The meaning of blood pressure.

Measurement of arterial pressure is one of the most basic elements of patient management. Arterial pressure is determined by the volume ejected by the heart into the arteries, the elastance of the walls of the arteries, and the rate at which the blood flows out of the arteries. This review will discuss the three forces that determine the pressure in a vessel: elastic, kinetic, and gravitational energy. Emphasis will be placed on the importance of the distribution of arterial resistances, the elastance of the walls of the large vessels, and critical closing pressures in small arteries and arterioles. Regulation of arterial pressure occurs through changes in cardiac output and changes in vascular resistance, but these two controlled variables can sometimes be in conflict.

Volume and its relationship to cardiac output and venous return.

Volume infusions are one of the commonest clinical interventions in critically ill patients yet the relationship of volume to cardiac output is not well understood. Blood volume has a stressed and unstressed component but only the stressed component determines flow. It is usually about 30 % of total volume. Stressed volume is relatively constant under steady state conditions. It creates an elastic recoil pressure that is an important factor in the generation of blood flow. The heart creates circulatory flow by lowering the right atrial pressure and allowing the recoil pressure in veins and venules to drain blood back to the heart. The heart then puts the volume back into the systemic circulation so that stroke return equals stroke volume. The heart cannot pump out more volume than comes back. Changes in cardiac output without changes in stressed volume occur because of changes in arterial and venous resistances which redistribute blood volume and change pressure gradients throughout the vasculature. Stressed volume also can be increased by decreasing vascular capacitance, which means recruiting unstressed volume into stressed volume. This is the equivalent of an auto-transfusion. It is worth noting that during exercise in normal young males, cardiac output can increase five-fold with only small changes in stressed blood volume. The mechanical characteristics of the cardiac chambers and the circulation thus ultimately determine the relationship between volume and cardiac output and are the subject of this review.

A further analysis of why pulmonary venous pressure rises after the onset of LV dysfunction.

Based on a dynamic computational model of the circulation, Burkhoff and Tyberg (Am J Physiol Heart Circ Physiol 265: H1819-H1828, 1993) concluded that the rise in pulmonary venous pressure (Pvp) with left ventricular (LV) dysfunction requires a decrease in vascular capacitance and transfer of unstressed volume to stressed volume (nu). We argue that the values they used for venous resistance (Rvs), venous compliance (Cvs), and nu were too low, and changing these values significantly changes the conclusion. We used a computational model of the circulation that was similar to theirs, but we made Rvs four times higher (0.06 versus 0.015 mmHg.s.ml(-1)), Cvs larger (110 versus 70 ml/mmHg), and nu larger (1,400 versus 750 ml); all other parameters, including those for the heart, were essentially the same. We simulated left ventricular dysfunction by decreasing end-systolic elastance (Eeslv) as they did and examined changes in cardiac output, arterial blood pressure, and Pvp. We then examined the effect of changes in Rvs, heart rate, and nu when Eeslv was depressed with and without pericardial constraint. In contrast to their findings, with our parameters the model predicts that decreasing Eeslv substantially increases Pvp. Furthermore, increasing systemic vascular resistance or decreasing Rvs or heart rate produces large increases in Pvp when Eeslv is reduced. Pericardial constraint limits the changes in Pvp. In conclusion, when Rvs and Cvs are increased, baseline nu must be higher to maintain normal cardiac output. This increased volume can shift between compartments under flow conditions and account for the increase in Pvp with decreased left ventricular function even without recruitment of unstressed volume.

Estrogen decreases TNF-alpha and oxidized LDL induced apoptosis in endothelial cells.

