Arterial Pressure Curve Research Articles

Effect of a single dose of esmolol on the bispectral index scale (BIS) during propofol/fentanyl anaesthesia

Esmolol, a short-acting beta 1-antagonist, can reduce anaesthetic requirements and decrease seizure activity during electroconvulsive therapy even after a single dose of 80 mg. We studied the effect of esmolol on the bispectral index scale (BIS), which is a processed EEG recently introduced to monitor depth of anaesthesia. We gave esmolol 80 mg to 30 healthy male patients after induction of anaesthesia using propofol, with either fentanyl (group 1) or placebo (group 2). Patients were ventilated mechanically through a laryngeal mask airway and anaesthesia was maintained using propofol to keep the BIS value between 55 and 60. Esmolol did not affect the BIS index value in either group. In group 1, the areas (mean (SD)) under the BIS vs time curve 3 min before and 3 min after esmolol administration were 145 (9) and 146 (8) respectively (P = 0.116). In group 2 values were 147 (8) and 146 (7) respectively (P = 0.344). In contrast, in group 1 the area under the systolic arterial pressure (SAP) curve was 299 (31) before and 270 (29) after esmolol (P < 0.001), and 156 (17) and 141 (17) respectively for heart rate (P < 0.001). In group 2 values were 326 (36) and 302 (41) for SAP (P < 0.001) and 182 (25) and 155 (22) for heart rate (P < 0.001). The results suggest that a single dose of esmolol affects the SAP and heart rate but does not affect BIS values.

Comparaison de deux techniques de monitorage du débit cardiaque : méthode du contour de pouls et thermodilution artérielle pulmonaire continue

Two devices for continuous cardiac output (CO) monitoring at patient bedside were evaluated. Vigilance™ monitor (Baxter Lab.) provides CO measurements by intermittent bolus (TDCO Vig) and continuous thermodilution (CCO Vig) methods, curves are both collected using a pulmonary artery catheter ; PICCO™ monitor (Pulsion Lab.) also provides continuous CO by pulse contour analysis (CCO Pic) and intermittent trans-thoracic thermodilution CO measurements (TDCO Pic), which is used to calculate a calibration factor for further beat-to-beat estimations of CCO Pic. Both systemic arterial pressure and thermodilution curves are collected using a femoral arterial catheter. The objectives of the study were : 1) to compare both methods, 2) to identify the situations possibly responsible for a poor reliability of the pulse contour method. CO measurements ( n=301) were recorded simultaneously with both devices in 10 ICU patients : 44 conflicting data pairs, measured after vaso-active drugs initiation or following a calibration procedure performed during cardiac arythmia, were excluded. 257 data pairs for continuous CO measurements were compared using linear regressions and Bland-Altman plots method. Mean values for CCO Vig and CCO Pic were 7,3±2,63 and 7,8±3,04 l. min −1 respectively, and the correlation was significant ( r=0,94, p<10 −4). The average difference (bias) was 0,5± 1,06 l. min −1, i.e 7 % overestimation of CO by CCO Pic, and the 95 % confidence interval was large. For 9 among 10 patients the correlation between CCO Vig and CCO Pic was good (Spearman test). For CO values less than 8 l.min −1, the bias and 95 % confidence interval were smaller (0,2±0,66 l. min −1, n=180). Moreover, 108 data pairs for intermittent CO measurements were collected. The correlation between TDCO Vig (7,4±2,7 l. min −1) and TDCO Pic (8,1±1,06 l. min −1) was significant ( r=0,97, p<10 −4). The bias was 0,76±0,86 l. min −1 and could be related to a thermal loss between pulmonary and femoral arterial collection. On the whole, the agrement between both continuous CO measurments is acceptable. Since TDCO Pic is used for CCO Pic calibration, the difference between the two CO continuous methods could be partly explained by an overestimation of TDCO Pic. Consequently, the software calibration process should be refined. Moreover, we identified two situations that are responsible for erroneous values of CCO Pic and require a new calibration : cardiac arythmia during PICCO™ calibration, vaso-active drugs initiation.

