Changes In Venous Return Research Articles

Effects of the knee-chest position on cardiac index and propofol requirements during bispectral index (BIS)-guided spine surgery

The knee-chest (KC) position is often used for spine surgery. It is considered to promote significant changes in venous return and cardiac output. However, the magnitude of these changes and their consequences on intraoperative haemodynamics and anaesthetic requirements remain to be determined. The goal of the present study was to determine the changes in cardiac index and propofol requirements of patients undergoing spine surgery in the KC position. Twenty ASA 1-3 patients scheduled for elective spine surgery were included in the study. A radial artery catheter and an oesophageal Doppler probe were properly positioned after induction of anaesthesia. Anaesthesia consisted of bispectral index (BIS)-guided, plasma target-controlled, propofol-remifentanil anaesthesia. After positioning the patient KC, remifentanil target concentration was maintained throughout the case as in the supine position whilst propofol target concentration was adjusted to maintain BIS values between 40 and 50. Cardiac index, stroke volume, heart rate, end-tidal CO(2) (ETCO(2)), mean arterial pressure, peak and plateau airway pressures, BIS values and plasma target concentrations of propofol and remifentanil were compared 15 min after induction of anaesthesia (in the supine position) and 15 min after placing the patients KC. Data are expressed as mean+/-S.D. except for DeltaPP expressed as a number of patients with DeltaPP greater than 13%. Cardiac index, stroke volume, mean arterial pressure and propofol target concentration were significantly decreased from supine to KC position: 2.6+/-0.03 to 1.7+/-0.04 l/min/m(2), p<0.0001; 68+/-1.2 to 45+/-1 ml, p<0.0001; 83+/-1.2 to 76+/-1.4 mmHg, p<0.0001 and 3+/-0.06 to 2+/-0.05 microg/ml, p<0.0001, respectively. The number of patients with DeltaPP greater than 13% was zero in the supine position and 18 (90%) in the KC position (p<0.0001). Placing surgical patients in the KC position during BIS guided anaesthesia was associated with marked decrease in cardiac index and propofol requirements. These results suggest that monitoring intraoperative cardiac index via an oesophageal Doppler and depth of anaesthesia with the BIS may be useful in patients undergoing spine surgery in the KC position.

Heart???lung interactions

Assessment of cardiovascular stability using ventilation-induced changes in measured physiological variables, referred to as functional hemodynamic monitoring, usually requires measurement of ventilation-induced changes in venous return. Thus, it is important to understand the determinants of these complex heart-lung interactions. Several animal and human studies have recently documented that ventricular interdependence plays an important role during positive-pressure breathing, causing acute cor pulmonale. With the use of lower tidal volume ventilation in patients with acute respiratory failure, the incidence of acute cor pulmonale is decreasing proportionally. When present, however, it induces a stroke volume variation that is 180 degrees out of phase with that seen in hypovolemic states, such that left ventricular stroke volume increases during inspiration rather than decreasing as seen in hypovolemia. Further, when either tidal volume or positive end-expiratory pressure levels are varied, both stroke volume variation and pulse pressure variation are affected in a predictable manner. The greater the swing in intrathoracic pressure, the greater the change in venous return. Functional hemodynamic monitoring is becoming more prevalent. For it to be used effectively, the operator needs to have a solid understanding of how ventilation induces both pulse pressure variation and stroke volume variation in that specific patient.

The sitting position in neurosurgery — Unresolved hemodynamic consequences!

