Changes In Central Hemodynamics Research Articles

Atrial Natriuretic Peptide Attenuates Pacing-Induced Myocardial Ischemia During General Anesthesia in Patients with Coronary Artery Disease

Atrial natriuretic peptide (ANP) exerts a dilatory effect on coronary arteries in humans.We investigated the effects of ANP on pacing-induced myocardial ischemia during enflurane anesthesia in patients with coronary artery disease (CAD). In 20 patients with CAD, myocardial ischemia was induced by atrial pacing before and after an iv infusion of ANP (50 mg [center dot] kg-1 [center dot] min-1, n = 10) or placebo (n = 10). We studied the effects of ANP or placebo on pacing-induced changes in central hemodynamics, myocardial blood flow and regional myocardial indices of lactate uptake (RMLU), and oxygen consumption (RMVO2) and extraction (RMO (2) E). ST-segment depression was less pronounced during pacing with ANP compared with control pacing (-0.09 +/- 0.01 vs -0.24 +/- 0.02 mV; P < 0.001). RMLU decreased to -11.1 [micro sign]mol/min during control pacing compared with -0.7 [micro sign]mol/min during pacing with ANP (P < 0.01). ANP did not affect pacing-induced changes in RMVO (2), RMO2 E, or the rate pressure product. Placebo did not affect pacing-induced changes in ST-segment depression or RMLU. In conclusion, ANP attenuates ischemic ST-segment depression and lactate release during pacing-induced myocardial ischemia in patients with CAD. The antiischemic effect of ANP was not accompanied by any improvement in the regional myocardial oxygen supply/demand relationship. Implications: We evaluated the effects of IV atrial natriuretic peptide (50 ng [center dot] kg-1 [center dot] min-1) on pacing-induced myocardial ischemia during general anesthesia in patients with coronary artery disease. In contrast to placebo, atrial natriuretic peptide attenuated ST-segment depression and myocardial lactate production and improved left ventricular function during pacing-induced ischemia. (Anesth Analg 1999;88:279-85)

Central Hemodynamic Changes in Experimental Muscle Crush Injury in Pigs

To investigate central and pulmonary hemodynamics in a standardized normovolemic experimental muscle injury model, 8 anesthetized and mechanically ventilated test pigs were intracavally infused with 100 ml of autologous muscle extract over a period of 100 min; 8 control pigs received Ringer’s solution. The cardiac index decreased 20% and the heart rate decreased 10% within 30 min of starting the infusion in the muscle extract group and remained depressed. Mean arterial pressure increased significantly in both groups. The pulmonary capillary wedge pressure and central venous pressure remained relatively unchanged during the 5-hour study. A 2-fold increase in mean pulmonary arterial pressure and a nearly 4-fold increase in the pulmonary vascular resistance index was seen in the muscle extract infusion group, which however returned to normal. Arterial hemoglobin concentration and systemic vascular resistance index remained fairly stationary in both groups. Immediate significant decreases in both arterial oxygen saturation and arterial oxygen tension were observed in the muscle extract group, however both variables recovered towards the end of the experiment. A slight increase in arterial blood pH value was noted during the experiment. In conclusion, autologous muscle extract infusion causes decreases in heart rate and cardiac index, as well as a significant increase in pulmonary vascular tone and systemic hypoxemia, emphasizing the detrimental effects of skeletal muscle injury following severe trauma.

Changes in Central and Peripheral Hemodynamics Induced by Long-Term Physical Exercise Training in Patients With Chronic Heart Failure

Changes in Central and Peripheral Hemodynamics Induced by Long-Term Physical Exercise Training in Patients With Chronic Heart Failure

Changes in central and peripheral hemodynamics induced by long-term physical exercise training in patients with chronic heart failure

Changes in central and peripheral hemodynamics induced by long-term physical exercise training in patients with chronic heart failure

Positive pressure inspiration differentially affects right and left ventricular outputs in postoperative cardiac surgery patients

