We considered that a moderate reduction of the central blood volume (CBV) may activate the coagulation system. Lower body negative pressure (LBNP) is a non-invasive means of reducing CBV and, thereby, simulates haemorrhage. We tested the hypothesis that coagulation markers would increase following moderate hypovolemia by exposing 10 healthy male volunteers to 10 min of 30 mmHg LBNP. Thoracic electrical impedance increased during LBNP (by 2·6 ± 0·7 Ω, mean ± SD; P < 0·001), signifying a reduced CBV. Heart rate was unchanged during LBNP, while mean arterial pressure decreased (84 ± 5 to 80 ± 6 mmHg; P < 0·001) along with stroke volume (114 ± 22 to 96 ± 19 ml min−1; P < 0·001) and cardiac output (6·4 ± 2·0 to 5·5 ± 1·7 l min−1; P < 0·01). Plasma thrombin–antithrombin III complexes increased (TAT, 5 ± 6 to 19 ± 20 μg l−1; P < 0·05), indicating that LBNP activated the thrombin generating part of the coagulation system, while plasma D-dimer was unchanged, signifying that the increased thrombin generation did not cause further intravascular clot formation. The plasma pancreatic polypeptide level decreased (13 ± 11 to 6 ± 8 pmol l−1; P < 0·05), reflecting reduced vagal activity. In conclusion, thrombin generation was activated by a modest decrease in CBV by LBNP in healthy humans independent of the vagal activity.
haemorrhage; hypovolemia; pancreatic polypeptide; thrombin generation; vagal activity
In the assessment of hypovolemia the value of functional hemodynamic monitoring during spontaneous breathing is debated. The aim of our study was to investigate in spontaneously breathing subjects the changes in hemodynamic parameters during graded central hypovolemia and to test whether slow patterned breathing improved the discriminative value of stroke volume (SV), pulse pressure (PP), and their variations (SVV, PPV). In addition, we tested the alterations in labial microcirculation.
20 healthy volunteers participated in our study. Central hypovolemia was induced by lower body negative pressure (LBNP). Continuous signals of ECG, non-invasive blood pressure and central venous pressure were recorded. During baseline and each stage of LBNP the labial microcirculation was investigated by orthogonal polarization spectral imaging, 3 minute periods of patterned breathing at 6 and 15/min respiratory rate were performed, and central venous blood gas analysis was done. Data from baseline and those of different LBNP levels were compared by analysis of variance and those of different breathing rates by t-test. Finally, we performed ROC analysis to assess the discriminative values of SV, PP, SVV and PPV.
Moderate central hypovolemia induced by LBNP caused significant, clinically relevant falls in PP (p < 0.05) and SV and central venous oxygen saturation (ScvO2) (p < 0.001). The proportion of perfused vessels (p < 0.001) and microvascular flow index decreased (p < 0.05). PPV increased (p < 0.001), however the magnitude of fluctuations was greater during slow patterned breathing (p < 0.001). SVV increased only during slow patterned breathing (p < 0.001). ROC analysis confirmed the best predictive value for SV (at 56 ml cut-off AUC 0.97, sensitivity 94%, specificity 95%). Slow patterned breathing improved the discriminative value of SVV (p = 0.0023).
Functional hemodynamic monitoring with slow patterned breathing to control spontaneous respiration may be worthy for further study in different populations for the assessment of hypovolemia and the prediction of volume responsiveness.
Hypovolemia; Functional hemodynamic monitoring; Spontaneous breathing; Microcirculation
To test the hypothesis that the sensitivity of near-infrared spectroscopy (NIRS) in reflecting the degree of (compensated) hypovolemia would be affected by the application site and probing depth. We simultaneously applied multi-site (thenar and forearm) and multi-depth (15–2.5 and 25–2.5 mm probe distance) NIRS in a model of simulated hypovolemia: lower body negative pressure (LBNP).