What factors are associated with hyperlactatemia after cardiac surgery characterized by well-maintained oxygen delivery and a normal postoperative course? A retrospective study

Background and objective The purpose of this study was to investigate retrospectively what factors contribute to the development of the type of hyperlactatemia which may follow cardiopulmonary bypass despite well-maintained oxygen delivery and a normal perioperative course. Methods The medical records of 124 patients undergoing elective cardiac surgery using cardiopulmonary bypass were reviewed. The patients were divided into a hyperlactatemia group (n =34), where the serum lactate concentration was > 5.0 mmol L−1 perioperatively, and a normal lactatemia group (n =90), which comprised the remaining patients. Results The duration of cardiopulmonary bypass in the hyperlactatemia group was significantly longer than for the normal lactatemia group. Significant differences of lactate concentrations between the groups, and significant elevations of serum lactate had been observed after the start of cardiopulmonary bypass. Oxygen extraction rates were significantly reduced during the period of cardiopulmonary bypass but, on the contrary, increased in the hyperlactatemia group after surgery. The area under the curve of mean arterial pressure consisted of 5-min interval plots during the initial period of cardiopulmonary bypass in the hyperlactatemia group. This was significantly smaller than for the normal lactatemia group. Weakly significant correlations between maximal lactate and duration of cardiopulmonary bypass, and especially the area under the curve, were observed. Conclusions It is suggested that the pathophysiology observed is based on impairment of tissue oxygen utilization. The duration of cardiopulmonary bypass and especially the occurrence of hypotension at the start of the bypass period appears to be related to the development of lactic acidosis.

What factors are associated with hyperlactatemia after cardiac surgery characterized by well-maintained oxygen delivery and a normal postoperative course? A retrospective study.

and objective The purpose of this study was to investigate retrospectively what factors contribute to the development of the type of hyperlactatemia which may follow cardiopulmonary bypass despite well-maintained oxygen delivery and a normal perioperative course. The medical records of 124 patients undergoing elective cardiac surgery using cardiopulmonary bypass were reviewed. The patients were divided into a hyperlactatemia group (n=34), where the serum lactate concentration was > 5.0 mmol L(-1) perioperatively, and a normal lactatemia group (n=90), which comprised the remaining patients. The duration of cardiopulmonary bypass in the hyperlactatemia group was significantly longer than for the normal lactatemia group. Significant differences of lactate concentrations between the groups, and significant elevations of serum lactate had been observed after the start of cardiopulmonary bypass. Oxygen extraction rates were significantly reduced during the period of cardiopulmonary bypass but, on the contrary, increased in the hyperlactatemia group after surgery. The area under the curve of mean arterial pressure consisted of 5-min interval plots during the initial period of cardiopulmonary bypass in the hyperlactatemia group. This was significantly smaller than for the normal lactatemia group. Weakly significant correlations between maximal lactate and duration of cardiopulmonary bypass, and especially the area under the curve, were observed. It is suggested that the pathophysiology observed is based on impairment of tissue oxygen utilization. The duration of cardiopulmonary bypass and especially the occurrence of hypotension at the start of the bypass period appears to be related to the development of lactic acidosis.

Dynamic cerebral autoregulation in sick newborn infants.

The sick newborn infant is vulnerable to brain injury and impaired cerebral autoregulation is thought to contribute to this. Coherent averaging is a method of measuring the dynamic cerebral autoregulatory response that is particularly suitable for neonates. We used this method in combination with a measure of the gradient of the cerebral blood flow velocity (CBFV) response following transient blood pressure (BP) peaks to study dynamic autoregulation in infants undergoing intensive care. Term and preterm infants at high risk of neurologic injury were compared with a control group of infants, also undergoing intensive care. Simultaneous video-EEG, CBFV (using transcranial Doppler), and arterial blood pressure measurements were obtained intermittently during a study period of at least 2 h. Cerebral autoregulatory response curves were constructed for high risk and control groups. Intact cerebral autoregulation produces a characteristic response consisting of a brief period when CBFV follows arterial blood pressure but quickly returns to baseline value. An impaired autoregulatory response shows CBFV mirroring the arterial blood pressure curve closely. Thirteen high-risk infants, who also had seizures (10 term and 3 preterm) and 12 control infants (6 term and 6 preterm) were studied. Autoregulation was absent in high-risk term and preterm infants. It was also absent in preterm control infants. Term, neurologically healthy infants undergoing intensive care have an intact autoregulatory response. The constant passive response seen in high-risk infants may reflect the severity of the underlying neurologic disease.