Apoptosis induced by oxidized low-density lipoproteins (oxLDL) and tumor necrosis factor-alpha (TNF-alpha) is believed to contribute to atherosclerosis and vascular dysfunction. Estrogen treatment reduces apoptosis due to TNF-alpha and we hypothesized that it would also reduce apoptosis due to oxLDL. We also explored the anti-apoptotic mechanisms. We used early passage human umbilical vein endothelial cells (HUVEC) grown in steroid-depleted, red phenol-free medium. Cells were synchronized by starvation for 6h and then treated with oxLDL (75microg/ml) or TNF-alpha (20ng/ml) in the presence of 17-beta-estradiol (E2) (20nM). Apoptosis was analyzed by flow cytometry and caspase-3 cleavage. We also assessed expression of Bcl-2 and Bcl-xL and phosphorylation of BAD. At 6h TNF-alpha induced apoptosis but oxLDL did not; E2 did not affect this TNF-alpha induced apoptosis and there was no change in Bcl-2 or Bcl-xL expression. At 24h both TNF-alpha and oxLDL increased apoptosis and E2 reduced the increase. E2 also increased expression of the anti-apoptotic Bcl-2 and Bcl-xL and increased phosphorylation of proapoptotic BAD which reduces its proapoptotic activity at 1h. However at 24h there was also an increase in total BAD so that the proportion of phosphorylation of BAD decreased. oxLDL induced apoptosis occurs later than that of TNF-alpha. E2 decreased this late phase apoptosis and this likely requires the production of anti-apoptotic proteins.

Diagnostic workup, etiologies and management of acute right ventricle failure : A state-of-the-art paper.

INTRODUCTION: This is a state-of-the-art article of the diagnostic process, etiologies and management of acute right ventricular (RV) failure in critically ill patients. It is based on a large review of previously published articles in the field, as well as the expertise of the authors. RESULTS: The authors propose the ten key points and directions for future research in the field. RV failure (RVF) is frequent in the ICU, magnified by the frequent need for positive pressure ventilation. While no universal definition of RVF is accepted, we propose that RVF may be defined as a state in which the right ventricle is unable to meet the demands for blood flow without excessive use of the Frank-Starling mechanism (i.e. increase in stroke volume associated with increased preload). Both echocardiography and hemodynamic monitoring play a central role in the evaluation of RVF in the ICU. Management of RVF includes treatment of the causes, respiratory optimization and hemodynamic support. The administration of fluids is potentially deleterious and unlikely to lead to improvement in cardiac output in the majority of cases. Vasopressors are needed in the setting of shock to restore the systemic pressure and avoid RV ischemia; inotropic drug or inodilator therapies may also be needed. In the most severe cases, recent mechanical circulatory support devices are proposed to unload the RV and improve organ perfusion CONCLUSION: RV function evaluation is key in the critically-ill patients for hemodynamic management, as fluid optimization, vasopressor strategy and respiratory support. RV failure may be diagnosed by the association of different devices and parameters, while echocardiography is crucial.

Measurement of pleural pressure swings with a fluid-filled esophageal catheter vs pulmonary artery occlusion pressure.

PURPOSE: Pleural pressure measured with esophageal balloon catheters (Peso) can guide ventilator management and help with the interpretation of hemodynamic measurements, but these catheters are not readily available or easy to use. We tested the utility of an inexpensive, fluid-filled esophageal catheter (Peso) by comparing respiratory-induced changes in pulmonary artery occlusion (Ppao), central venous (CVP), and Peso pressures. METHODS: We studied 30 patients undergoing elective cardiac surgery who had pulmonary artery and esophageal catheters in place. Proper placement was confirmed by chest compression with airway occlusion. Measurements were made during pressure-regulated volume control (VC) and pressure support (PS) ventilation. RESULTS: The fluid-filled esophageal catheter provided a high-quality signal. During VC and PS, change in Ppao (∆Ppao) was greater than ∆Peso (bias = -2 mm Hg) indicating an inspiratory increase in cardiac filling. During VC, ∆CVP bias was 0 indicating no change in right heart filling, but during PS, CVP fell less than Peso indicating an inspiratory increase in filling. Peso measurements detected activation of expiratory muscles, development of non-west zone 3 lung conditions during inspiration, and ventilator-triggered inspiratory efforts. CONCLUSIONS: A fluid-filled esophageal catheter provides a high-quality, easily accessible, and inexpensive measure of change in pleural pressure and provided insights into patient-ventilator interactions.

Predicting volume responsiveness in spontaneously breathing patients: still a challenging problem.

The prediction of which patients respond to fluid infusion and which patients do not is an important issue in the intensive care setting. Assessment of this response by monitoring changes in some hemodynamic characteristics in relation to spontaneous breathing efforts would be very helpful for the management of the critically ill. This unfortunately remains a difficult clinical problem, as discussed in the previous issue of the journal. Technical factors and physiological factors limit the usefulness of current techniques.

Experts' opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation.