The study group comprised 24 healthy male volunteers who were subjected to an LBNP protocol in which a baseline period of 30 min was followed by a step-wise manipulation of negative pressure in the following steps: 0, −20, −40, −60, −80 and −100 mmHg. Stroke volume and heart rate were measured using volume-clamp finger plethysmography. Two multi-depth NIRS devices were used to measure tissue oxygen saturation (StO2) and tissue hemoglobin index (THI) continuously in the thenar and the forearm. To monitor the shift of blood volume towards the lower extremities, calf THI was measured by single-depth NIRS.
The main findings were that the application of LBNP resulted in a significant reduction in stroke volume which was accompanied by a reduction in forearm StO2 and THI.
NIRS can be used to detect changes in StO2 and THI consequent upon central hypovolemia. Forearm NIRS measurements reflect hypovolemia more sensitively than thenar NIRS measurements. The sensitivity of these NIRS measurements does not depend on NIRS probing depth. The LBNP-induced shift in blood volume is reflected by a decreased THI in the forearm and an increased THI in the calf.
Electronic supplementary material
The online version of this article (doi:10.1007/s00134-010-2128-6) contains supplementary material, which is available to authorized users.
Near-infrared spectroscopy; Lower body negative pressure; Hypovolemia; Tissue oxygenation; Microcirculation; Tissue hemoglobin content
Arrhythmias in patients with repaired tetralogy of Fallot (ToF) might be due in part to altered autonomic heart rate (HR) control caused by altered right ventricle hemodynamics. This study investigated autonomic HR control in ToF adolescents at rest and during unloading of the right ventricle. A total of 17 ToF patients and 56 healthy controls aged 12 to 18 years underwent orthostatic stress with lower body negative pressure (LBNP) of −20 mm Hg. HR, blood pressure and stroke volume were recorded non-invasively. Indices of HR variability were computed in time and frequency domains. All ToF patients also underwent cardiac magnetic resonance imaging, demonstrating pulmonary regurgitation and right ventricular dilation. At rest, HR variability indices of vagal heart rate control were non-significantly lower in the ToF patients compared to controls. During LBNP, HR increased more in controls than ToF patients (p ≤ 0.001). Further, most HR variability indices decreased among controls, but increased among ToF patients (p ≤ 0.01 or p ≤ 0.001 for all variables), suggesting vagal activation in the ToF patients. In conclusion, adolescents after ToF repair have fairly normal HR control at rest despite altered right ventricular hemodynamics. During unloading of the right ventricle, however, vagal HR control increases in the ToF patients and decreases in the controls.
Tetralogy of Fallot; autonomic nervous system; heart rate variability; adolescence
Adequate volume expansion (VE) in patients with evidence of hypoperfusion should be aimed not only at achieving an increase in stroke volume (SV) and cardiac index (CI) but also at improved tissue perfusion and oxygenation. Our aim in this study was to assess the dynamic changes in muscle tissue oxygen saturation (StO2) during hypovolaemia and in response to VE.
We conducted a prospective study of 42 fluid challenges in patients undergoing major abdominal surgery with evidence of hypovolaemia, defined as pulse pressure variation (PPV) >13% and SV variation (SVV) >12%. CI, SV, SVV (FloTrac/Vigileo) and PPV were measured before and after VE. Fluid responsiveness was defined as an increase of SV >15% after a 500-mL colloid infusion over 15 minutes. In all patients, the muscle StO2 and its changes during a standardised vascular occlusion test were analysed using a near-infrared spectroscopy device after anaesthesia induction (which defined the baseline state) and before and after each VE.
No patients were preload-responsive after anaesthesia induction. Twenty-nine of forty-two fluid challenges (69%) were positive for VE, with a statistically significant (P < 0.001) difference in SV changes between positive and negative responses to VE. There was a statistically significant difference in PPV and SVV values before VE in the positive and negative fluid responses [PPV: 16% (15% to 18%) vs. 14% (13% to 15%), P = 0.001; and SVV: 14% (13% to 16%) vs. 16% (15% to 16%), P = 0.03 or positive and negative fluid responses, respectively]. Data are presented as medians and 25th and 75th percentiles Before VE there was no significant difference in StO2 values relative to baseline [86% (78% to 88%) vs. 84% (77% to 91%), P = 0.83], without a significant difference (P = 0.36) between positive and negative fluid challenges. Hypovolaemia was associated with a significant reduction (P = 0.004) in StO2 recovery slope, with a significant difference (P = 0.02) between positive and negative fluid challenges. The VE-induced increase in the StO2 recovery slope was 62 ± 49% (P < 0.001) for positive fluid challenges and 26 ± 34% (P = 0.04) for negative fluid challenges.