Cardiac function evaluated by transesophageal echocardiography during cardiopulmonary bypass

To evaluate cardiac function at cardiopulmonary bypass weaning, we applied a new technique clinically to determine the approximated Emax without using a conductance catheter. Subjects were 5 patients. The left ventricular end-systolic pressure was obtained by overlaying the radial arterial pressure curve on the left ventricular pressure curve. Left ventricular end-systolic volume was assessed by a transesophageal echographic apparatus. At cardiopulmonary bypass weaning, volume loading was applied to increase left atrial pressure by a few mmHg while fixing the pump flow rate at half flow. Changes in left ventricular end-systolic volume and approximated left ventricular end-systolic pressure for total heart beat were plotted during this period, and the gradient of the regression line was taken as approximated Emax. Approximated Emax ranged from 1.29 to 3.28 (mean 2.13 +/- 0.72), and its correlation coefficient was 0.80 +/- 0.06. Our new technique is useful in evaluating cardiac function during cardiopulmonary bypass.

Systolic and diastolic changes in human coronary blood flow during Valsalva manoeuvre.

Valsalva manoeuvre is reported to be sometimes successful for the relief of angina pectoris. The present study investigated how haemodynamic changes produced by Valsalva manoeuvre can interact to improve the relationship between cardiac work and coronary blood flow. Ten male subjects aged 53 +/- 12 years (SD) were considered. Blood velocity in the internal mammary artery, previously anastomosed to the left descending coronary artery, was studied with Doppler technique. The subjects performed Valsalva manoeuvres by expiring into a tube connected to a mercury manometer, to develop a pressure of 40 mmHg. The arterial blood pressure curve was continuously monitored with a Finapres device from a finger of the left hand. During expiratory effort, an increase in heart rate and a decrease in arterial pulse pressure were followed by a more delayed and progressive increase in mean and diastolic pressures. Systolic blood velocity markedly decreased along with the reduction in pulse pressure and increase in heart rate. By contrast, diastolic and mean coronary blood velocities did not show any significant change. Since it is known that the Valsalva manoeuvre strongly reduces stroke volume and cardiac output, it is likely that a reduction in cardiac work also takes place. Since in diastole, i.e. when the myocardial wall is better perfused, coronary blood velocity did not show any significant reduction, it is likely that unchanged perfusion in the presence of reduced cardiac work is responsible for the relief from angina sometimes observed during Valsalva manoeuvre. It is also likely that the increase in heart rate prevents the diastolic and mean blood coronary velocity from decreasing during the expiratory strain, when an increased sympathetic discharge could cause vasoconstriction through the stimulation of the coronary alpha-receptors.

Assessment of right ventricular function by right ventricular systolic time intervals in acute respiratory failure.

Whether right ventricular systolic time intervals accurately reflect right ventricular function in patients with acute respiratory failure was determined by assessing the correlation between right ventricular systolic time intervals and the right ventricular end-systolic pressure-volume relationship. A prospective study. A surgical intensive care unit in a university hospital. Twenty patients with acute respiratory failure. Right ventricular systolic time intervals were determined by the simultaneous graphic display of the electrocardiogram, the phonocardiogram, and the pulmonary artery pressure curve and were expressed as a ratio of the pre-ejection period/right ventricular ejection time. The total electromechanical systole was measured from the onset of the electrocardiographic wave complex to the pulmonic component of the second heart sound. Right ventricular ejection time was measured from the rapid upstroke of the pulmonary artery pressure curve to the dicrotic notch. Right ventricular ejection fraction, from which right ventricular end-systolic volume was derived, was measured by the thermodilution technique. Pulmonary artery dicrotic notch pressure was used as an estimate of right ventricular end-systolic pressure. Data were collected at the baseline and after one or two alterations in preload, to define the right ventricular end-systolic pressure-volume relationship line. There was an inverse correlation between the pre-ejection period/right ventricular ejection time ratio and the slope of the right ventricular end-systolic pressure-volume relationship line (r2 = .67; p < .0001). When patients were divided into two groups, based on the pre-ejection period/right ventricular ejection time ratio, the slope of the right ventricular end-systolic pressure-volume relationship line was lower in the group with a high pre-ejection period/right ventricular ejection time ratio (p < .0001). No difference in other hemodynamic data, between the two groups, was noted. These data suggest that right ventricular systolic time intervals reflect right ventricular performance accurately in patients with acute respiratory failure.

