Effects of changing haematocrit, ventricular rate and myocardial inotropy on the accuracy of impedance cardiography.

1. The accuracy and limitations of the non-invasive impedance cardiograph technique were examined in dogs with electromagnetic flow-transducers mounted on the aortic root over a wide range of physiological conditions of anaemia, heart rate, stroke volume and myocardial inotropy. 2. The in vivo blood resistivity (rho-haematocrit relationship is linear and slightly inverse, and is thus opposite to the curvilinear, direct relationship of the bench-derived rho-haematocrit relationship. At haematocrit 41%, in vivo rho is 135 ohm.cm (s.e.m. = 1.0, n = 134) and rises only to 143 ohm.cm (s.e.m. = 1.6, n = 134) as haematocrit falls to 26%. 3. When in vivo rho is used in the Kubicek formula for stroke volume (SV) calculation, the instrument is linear and accurate for heart rates over 38-156 min-1. Thus 82% of all points fall within +/- 20% of the line of equal value over stroke volumes ranging from 8-46 ml (N = 3, n = 105). The standard error of the estimate for pooled data is +/- 2% of the mean impedance stroke volume value of 22.2 ml. The instrument tends to overread at heart rates lower than 60 min-1.

Central nervous system 5-hydroxytryptamine and noradrenaline specificity of ear vascular and ventilation reflexes in thermoregulating rabbits.

Contrasting hypotheses of mammalian thermoregulation were tested in unanesthetized rabbits in relation to the role of the central nervous (CNS) monoamines 5-hydroxytryptamine (5-HT) and noradrenaline (NA) in regulating lung function and ear skin blood flow (Doppler flowmeter). Normal rabbits and rabbits with CNS depletion of 5-HT and NA (caused by the neurotoxins 5,7-dihydroxytryptamine and 6-hydroxydopamine) were studied in an airconditioned chamber at ambient temperatures of 12 degrees, 22 degrees and 35 degrees C. The results suggest that CNS 5-HT plays an excitatory role in the heat conservation mechanism of cold-induced ear skin vasoconstriction, and that this effect is inhibited by CNS NA to cause heat dissipation during heat stress. Both CNS 5-HT and NA appear to exert a mild inhibitory restraint on ventilation even during heat stress. The data support the theory that CNS 5-HT is concerned with heat conservation and CNS NA with heat loss mechanisms in the cutaneous circulation, and that both monoamines moderate heat loss through panting. CNS monoamine-dependent thermoregulation in the rabbit thus resembles the model postulated for the cat, dog and monkey rather than, as previously proposed, for the sheep and goat.

Suprabulbar and bulbar integration of ventilation and ear vascular control during thermoregulation in the rabbit.

Suprabulbar and bulbospinal integration of cardiorespiratory responses to cold and heat stress was studied in groups of normal, thalamic and pontine rabbits. The animals sat in an airconditioned environmental chamber in which ambient temperature (TA) was maintained sequentially at 22 degrees C, 12 degrees C, 22 degrees C and 35 degrees C, with an accuracy of +/- 1 degree C. Neither thalamic nor pontine rabbits could maintain core temperature in cold or heat. At TA 35 degrees C, thalamic and pontine animals did not pant, indicating that telencephalic responses were necessary for the integration of mechanisms promoting respiratory heat loss. Thalamic animals, however, could inhibit ear vascular sympathetic tone in the heat, but the response was absent in pontine animals, suggesting diencephalic responses were essential for the integration of mechanisms promoting ear skin heat loss. Thus, the neural adjustments to thermal stress depend on mechanisms of integration distributed longitudinally throughout the central nervous system, and different components of the reflex cardiorespiratory response depend on different sites in the central nervous system for their full expression.

Hypoxaemia during postoperative recovery using continuous pulse oximetry.

