Assessment of right ventricular contractile state with the conductance catheter technique in the pig.

OBJECTIVE: Since the conductance catheter method has facilitated evaluation of left ventricular contractile state in both laboratory and clinical studies, the aim of this study was to determine whether the technique is similarly useful for the right ventricle. METHODS: A series of right ventricular pressure-volume loops was obtained in seven open chest pigs during transient vena caval occlusion using a 12-electrode conductance catheter. End systolic pressure-volume relationships, stroke work-end diastolic volume relationships, and dP/dt-end diastolic volume relationships were compared at control and during infusion of dobutamine and esmolol. RESULTS: Right ventricular pressure-volume loops generated with the conductance catheter were of a shape consistent with those previously reported by other volume measurement techniques, and responded to changes in inotropic state in a predictable fashion. Dobutamine shifted the three contractile relationships leftward, whereas esmolol shifted them rightward. Comparisons of stroke volume derived with the conductance catheter and with a pulmonary artery flow probe demonstrated the ability of the conductance technique to measure relative volume changes. CONCLUSIONS: The conductance catheter provides a continuous measure of right ventricular volume that was used to detect changes in right ventricular contractile state in pigs. This represents a promising and much needed method for the evaluation of right ventricular function.

Heart reduction surgery: an analysis of the impact on cardiac function.

OBJECTIVES: Reports of improved ejection fraction, coupled with decreased filling pressures, have prompted a number of centers to begin evaluating the efficacy of heart reduction surgery to ameliorate symptoms of heart failure. However, the impact of this operation on cardiac mechanics is unknown. We applied a multiple compartment elastance model to simulate the effects of excising cardiac mass on heart function. METHODS: The left ventricle was divided into two functional compartments to simulate excision of part of the wall. At multiple increments of mass reduction, the resulting end-systolic elastance, ejection fraction, stroke volume, end-diastolic pressure and volume, and diastolic stiffness were determined. RESULTS: Changes in systolic function were accompanied by offsetting changes in diastolic function; consequently, overall pump function (the Frank-Starling Relationship) was found to be depressed. The geometric rearrangement associated with this operation leads to a reduction in wall stress for a given level of pressure generation, thus implying an increase in the efficiency with which wall stress is transduced into intraventricular pressure. CONCLUSIONS: Overall pump function is depressed in the short run after heart reduction surgery. However, on the basis of theoretic arguments, heart reduction surgery may have long-term beneficial implications. Importantly, this analysis revealed that changes in parameters of ventricular function have different implications during heart reduction surgery than when such changes are observed with inotropism caused by acute pharmacologic therapy.

Retrograde cardioplegia preserves myocardial function after induced coronary air embolism.

Coronary air embolism is a potential complication of cardiopulmonary bypass. We compared left ventricular function before and after the administration of antegrade or retrograde cardioplegic solution in a porcine model of coronary air embolism. Nineteen pigs were placed on cardiopulmonary bypass support and cooled to 32 degrees C. The heart was initially arrested with antegrade cold blood cardioplegic solution. The aortic crossclamp was released at 30 minutes and 0.02 cc/kg body weight of air was injected into the left anterior descending artery distal to the first diagonal branch. After 5 minutes the aorta was reclamped and the animals treated with 15 ml/kg body weight of 1:4 blood cardioplegic solution delivered by the antegrade (n = 6) or retrograde (n = 7) method. Control animals (n = 6) were not treated. Changes in regional preload recruitable stroke work were used to assess left ventricular performance before and after cardiopulmonary bypass. Two control animals could not be weaned from cardiopulmonary bypass. Left ventricular function was best preserved after treatment of induced coronary air embolism with retrograde cardioplegia (90% of baseline). Coronary air embolism treatment with antegrade cardioplegia resulted in diminished left ventricular performance (68% of baseline). In control animals left ventricular contractility was significantly impaired (39% of baseline). We conclude that administration of retrograde cardioplegic solution may be an effective method of treating coronary air embolism. The favorable outcome seen with cardioplegia may be in part because of its ability to protect the ischemic myocardium while the solution mechanically dislodges air from the vascular bed.