Blood pressure and hormonal responses to short whole body cold exposure in subjects with high dietary salt intake.

The objective of the present study was to test a hypothesis that a high dietary salt intake potentiates a cold induced increase in blood pressure in normotensive men. Male subjects (n = 12) were given 7 g day-1 sodium chloride during the cold months of the year, divided in 3-4 doses per day and dissolved in water, for 14 days additional to their normal diet which contained on the average 9.7 g sodium chloride per day. The same subjects, having their normal diet, served as controls. The resting blood pressure was measured on the fourteenth day seven times at the intervals of five minutes in a climatic chamber in thermoneutral conditions. Then the subjects, wearing a three-layer winter clothing, moved into a wind tunnel (-15 degrees C, air velocity 3.5 ms-1) in which they stayed for fifteen minutes and the blood pressure was recorded at the intervals of three minutes. After the cold exposure, the subjects moved back into the climatic chamber for 30 min and the blood pressure was measured as before the cold exposure. Blood samples were drawn before and after the experiment for ion and hormone measurements. A 12 h urine sample was collected just prior to the cold exposure. A significant difference both in systolic (7 mmHg) and in diastolic (7 mmHg) blood pressure was found between a salt load group and control group under thermoneutral conditions, repeatedly measured over 30 min (paired Student's t-test; p < 0.05). During the whole body cold exposure, blood pressure significantly increased both with and without the extra salt load (repeated measures ANOVA, Student-Newman-Keuls; p < 0.05). The level to which the mean arterial pressure increased during the exposure was independent of the salt intake and the profile of the mean arterial pressure curve was similar in both groups. The systolic pressure increased by a 25 mmHg in both groups during the cold exposure. The increase in the diastolic pressure was significantly (paired Student's t-test, p < 0.05) higher in the high salt group (18 +/- 4 mmHg) than in the control group (12 +/- 3 mmHg) thus supporting partly our hypothesis. After the two-week high salt intake, serum Na+, K+, Cl-, Hct, and plasma Hb were at the similar level as before the extra salt intake. Plasma renin activity, NT-proANP, ANP, and serum aldosterone were not different between the groups, both before and after the cold exposure. The main findings are: 1) the mean arterial pressure increases to the same level and in the same manner independent of the salt load during a short whole body cold exposure and 2) in cold the diastolic blood pressure increases significantly more in people under a very high salt diet.

Doppler derivation of complete pulmonary artery pressure curves in patent ductus arteriosus

In this study, we have demonstrated a method of obtaining complete, accurate PA pressure curves from a PDA Doppler flow velocity signal and a simultaneous aortic pressure tracing. This technique provides a dynamic evaluation of changes in PA pressures throughout the cardiac cycle and provides more hemodynamic information than single-point Doppler velocity methods of estimating PA pressures.

Spectral analysis of cyclic fluctuations in haemodynamic parameters in critically ill patients.

In critically ill patients haemodynamic parameters are being routinely monitored. All of the fluctuations in blood pressures cannot be visualised since on most monitors the time window is too short and trend curves do not have a sufficient time resolution. Therefore, frequency analysis was applied to an 800-second window. Systemic artery pressure, central venous pressure and pulmonary artery pressure curves of 6 patients were sampled with a frequency of 40 Hz. The signals were transformed into the frequency domain by the Fast Fourier Transform method. Bispectral analysis was applied to determine the origin of higher frequencies. There were three main frequencies present: heart stroke rate, respiratory frequency and a slow frequency (< 0.05 Hz), which was equal to the used infusion rate (2-10 ml/h) of vaso-active drugs. Continuous infusion of short-acting vaso-active drugs delivered by pulsatile diaphragm pumps to produce slow significant fluctuations in especially the arterial blood pressures (range: 5-40 mmHg). The periodicity of these slow fluctuations is not visualised during routine monitoring, so the observer may misinterpret the cause of changes in blood pressure and make inappropriate clinical decisions. A solution for detection of such slow waves is Fast Fourier Transform combined with bispectral analysis.

