Peripheral Arterial Pressure Research Articles

Continuous cardiac output monitoring in humans by invasive and noninvasive peripheral blood pressure waveform analysis

We present an evaluation of a novel technique for continuous (i.e., automatic) monitoring of relative cardiac output (CO) changes by long time interval analysis of a peripheral arterial blood pressure (ABP) waveform in humans. We specifically tested the mathematical analysis technique based on existing invasive and noninvasive hemodynamic data sets. With the former data set, we compared the application of the technique to peripheral ABP waveforms obtained via radial artery catheterization with simultaneous thermodilution CO measurements in 15 intensive care unit patients in which CO was changing because of disease progression and therapy. With the latter data set, we compared the application of the technique to noninvasive peripheral ABP waveforms obtained via a finger-cuff photoplethysmography system with simultaneous Doppler ultrasound CO measurements made by an expert in 10 healthy subjects during pharmacological and postural interventions. We report an overall CO root-mean-squared normalized error of 15.3% with respect to the invasive hemodynamic data set and 15.1% with respect to the noninvasive hemodynamic data set. Moreover, the CO errors from the invasive and noninvasive hemodynamic data sets were only mildly correlated with mean ABP (rho = 0.41, 0.37) and even less correlated with CO (rho = -0.14, -0.17), heart rate (rho = 0.04, 0.19), total peripheral resistance (rho = 0.38, 0.10), CO changes (rho = -0.26, -0.20), and absolute CO changes (rho = 0.03, 0.38). With further development and successful prospective testing, the technique may potentially be employed for continuous hemodynamic monitoring in the acute setting such as critical care and emergency care.

Therapy Insight: cirrhotic cardiomyopathy

Liver cirrhosis is associated with several cardiovascular disturbances. These disturbances include hyperdynamic systemic circulation, manifested by an increased cardiac output and decreased peripheral vascular resistance and arterial pressure. Despite the baseline increase in cardiac output, cardiac function in patients with cirrhosis is abnormal in several respects. Patients show attenuated systolic and diastolic contractile responses to stress stimuli, electrophysiological repolarization changes, including prolonged QT interval, and enlargement or hypertrophy of cardiac chambers. This constellation of cardiac abnormalities is termed cirrhotic cardiomyopathy. It has been suggested that cirrhotic cardiomyopathy has a role in the pathogenesis of cardiac dysfunction and even overt heart failure after transjugular intrahepatic portosystemic shunt placement, major surgery and liver transplantation. Cardiac dysfunction contributes to morbidity and mortality after liver transplantation, even in many patients who have no prior history of cardiac disease. Depressed cardiac contractility contributes to the pathogenesis of hepatorenal syndrome, especially in patients with spontaneous bacterial peritonitis. Pathogenic mechanisms underlying cirrhotic cardiomyopathy include cardiomyocyte-membrane biophysical changes, attenuation of the stimulatory beta-adrenergic system and overactivity of negative inotropic systems mediated via cyclic GMP. The clinical features, general diagnostic criteria, pathogenesis and treatment of cirrhotic cardiomyopathy are discussed in this review.

Continuous blood pressure-derived cardiac output monitoring—should we be thinking long term?

Cardiac output, along with cardiac filling pressure, arterial blood pressure, and heart rate, is one of the most important hemodynamic variables to monitor continuously in patients with compromised cardiovascular performance. This point is illustrated strikingly in [Fig. 1][1], which shows an

Lowering of Central Aortic Blood Pressure-Not All Antihypertensive Agents Are Created Equal: Differential Impact of Blood Pressure-Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study. Circulation 113: 1213-1225, 2006.

Lowering of Central Aortic Blood Pressure-Not All Antihypertensive Agents Are Created Equal: Differential Impact of Blood Pressure-Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study. Circulation 113: 1213-1225, 2006.