RATIONALE: Acute respiratory distress syndrome (ARDS) is frequently associated with hemodynamic instability which appears as the main factor associated with mortality. Shock is driven by pulmonary hypertension, deleterious effects of mechanical ventilation (MV) on right ventricular (RV) function, and associated-sepsis. Hemodynamic effects of ventilation are due to changes in pleural pressure (Ppl) and changes in transpulmonary pressure (TP). TP affects RV afterload, whereas changes in Ppl affect venous return. Tidal forces and positive end-expiratory pressure (PEEP) increase pulmonary vascular resistance (PVR) in direct proportion to their effects on mean airway pressure (mPaw). The acutely injured lung has a reduced capacity to accommodate flowing blood and increases of blood flow accentuate fluid filtration. The dynamics of vascular pressure may contribute to ventilator-induced injury (VILI). In order to optimize perfusion, improve gas exchange, and minimize VILI risk, monitoring hemodynamics is important. RESULTS: During passive ventilation pulse pressure variations are a predictor of fluid responsiveness when conditions to ensure its validity are observed, but may also reflect afterload effects of MV. Central venous pressure can be helpful to monitor the response of RV function to treatment. Echocardiography is suitable to visualize the RV and to detect acute cor pulmonale (ACP), which occurs in 20-25 % of cases. Inserting a pulmonary artery catheter may be useful to measure/calculate pulmonary artery pressure, pulmonary and systemic vascular resistance, and cardiac output. These last two indexes may be misleading, however, in cases of West zones 2 or 1 and tricuspid regurgitation associated with RV dilatation. Transpulmonary thermodilution may be useful to evaluate extravascular lung water and the pulmonary vascular permeability index. To ensure adequate intravascular volume is the first goal of hemodynamic support in patients with shock. The benefit and risk balance of fluid expansion has to be carefully evaluated since it may improve systemic perfusion but also may decrease ventilator-free days, increase pulmonary edema, and promote RV failure. ACP can be prevented or treated by applying RV protective MV (low driving pressure, limited hypercapnia, PEEP adapted to lung recruitability) and by prone positioning. In cases of shock that do not respond to intravascular fluid administration, norepinephrine infusion and vasodilators inhalation may improve RV function. Extracorporeal membrane oxygenation (ECMO) has the potential to be the cause of, as well as a remedy for, hemodynamic problems. Continuous thermodilution-based and pulse contour analysis-based cardiac output monitoring are not recommended in patients treated with ECMO, since the results are frequently inaccurate. Extracorporeal CO2 removal, which could have the capability to reduce hypercapnia/acidosis-induced ACP, cannot currently be recommended because of the lack of sufficient data.

Validity of the hepatojugular reflux as a clinical test for congestive heart failure.

This study describes observations designed to test the validity of the hepatojugular reflux as an indicator of actual or incipient heart failure. The central venous pressure (CVP) could be predicted from the height of the jugular venous pulsations in 44 of 48 comparisons. In the remaining comparisons, discrepancies ranged from 5 to 7 mm Hg. In patients with normal resting cardiac function, abdominal compression did not cause an increase in CVP of greater than 2 mm Hg (2.7 mm H2O). In 16 of 19 patients with impaired function, CVP increased by greater than or equal to 3 mm Hg. The increase in CVP was estimated from neck veins to within 2 mm Hg in all but 3 instances. CVP stabilized by 10 seconds and did not change over the subsequent 60 seconds. Abdominal compression caused no consistent change in cardiac output. Changes in venous pressure could not be attributed to changes in esophageal pressure or to compression of the heart by elevation of the diaphragm. Observations were consistent with the hypothesis that an increase in right-sided cardiac filling pressures resulting from abdominal compression carried out as described here, reflects both the volume of blood in the abdominal veins and the ability of the ventricles to respond to increased venous return, and constitutes a useful clinical test for detecting congestive cardiac failure. An increase of 3 cm in the height of neck vein distention is a reasonable upper limit of normal.

Comparison of the effects of pindolol and propranolol on exercise performance in patients with angina pectoris.