Hypovolaemia significantly affects the muscle StO2 recovery slope. Restoring effective intravascular volume with fluid loading significantly improves the StO2 recovery slope, despite apparently ineffective changes in systemic haemodynamics.
Two commercial automated, non-invasive systems for estimation of cardiac output were evaluated. Values of cardiac output obtained by electrical bioimpedance cardiography (BoMed NCCOM3 machine) were compared with values derived from an indirect Fick technique that uses carbon dioxide rebreathing (Gould 9000 IV system) during 103 simultaneous measurements made at rest in 19 randomly selected subjects and on exercise in 11 subjects. Cardiac output values obtained with impedance cardiography were significantly correlated with those measured by the indirect Fick method, although there was a wide scatter with over 73% of the readings lying outside the limits defined by the line of identity +/- 20%. This correlation was greatly reduced when stroke volume index was used instead of cardiac output. Indirect Fick results were linearly related to oxygen uptake both at rest and on exercise, while impedance cardiography results did not correlate with oxygen uptake. Impedance cardiography gave consistently lower results for cardiac output than indirect Fick at all levels of exercise. Both machines were easy to use and produced acceptable mean (SE) coefficients of variation (BoMed NCCOM3 7.7 (1.0)%, Gould 9000 IV 10.6 (1.4)%). Further validation is required before either of these machines can be recommended as an alternative to invasive monitoring in clinical practice.
Orthostatic stress activates the coagulation system. The extent of coagulation activation with full orthostatic load leading to presyncope is unknown. We examined in 7 healthy males whether presyncope, using a combination of head up tilt (HUT) and lower body negative pressure (LBNP), leads to coagulation changes as well as in the return to baseline during recovery. Coagulation responses (whole blood thrombelastometry, whole blood platelet aggregation, endogenous thrombin potential, markers of endothelial activation and thrombin generation), blood cell counts and plasma mass density (for volume changes) were measured before, during, and 20 min after the orthostatic stress. Maximum orthostatic load led to a 25% plasma volume loss. Blood cell counts, prothrombin levels, thrombin peak, endogenous thrombin potential, and tissue factor pathway inhibitor levels increased during the protocol, commensurable with hemoconcentration. The markers of endothelial activation (tissue factor, tissue plasminogen activator), and thrombin generation (F1+2, prothrombin fragments 1 and 2, and TAT, thrombin-antithrombin complex) increased to an extent far beyond the hemoconcentration effect. During recovery, the markers of endothelial activation returned to initial supine values, but F1+2 and TAT remained elevated, suggestive of increased coagulability. Our findings of increased coagulability at 20 min of recovery from presyncope may have greater clinical significance than short-term procoagulant changes observed during standing. While our experiments were conducted in healthy subjects, the observed hypercoagulability during graded orthostatic challenge, at presyncope and in recovery may be an important risk factor particularly for patients already at high risk for thromboembolic events (e.g. those with coronary heart disease, atherosclerosis or hypertensives).
In ICUs, fluid administration is frequently used to treat hypovolaemia. Because volume expansion (VE) can worsen acute respiratory distress syndrome (ARDS) and volume overload must be avoided, predictive indicators of fluid responsiveness are needed. The purpose of this study was to determine whether passive leg raising (PLR) can be used to predict fluid responsiveness in patients with ARDS treated with venovenous extracorporeal membrane oxygenation (ECMO).