ONTROVERSY continues to surround use of the sitting position for neurosurgical procedures. 1–3 The seated position, while presenting a number of challenges for the anesthesiologist, offers many surgical advantages for patients undergoing posterior fossa and cervical spine procedures. Specifically, the upright position improves operator orientation and surgical access to midline lesions in many posterior fossa cases. Gravitational drainage of venous blood from the surgical field and lowering of intracranial pressure increases technical ease and allows more rapid access to bleeding points. 4 An unobstructed view of the face allows motor responses to cranial nerve stimulation to be directly observed in the sitting position, and access to the anterior chest wall is facilitated in the event of cardiovascular collapse. Despite the many advantages offered from the surgical perspective, the sitting position presents unique physiological challenges for the anesthesiologist with the potential for serious complications. 1,5 Venous air embolism, with or without paradoxical air embolism, is a major concern in relation to the use of this position. 2,6 Hemodynamic instability with hypotension and potential compromise of cerebral and myocardial perfusion may occur. Reduction of inhaled volatile anesthetic agent and decreasing depth of anesthesia may predispose the seated patient to the risk of intraoperative awareness. Peripheral neuropathy 1 tension pneumocephalus, 7 and quadriplegia 1,2 are additional reported associated complications. The hemodynamic effects of anesthesia in the sitting position may be influenced by choice of ventilatory technique. Spontaneous ventilation with a volatile anesthetic agent in nitrous oxide/oxygen was popular in the 1960’s to provide signs of surgical encroachment on vital medullary and pontine structures. 8 The problems of cardiovascular instability and arterial hypotension associated with the upright position may be aggravated by the depressant effects of intravenous induction and volatile agents on myocardial contractility during general anesthesia and changes in venous return following intermittent positive pressure ventilation. 9 The volume of blood accumulating in the venous system may be influenced by patient factors - body mass index, intravascular volume status, pre-existing hypertension and mode of ventilation. As much as 1500 mL may be sequestered in the venous system of the lower limbs due to the effect of gravity 10 and increased diffusion through the capillary walls and venous dilatation associated with the use of volatile anesthetic agents. 11 Indicator dilution technique studies have confirmed a 14% redistribution of blood volume from the intra- to the extrathoracic compartment in anesthetized patients after a change from the supine to the sitting position. 12 Concomitant changes in arterial pressure and stroke volume index were thus attributed to alterations in cardiac preload. A number of techniques have been advocated to attenuate the hemodynamic effects of patient placement in the sitting position. Colloid preloading (10 mL·kg –1 ) 30 min before starting general anesthesia was reported to prevent decreases in systolic and central venous pressures during sitting patient positioning without adverse effects. 13 Compensatory mechanisms, perhaps mediated by the renin-angiotensin-aldosterone system or the sympathetic nervous system, may be operative in the awake or anesthetized state to attenuate adverse hemodynamic changes associated with the sitting position. Wrapping of the legs, application of anti-gravity suits and positioning of the knees at right heart level may all have potential benefits.

Objective evaluation of changes in left ventricular and atrial volumes during parabolic flight using real-time three-dimensional echocardiography

We tested the feasibility of real-time three-dimensional (3D) echocardiographic (RT3DE) imaging to measure left heart volumes at different gravity during parabolic flight and studied the effects of lower body negative pressure (LBNP) as a countermeasure. Weightlessness-related changes in cardiac function have been previously studied during spaceflights using both 2D and 3D echocardiography. Several technical factors, such as inability to provide real-time analysis and the need for laborious endocardial definition, have limited its usefulness. RT3DE imaging overcomes these limitations by acquiring real-time pyramidal data sets encompassing the entire ventricle. RT3DE data sets were obtained (Philips 7500, X3) during breath hold in 16 unmedicated normal subjects in upright standing position at different gravity phases during parabolic flight (normogravity, 1 Gz; hypergravity, 1.8 Gz; microgravity, 0 Gz), with LBNP applied (-50 mmHg) at 0 Gz in selected parabolas. RT3DE imaging during parabolic flight was feasible in 14 of 16 subjects. Data were analyzed (Tomtec) to quantify left ventricular (LV) and atrial (LA) volumes at end diastole and end systole, which significantly decreased at 1.8 Gz and increased at 0 Gz. While ejection fraction did not change with gravity, stroke volume was reduced by 16% at 1.8 Gz and increased by 20% at 0 Gz, but it was not significantly different from 1 Gz values with LBNP. RT3DE during parabolic flight is feasible and provides the basis for accurate quantification of LV and LA volume changes with gravity. As LBNP counteracted the increase of LV and LA volumes caused by changes in venous return, it may be effectively used for preventing cardiac dilatation during 0 Gz.

