and the sympathetically mediated component, LFPn were significantly lower than during the following recovery phase (ANOVA, p < 0.0001, p < 0.01 respectively). Both APACHE II (Acute Physiological and Chronic Health Evaluation) and TISS (Therapeutic Intervention Scoring System) scores showed an inverse correlation with total heart rate variability, logLFP, LFPn and the LFP/RFP ratio (p < 0.002 to 0.0001). Sympathetically mediated heart rate variability was significantly lower during the sepsis syndrome and was inversely proportional to disease severity.

Lipopolysaccharide prolongs action potential duration in HL-1 mouse cardiomyocytes

“…Considering that murine heart rates range from 400 to 800 beats/min (20), an increase in action potential duration of this magnitude could account for LPS-induced bradycardia (22). Projecting in vitro observations to heart function in situ, these findings account at least in part for reduced heart rate variability (8,30,31,38) and depressed cardiac function that accompanies sepsis (36,44). This may be particularly relevant to neonatal sepsis where mortality is often preceded by reduced heart rate variability and transient decelerations (10,11).…”

“…This is attributable in part to the volume loading that is frequently the initial treatment for septic shock patients to maintain cardiac output and organ perfusion (15, 28). As is often the case in the complexity of sepsis, the prevailing symptoms can mask organ and system failure occurring at a deeper level in the clinical spectrum.The most prevalent sign of myocardial depression in the septic patients, in spite of their increased heart rates, is reduced heart rate variability (HRV), which is prodromal to unfavorable outcome (8,30,31,38). Based on telemetry studies in mice, this reduction in HRV is attributable to lipopolysaccharide (LPS; Ref.…”

“…The most prevalent sign of myocardial depression in the septic patients, in spite of their increased heart rates, is reduced heart rate variability (HRV), which is prodromal to unfavorable outcome (8,30,31,38). Based on telemetry studies in mice, this reduction in HRV is attributable to lipopolysaccharide (LPS; Ref.…”

Physiology of Vasopressin Relevant to Management of Septic Shock

“…First, depletion of neurohypophyseal stores of vasopressin in advanced shock due to excessive baroreceptor firing has been postulated. Second, others 56,57 have postulated autonomic insufficiency, citing lack of baroreflex-mediated bradycardia after vasopressin infusion as evidence. 1 Third, low concentrations of norepinephrine excite central vasopressin- Figure 2.…”

“…Landry and coworkers 1 showed that increased metabolism or clearance of vasopressin is not a mechanism of the low vasopressin levels in patients with septic shock. The potential mechanisms of vasopressin deficiency include (1) depletion of pituitary stores of vasopressin after exhaustive release of vasopressin in early septic shock, (2) autonomic dysfunction in patients with septic shock, 56,57 and (3) increased vascular endothelial release of NO within the posterior pituitary, which may downregulate vasopressin production (Table 3). 37 The mechanisms of the exquisite sensitivity of vasodilatory shock patients to vasopressin may also be multifactorial.…”