Use of antihypertension agents for the suppression of arterial pulse pressure waveforms in patients with intracranial aneurysms

Patients with intracranial aneurysms tend toward raised blood pressure and abnormal pulse pressure profiles. The authors have investigated the influence of three antihypertension agents on blood pressure and pulse pressure waveforms in patients with known intracranial aneurysms, with a view to assessing the potential benefits of longterm antihypertension therapy on the progression of unruptured intracranial aneurysms. Nineteen patients with a mean age of 56 years (range 38-76 years) were recruited for this study. All patients had confirmed intracranial aneurysms. A double-blind, randomized, crossover study was performed using perindopril, irbesartan, isosorbide mononitrate, and a placebo. Blood pressure and pulse pressure waveforms were assessed at the end of each 4-week treatment period. Perindopril and irbesartan were well tolerated. For all measured parameters except heart rate (p = 0.03), no significant difference between baseline and placebo was identified. Each drug when compared with placebo reduced peripheral arterial blood pressure. Perindopril significantly decreased mean blood pressure by 10 mm Hg (p = 0.004), irbesartan by 9 mm Hg (p = 0.004), and isosorbide mononitrate by 13 mm Hg (p = 0.005). The administration of each drug effected a significant reduction in the carotid artery augmentation index (AIX) compared with baseline values (perindopril p = 0.01, irbesartan p = 0.0002, and isosorbide mononitrate p = 0.03). There was also a significant difference in the AIX between irbesartan and the placebo (p = 0.05). Compared with the placebo, there was a significant difference in AIX (adjusted for heart rate) following the administration of irbesartan (p = 0.003) and isosorbide mononitrate (p = 0.01), but not with perindopril (p = 0.17). Irbesartan appears to be the most effective treatment for the combined suppression of blood pressure and AIX in patients with intracranial aneurysms and has a high degree of patient tolerance.

Continuous Cardiac Output Monitoring by Peripheral Blood Pressure Waveform Analysis

A clinical method for monitoring cardiac output (CO) should be continuous, minimally invasive, and accurate. However, none of the conventional CO measurement methods possess all of these characteristics. On the other hand, peripheral arterial blood pressure (ABP) may be measured reliably and continuously with little or no invasiveness. We have developed a novel technique for continuously monitoring changes in CO by mathematical analysis of a peripheral ABP waveform. In contrast to the previous techniques, our technique analyzes the ABP waveform over time scales greater than a cardiac cycle in which the confounding effects of complex wave reflections are attenuated. The technique specifically analyzes 6-min intervals of ABP to estimate the pure exponential pressure decay that would eventually result if pulsatile activity abruptly ceased (i.e., after the high frequency wave reflections vanish). The technique then determines the time constant of this exponential decay, which equals the product of the total peripheral resistance and the nearly constant arterial compliance, and computes proportional CO via Ohm's law. To validate the technique, we performed six acute swine experiments in which peripheral ABP waveforms and aortic flow probe CO were simultaneously measured over a wide physiologic range. We report an overall CO error of 14.6%.

Peripheral arterial blood pressure monitoring adequately tracks central arterial blood pressure in critically ill patients: an observational study

IntroductionInvasive arterial blood pressure monitoring is a common practice in intensive care units (ICUs). Accuracy of invasive blood pressure monitoring is crucial in evaluating the cardiocirculatory system and adjusting drug therapy for hemodynamic support. However, the best site for catheter insertion is controversial. Lack of definitive information in critically ill patients makes it difficult to establish guidelines for daily practice in intensive care. We hypothesize that peripheral and central mean arterial blood pressures are interchangeable in critically ill patients.MethodsThis is a prospective, observational study carried out in a surgical-medical ICU in a teaching hospital. Fifty-five critically ill patients with clinical indication of invasive arterial pressure monitoring were included in the study. No interventions were made. Simultaneous measurements were registered in central (femoral) and peripheral (radial) arteries. Bias and precision between both measurements were calculated with Bland-Altman analysis for the whole group. Bias and precision were compared between patients receiving high doses of vasoactive drugs (norepinephrine or epinephrine >0.1 μg/kg/minute or dopamine >10 μg/kg/minute) and those receiving low doses (norepinephrine or epinephrine <0.1 μg/kg/minute or dopamine <10 μg/kg/minute).ResultsCentral mean arterial pressure was 3 ± 4 mmHg higher than peripheral mean arterial pressure for the whole population and there were no differences between groups (3 ± 4 mmHg for both groups).ConclusionMeasurement of mean arterial blood pressure in radial or femoral arteries is clinically interchangeable. It is not mandatory to cannulate the femoral artery, even in critically ill patients receiving high doses of vasoactive drugs.

Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model

Rewarming from accidental hypothermia is often complicated by "rewarming shock," characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study, we tested whether epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1, 2, and 3 for dose-finding studies, and hypothermic groups 4, 5, and 6. At 20 and 24 degrees C during rewarming, group 4 (low-dose Epi) and group 5 (high-dose Epi) received bolus injections of 0.1 and 1.0 microg Epi, respectively. At 28 degrees C, Epi infusion was started in groups 4 and 5 with 0.125 and 1.25 microg/min, respectively. Group 6 served as saline control. After rewarming, both CO and stroke volume were restored in group 4, in contrast to groups 5 and 6, in which both CO and stroke volume remained significantly reduced (30%). Total peripheral resistance was significantly higher in group 5 during rewarming from 24 to 34 degrees C, compared with groups 4 and 6. This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature-dependent adrenoreceptor affinity.

Ungewöhnliche Ursache pektanginöser Beschwerden nach Bypassoperation

The coronary subclavian-steal-syndrome is a rare cause for angina pectoris following A. mammaria interna bypass operation. A 72-year-old male patient presented with vertigo and angina pectoris. A three vessel coronary artery disease was known and coronary artery surgery with three aortocoronary bypasses had been performed a year prior to presentation. A difference in peripheral arterial pressure between the right (150/80 mmHg) and the left (125/75 mmHg) arm was noted at physical examination. Color Doppler sonography of the left vertebral arteria exhibited a retrograde flow suggesting a coronary subclavian-steal-syndrome. Angiography revealed a significant stenosis of the left arteria subclavia. The stenosis was successfully treated with percutaneous transluminal angioplasty and stent implantation.

Non‐invasive pulsatile arterial pressure and stroke volume changes from the human finger

In this paper we review recent developments in the methodology of non-invasive finger arterial pressure measurement and the information about arterial flow that can be obtained from it. Continuous measurement of finger pressure based on the volume-clamp method was introduced in the early 1980s both for research purposes and for clinical medicine. Finger pressure tracks intra-arterial pressure but the pressure waves may differ systematically both in shape and magnitude. Such bias can, at least partly, be circumvented by reconstruction of brachial pressure from finger pressure by using a general inverse anti-resonance model correcting for the difference in pressure waveforms and an individual forearm cuff calibration. The Modelflow method as implemented in the Finometer computes an aortic flow waveform from peripheral arterial pressure by simulating a non-linear three-element model of the aortic input impedance. The methodology tracks fast changes in stroke volume (SV) during various experimental protocols including postural stress and exercise. If absolute values are required, calibration against a gold standard is needed. Otherwise, Modelflow-measured SV is expressed as change from control with the same precision in tracking. Beat-to-beat information on arterial flow offers important and clinically relevant information on the circulation beyond what can be detected by arterial pressure.

Respiration can be monitored by photoplethysmography with high sensitivity and specificity regardless of anaesthesia and ventilatory mode

Photoplethysmography (PPG) is a non-invasive optical technique used, for instance, in pulse oximetry. Beside the pulse synchronous component, PPG has a respiratory synchronous variation (PPGr). Efforts have been made to utilize this component for indirect monitoring of respiratory rate and volume. Assessment of the clinical usefulness as well as of the physiological background of PPGr is required. We evaluated if anaesthesia and positive-pressure ventilation would affect PPGr. We recorded reflection mode PPGr, at the forearm, and the respiratory synchronous changes in central venous pressure (CVP), peripheral venous pressure (PVP) and arterial blood pressure (ABP) in 12 patients. Recordings for each patient were made on three occasions: awake with spontaneous breathing; anaesthetized with spontaneous breathing; and anaesthetized with positive-pressure ventilation. We analyzed the sensitivity, specificity, coherence and time relationship between the signals. PPGr sensitivity for breath detection was [mean (SD)] >86(21)% and specificity >96(12)%. Respiratory detection in the macrocirculation (CVP, PVP and ABP) showed a sensitivity >83(29)% and specificity >93(12)%. The coherence between signals was high (0.75-0.99). The three measurement situations did not significantly influence sensitivity, specificity or time shifts between the PPGr, PVP, ABP, and the reference CVP signal despite changes in physiological data between measurements. A respiratory synchronous variation in PPG and all invasive pressure signals was detected. The reflection mode PPGr signal seemed to be a constant phenomenon related to respiration regardless of whether or not the subject was awake, anaesthetized or ventilated, which increases its clinical usefulness in respiratory monitoring.