Left Ventricular Ejection Time and End-Systolic Pressure Revisited

Left Ventricular Ejection Time and End-Systolic Pressure Revisited

Angiotensin II exerts differential actions on renal nerve activity and heart rate.

Angiotensin II (Ang II) exerts complex actions on sympathetic nerve activity and heart rate, but these actions are incompletely understood. We performed three series of experiments in conscious rabbits to analyze the actions of exogenous and endogenous Ang II on renal sympathetic nerve activity and heart rate. (1) Graded intravenous doses of phenylephrine and Ang II suppressed renal sympathetic nerve activity to the same degree, whereas Ang II decreased heart rate much less than phenylephrine. (2) Ang II infusion at 10 ng/kg per minute increased mean arterial pressure by 13 +/- 2 mm Hg (P < .01) and decreased renal sympathetic nerve activity by 67 +/- 13% (P < .01) but did not change heart rate. In the same rabbits, nitroprusside and phenylephrine infusions were used to generate baroreceptor reflex curves. Ang II shifted the heart rate-mean arterial pressure curve to the right but did not alter the renal nerve activity-mean arterial pressure curve. (3) The Ang II type 1 receptor antagonist losartan decreased mean arterial pressure by 8 +/- 3 mm Hg (P < .01) and increased renal sympathetic nerve activity by 63 +/- 15% (P < .05) but did not change heart rate. Losartan shifted the heart rate-mean arterial pressure curve to the left but did not alter the renal nerve activity-mean arterial pressure curve. These results demonstrate that whereas exogenous Ang II resets the baroreceptor reflex control of heart rate to a higher pressure, it does not increase resting renal sympathetic nerve activity or alter the baroreceptor reflex control of renal nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of left ventricular filling profile during preceding control beats on pulse pressure during ventricular premature contractions.

We investigated whether the left ventricular filling profile, defined as the early to late diastolic left ventricular filling volume ratio, during the preceding control beats actually affects the pulse pressure during a ventricular premature contraction (PVC). Twenty patients underwent invasive electrophysiological study for sinus bradycardia. VPCs with various coupling intervals were induced by right ventricular electrical stimulation, and the mitral filling flow velocity by pulsed Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which preceded the VPC was measured as an index characterizing left ventricular filling profile. The coupling interval of each VPC and the extrasystolic beat pulse pressure were measured. The ratio of the extrasystolic beat pulse pressure to the control beat pulse pressure was expressed in % (% extrasystolic beat pulse pressure). The correlation between the coupling interval and the % extrasystolic beat pulse pressure was investigated. Coupling intervals of 0.80, 0.70, 0.60, 0.50, and 0.45 s were used. At a coupling interval of 0.80 or 0.45 s, the % extrasystolic beat pulse pressure showed no significant correlation with the Ei/Ai ratio. In contrast, the % extrasystolic beat pulse pressure with coupling intervals of 0.70, 0.60, and 0.50 s showed a significant positive correlation with the Ei/Ai ratio (r = 0.67, 0.74, and 0.66, P < 0.01, respectively). In addition to the prematurity and the site of origin of the VPCs, the left ventricular filling profile during the preceding control beats may significantly affect the height of the pulse pressure during extrasystoles with medium length coupling intervals.