Purpose : The purpose of this study was to determine the dynamic changes in right ventricular (RV) and left ventricular (LV) output during positive airway pressure inspiratory hold maneuvers so as to characterize the interaction of processes in creating steady-state cardiac output during positive pressure ventilation. Materials and Methods : We examined the disparity of RV and LV outputs at 5 seconds (early) and 20 seconds (late) into a 25-second inspiratory hold maneuver in 14 subjects in the intensive care unit immediately following coronary artery bypass surgery. RV output was measured by the thermodilution technique, whereas LV output was measured by the arterial pulse contour method. RV and LV volumes were also measured by thermal and radionuclide ejection fraction techniques, respectively. Results : As P aw was progressively increased from 0 to 20 cm H 2O in sequential inspiratory hold maneuvers, both RV and LV outputs changed differently both at 5 seconds and 20 seconds into the inspiratory hold maneuvers. When expressed as change in cardiac output (L/min) for every cm H 2O Paw increase relative to end-expiratory values, RV output increased at 5 seconds (0.05 ± 0.15 L/min) then decreased at 20 seconds (−0.08 ± 0.21, P < .05). LV output decreased slightly at 5 seconds (−0.14 ± 0.22) and did not change from this minimal depressed level at 20 seconds ( P < .05). Changes in RV and LV output were paralleled by changes in RV and LV end-diastolic volumes, respectively. Conclusion : Positive pressure inspiration induces time-dependent changes in central hemodynamics, which are dissimilar between RV and LV function. Initially, inspiration increases RV output but decreases LV output, such that intrathoracic blood volume increases. However, sustained inspiratory pressures induce proportionally similar decreases in both RV and LV outputs. Thus, the hemodynamic effects of positive pressure ventilation will depend on the degree of lung inflation, the inspiratory time, and when measurements are made within the ventilatory cycle. These data also suggest that positive pressure ventilation with up to 20 cm H 2O P aw does not significantly impair ventricular performance in humans.

Electrical stimulation-induced contraction to reduce blood stasis during arthroplasty

Deep venous thrombosis and subsequent pulmonary embolism due to venous pooling/stasis commonly occur in patients during hip and/or knee arthroplasty (i.e., replacement). This problem may be alleviated by using techniques to promote lower limb blood flow. Electrical stimulation-induced contractions have been shown to activate the skeletal muscle pump, promote limb blood flow, and may be effective for reducing venous pooling/stasis and edema. Therefore, electrical stimulation may reduce the incidence of deep venous thrombosis (DVT) and pulmonary embolism (PE) during and following surgery. The overall goal of this project was to evaluate the clinical efficacy of sequential electrical stimulation-induced leg muscle contractions on the venous blood flow during surgery. The degree of venous pooling/stasis was monitored via electrical impedance changes in the thorax. The changes in the patient's central hemodynamics were then calculated. Thirty patients were recruited and randomly assigned to either a control group (n = 15, mean age = 66.4 +/- 7.3) or experimental group (n = 15, age = 60.7 +/- 9.7). Both groups received the standard medical treatment for prevention of DVT (i.e., coumadin, heparin, etc.) and compression stockings (TED, Kendall). The control group used the sequential compression device (SCD + TED) and the experimental group used electrical stimulation (ES + TED). Electrical stimulation was applied via surface electrodes to the lower-limb muscles (tibialis anterior and gastrocnemius) and upper limb muscles (quadriceps femoris and hamstrings). These muscles contracted sequentially, using an eight-channel electrical stimulator. Four seconds of calf (contraction/compression) were followed by 7-s of calf and thigh (contraction/compression) interspersed by 60-s rest period during both electrical stimulation or sequential compression device. This cycle continued throughout the surgery (60-75 min) for both groups. At 15 min intervals, venous return was monitored by impedance cardiograph. Physiologic responses including ventricular stroke volume (SV), cardiac output (CO), heart rate (HR), total peripheral resistance (TPR), as well as mean arterial pressure (MAP) were monitored. These responses were statistically analyzed and compared throughout the surgery within each group and between the two groups. The results show stroke volume and cardiac output to be higher throughout surgery in the electrical stimulation group as compared with the sequential compression device group. The heart rate was consistently lower during electrical stimulation for both groups. Total peripheral resistance did not change in the electrical stimulation group; but increased in the sequential compression device group. The data suggest that continuous electrical stimulation-induced contractions could improve lower leg circulation by eliciting the physiologic muscle pump. This will lead to improved venous circulation and reduction of blood stasis during total hip and/or knee surgery. This technique may offer greater protection against DVT and PE during surgery than the commonly used sequential compression device.