Inhaled nitric oxide is not a negative inotropic agent in a porcine model of pulmonary hypertension.

BACKGROUND: Reports of pulmonary edema complicating inhaled nitric oxide therapy in patients with chronic heart failure and pulmonary hypertension have raised the concern that inhaled nitric oxide may have negative inotropic effects. METHODS AND RESULTS: We investigated the effect of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on left ventricular contractile state in 10 open-chest pigs. Pressure-volume loops were generated during transient preload reduction to determine the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relation. Inhaled nitric oxide had no effect on systemic vascular resistance, cardiac output, end-systolic pressure volume relationship or stroke work-end-diastolic volume relation under normal conditions. After induction of pulmonary hypertension (intravenous thromboxane A2 analog), inhalation of nitric oxide (80 ppm) resulted in a reduction in pulmonary vascular resistance (mean +/- standard error of the mean) from 10.4 +/- 3 to 6.5 +/- 2 Wood units (p < 0.001) and in pulmonary artery pressure from 44 +/- 4 to 33 +/- 4 mm Hg (p < 0.05). Left ventricular end-diastolic volume rose from 53 +/- 9 ml to 57 +/- 10 ml (p = 0.02). No statistically significant change in cardiac output or systemic vascular resistance was observed. Inhaled nitric oxide had no effect on end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation. CONCLUSIONS: In a porcine model of pulmonary hypertension, inhaled nitric oxide does not impair left ventricular contractile function. Therefore the cause of pulmonary edema observed in some patients receiving inhaled nitric oxide is not due to a negative inotropic action of this therapy.

Reversal of iatrogenic myocardial edema and related abnormalities of diastolic properties in the pig left ventricle.

OBJECTIVE: This study examines the resolution of iatrogenic edema and related changes in systolic and diastolic properties in the intact pig left ventricle. METHODS: The coronary arteries were perfused for 50 to 60 seconds with diluted blood (hematocrit value 10% +/- 1%, edema group, n = 5) or whole blood (hematocrit value 28% +/- 1%, control group, n = 6) infused into the aortic root during aortic crossclamping in conditioned, anesthetized pigs. After whole blood reperfusion, preload reduction by vena caval occlusion was used to define systolic and diastolic properties at 15-minute intervals. Left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography were recorded. RESULTS: Left ventricular mass (wall volume) in the edema group increased significantly compared with that in control pigs after crossclamp removal. Mass returned to preperfusion levels after 45 minutes. The ventricular stiffness constant (beta) increased significantly in the edema group versus the control group, returning to baseline by 30 minutes. The diastolic relaxation constant (tau) and base constant (alpha) did not differ between groups. There was no significant change in contractility. CONCLUSION: Increases in left ventricular mass and diastolic stiffness induced by coronary perfusion with hemodiluted blood resolve after 45 minutes of whole blood perfusion in pigs. This study defines physiologic effects of edema in the normal heart while eliminating most common confounding experimental errors.

Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure.

BACKGROUND: Inhaled nitric oxide has been shown to be a potent and selective pulmonary vasodilator. Reports of increases in left ventricular end-diastolic pressure and episodes of pulmonary edema during the clinical use of inhaled nitric oxide in patients with preexisting left ventricular dysfunction have raised concerns that this agent may have myocardial depressant effects. We therefore undertook a study of the effects of inhaled nitric oxide on myocardial contractility in a porcine model of ventricular failure and pulmonary hypertension. METHODS: After inducing heart failure in 10 pigs by rapid ventricular pacing, hemodynamic measurements and pressure-volume diagrams (by the conductance method) were obtained in six animals at baseline and during administration of inhaled nitric oxide at concentrations of 20 and 40 ppm. Myocardial contractile state was assessed by the end-systolic pressure-volume relationship and preload-recruitable stroke work, whereas diastolic function was measured in terms of the end-diastolic pressure-volume relationship and the pressure decay time constant T. RESULTS: Baseline hemodynamics reflected heart failure and pulmonary hypertension, and inhaled nitric oxide induced significant reductions in mean pulmonary artery pressure and pulmonary vascular resistance. Although left ventricular end-diastolic pressure increased during administration of inhaled nitric oxide, no changes were observed in measures of systolic or diastolic function. CONCLUSIONS: Inhaled nitric oxide reduced pulmonary vascular resistance but did not alter myocardial contractility or diastolic function. Increases in left ventricular end-diastolic pressure during inhaled nitric oxide therapy are therefore not due to myocardial depression and may be related to increases in volume delivery to the left side of the heart resulting from reduced pulmonary vascular resistance.