Right Atrial Pressure: Determinant or Result of Change in Venous Return?

According to the concept of Guyton, cardiac output is largely controlled by venous return, which is determined by the difference between mean systemic venous pressure and right atrial pressure. In the analysis of the venous return curve, other authors have suggested that right atrial pressure is the dependent variable and venous return is the independent variable (right atrial pressure decreased because cardiac output increased). The present report analyzes this historical debate, which has already lasted > 50 years.

Structural Analysis of Heart Rhythm Spectrogram in Narcotized Cats

Eight types of peaks were revealed in the cardiac rhythm spectrum during acute experiments on vagotomized cats. Some peaks had no physiological nature and resulted from specificity of ECG processing by Fourier analysis, while others reflected myogenic reaction of the sinoatrial node (length-dependence of automaticity) to changes in venous return caused by respiratory-induced and other variations of the blood flow in the cardiovascular system.

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

Quantification of left ventricular modification in weightlessness conditions from the spatio-temporal analysis of 2D echocardiographic images

Two-dimensional echocardiography (2DE) performed during flights with a parabolic trajectory to simulate weightlessness provides a unique means to study left ventricular (LV) modifications to prevent post-flight orthostatic intolerance in astronauts. However, conventional analysis of 2DE is based on manual tracings and depends on experience. Accordingly, the aim was objectively to quantify, from 2DE images, the LV modifications related to different gravity levels, by applying a semi-automated level-set border detection technique. The algorithm validation was performed by the comparison of manual tracing results, obtained by two independent observers with 20 images, with the semi-automated measurements. To quantify LV modifications, three consecutive cardiac cycles were analysed for each gravity phase (1 Gz, 1.8 Gz, 0 Gz). The level-set procedure was applied frame-by-frame to detect the LV endocardial contours and obtain LV area against time curves, from which end-diastolic (EDA) and end-systolic (ESA) areas were computed and averaged to compensate for respiratory variations. Linear regression (y = 0.91x + 1.47, r = 0.99, SEE:0.80cm2) and Bland-Altman analysis (bias = -0.58 cm2, 95% limits of agreement= +/- 2.14cm2) showed excellent correlation between the semi-automatic and manually traced values. Inter-observer variability was 5.4%, and the inter-technique variability was 4.1%. Modifications in LV dimensions during the parabola were found: compared with 1 Gz values, EDA and ESA were significantly reduced at 1.8 Gz by 8.8 +/- 5.5% and 12.1 +/- 10.1%, respectively, whereas, during 0 Gz, EDA and ESA increased by 13.3 +/- 7.3% and 11.6 +/- 5.1%, respectively, owing to abrupt changes in venous return. The proposed method resulted in fast and reliable estimations of LV dimensions, whose changes caused by different gravity conditions were objectively quantified.

Flow dependency of error in thermodilution measurement of cardiac output during acute tricuspid regurgitation

Objective: To evaluate the effect of variable degrees of tricuspid regurgitation on thermodilution cardiac output measurements during changes in venous return. Design: Prospective, controlled animal study. Setting: University laboratory. Participants: Eight anesthetized mongrel dogs instrumented for simultaneous measurement of cardiac output by thermodilution and ascending aortic electromagnetometry. Interventions: Data were collected before and after induction of moderate and severe tricuspid regurgitation. Under each condition, measurements were obtained at baseline and after opening 2 peripheral arteriovenous shunts to increase venous return. Measurements and Main Results: Baseline electromagnetic flow ranged from 1.74 to 3.62 L/min (median 2.73 L/min). Moderate and severe regurgitation reduced median electromagnetic flow values by 31% and 51%. Applying generalized estimating equations to model thermodilution cardiac output as a function of electromagnetic flow, arteriovenous shunt, and severity of tricuspid regurgitation revealed that (1) moderate and severe regurgitation changed the slope and intercept of the thermodilution/electromagnetic regression, but the differences between them were not significant, and (2) arteriovenous shunt alone had no effect under any condition. A simplified model independent of shunt and containing just 2 levels of tricuspid regurgitation (none or present) crossed with electromagnetic flow was applied. This analysis showed that regurgitation caused thermodilution to significantly underestimate electromagnetic flow at cardiac outputs >2.27 L/min (99 mL/kg/min) and overestimate it at flows <1.02 L/min (44 mL/kg/min). Conclusions: These data show that acute tricuspid regurgitation may produce underestimation of cardiac output by thermodilution when flow is relatively high, produce overestimation when flow is relatively low, or have minimal effect when flow is in the midrange. Copyright © 2001 by W.B. Saunders Company