Central and peripheral haemodynamic changes in post-term fetuses: correlation with oligohydramnios and abnormal fetal heart rate pattern.

To assess the hypothesis that the occurrence of oligohydramnios and abnormal fetal heart rate (FHR) pattern in post-term fetuses is associated with impaired fetal cardiac function. A cross sectional study was performed on post-term and term fetuses. Fetal tests included a computerised analysis of the FHR, a biophysical profile and Doppler studies of the abdominal aorta, umbilical artery, middle cerebral artery and the fetal heart. Pulsatility index (PI) was calculated from the abdominal aorta, umbilical and middle cerebral artery flow velocity waveforms. Peak velocity, velocity time integral (VTI), E:A ratio, and heart rate (HR) were calculated from the flow velocity waveforms obtained from the aortic and pulmonic outflow, and from the mitral and tricuspid valves. Maternal fetal laboratory, Department of Obstetrics. One hundred and twenty post-term and 42 term fetuses. Only the tricuspid E:A ratio was significantly higher (P < 0.05) in post-term fetuses with a normal amniotic fluid index compared with term fetuses. Post-term fetuses with an abnormal amniotic fluid index had a significantly lower aortic peak velocity (P < 0.01), aortic VTI x HR (P < 0.01), and mitral VTI x HR (P < 0.05) compared with post-term fetuses with a normal amniotic fluid index or compared with term fetuses. Post-term fetuses with reduced FHR variation had a significantly lower aortic peak velocity (P < 0.01), pulmonic peak velocity (P < 0.05), aortic VTI x HR (P < 0.01), pulmonic VTI x HR (P < 0.05) and a significantly lower mitral VTI x HR (P < 0.05) when compared with post-term fetuses with normal FHR variation. Similar results were obtained in comparing fetuses with normal and adverse perinatal outcome. The occurrence of oligohydramnios and abnormal FHR pattern in post-term fetuses appears to be associated with impaired fetal cardiac function. This finding should allow further investigations of post-term fetuses.

Central hemodynamic changes associated with pregnancy in a long-term cardiac transplant recipient

We present a case of pregnancy in a woman who had undergone cardiac transplantation and was monitored by “surveillance” biopsy at intervals during the entire course of pregnancy and the immediate postpartum period. Exercise reserve remained normal during these periods despite angiographic evidence of coronary disease and episodes of rejection. Central hemodynamic changes were similar to those expected during normal pregnancy. Hemodynamic stability was maintained during epidural anesthesia for labor and subsequent cesarean section. (A M J O BSTET G YNECOL 1996;174:1651-3.)

Severe hemorrhagic fever with renal syndrome in a pregnant woman

Hemorrhagic fever with renal syndrome (HFRS) is a disease of viral etiology, which is based on the defeat of small vessels with the development of DIC syndrome. The severity of the condition and the outcome of severe HFRS are determined by acute renal failure (ARF). Cases of eclampsia with HFRS, which are not associated with hemodialysis, are described, during which, as is known, the appearance of seizures is possible due to the development of an imbalance syndrome. In the period of oligoanuria and polyuria with HFRS, there is an increase in peripheral vascular resistance with normal or reduced BCC with the formation of arterial hypertension in some cases. Changes in central hemodynamics in HFRS are close to those in preeclampsia and eclampsia of pregnant women. In addition, coagulopathy is characteristic of HFRS and late gestosis.