A theoretic analysis of the effect of pulmonary vasodilation on pulmonary venous pressure: implications for inhaled nitric oxide therapy.

BACKGROUND: Although the use of inhaled nitric oxide offers certain advantages over more traditional pulmonary vasodilators, concerns have emerged because of reports of acute pulmonary edema during nitric oxide administration in patients with chronic heart failure. It is unclear whether the pulmonary vasodilating action of nitric oxide could, by itself, cause venous pressures to rise in the lung and why patients with preexisting chronic heart failure are at greatest risk for the development of pulmonary edema during inhaled nitric oxide therapy. METHODS: The cardiovascular system was modeled as time-varying elastances; the pulmonary and systemic vascular systems were each modeled as a series of resistive and compliance elements. Protocols were devised to examine the effects of a decrease in pulmonary vascular resistance on pulmonary venous pressure under different conditions of contractile state and volume status. RESULTS: Under all conditions studied, pulmonary venous pressure increased as pulmonary vascular resistance decreased. Increases in pulmonary venous pressure were caused by volume shifts between pulmonary arterial and venous compartments. These volume shifts were accentuated by high volume status. The impact of alterations in contractile state was minimal. CONCLUSIONS: Pulmonary vasodilation by itself can lead to an increase in pulmonary venous pressure that is mediated by shifts of blood between arterial and venous compartments of the pulmonary bed. Furthermore, impairment in ventricular contractile state by itself has relatively little effect on pulmonary venous pressure. The magnitude of the increase in pulmonary venous pressure is largely determined by the volume status and the initial value of pulmonary vascular resistance.

Desaturated venous-to-arterial shunting reduces right-sided heart failure after cardiopulmonary bypass.

BACKGROUND: Right-sided circulatory failure is a major cause of morbidity in heart transplant and ventricular assist device recipients. METHODS: Several systems for managing right-sided circulatory failure with use of a right-to-left shunt without need for an oxygenator or systemic heparinization were designed and used clinically. RESULTS: A right-to-left shunt was successfully used to treat severe right-sided circulatory failure in both a transplant and a left ventricular assist device recipient. CONCLUSIONS: If constructed between the femoral vein and artery, such a shunt could (1) be easily inserted and removed, (2) selectively infuse the lower extremities with desaturated blood while maintaining cerebral and cardiac perfusion with saturated blood, (3) selectively reduce the risk of paradoxical emboli to the head and heart, and (4) provide a known and adjustable degree of shunting depending on the condition of the patient, a major advantage of this system compared with creation of an atrial septal defect.

Right ventricular obstruction in aortic dissection: a mechanism of hemodynamic collapse.

The main and right pulmonary arteries may be compressed by the false lumen of a type I aortic dissection. We report a 73-year-old women with a dissection of the aorta in whom echocardiographic examination revealed acute pulmonary arterial compression causing right ventricular failure and hemodynamic collapse.

Systolic arterial pressure recovery after ventricular fibrillation in pigs.