Second derivative of the finger arterial pressure waveform: an insight into dynamics of the peripheral arterial pressure pulse.

The study investigated second derivative of the finger arterial pressure waveform (SDFAP) in 120 healthy middle-aged subjects and in 24 subjects with essential hypertension. SDFAP consists of 5 sequential waves 'a'-'e'. Their normalized magnitudes (B/A, C/A, D/A, and E/A) were calculated. In multivariate regression analysis, B/A and C/A correlated only with age. D/A independently correlated with age, heart period, mean blood pressure (MBP), body height, and gender. E/A independently correlated with age and MBP. D/A and E/A were higher (0.42+/-0.16 vs. 0.33+/-0.14, p = 0.05 and 0.63+/-0.15 vs. 0.45+/-0.14, p < 0.001), while B/A and C/A were lower (1.04+/-0.16 vs. 1.20+/-0.17, p = 0.002 and 0.09+/-0.15 vs. 0.26+/-0.20, p = 0.001) in hypertensives compared to sex- and age-matched controls. After the adjustment for MBP, heart period, and body mass index (ANCOVA), independent discriminative power was preserved only for indices B/A and C/A (p = 0.001 and 0.021, respectively). Therefore, B/A and C/A provide additional information about simple clinical characteristics and might reflect the structural alteration of the arterial wall in hypertensive subjects.

Pulse oximeter as a sensor of fluid responsiveness: do we have our finger on the best solution?

The pulse oximetry plethysmographic signal resembles the peripheral arterial pressure waveform, and the degree of respiratory variation in the pulse oximetry wave is close to the degree of respiratory arterial pulse pressure variation. Thus, it is tempting to speculate that pulse oximetry can be used to assess preload responsiveness in mechanically ventilated patients. In this commentary we briefly review the complex meaning of the pulse oximetry plethysmographic signal and highlight the advantages, limitations and pitfalls of the pulse oximetry method. Future studies including volume challenge must be performed to test whether the pulse oximetry waveform can really serve as a nonivasive tool for the guidance of fluid therapy in patients receiving mechanical ventilation in intensive care units and in operating rooms.

Stiffening Our Resolve Against Adult Weight Gain

Increasing adiposity with a clinical endpoint of obesity is associated with a progressive increase in risk of cardiovascular diseases (CVD). However, we are only beginning to understand the physiological and pathophysiological mechanisms by which excessive body fat storage causes CVD. In this issue of Hypertension , the findings of Wildman et al1 extend and strengthen previous observations2–5 by showing that changes in arterial stiffness, as measured by aortic pulse-wave velocity (PWV), are related to changes in body weight over a 2-year follow-up period in healthy men and women aged 20 to 40 years. Weight gain was associated with an increase, whereas weight loss was associated with a decrease in aortic PWV, independent of changes in blood pressure. The greatest increases in aortic PWV were observed in those subjects who gained the most weight (≥4.5 kg). Importantly, the changes in aortic PWV were related to changes in body mass index (BMI), indicating that the associations with body weight were mediated by changes in adiposity (rather than fat-free mass). Changes in aortic PWV over time also were related to baseline body weight, BMI, and waist circumference (an indirect measure of abdominal adiposity), providing evidence that higher initial levels of total and abdominal body fatness are associated with greater future increases in arterial stiffness. The study included subjects with a broad range of BMI, suggesting that the findings are applicable to both nonobese and obese adults in the general population. An important finding was that black adults demonstrated greater increases in weight gain-adjusted and blood pressure-adjusted aortic PWV over time, suggesting that they undergo greater increases in arterial stiffness in response to the same age-associated weight gain compared with whites. These observations provide further support for the emerging concept that adiposity-driven weight gain during adulthood contributes significantly to the adverse changes …

A bridge from short-term to long-term left ventricular assist device--experimental verification of a physiological controller.