Effects of Acute Plasma Volume Expansion on Maternal Renal and Central Hemodynamics and Atrial Natriuretic Peptide Concentrations in Normal and Preeclamptic Pregnancies

Objective: To evaluate the maternal renal hemodynamic response to acute plasma volume expansion in normal and hypertensive pregnancies, and relate it to changes in central hemodynamics and plasma atrial natriuretic peptide (ANP) concentrations.Methods: Seven women with pregnancy-induced hypertension (PIH)/ preeclampsia and 10 healthy pregnant controls in the last trimester were studied. Renal Doppler and echocardiographic investigations were performed, and maternal venous blood was sampled for determination of ANP concentrations before and after 30 min infusion of a crystalloid solution (15 mL/kg).Results: Baseline renal artery pulsatility index (PI) did not differ between the normal group (1.10 ± 0.13, mean and SD) and the PIH/preeclampsia group (1.12 ± 0.08). After volume expansion PI increased (P < 0.01) to 1.43 ± 0.23 in the normal group, but it remained unchanged in the PIH/preeclampsia group. After volume expansion, both normal and PIH/preeclamptic women showed an increase in cardiac output and stroke volume, and a decrease in total systemic resistance, while blood pressure and heart rate remained fairly unchanged. Baseline plasma concentrations of ANP before volume expansion in the normal (4.1 ± 1.3 pmol/L) and the PIH/preeclamptic (6.1 ± 3.9 pmol/L) groups did not differ significantly. Following volume expansion, concentrations of ANP increased (P < 0.05) in both groups to 6.3 ± 3.2 pmol/L and to 9.9 ± 6.1 pmol/ L, respectively. In the normal group there was a positive linear relationship between increased ANP concentrations and changes in PI (r = 0.68, P < 0.05).Conclusions: Despite similar changes in central hemodynamics and increases in plasma ANP in the two groups during volume expansion, renal vascular resistance, as estimated by renal artery pulsatility index, increased only in healthy pregnant women and not in patients with PIH/preeclampsia.

Monitoring of mixed venous oxygen saturation and pressure from biosensors in the right ventricle A 24 hour study in patients with heart failure

Right ventricle venous oxygen saturation was studied in 10 heart failure patients over 24 h using a lead equipped with an oxygen biosensor inserted temporarily. At the same time a pressure sensor, incorporated in the same lead to measure right ventricular pulse pressure and maximum positive and negative rate of pressure development (RV dP/dt), was tested to see whether it would interfere with the oxygen sensor. Data from the biosensor lead were continuously compared with mixed venous oxygen saturation obtained from a fibreoptic Swan-Ganz catheter with the tip in the pulmonary artery. For reference, blood samples were drawn at regular intervals from this catheter. A provocative protocol was used to cause haemodynamic changes. There was good correlation between oxygen saturation in the right ventricle (biosensor-derived) and mixed venous oxygen saturation in the pulmonary artery (fibreoptic-derived) (r = 0.86) and between sensor-obtained right ventricular oxygen saturation and oxygen saturation in the blood samples from the pulmonary artery (r = 0.90). Changes in central haemodynamics were also well reflected by changes in pulse pressure and dP/dt derived from the pressure sensor. As it was not possible to obtain absolute pressures no attempt was made to compare the pressure changes with conventional haemodynamics. These 24 h haemodynamic measurements suggest that a biosensor-equipped lead placed in the right ventricle could be a valuable tool for long-term monitoring of mixed venous oxygen saturation and pressure in patients with congestive heart failure.

Responses of the circulatory system and muscle sympathetic nerve activity to head-down tilt in humans

These experiments were conducted to examine whether changes in central and peripheral hemodynamics were proportional to muscle sympathetic nerve activity (MSNA) during graded head-down tilt (HDT). Twelve healthy males (19-42 yr old) underwent HDT at 15 degrees and 30 degrees for 10 min each with a 10-min rest period between the trials. MSNA at 15 degrees HDT declined by 31 +/- 5% (P < 0.05) for burst rate and by 37 +/- 3% (P < 0.05) for total activity. At 30 degrees HDT, the reduction in MSNA was 51 +/- 5% for burst rate (P < 0.05 vs. 15 degrees HDT) and 46 +/- 5% for total activity (P < 0.05 vs. 15 degrees HDT). Stroke volume increased (P < 0.05) during both 15 degrees and 30 degrees HDT, but heart rate and blood pressure remained unchanged. A concurrent increase in central venous pressure (P < 0.05) and stroke volume with a reduction of thoracic impedance (P < 0.05) suggests that both pressure and volume in the atrium were elevated during HDT, and the magnitude of these changes was greater (P < 0.05) at 30 degrees HDT than at 15 degrees HDT. Forearm blood flow increased during HDT at both 15 degrees and 30 degrees, and the magnitude of the increase was greater (P < 0.05) at 30 degrees HDT. It is concluded that the magnitude of the loading of the cardiopulmonary mechanoreceptors during HDT was higher at 30 degrees in comparison to 15 degrees. This increased the afferent firing rate by the cardiopulmonary receptors and probably inhibited sympathetic outflow in the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of Skeletal Muscle Laser Doppler Flowmetry to Changes in Central Hemodynamics in Detecting the Physiological Response to Moderate Hemorrhage