The effects of pindolol (mean dose 17 +/- 8 mg/day), a beta-blocking drug with intrinsic sympathomimetic activity (ISA), and propranolol (130 +/- 40 mg/day) on exercise performance in 11 patients with stable angina pectoris were compared. Doses were titrated to symptoms. The design was a randomized, double-blind, crossover protocol with 8 weeks of treatment with each drug. At the end of each drug period, subjects performed 3 exercise tests: a symptom-limited test on a cycle ergometer with measurement of gas exchange parameters; a steady-state exercise test to measure cardiac output by the CO2 rebreathing method; and a supine exercise test with radionuclide angiography. The ISA effect of pindolol was evident at rest in that the heart rate of 82 +/- 4 beats/min was higher than with propranolol (70 +/- 3). At low levels of exercise heart rate, cardiac output and O2 consumption (VO2) were still higher. However, there was no difference in cardiac output or VO2 at higher levels of exercise and no difference in the VO2 at the anaerobic threshold and peak exercise. Peak VO2 was 1,344 +/- 108 ml/min with propranolol and 1,350 +/- 116 with pindolol therapy. There were also no differences in ejection fraction or cardiac volumes at rest or during exercise. The incidence of side effects was similar with both drugs and there was no significant preference for either medication. In conclusion, patients with angina treated with pindolol had the same peak exercise performance as with an 8:1 equivalent dose of propranolol (clinically equivalent), although at lower levels of exercise, VO2, cardiac output and heart rate were higher from the ISA of pindolol.

Effect of negative pleural pressure on left ventricular hemodynamics.

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 +/- 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 +/- 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 +/- 21 to 47 +/- 21 (p less than 0.001) and then returned to control levels. During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration. Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.

Presence of nitrotyrosine with minimal inducible nitric oxide synthase induction in lipopolysaccharide-treated pigs.

The production of large amounts of nitric oxide (NO) by the inducible form of nitric oxide synthase (iNOS) and the subsequent production of peroxynitrite (OONO-) are believed to be major factors in the hemodynamic abnormalities of sepsis. This finding is based on data from rats and mice but has not been established in other species. Therefore, we examined the role of iNOS in lipopolysaccharide (LPS)-treated pigs, which have a hemodynamic pattern with sepsis that is more similar to humans than rats. Pigs were anesthetized, ventilated, and given LPS (n = 12), 20 microg/kg over 2 h, or saline (n = 7). They were killed after 2 (n = 8 LPS, 7 control) or 4 h (4 LPS). We measured cardiac output (CO), mean arterial (Part), and pulmonary and central venous pressures. We evaluated NO production by measuring expired NO, and plasma nitrate/nitrite concentration, NOS activity (in lung tissue), and iNOS protein by Western analysis, and immunohistochemistry (lung and liver), as well as iNOS mRNA by Northern analysis (liver and lung). We also measured nitrotyrosine as evidence of OONO- production by slot blot, Western analysis, and immunohistochemistry. By 2 h, Part fell and CO did not change so that systemic vascular resistance decreased from 21.5+/-2.9 to 12.7+/-3.1 mmHg x L(-1) x min (P < 0.05) and remained at 11.3+/-1.7 mmHg x L(-1) x min in the animals observed for 4 h. Plasma nitrate/nitrite, expired NO, and NOS activity did not change. We found no iNOS in tissues by Western analysis with 5 different antibodies but detected a small amount of iNOS by immunohistochemistry in inflammatory cells and small vessels. There was a small increase in iNOS mRNA in liver and lung. Despite the minimal increase in iNOS, nitrotyrosine was increased in small vessels and in inflammatory cells. In conclusion, caution should be used when extrapolating the septic response in rodents to other species, for the pattern of iNOS induction is very different.

Regional changes in constitutive nitric oxide synthase and the hemodynamic consequences of its inhibition in lipopolysaccharide-treated pigs.