A physiological controller is a key component to optimize the performance of left ventricular assist devices (LVADs) from short term to long term (10-20 years). The difficulties of its design lie in the inaccurate modeling of any particular human cardiovascular system because of limited knowledge, the large fluctuation of systemic parameters in normal daily life, nonlinearity introduced by one-way heart valves, and restriction on available sensors. The desired physiological controller for a permanent LVAD is expected to handle different activity levels such as sleeping, resting and exercising, and different pathological levels of left ventricular failure. In this study, a physiological controller designed for a long-term continuous flow (CF) LVAD was tested in a mock circulatory loop. The pressure head across the LVAD and motor signals were used as feedback signals, which were obtained from long-term reliable sensors. Three activities and five different pathological levels of left ventricular failure were simulated to test the performance of the designed controller. The experimental results showed that the designed controller restored the total peripheral flow and arterial pressure, and decreased the left ventricular end-diastolic pressure to a safe range. The suction of the left ventricle was successfully reversed by the designed controller. The controller thus was proven to be able to control the LVAD properly in many of the possible physiological conditions experienced by LVAD recipients in long term.

Significantly higher incidence of carotid atherosclerosis found in Japanese type 2 diabetic patients with early nephropathy

We have tried to evaluate the clinical incidence of carotid atherosclerosis found in Japanese type 2 diabetic patients with early diabetic nephropathy. 123 diabetic patients with micro-albuminuria (group A) were investigated during 2-week hospitalization. As a control group, 50 diabetic patients without nephropathy (group B) were investigated. Carotid arteries were examined by B-mode ultrasonography (7.5MHz), and peripheral arterial blood flow and pressure was examined at the same time with Doppler ultrasonography by a single examiner. Fasting blood samples and 24-h urine samples were taken to analyze biochemical data and urinary albumin excretion rate. In group A, 77 patients were found to have either carotid plaque lesions or increased thickness of carotid wall. And this was found significantly higher than in the control group B (18 cases, P < 0.01). To clarify the clinical risk factors for carotid atherosclerosis in diabetic patients with early nephropathy, 123 group A patients were divided into two groups with (group C, n = 76) or without carotid atherosclerosis (group D, n = 47) and comparative analysis was carried out. From this study, significantly higher incidence of carotid atherosclerosis was confirmed in the diabetic patients with early nephropathy. And it was suggested that the age, lipid levels, presence of hypertension would be important clinical risk factors for carotid atherosclerosis found in diabetic patients with early nephropathy.

Is PA-PWRmax Truly a Preload-Independent Index of Myocardial Contractility in Anesthetized Humans?

This study tested the hypothesis that the preload-adjusted maximal power index (PA-PWRmax) is a load-independent index of human myocardial contractility. Based on the ventricular pressure-volume relationship and derived from stroke work, the index is the product of instantaneous ventricular pressure and volume changes, divided by a correction term of end-diastolic volume (EDV²) or end-diastolic area (EDA^3/2) to adjust for preload effects. Echocardiographic measures of instantaneous ventricular area change may be used to obtain PA-PWRmax noninvasively. We prospectively evaluated 28 human subjects undergoing cardiac evacuation before cardiopulmonary bypass procedures. Continuous peripheral arterial pressure, pulmonary arterial pressure, and echocardiographic views of the left ventricle in the transgastric short-axis view were recorded. Simultaneously gated instantaneous fractional shortening (FS) and PA-PWRmax indices were calculated, with FS = (EDA – ESA)/EDA and PA-PWRmax = [MAP (EDA – ESA)]/ EDA^3/2, where ESA = end-systolic area and MAP = instantaneous mean arterial pressure. FS decreased uniformly with cardiac evacuation and decreasing pulmonary artery diastolic pressure (t = –5.4; 95% confidence interval, –10 to –0.046; p < 0.001), as did PA-PWRmax (t = –5.8; 95% confidence interval, –2.25 to –1.08; p < 0.001). FS and PA-PWRmax showed a strong downward correlation (r = 0.81). Unlike previous studies of autonomically denervated animals, our study did not find PA-PWRmax to be preload independent, perhaps because of the instantaneous homeostatic mechanisms of the human autonomic nervous system linking contractility to loading conditions.