Previous studies have demonstrated that laser Doppler (LD) flowmetry is a useful technique for following changes in blood flow in a tissue bed, but the potential role of LD flowmetry in management of the critically ill patient is unclear. This study sought to establish the sensitivity of LD flowmetry compared to changes in centrally measured hemodynamic parameters in response to a mild hemorrhagic episode. In order to establish the correlation between LD flow and actual blood flow, livers from Sprague-Dawley rats were isolated and perfused via the portal vein with citrate anticoagulated rat blood. Changes in LD flow were recorded while changing blood flow via the perfusion pump. There was a strong correlation between pump flow and LD flow (for N = 5 livers, r > 0.9; P < 0.05). This relationship was stable at hematocrits >20. The second part of this study tested the sensitivity of LD flowmetry in anesthesized baboons. An LD probe was placed on the surface of the gracilis muscle of the adult male baboons. LD flow and hemodynamic parameters were measured following two episodes of bleeding and reinfusing 250 cc of blood. During the first bleed there were significant changes in heart rate (97 + 8 to 159 + 12), mean arterial pressure (125 + 6 to 105 + 9), and LD flow (20.6 + 4.6 to 11.9 + 3.6); these parameters returned to normal after reinfusion of blood. During the second bleed, the only parameters that showed significant changes were heart rate (118 + 5 to 135 + 12) and LD flow (17.5 + 8 to 10.7 + 3.4). Cardiac output, pulmonary artery wedge pressure, and arterial blood pH by blood gas determination did not change significantly during either bleeding episode. This study suggests that LD flowmetry is more sensitive to tissue hypoperfusion than commonly measured central parameters and may be useful in aiding the resuscitation of critically ill patients.

Effects of enalapril versus losartan on regression of volume overload-induced cardiac hypertrophy in rats.

The role of nonhemodynamic cardiac trophic mechanisms differs not only between different models of cardiac hypertrophy but also within the same model for development versus maintenance of cardiac hypertrophy. Our previous studies pointed to a major role for the renin-angiotensin system (RAS) as a cardiac trophic stimulus in the remodeling of the heart in response to volume overload by aortocaval shunt or minoxidil treatment. In the present study, we evaluated the effects of blockade of the RAS by the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan on left ventricular (LV) and right ventricular mass and LV dilation in relation to changes in central hemodynamics during the maintenance of minoxidil and aortocaval shunt-induced cardiac hypertrophy. Both blockers similarly decreased LV end-diastolic pressure (LVEDP) and LV peak systolic pressure, whereas cardiac output remained unchanged in both models of volume overload. This suggests a major contribution of improved LV performance and decreased afterload to the decrease in cardiac preload by the two blockers rather than decreased venous return. Both blockers reversed LV hypertrophy in parallel to their effects on LVEDP in both models of volume overload. In minoxidil-treated rats, the extent of reversal in LV mass and dilation by the two blockers was similar to "spontaneous regression" after discontinuation of minoxidil treatment. These results indicate that in contrast to the development phase of cardiac hypertrophy, the RAS does not contribute to the maintenance of volume overload-induced cardiac hypertrophy in these two models via direct cardiac trophic effects. The RAS, however, maintains cardiac hypertrophy indirectly by contributing to the persistence of high filling pressures.