The role of constitutive nitric oxide synthases (cNOS) in sepsis remains controversial. Part of the problem is that many of the studies have been performed in rats, which respond differently than larger animals. Our objective, therefore, was to determine whether cNOS, i.e. ecNOS (NOS-3) and nNOS (NOS-1) are still active in vessels of pigs treated with lipopolysaccharide (LPS) from Escherichia coli. We also characterized the dose-response relationship of the NOS inhibitor N(G)-nitro-L-arginine-methyl-ester (L-NAME) in the arterial, venous, and pulmonary circuits as a reflection of NO production. We anesthetized and ventilated 14 pigs, which were instrumented for hemodynamic measurements. We measured mean circulatory filling pressure and resistance to venous return by transiently arresting the circulation with a balloon in the right atrium. Animals were given 20 microg/kg of LPS (n = 8) or saline (n = 6) over 2 h. They were then given progressively increasing doses of L-NAME (0.5 to 16 microg/kg). We injected 20 microg boluses of norepinephrine at baseline, after 2 h, and after 0.5, 4, and 16 microg of L-NAME to test the pressor response. Tissue was obtained from six control animals followed for 2 h, eight animals treated with LPS for 2 h and then sacrificed, and four animals treated for 2 h and sacrificed after 2 more h. Cardiac output did not change, and the systemic vascular resistance fell in LPS animals. By Western analysis, ecNOS was increased in LPS animals at 2 and 4 h in the aorta and vena cava, and this was paralleled by changes in nNOS in the vena cava. In contrast, ecNOS decreased in the pulmonary artery and nNOS did not change. Calcium-dependent NOS activity increased with LPS in the aorta and vena cava but decreased in pulmonary artery at 4 h. The dose-response relationships to L-NAME for systemic vascular resistance, resistance to venous return, and cardiac output were shifted to the left after LPS in support of increased sensitivity supporting increased NO. The pressor response to norepinephrine was depressed after LPS and was partially restored with 4 mg/kg of L-NAME, but this dose produced 90% of the fall in cardiac output. In conclusion, in contrast to rats, cNOS activity is present in the systemic vessels of LPS-treated pigs and could play a role in the pathophysiology of sepsis.

Regional distribution of endothelin-1 and endothelin converting enzyme-1 in porcine endotoxemia.

Endothelin-1 (ET-1) levels are markedly increased in sepsis. Since ET-1 is primarily transcriptionally regulated, there should be a corresponding increase in pre-pro-endothelin-1 (ppET-1). Our objective was to determine whether ppET-1 is increased in pigs with a low systemic vascular resistance. We also examined the distribution of ET-1 and the regulation of endothelin-converting enzyme 1 (ECE-1), the rate limiting enzyme in ET-1 production. We anesthetized and ventilated 16 pigs. We measured arterial, pulmonary, and central venous pressures, as well as cardiac output. ET-1 was measured by radioimmunoassay in plasma and in multiple tissues. We infused 20 microg/kg of endotoxin over 2 h and then sacrificed the animals. ppET-1 and ECE-1 mRNA were assessed by Northern analysis. We performed immunohistochemistry for the assessment of tissue ET-1 and ECE-1. The systemic vascular resistance rose at 30 min, but fell by 120 min. Plasma ET-1 more than doubled by 2 h. However, there was no change in the concentration of ET-1 in any tissue except in the pulmonary artery. By immunohistochemistry, there was also no change in ET-1 in aorta, vena cava, heart, lung, liver, and kidney. Distribution of ECE-1 followed that of ET-1 on immunohistochemistry. There was a significant increase in ppET-1 mRNA in liver, kidney papillae, and vena cava, and a tendency for an increase in other tissues. This was paralleled by an increase in ECE-1 mRNA. In conclusion, the amount of ECE-1 mRNA and protein parallel those of ET-1. Endotoxemia is associated with a marked increase in plasma ET-1 and an increase in ppET-1 and ECE-1 mRNA in multiple tissues; however, there was no significant change in tissue ET-1 except in the pulmonary artery. The rise in plasma levels without a change in tissue levels suggests a greater release into the vasculature in sepsis than under normal conditions.

Assessment of myocardial stress from early ambulatory activities following myocardial infarction.

Little is known of the magnitude of the stress imposed on the heart by ambulatory activities following infarction. Heart rate, blood pressure, and rhythm provide simple and important estimates of these potential stresses. We therefore measured these variables in 32 patients during sitting, standing, and walking in the first two days following myocardial infarction. Ambulatory activities caused only a small increase in heart rate, with a maximum increase of 9 beats/minute during walking. The blood pressure was either unchanged or decreased during activity. In six other patients, we also measured central hemodynamics during the same activities. The wedge pressure fell with sitting and standing and remained low after walking. All activities were well tolerated. The major problem was hypotension; this was associated with chest pain in one patient, dizziness in four and shortness of breath in two. Most of the patients with hypotension were taking nitrates. In conclusion, mild ambulatory activities produce little stress for the myocardium and can be permitted in the first few days following infarction as long as blood pressure is measured.

The effects of changes in ventilation and cardiac output on expired nitric oxide.