Ventricular fibrillation (VF) is induced during implantable cardioverter defibrillator insertion and can result in cardiovascular collapse. The relation between repeated VF trials of varying duration and systolic blood pressure (SBP) recovery rate was studied in 6 pigs. Two implantable cardioverter defibrillator patches were placed on the heart, and VF was varied in a cyclic pattern until cardiovascular collapse occurred. A negative logarithmic relation between SBP recovery rate and duration of VF was found in 4 of the pigs with correlation coefficients of 0.62 to 0.97 (p < 0.05). The overall correlation coefficient was 0.51 for all 116 data points (p < 0.001). Although there was a significant (p < 0.05) decrease in average (+/- standard error of the mean) baseline SBP in the second half of each experiment (83 +/- 5 mm Hg versus 77 +/- 6 mm Hg), no significant difference in SBP was observed during VF (17 +/- 1 mm Hg versus 16 +/- 1 mm Hg) or after 15 seconds of SBP recovery (51 +/- 4 mm Hg versus 46 +/- 3 mm Hg) between the two halves of the experiments. Cardiovascular collapse occurred without warning; epinephrine was effective in reversing it. In conclusion, SBP recovery rate and duration of VF have a negative logarithmic relation consistent with a negative effect on left ventricular contractility with prolongation of VF. The onset of cardiovascular collapse during implantable cardioverter defibrillator testing cannot be predicted on the basis of monitored blood pressure alone.

Iatrogenic myocardial edema: increased diastolic compliance and time course of resolution in vivo.

BACKGROUND: Perfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals. METHODS: Edema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion. RESULTS: In the edema group, average left ventricular mass (132 +/- 7 [standard error of the mean] versus 106 +/- 4 g) and ventricular stiffness constant (0.15 +/- 0.02 versus 0.05 +/- 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 +/- 6 versus 116 +/- 4 g) and ventricular stiffness (0.06 +/- 0.01 versus 0.05 +/- 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups. CONCLUSIONS: Crystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction.

Electrical isolation of the heart. Stabilizing parallel conductance for left ventricular volume measurement.

Modern indices of left ventricular function require accurate measurement of left ventricular volume (LVV). Although conductance catheter (COND) measurements of LVV have been found to be reproducible under steady state conditions in closed chest animals, after median sternotomy, measurements of LVV are subject to exaggerated variation in parallel conductance (alpha Vc) outside of the left ventricle. Current calibration methods for measuring alpha Vc include hypertonic saline injection and quantitative two dimensional echocardiography. Unfortunately, these methods are hampered by imprecision, since frequent changes in alpha Vc in the open chest make recalibration impractical. Accordingly, a latex wrap technique was developed to insulate the left ventricle from extracardiac sources of alpha Vc in the open chest. Anesthetized pigs (n = 5) underwent a median sternotomy with insertion of a 6 French COND-micromanometer combination catheter into the left ventricle. Three conditions were tested: 1) unaltered; 2) metallic retractor outside of the pericardium (metal); and 3) latex wrap between the metal and pericardium. Pressure/COND loops showed that the insulator improved the shape of the loops and decreased alpha Vc, as measured by an echo-area/COND relationship, whereas metal increased alpha Vc and produced artifacts in the loops. In conclusion, electrical isolation eliminates distortion of pressure/COND loops related to extracardiac sources of alpha Vc, therefore allowing for accurate COND measurements in the open chest.

Validation study of a new transit time ultrasonic flow probe for continuous great vessel measurements.

Continuous measurement of cardiac output is important during experimental and clinical cardiac surgery as an indicator of ventricular function. Previous flow probes underestimated flow secondary to position and flow (S-series probes; Transonic Systems, Inc., Ithaca, NY), required frequent calibrations (electromagnetic), and were cumbersome to use. The new A-series probe (ASP) by Transonic Systems, Inc., uses a new X method of ultrasonic illumination insensitive to perturbations in flow. The ASPs were found to be accurate during in vitro studies, but have not been validated in vivo. Six anesthetized pigs were instrumented for right atrium to left atrium bypass, and ASPs were placed on the ascending aorta and pulmonary artery. Baseline measurements included aortic (Ao) and pulmonic flow (P), and thermodilution (Td) cardiac output. Animals then were placed on right heart bypass, and flow was randomly varied from 1 to 6 L/min, and Ao flow was recorded. In addition, ASPs were rotated and their direction reversed. After data collection, the occlusive roller pump (RP) was calibrated using a timed collection method. Calibrated RP flows were plotted versus ASP flows, and regression was applied. There was no difference between mean Ao, P, and Td cardiac outputs at baseline. In addition, changes in position and direction of the probe did not affect measurement of flow. The ASPs showed a highly linear correlation with RP ([r = 0.98, p < 0.01] ASP[L/min] = 0.98 RP-0.032). During laminar flow states, ASPs are accurate and insensitive to position on the great vessels.