Relationship between Venous and Arterial Haemodynamics during Postural Changes in Venous Insufficiency

Objective: To study the changes in central haemodynamics and the relationship between arterial blood pressure and the venous dynamics of the lower limbs in patients with venous insufficiency. Design: Prospective haemodynamic study during postural changes in 14 patients with venous insufficiency with no other concomitant cardiovascular disease or disturbances in autonomic nervous system. Setting: Department of Cardiology and Angiology, University Hospital, Gent, Belgium. Patients: Fourteen patients with venous valve insufficiency in the lower limbs. Interventions: Measurements of arterial blood pressure, heart rate, stroke volume and cardiac output were performed in the supine position after 30 min rest and 5, 15 and 30 min after standing and during the recovery. Venous pressure at the ankle and calf circumference were also measured. Main outcome measures: Changes in cardiac output and total peripheral vascular resistance in order to maintain blood pressure during postural changes. Results: Arterial blood pressure was maintained constant owing to an increase in total peripheral vascular resistance despite a decrease in cardiac output. Venous pressure is also related to arterial blood pressure. Conclusions: The arterial and venous systems, even in venous insufficiency, are integrated to maintain blood pressure constant during postural changes.

Iloprost attenuates trauma-related pulmonary sequestration of leucocytes and platelets

The purpose of this study was to investigate the effects of iloprost, a synthetic prostacyclin analogue, on the pulmonary cellular trapping after a standardized soft tissue trauma. In two groups 1 and 2 iloprost was given in doses of 100 ng/kg/min commencing 30 and 20 min respectively prior to trauma and ceasing 10 min after trauma. 111Indium-oxine was used to label neutrophils in 6 animals from each group. Platelets were labelled in 6 and 7 animals respectively. A third group of 11 pigs served as a control and did not receive iloprost. The pulmonary sequestration of platelets and neutrophils was studied dynamically with a gamma camera and directly after trauma was significantly less in group 1 when compared to the control group. A rise in pulmonary vascular resistance and pulmonary arterial pressure was seen in the control group immediately after trauma but this was not evident in the iloprost groups. PaO 2 decreased significantly in group 1 and 2 during the iloprost infusion. The results indicate that iloprost attenuates the pulmonary cellular sequestration and changes in central hemodynamics during trauma in this model.

Central and peripheral hemodynamic changes in fetuses with absent end-diastolic velocity in umbilical artery: Correlation with computerized fetal heart rate pattern

OBJECTIVES: Our purpose was to study hemodynamic changes in peripheral and central blood vessels and to correlate these changes with the computerized fetal heart rate pattern in fetuses with absent end-diastolic velocity in the umbilical artery. STUDY DESIGN: Doppler studies of the umbilical artery, the middle cerebral artery, and aortic and pulmonic outflow, together with computerized fetal heart rate monitoring, were performed every 2 to 4 days until delivery in 13 fetuses with absent end-diastolic velocity in the umbilical artery. The pulsatility index was calculated from the flow velocity waveforms obtained from the umbilical and middle cerebral arteries. The velocity time integral (an index of cardiac output) and the heart rate were calculated from the flow velocity waveforms obtained from the aortic and pulmonic outflow. RESULTS: Two fetuses were delivered immediately after the first examination because of repetitive fetal heart rate decelerations. One fetus was excluded from the study because of major malformations. Ten had three to eight tests each. Six had a biphasic change of the middle cerebral artery, which consisted of a decrease (p < 0.001) followed by an increase in the pulsatility index (p < 0.05). When the middle cerebral artery lost its vasodilation, there was an increase in the middle cerebral artery/umbilical artery pulsatility index ratio (p < 0.05). Left cardiac output decreased (p < 0.05), resulting in an increase in the pulmonary/aortic velocity time integral × heart rate ratio (p < 0.05). Reduced fetal heart rate variation (< 30 msec) developed in all six fetuses, and they were delivered because of repetitive fetal heart rate decelerations. Four fetuses with only a decrease in the middle cerebral artery pulsatility index did not have reduced fetal heart rate variation or decelerations, the aortic velocity time integral × heart rate didn't decrease, and the pulmonic/aortic velocity time integral × heart rate ratio didn't increase. These fetuses were delivered for reasons other than fetal distress. The middle cerebral artery pulsatility index correlated with the aortic velocity time integral × heart rate (r = -0.53, p < 0.0001), and the middle cerebral artery/umbilical artery pulsatility index correlated with the pulmonic/aortic velocity time integral × heart rate (r = 0.56, p < 0.0001). CONCLUSION: Abnormal fetal heart rate patterns occur in fetuses with absent end-diastolic velocity in the umbilical artery when the middle cerebral artery begins to lose its compensatory maximal dilation. The increase in the middle cerebral artery pulsatility index is associated with a significant reduction in left ventricular output without significant changes in right ventricular function. Thus it appears that a loss of autonomic reactivity occurs in the brain first and is followed within a few days by a similar response in the heart, as shown by the decreased fetal heart rate variation. (AM J OBSTET GYNECOL 1994;170:509-15.)