The measurement of nitric oxide (NO) in expired gas is being increasingly reported in disease states such as sepsis, heart failure, and asthma. However, the effects of changes in ventilatory and cardiac parameters on expired NO are not known. Therefore, we assessed the effects of changes in minute ventilation (VE), ventilatory pattern, and cardiac output on expired gas NO levels in five anesthetized, intubated pigs. The animals were mechanically ventilated at three settings for each of respiratory rate (12 to 14, 16 to 18, and 22 to 24/min) and tidal volume (10, 15, and 20 mL/kg) applied in random sequence, yielding nine ventilatory patterns and a range of VE (3.7+/-0.1 to 13.2+/-0.8 L/min). When VE was increased, expired NO concentration declined slightly (r=-0.40, p<0.01), but the rate of excretion of NO in expired gas increased significantly (r=0.60, p<0.01). In contrast, when cardiac output was increased progressively from 3.6+/-0.1 to 4.7+/-0.3 and 5.8+/-0.4 L/min (p<0.01) by volume loading during constant eucapneic ventilation, there was no change in expired NO. Changes in VE over a physiologic range significantly affect the measurement of NO in expired gas, whereas short-term changes in cardiac output do not. To facilitate comparison between studies, we suggest that the measurement of expired NO should be reported in conjunction with data on VE.

Thoracicoabdominal mechanics during resuscitation maneuvers.

The importance of intrathoracic pressure in generating blood flow during cardiopulmonary resuscitation has recently been emphasized. The purpose of this study was to investigate the factors involved in generating intrathoracic pressure. Studies were performed in anesthetized paralyzed dogs with the circulation intact. Balloon-tipped catheters were placed in the abdomen and esophagus for measurement of intra-abdominal and intrathoracic pressures and cannula placed in the airway for airway pressure. The following four maneuvers were studied: (1) chest compression with open airway; (2) chest compression with closed airway; (3) pulmonary inflation to transpulmonary pressure (TP) of 30 cm H2O (TP = 30); and (4) chest compression plus pulmonary inflation (TP = 30). We found that under static conditions, chest compression alone produced small positive intrathoracic pressures (9 +/- 8 cm H2O), but these could be increased by closing the airway pressure (18 +/- 6 cm H2O) or inflating the lungs (15 +/- 7 cm H2O). The combination of inflating the lung and compressing the chest produced the highest intrathoracic pressure (48 +/- 18 cm H2O; p less than 0.001). The pressure developed was highly variable and the distribution of pressures within the thorax was not uniform. As the intrathoracic pressure became large, a pressure gradient developed from thorax to abdomen, and the diaphragm everted; this pressure gradient could divert blood from the brain.

Interposed abdominal compressions and carotid blood flow during cardiopulmonary resuscitation. Support for a thoracoabdominal unit.

To determine if the timing of interposed abdominal compressions (IAC) affects the augmented blood flow during this form of cardiopulmonary resuscitation (CPR), we performed early-onset or late-onset abdominal compressions at three vascular volumes in nine dogs. Early-onset IAC began immediately following chest compression; we predicted that this would act primarily by emptying the aorta and sustaining the elevated intrathoracic pressure. Late-onset IAC began one-fourth to one-third of the time into diastole; this would have primarily increased venous return. We measured carotid blood flow (electromagnetic flow probe) and right atrial (Pra), thoracic aortic (Pta), abdominal aortic (Paa), and intra-abdominal pressures. The IAC-CPR increased carotid blood flow compared with conventional CPR (22.8 +/- 13.1 percent vs 8.7 +/- 5.8 percent of control; p less than 0.003), but there was no difference between the early and late modes of IAC (22.7 +/- 11.6 percent vs 22.9 +/- 14.7 percent of control). The increase in carotid blood flow was present with the first abdominal compression and was constant over the 40 to 60 seconds of CPR. Peak Pra, Pta, and Paa were similar during abdominal compression (91.8 +/- 16.9 mm Hg, 96.1 +/- 16.0 mm Hg, and 102.4 +/- 15.2 mm Hg, respectively; p less than 0.001). The Pta-Pra diastolic gradient was 18.0 +/- 8.2 mm Hg for early-onset and 20.6 +/- 7.5 mm Hg for late-onset compression (not significant). We conclude that increased carotid blood flow in IAC-CPR in the dog is principally due to the increased pressure in a common thoracoabdominal unit.