Perioperative management of the left ventricular assist device recipient.

An understanding of the unique preoperative, intraoperative, and postoperative considerations of left ventricular assist device implantation is essential for the successful anesthetic management of these challenging cases. This article discusses the different stages of anesthetic care of the left ventricular assist device recipient, including preoperative assessment, lining, induction, separation from cardiopulmonary bypass, and the postbypass period.

Left-to-right systolic and diastolic ventricular interactions are dependent on right ventricular volume.

Three-compartment elastance modeling predicts that the magnitude of gain is solely dependent on the ratio of free wall and septal elastances. However, when nonlinearities in pressure-volume relationships are considered, the same model predicts that gain is load dependent. We therefore studied left-to-right ventricular interactions in the isolated cross-perfused canine heart preparation to determine whether, in fact, right ventricular volume modulates left-to-right ventricular interaction. We found that left-to-right systolic gain increased from 0.035 +/- 0.022 to 0.073 +/- 0.017 (P = 0.003) and left-to-right diastolic gain increased from 0.067 +/- 0.050 to 0.186 +/- 0.097 (P = 0.03) in response to increased right ventricular volume. This degree of volume dependency of gain is predicted by the three-compartment model when measured nonlinearities in time-varying elastance are taken into account. Future studies will need to account for changes in loading conditions when interpreting changes in systolic and diastolic interactions.

Disparity of isoflurane effects on left and right ventricular afterload and hydraulic power generation in swine.

UNLABELLED: The interaction between myocardial and vascular effects of anesthetics has a potential impact on how these drugs influence performance of the heart. Most studies have focused on volatile anesthetic effects on the left ventricle (LV) and systemic circulation. Whether the right ventricle (RV) and pulmonary circulation respond in a similar fashion, however, is unclear. In the present study, we therefore examined the dose-related effects of isoflurane on LV and RV contractility and total afterload and related changes to simultaneous effects on the hydraulic power generated by each chamber. Two groups of swine were studied: one received no additional treatment before isoflurane (ISO, n = 6), and the other received hexamethonium, atropine, and propranolol to produce autonomic blockade before isoflurane administration (ISO+AB, n = 4). For each experiment, measurements were made of RV and LV regional segment lengths and pressures, along with proximal aortic and pulmonary arterial (PA) blood flow and pressure during the administration of 0, 0.5, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC) isoflurane. Contractility was assessed by calculating the regional preload recruitable stroke work slope (PRSW). Afterload was characterized in both nonpulsatile and pulsatile terms by calculating aortic input impedance magnitude (Z). From these data, total arterial resistance (R), characteristic impedance (ZC), and vascular compliance (C) were determined with reference to a three-element Windkessel model of the circulation. Additionally, steady-state (WSS), oscillatory (WOS), and total (WT) hydraulic power output of each ventricle was calculated. In the ISO group, isoflurane produced a nearly threefold greater decrease of peak systolic pressure in the LV than in the RV, yet the dose-related decrease of regional PRSW was virtually the same in both chambers. In the aorta, isoflurane produced a maximal 25% reduction in R at 1.0 MAC and doubled C without a significant change in ZC. Alternatively, PA R was increased from baseline at 1.0 and 1.5 MAC, whereas ZC was increased from all other values at 1.5 MAC. PA C was not altered by isoflurane. In ISO+AB pigs, PA ZC at baseline was higher than that evident in ISO animals but was not altered by isoflurane. In contrast, baseline aortic R was lower in ISO+AB pigs but was still modestly reduced by 1.0 MAC isoflurane. In ISO animals, WT and WSS from both ventricles demonstrated dose-related decreases, but the reductions in LV WTand WSS were greater than those for the RV at all doses. Accordingly, the power requirement per unit flow decreased for the LV but remained constant for the RV. WOS for both ventricles was also reduced by isoflurane. However, the LV WOS to WT ratio increased, which indicates that more power was lost to the system by pulsation. In contrast, reductions in RV WT and WOS were nearly parallel at all isoflurane doses, and the WOS to WT ratio was unchanged. In the ISO+AB group, isoflurane-induced alterations in LV and RV power characteristics were similar to those in the ISO group. These data indicate that, despite similar effects on biventricular contractility, isoflurane exerts qualitatively different effects on RV and LV afterload, in part via alteration in autonomic nervous activity, that influence the distribution of power output between steady-state and pulsatile components. IMPLICATIONS: In this study, we examined the effects of isoflurane on cardiac performance in swine and found that, although the drug depresses contraction of both the left and right ventricles similarly, it has different effects on forces that oppose the ejection of blood. These findings demonstrate that the two interdependent pumps that comprise the heart can be influenced differently by anesthetic drugs.