Congestion of superior mesenteric veins and small bowel mucosal injury after endoscopic treatment of esophageal varices in patients with portal hypertension.

We investigated treatment-induced changes in venous return from the small bowel and small bowel intestinal mucosal injury induced by the treatment of esophageal varices in patients with portal hypertension. A total of 14 patients (age 59.8+/-9.5 years, five women and 9 men) who received prophylactic treatment of esophageal varices between December 1998 and March 1999 were investigated. Diamine oxidase (DAO) activity was measured before and after treatment. Changes in blood flow of the portal and superior mesenteric veins were investigated by Doppler ultrasonography in six patients. A significant decrease in DAO activity was observed three days after treatment (11.5+/-1.6 units/liter prior to treatment versus 8.6+/-1.6 units/liter three days after treatment; P < 0.001). Decreases in superior mesenteric and portal venous flow velocity were observed in four and three patients, respectively. In two patients with an increase in the cross-sectional area of the superior mesenteric vein with delayed venous return, a marked decrease in DAO activity was observed three days after treatment. In patients with portal hypertension, rapid reduction of pooling of portal flow caused by the treatment of esophageal varices can induce transient congestion of the mesenteric venous system which can produce some small bowel mucosal injury.

Relationship between venous return and right-atrial pressure.

The dynamics and amplitude of changes in venous return and right atrial pressure (central venous pressure) in response to pressor stimuli were studied in acute experiments on cats. The increase in venous return was accompanied by either increase, or decrease in the central venous pressure. Thus, shifts in systemic venous return were not accompanied by simultaneous and co-directed changes in the central venous pressure. These findings suggest the absence of a direct relationship between these parameters.

Load dependent diastolic dysfunction in heart failure.

Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processes such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to aggressively treat CHF patients with diuretics and vasodilators.

Systemic filling pressure in the intact circulation determined with a slow inflation procedure.

In eight mechanically ventilated, anaesthetized pigs weighing 10.3 +/- 0.8 kg (mean +/- SD) we studied the effect of the inflation time of the lung on the estimation of the mean systemic filling pressure (Psf) from the changes in venous return and central venous pressure during inflation of the lung. For this purpose we applied slow inflation procedures (SIP) to the lung with inflation times of 2.4, 4.8, 7.2, 9.6 and 12 s at tidal volumes (VT) of 15 and 30 ml/kg. The data were compared with the values of Psf obtained from inspiratory pause procedures (IPPs). A linear regression between venous return and central venous pressure applied during a SIP underestimated Psf compared with the value obtained with IPPs. An exponential fit through the values of Psf obtained from the different SIPs predicted an inflation time of about 15 s for an estimation of Psf that is not different from the Psf (IPP). The advantage of the SIP method is that the Psf can be determined much faster than with the method based on IPPs. However, due to the rather long inflation time needed, the method may be only applicable under circumstances where neurohumoral control mechanisms are suppressed as during intensive care and anaesthesia.

Semi-continuous versus injectate cardiac output measurement in intensive care patients after cardiac surgery.