Feasibility of generating hemodynamic pressure curves from noninvasive Doppler echocardiographic signals

Objectives. This study was designed to determine the feasibility of Doppler generation of accurate, complete right ventricular and pulmonary artery pressure curves in patients with Dopplermeasurable tricuspid and pulmonary regurgitation.Background. Doppler-derived flow velocities have been used to assess right ventricular systolic pressure; pulmonary artery systolic, diastolic and mean pressures, and left ventricular systolic and diastolic pressures. Instantaneous gradient across any area of discrete narrowing is accurately derived using the simplified Bernoulli equation (4V2). Invasive catheterization is currently the only means of generating intracardiac pressure curves. Noninvasively derived pressure curves using Doppler echocardiography would be a considerable advance in the assessment of normal and pathologic cardiac hemodynamics.Methods. Right ventricular and pulmonary artery pressure curves were generated in 18 of 22 patients with measurable tricuspid and pulmonary valve regurgitation using superimposition of Doppler-measured tricuspid and pulmonary valve blood flow velocities on an assumed right atrial pressure. Dopplermeasured right ventricular and pulmonary artery pressure curves were compared with simultaneous catheterization-measured curves.Results. Doppler-derived pulmonary artery systolic pressure (Doppler PAP) correlated with simultaneous catheter-measured pulmonary artery pressure (Cath PAP) by the equation Doppler PAP = 0.92(Cath PAP) + 4.5, r = 0.98. Other Doppler-derived pressure measurements that correlated at near identity with the catheterization-measured corresponding measurement include Doppler-derived pulmonary artery mean pressure (Doppler mean PAP) [Doppler mean PAP = 0.85(Cath mean PAP) + 2.6, r = 0.97], and Doppler-derived right ventricular pressure (Doppler RVP) [Doppler RVP = 0.84(Cath measured RVP) + 7.9, r = 0.98]. Doppler-derived pulmonary artery diastolic pressure (Doppler PAP diast) did not correspond as well in this study [Doppler PAP diast = 0.45(Cath PAP diast) + 6.6, r = 0.83].Conclusions. Clinically usable right ventricular and pulmonary artery pressure curves can be derived by superimposing Dopplermeasured tricuspid and pulmonary valve blood flow velocities in patients with tricuspid and pulmonary valve regurgitation.

Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions.

This study was designed to investigate whether the left ventricular filling profile during preceding control beats significantly affects the pulse deficit caused by ventricular premature contractions (VPCs). The study group consisted of 18 patients (10 men, eight women, 15-85 years old) who underwent electrophysiological catheterization because of sinus bradycardia. Using a temporary pacing lead inserted in the right ventricular apex, isolated VPCs with various coupling intervals were produced by electrical stimulation of the right ventricle. During the production of the VPCs, the mitral filling flow velocity using pulsed wave Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The right ventricle was stimulated 800, 750, 700, 650, 600, 550, 500, 450 and 400 ms after the triggered control beat QRS complex. Pulse pressures during VPCs gradually decreased in relation to the shortening of the extrasystolic beat coupling interval. The longest coupling interval for each subject, which caused complete abolition of the pressure pulse during the VPC, was defined as the pulse deficit coupling interval. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which precede the VPC was obtained as an index expressing the left ventricular filling profile. The Ei/Ai ratio of the mitral filling flow velocity ranged from 0.7 to 4.5 (1.8 +/- 1.0). The pulse deficit coupling interval ranged from 440 to 640 ms (510 +/- 60 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

37 Doppler derived complete pulmonary artery pressure curves from a patient ductus arteriosus

37 Doppler derived complete pulmonary artery pressure curves from a patient ductus arteriosus

Right ventricular systolic time intervals determined by means of a pulmonary artery catheter.

To evaluate the right ventricular systolic time interval as an index of right ventricular function and also to ascertain whether the right ventricular ejection fraction may be determined by means of a conventional pulmonary artery catheter. Prospective study. Intensive care unit. Eight, consecutive critically ill adult patients. Simultaneous blind measurements, performed by two investigators, of the right ventricular systolic time interval and right ventricular ejection fraction, determined by means of a pulmonary artery catheter. Two studies, separated by an interval of 24 hrs, per patient. Linear regression analysis. Multiple regression test. Of the 16 studies performed, two determinations of right ventricular systolic time intervals were technically inadequate. In the remaining 14 valid studies, we found one close linear correlation between the right ventricular ejection fraction and the preejection period/ejection time quotient measured using the simultaneous display of the electrocardiogram (EKG) and pulmonary arterial pressure curve (r2 = .90, p < .001, right ventricular ejection fraction = 68.96-60.59 x [right ventricular preejection period/right ventricular ejection time]). The method proved to be simple, very accurate, with little interobserver variation (8.09 +/- 10.6% interobserver variation for right ventricular preejection period/right ventricular ejection time) and provided adequate information regarding situations in which the performance of the right ventricle is modified in a given patient. The right ventricular preejection period/right ventricular ejection time quotient was the only variable that displayed a significant relationship with the right ventricular ejection fraction in the multivariate analysis (p < .001). Right ventricular systolic time intervals, measured using the simultaneous display of the pulmonary artery catheter curve and EKG, provide adequate information regarding right ventricle performance in critically ill patients. The close linear correlation between the right ventricular preejection period/right ventricular ejection time quotient and the right ventricular ejection fraction enables the investigator to estimate, with a high degree of accuracy, the right ventricular ejection fraction and the values derived from the preload of the right ventricle, without the need for a modified pulmonary artery catheter.