Management strategies for high-risk cardiac surgery: improving outcomes in patients with heart failure.

BACKGROUND: Surgical heart failure management is the fastest growing aspect of cardio-vascular surgery. Advances in cardiac surgical techniques have changed the number and types of operations permitted physicians and thus broadened the complexity of patients recommended for operation. METHODS: Surgeons, anesthesiologists and cardiologists face hemodynamic and patho-physiological challenges that can be optimally overcome only by modifying treatment strategies. Because many treatment standards are still evolving in this rapidly advancing field, a team of cardiovascular surgeons and anesthesiologists convened to share clinical experience and impressions and discuss practical issues related to high-risk patients undergoing heart surgery. RESULTS: Heart failure pathophysiology, surgical heart failure management, including mitral reconstruction and left ventricular remodeling, cardiopulmonary bypass weaning, inotropic support, transesophageal echocardiography and acute cardiovascular collapse after cardiac surgery are discussed. CONCLUSION: This article is intended to guide clinicians to improve patient care and outcomes in this special population by providing specific guidance on the appropriate use of inotropic and mechanical support in patients undergoing high-risk procedures using innovative techniques.

Selective reduction of PVR by inhalation of a cGMP analogue in a porcine model of pulmonary hypertension.

Selective reduction of pulmonary vascular resistance (PVR) remains a therapeutic goal for the treatment of pulmonary hypertension, but current therapeutic options remain limited. Although the gas nitric oxide (NO) selectively dilates the pulmonary vascular bed, it requires special equipment for administration, has a short biologic half-life, and is potentially toxic. We hypothesized that stimulation of the NO pathway at the level of its second messenger, guanosine 3',5'-cyclic monophosphate (cGMP), by targeted pulmonary delivery of a membrane-permeable nonhydrolyzable cGMP analogue would cause selective pulmonary vasodilation. Pulmonary hypertension was induced in 21 pigs by the intravenous infusion of a thromboxane A2 analogue (9,11-dideoxy-9 alpha,11 alpha-epoxymethanoprostaglandin F2 alpha). Inhaled 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) lowered PVR in a time- and dose-dependent manner, with maximal effect achieved after 20 min. Compared with physiological saline control, 8-BrcGMP inhalation (3.0 micrograms/kg) lowered PVR by 25 +/- 3% (P < 0.01), whereas there was no significant decline in systemic vascular resistance (4 +/- 6%); mean pulmonary arterial pressure declined 13 +/- 3% (P < 0.01), whereas there was little change in mean arterial pressure; cardiac output increased 10 +/- 4% (P < 0.05). PVR did not decrease after inhalation of noncyclic 8-bromoguanosine 5'-monophosphate, indicating that stimulation of the NO-cGMP pathway beyond the level of NO results in pulmonary vasodilation independent of stimulation of purinergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Systolic arterial pressure recovery after ventricular fibrillation/flutter in humans.

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 +/- 2, and the mean drop in systolic pressure was 84 +/- 16 mmHg. The mean recovery time for systolic pressure was 10 +/- 6 seconds, the average systolic pressure recovery rate was 13 +/- 14 mmHg/sec, and the mean percent systolic pressure recovery was 94% +/- 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.