Continuous pulse oximetry monitoring was used to determine the incidence of hypoxaemia (arterial oxygen saturation less than or equal to 90%) occurring in the first hour of postoperative recovery. Of 107 patients studied, hypoxaemia was recorded in 80%. Twenty-eight (26%) of these patients had saturations below 80%. The average frequency (i.e., the number of desaturations per patient) and the total duration of these desaturations was 7.7 desaturations and 182 seconds respectively. Intermittent measurements taken preoperatively and at 5 and 30 minutes postoperatively revealed hypoxaemia in 2%, 4% and 6% of patients respectively. In 39 patients who received oxygen therapy throughout the monitoring period, 64% experienced hypoxaemia within the first 15 minutes of recovery as opposed to only 18% in the final 15 minutes monitoring period. Of the factors assessed, only patients with a body mass index greater than 25 had an increased risk of hypoxaemia (P less than 0.01). Four patients required active intervention and ventilatory assistance. We conclude that postoperative hypoxaemia is a particularly common occurrence even in patients otherwise considered healthy. Hence, pulse oximetry should be employed routinely during recovery. Where possible, monitoring should be performed continuously for at least 45 minutes.

Role of central nervous system monoamines in cardiopulmonary effects of Althesin in rabbit and man.

The steroid induction agent, Althesin, infused intravenously in light anesthetic doses in otherwise unsedated man (84 micrograms kg-1 min-1) and rabbit (140 micrograms kg-1 min-1) causes similar autonomic and somatic effects. In the rabbit, the rise in heart rate (mainly due to central vagal blockade) and the selective depressant effects on respiratory rate are independent of CNS 5-hydroxytryptamine and noradrenaline. The rise in arterial pressure and the fall in hindlimb conductance is dependent on CNS 5-hydroxytryptamine and noradrenaline synthesizing neurons, which are probably arranged in series. These findings provide a working hypothesis for the mechanisms of action of Althesin on central cardiopulmonary controls in man.

Thoracic resistivity for stroke volume calculation in impedance cardiography.

Blood resistivity (rho) values used in the Kubicek formula for stroke volume (SV) calculation by impedance cardiography are bench derived and do not take into account complex blood velocity movements and dynamic hematocrit changes in systole. In this study, the relevance of rho has been questioned. Thoracic resistivity (rho tau) has been calculated in dogs from the rearranged Kubicek formula: rho tau = (SV . ZO2)/(L2 dZ/dtmax.T), where SV was measured by the electromagnetic flowmeter (EM). Hematocrit (Hct) in the dog was varied by hemorrhage and infusion. In contrast to the direct and exponential bench rho-Hct relationship, rho tau varies inversely with Hct, but by no more than +6.3 omega . cm (at Hct 26%) and -11.8 omega . cm (at Hct 66%) about a mean rho tau of 135 +/- 1.0 omega . cm (at Hct 40%). Impedance SV calculated using rho tau over a wide range of SV bears a linear relationship to EM values with a 95% prediction limit for a single SV estimate of +/- 0.84 about a mean value of 26.9 ml. The findings suggest that rho tau is virtually constant during a variety of physiological disturbances.

Impedance cardiography for cardiac output measurement: an evaluation of accuracy and limitations.

The Kubicek thoracic cylinder model of impedance cardiography (IC) for measuring beat-by-beat stroke volume (SV) was evaluated in controlled studies using the electromagnetic flowmeter (FM) as the reference technique. Assuming the validity of the Kubicek equation for stroke volume calculation, IC stroke volume was found to be a linear function of EM values at any one haematocrit over a wide range of SV, but the slope of the relationship fell as haematocrit fell. Experiments using the same equation in dogs, in which blood resistivity in vivo (rho tau) was made the dependent variable, and the EM-derived value was used for stroke volume, showed that rho tau was almost constant over a wide range of haematocrits. These findings were supported by studies in man and rabbit where Fick and thermodilution-derived values were used for stroke volume. When these data were applied to normotensive and hypertensive human subjects with normal hearts and lungs in controlled studies at rest, during tilting, with drug therapy and on exercise, IC measured stroke volume and cardiac output with a variability at least as good as the 9-11% acceptable for clinical use. This conclusion applied to thoracic configurations of different sizes and shapes from adult man to the neonate. In chronic disease states, while assessments of relative changes are valuable, absolute data are questionable. Further research is required under these conditions, as it is also for other models of IC, which are based on different assumptions.