Localization of the sites of pulmonary vasomotion by use of arterial and venous occlusion

In this study, we present a new approach for using the pressure vs. time data obtained after various vascular occlusion maneuvers in pump-perfused lungs to gain insight into the longitudinal distribution of vascular resistance with respect to vascular compliance. Occlusion data were obtained from isolated dog lung lobes under normal control conditions, during hypoxia, and during histamine or serotonin infusion. The data used in the analysis include the slope of the arterial pressure curve and the zero time intercept of the extrapolated venous pressure curve after venous occlusion, the equilibrium pressure after simultaneous occlusion of both the arterial inflow and venous outflow, and the area bounded by equilibrium pressure and the arterial pressure curve after arterial occlusion. We analyzed these data by use of a compartmental model in which the vascular bed is represented by three parallel compliances separated by two series resistances, and each of the three compliances and the two resistances can be identified. To interpret the model parameters, we view the large arteries and veins as mainly compliance vessels and the small arteries and veins as mainly resistance vessels. The capillary bed is viewed as having a high compliance, and any capillary resistance is included in the two series resistances. With this view in mind, the results are consistent with the major response to serotonin infusion being constriction of large and small arteries (a decrease in arterial compliance and an increase in arterial resistance), the major response to histamine infusion being constriction of small and large veins (an increase in venous resistance and a decrease in venous compliance), and the major response to hypoxia being constriction of the small arteries (an increase in arterial resistance). The results suggest that this approach may have utility for evaluation of the sites of action of pulmonary vasomotor stimuli.

Carotid sinus baroreceptor reflex in dogs with experimental heart failure.

We have previously demonstrated a decrease in baroreceptor discharge sensitivity in dogs with experimental heart failure. In the present study, we determined the sensitivity of the carotid sinus baroreceptor reflex in dogs with pacing-induced heart failure. The carotid sinus baroreceptor reflex sensitivity was determined by pressurizing one carotid sinus with all other baroreceptor and cardiopulmonary receptor inputs removed. The data were analyzed by plotting carotid sinus pressure-mean arterial pressure curves and carotid sinus pressure-renal sympathetic nerve activity curves in the two groups of dogs. The peak arterial pressure during carotid hypotension was significantly depressed in dogs with heart failure compared with normal dogs (107.1 +/- 5.7 versus 139.8 +/- 7.0 mm Hg, p less than 0.001). Mean arterial pressure range, renal sympathetic nerve activity range, and peak slope were significantly decreased in the heart-failure group. To determine if this depression was completely due to depression of baroreceptor discharge per se, or to alterations in central or end-organ responsiveness, similar experiments were performed by stimulating the carotid sinus nerve and evaluating frequency, voltage, and duration of stimulation on the resultant mean arterial pressure and renal sympathetic nerve activity. As was the case with carotid sinus pressurization, electrical stimulation caused a significantly smaller change in mean arterial pressure in heart-failure dogs compared with the normal dogs. However, there was no significant difference between normal and heart-failure dogs for the renal sympathetic nerve activity-electrical stimulation curves. These data strongly suggest that the depressed carotid sinus baroreceptor reflex in heart failure is not solely the result of depressed baroreceptor responsiveness but may be related to poor end-organ responses and normal central control of renal sympathetic outflow.