Increased Pulmonary Platelet Sequestration Due to Infusion of Cold Saline during Extracorporeal Circulation

We have previously documented that neutrophils (polymorphonuclear leukocytes) aggregate in the lungs 10-15 min after the start of dialysis. The aim of the present study was to investigate the corresponding platelet reaction and evaluate the effect of prewarmed priming solution on this reaction. The animals were divided into two groups, each consisting of 6 pigs. In group 1 the priming solution was prewarmed to 36-38 degrees C whereas it was maintained at room temperature in group 2. Platelets were selectively labelled with 111In-oxine. The activity over the lung was followed dynamically with a gamma camera and already after 2 min a significant difference in platelet sequestration showed between the groups. A significant increase in pulmonary vascular resistance was noted in group 2, but not in group 1. In conclusion, platelet aggregation occurs early on during dialysis in this model. The results also indicate that prewarming the priming solution attenuates the pulmonary platelet sequestration and also seems to decrease the changes in central hemodynamics.

Cardiac Effects of ACE Inhibition

Hypertension frequently is associated with a number of changes in heart structure and function, such as left ventricular hypertrophy, disturbed diastolic function, and subnormal stroke volume during exercise. Most of these changes probably are related to myocardial fibrosis. Antihypertensive agents reverse the structural and functional changes to different degrees. The hemodynamic changes in central hemodynamics at rest and during exercise were studied before and after angiotensin-converting enzyme (ACE) inhibition in 68 patients with essential hypertension (ranging from severe to moderately severe). In patients with moderately severe hypertension who were administered perindoprilat intravenously, mean arterial pressure was reduced by approximately 17% due to reduction in total peripheral resistance and no changes in heart pump function. Chronic treatment with captopril, enalapril, or lisinopril for 6-12 months induced reduction in blood pressure associated with decreased peripheral resistance. In general, there were only minor changes in cardiac output, stroke volume, and heart rate. Studies from other laboratories have shown that ACE inhibitors reverse left ventricular hypertrophy and improve left ventricular diastolic function. Captopril also appears to improve coronary circulation. The effect of ACE inhibitors on heart structure and function appears promising with regard to cardioprotection during chronic use, but long-term studies are needed to prove that this will occur in clinical practice.

Regional blood flow in human congestive heart failure

Despite the total-body consequences of congestive heart failure, little information is available on the distribution of cardiac output and regional-organ hemodynamics in this condition in humans. Technical and methodologic limitations probably account for the paucity of data in this area. Available data indicate that blood flow to the regions or organs studied, namely, the kidneys, hepatosplanchnic region, and upper limbs, decreases in proportion to the reduction in cardiac output. However, renal blood flow appears to be protected in human heart failure by a form of “autoregulation” during marked depression of cardiac output (<2.0 L/min/m 2). Results of preliminary studies suggest that the regulation of regional-organ hemodynamics is disturbed in this human condition. Cardioactive drugs profoundly affect regional-organ hemodynamics independent of changes in central hemodynamics and cardiac output. The determination of regional blood flow responses in human heart failure will become more important as we expand our knowledge base of the pathophysiology of heart failure, learn more about local vascular control mechanisms, and pursue the potential therapeutic objective of selectively augmenting regional-organ hemodynamics and function.