Load dependence of cardiac output in biventricular pacing: right ventricular pressure overload in pigs

Background The effect of biventricular pacing on stroke volume is believed to be dependent on right ventricular/left ventricular delay, but effects in individual patients are unpredictable. This variability may reflect relative right and left ventricular volume and/or pressure overloads. Accordingly, we tested the hypothesis that the relation of cardiac output to right ventricular/left ventricular delay is load dependent in a pig model of pulmonary stenosis. Methods After median sternotomy in 6 anesthetized, domestic pigs, complete heart block was induced by ethanol ablation. During epicardial, atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 180 ms in 30-ms increments. Right ventricular/left ventricular delay was varied at each atrioventricular delay from +80 ms (right ventricle first) to −80 ms (left ventricle first) in 20-ms increments. Aortic flow, right ventricular pressure, peripheral arterial pressure, and electrocardiogram were measured in the control state and during pulmonary stenosis, created by tightening a snare around the pulmonary artery until cardiac output decreased by 50%. Results Atrioventricular and right ventricular/left ventricular delay had no effect on cardiac output during the control state, but during pulmonary stenosis there was a statistically significant ( P = .0001, repeated-measures analysis of variance) right ventricular/left ventricular delay–related trend toward higher cardiac output with right ventricular pacing first. This effect was more pronounced when the optimal atrioventricular delay was determined first, resulting in a 20% increase in cardiac output when the optimal right ventricular/left ventricular delay was compared with simultaneous biventricular pacing. Conclusions Optimized biventricular pacing in swine is associated with increased cardiac output during acute pulmonary stenosis, but not during the control state. Further studies are needed to determine whether specific types of right ventricular and left ventricular overload predictably affect the relation between right ventricular/left ventricular delay and cardiac output.

The potential role of angiotensin-converting enzyme inhibition in peripheral arterial disease.

Peripheral arterial disease (PAD) is associated with significant morbidity and mortality, and yet remains under-recognized and under-treated. Atherosclerosis is the most common cause of lower extremity PAD and pharmacological interventions that alter this central pathogenic role of atherosclerosis may alter the natural history of PAD. There is growing evidence that the renin-angiotensin system (RAS) is a significant mediator of this disease process and that treatment with angiotensin-converting enzyme (ACE) inhibitors is associated with vasculoprotective effects that are independent of the antihypertensive properties of these agents. Numerous lines of evidence suggest that ACE inhibitors directly inhibit the atherosclerotic process and improve vascular endothelial function. In patients with PAD, ACE inhibitors have been shown to improve peripheral circulation as measured by peripheral arterial blood pressure and by increases in peripheral blood flow. Preliminary evidence suggests that ACE inhibitors might improve clinical symptoms in patients with PAD. Recent evidence has confirmed that ACE inhibition is associated with a decrease in morbidity and mortality in patients with arterial disease without left ventricular dysfunction; this benefit was at least as great for the subset of patients with PAD. Overall, these data support a significant role for the RAS in the pathogenesis of all atherosclerotic diseases (including PAD) and suggest that the benefit is independent of the blood pressure lowering properties of these agents. These studies suggest that ACE inhibitor therapy should be considered in the routine management of individuals with PAD, regardless of whether they have hypertension or left ventricular dysfunction.

Macrocirculation is not the sole determinant of respiratory induced variations in the reflection mode photoplethysmographic signal

Photoplethysmography (PPG) is a non-invasive optical technique sensitive to variations in blood volume and perfusion in the tissue. Reflection mode PPG may have clinical advantages over transmission mode PPG. To improve clinical usefulness and further development of the reflection mode PPG, studies on factors that modify the signal are warranted. We studied the coherence between the respiratory induced intensity variations (RIIV) of the PPG signal and respiratory synchronous pressure variations in central venous pressure (CVP), peripheral venous pressure (PVP) and arterial blood pressure (ABP) during positive pressure ventilation on 12 patients under anaesthesia and on 12 patients with spontaneous breathing. During positive pressure ventilation the coherence between all signals was high. Inspiration was followed first by an increase in CVP, then by increases in ABP and PVP and lastly by RIIV indicating less back-scattered light. In spontaneously breathing patients the coherence was high, but the phases between the signals were changed. During inspiration, ABP decreased slightly before CVP, followed by a decrease in RIIV and PVP. The phase relation between RIIV and respiratory induced variation in macrocirculation changed with ventilatory mode, but not in a uniform way, indicating the influence of mechanisms other than macrocirculation involved in generating the RIIV signal.