Commercially available semi-continuous cardiac output (SCCO) monitoring systems are based on the pulsed warm thermodilution technique. There is evidence that SCCO fails to correlate with standard intermittent bolus cardiac output (ICO) in clinical situations with thermal instability in the pulmonary artery. Furthermore, ventilation may potentially influence thermodilution measurements by enhanced respiratory variations in pulmonary artery blood temperature and by cyclic changes in venous return. Therefore, we evaluated the correlation, accuracy and precision of SCCO versus ICO measurements before and after extubation. Prospective cohort study. Intensive care unit (ICU) of a university hospital. 22 cardiac surgical ICU patients. None. SCCO and ICO data were obtained at nine postoperative time points while the patients were on controlled mechanical ventilation. Further sets of measurements were taken during the weaning phase 20 min before extubation, and 5 min, 20 min and 1 h after extubation. SCCO and ICO measurements yielded 286 data pairs with a range of 1.8-9.9 l/min for SCCO and 1.9-9.8 l/min for ICO. The correlation between SCCO and ICO was highly significant (r = 0.92; p < 0.01), accompanied by a bias of -0.052 l/min and a precision of 0.56 l/min. Correlation, accuracy and precision were not influenced by the mode of respiration. Our results demonstrate excellent correlation, accuracy and precision between SCCO and ICO measurements in postoperative cardiac surgical ICU patients. We conclude that SCCO monitoring offers a reliable clinical method of cardiac output monitoring in ICU patients following cardiac surgery.

Semi-continuous versus injectate cardiac output measurement in intensive care patients after cardiac surgery

ObjectiveCommercially available semi-continuous cardiac output (SCCO) monitoring systems are based on the pulsed warm thermodilution technique. There is evidence that SCCO fails to correlate with standard intermittent bolus cardiac output (ICO) in clinical situations with thermal instability in the pulmonary artery. Furthermore, ventilation may potentially influence thermodilution measurements by enhanced respiratory variations in pulmonary artery blood temperature and by cyclic changes in venous return. Therefore, we evaluated the correlation, accuracy and precision of SCCO versus ICO measurements before and after extubation.DesignProspective cohort study.SettingIntensive care unit (ICU) of a university hospital.Patients and participants22 cardiac surgical ICU patients.InterventionsNone.Measurements and resultsSCCO and ICO data were obtained at nine postoperative time points while the patients were on controlled mechanical ventilation. Further sets of measurements were taken during the weaning phase 20 min before extubation, and 5 min, 20 min and 1 h after extubation. SCCO and ICO measurements yielded 286 data pairs with a range of 1.8–9.9 l/min for SCCO and 1.9–9.8 l/min for ICO. The correlation between SCCO and ICO was highly significant (r=0.92;p<0.01), accompanied by a bias of −0.052 l/min and a precision of 0.56 l/min. Correlation, accuracy and precision were not influenced by the mode of respiration.ConclusionsOur results demonstrate excellent correlation, accuracy and precision between SCCO and ICO measurements in postoperative cardiac surgical ICU patients. We conclude that SCCO monitoring offers a reliable clinical method of cardiac ouput monitoring in ICU patients following cardiac surgery.

Demonstrable Cardiac Reinnervation After Human Heart Transplantation by Carotid Baroreflex Modulation of RR Interval

After heart transplantation, respiration-synchronous fluctuations (0.18 to 0.35 Hz, high frequency [HF]) in RR interval may result from atrial stretch caused by changes in venous return, but slower fluctuations (0.03 to 0.15 Hz, low frequency [LF]) not due to respiration suggest reinnervation. In normal subjects, sinusoidal neck suction selectively stimulates carotid baroreceptors and causes reflex oscillations of RR interval. To evaluate the presence of reinnervation, we measured the power of RR-LF and RR-HF in 26 heart transplant recipients and 16 control subjects before and during sinusoidal neck suction at 0.1 Hz and 0.20 Hz (similar to but distinct from that of controlled respiration, 0.25 Hz) and before and during administration of atropine or beta-blocker (esmolol hydrochloride) by spectral analysis. All transplant recipients showed small respiratory HF fluctuations. Nonrespiratory LF fluctuations were present in 13 of 26 transplant recipients and increased with months since transplantation (r = .53, P < .01). HF neck suction induced a 0.20-Hz component in all 16 control subjects and none of the 26 transplant subjects. LF neck suction increased RR-LF (from 0.73 +/- 0.20 to 1.30 +/- 0.26 ln ms2, P < .001), similar to but less than in control subjects (from 6.12 +/- 0.21 to 8.27 +/- 0.21 ln ms2, P < .001). Atropine reduced all fluctuations in control subjects and blocked the HF increase caused by 0.20-Hz neck suction but not the LF increase during 0.10-Hz stimulation. Neck suction-induced changes in LF fluctuations persisted after administration of atropine in transplant recipients but were attenuated by esmolol hydrochloride, suggesting sympathetic rather than vagal reinnervation. The presence of baroreceptor-induced RR oscillations is evidence of functional, although incomplete, autonomic reinnervation.

Pulmonary Artery Catheter Migration Causing Venous Cannula Obstruction during Cardiopulmonary Bypass

Pulmonary Artery Catheter Migration Causing Venous Cannula Obstruction during Cardiopulmonary Bypass

Neuroendocrine regulation of vascular capacitance.

Vascular capacitance of an organ or region is defined as the volume of blood contained in it at a particular distending pressure. Since the veins contain about 70% of the total blood volume, these are called the capacitance vessels (Green, 1950). A change in the diameter of the veins can cause a significant change in venous return and thus cardiac filling and cardiac output. The walls of the veins, contain a contractile (smooth muscle) and a viscoelastic element, and are very thin. Therefore, even a slight change in the transmural pressure can cause a great change in their diameters. Although the dominant influence on the veins and venous return of mechanical factors such as respiration, muscular exercise and posture has been well recognised for a very long time (see Brecher 1956, Karim 1987), the neurohumoral regulation of the venomotor tone and vascular capacitance has been the subject of great interest for the past thirty years (Shepherd & Vanhoutte, 1975, Rothe, 1983, Hainsworth, 1986). Generally, the veins (particularly those in the splanchnic bed) have rich sympathetic innervation, and numerous investigations have provided evidence that the individual veins or selected venous beds are under nervous control and react to the vasomotor centre activity in the same manner as do the arteries (see Folkow & Mellander 1964). Several investigations have clearly demonstrated that the capacitance vessels are more sensitive to changes in the sympathetic nerve activity than are the resistance vessels both in the hind limb of anaesthetised cats (Mellander, 1960) and dogs (Hainsworth et al., 1975, Karim et al., 1980) and in the abdomen of anaesthetized dogs (Karim & Hainsworth, 1976).KeywordsCarotid SinusSplanchnic NerveSuperficial VeinSympathetic TrunkCapacitance ResponseThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Cardiac output in conscious toads (Bufo marinus)

ABSTRACT Cardiac output and peripheral resistance have not been measured in conscious anuran amphibians, although some data exist for pithed and anaesthetized frogs (Shelton and Jones, 1965a,b; Shelton, 1970; Tazawa et al. 1979). The periodic lung ventilation characteristic of conscious anurans could increase cardiac output reflexively or by changes in venous return, as in mammals. Furthermore, because the undivided ventricle places the pulmonary and systemic vascular beds effectively in parallel, changes in the ratio of systemic to pulmocutaneous vascular resistance have the potential to alter the distribution of cardiac output. Therefore, the objectives of this study were to measure cardiac output and peripheral resistance in undisturbed, conscious Bufo marinus and to determine the effect of increased ventilation, stimulated by CO2, on pulmocutaneous blood flow and resistance.

Cardiac and respiratory arrest following aortocaval fistula.

Aortocaval fistula is an uncommon complication of lumbar disk surgery or is secondary to rupture of an ab­ dominal aortic aneurysm. We treated abrupt asystole in a patient with aor­ tocaval fistula which resulted from rup­ ture of an infrarenal aortic aneurysm into the vena cava. The sudden onset of extreme bradycardia or asystole has been reported to occur during dissec­ tion of an aneurysm associated with aortocaval fistulal-", It is postulated that acute decompensation due to a marked change in venous return to the heart or pulmonary embolism through the fistula may be the cause. We dis­ cuss here that reflex may be a poten­ tial mechanism for abrupt circulatory collapse.