We carried out a prospective study in a university hospital surgical ICU. All patients with ARDS treated with venovenous ECMO and exhibiting clinical and laboratory signs of hypovolaemia were enrolled. We measured PLR-induced changes in stroke volume (ΔPLRSV) and cardiac output (ΔPLRCO) using transthoracic echocardiography. We also assessed PLR-induced changes in ECMO pump flow (ΔPLRPO) and PLR-induced changes in ECMO pulse pressure (ΔPLRPP) as predictors of fluid responsiveness. Responders were defined by an increase in stroke volume (SV) > 15% after VE.
Twenty-five measurements were obtained from seventeen patients. In 52% of the measurements (n = 13), SV increased by > 15% after VE (responders). The patients' clinical characteristics appeared to be similar between responders and nonresponders. In the responder group, PLR significantly increased SV, cardiac output and pump flow (P < 0.001). ΔPLRSV values were correlated with VE-induced SV variations (r2 = 0.72, P = 0.0001). A 10% increased ΔPLRSV predicted fluid responsiveness with an area under the receiver operating characteristic curve (AUC) of 0.88 ± 0.07 (95% confidence interval (CI95): 0.69 to 0.97; P < 0.0001), 62% sensitivity and 92% specificity. On the basis of AUCs of 0.62 ± 0.11 (CI95: 0.4 to 0.8; P = 0.31) and 0.53 ± 0.12 (CI95: 0.32 to 0.73, P = 0.79), respectively, ΔPLRPP and ΔPLRPO did not predict fluid responsiveness.
In patients treated with venovenous ECMO, a > 10% ΔPLRSV may predict fluid responsiveness. ΔPLRPP and ΔPLRPO cannot predict fluid responsiveness.
acute respiratory distress syndrome; fluid responsiveness; passive leg raising; extracorporeal membrane oxygenation; venovenous
After cancer and cardio-vascular disease, stroke is the third greatest cause of death worldwide. Given the limitations of the current imaging technologies used for stroke diagnosis, the need for portable non-invasive and less expensive diagnostic tools is crucial. Previous studies have suggested that electrical bioimpedance (EBI) measurements from the head might contain useful clinical information related to changes produced in the cerebral tissue after the onset of stroke. In this study, we recorded 720 EBI Spectroscopy (EBIS) measurements from two different head regions of 18 hemispheres of nine subjects. Three of these subjects had suffered a unilateral haemorrhagic stroke. A number of features based on structural and intrinsic frequency-dependent properties of the cerebral tissue were extracted. These features were then fed into a classification tree. The results show that a full classification of damaged and undamaged cerebral tissue was achieved after three hierarchical classification steps. Lastly, the performance of the classification tree was assessed using Leave-One-Out Cross Validation (LOO-CV). Despite the fact that the results of this study are limited to a small database, and the observations obtained must be verified further with a larger cohort of patients, these findings confirm that EBI measurements contain useful information for assessing on the health of brain tissue after stroke and supports the hypothesis that classification features based on Cole parameters, spectral information and the geometry of EBIS measurements are useful to differentiate between healthy and stroke damaged brain tissue.
stroke; electrical bioimpedance spectroscopy; classification tree; cole parameters
Assessment of cardiac preload is important for clinical management of some emergencies related to hypovolemia. Effects of acute simulated hypovolemia on Doppler blood flow velocity indices of tricuspid valve (TV) and superior vena cava (SVC) were investigated in order to find sensitive Doppler indices for predicting right ventricular preload.
Doppler flow patterns of SVC and TV in 12 healthy young men were examined by transthoracic echocardiography (TTE) during graded lower body negative pressure (LBNP) of up to -60 mm Hg which simulated acute hypovolemia. Peak velocities of all waves and their related ratios (SVC S/D and tricuspid E/A) were measured, calculated and statistically analyzed.
Except for the velocity of tricuspid A wave, velocities of all waves and their related ratios declined during volume decentralization. Of all indices measured, the peak velocities of S wave and AR wave in SVC correlated most strongly with levels of LBNP (r = -0.744 and -0.771, p < 0.001).
The S and AR velocities are of good values in assessing right ventricular preload. Monitoring SVC flow may provide a relatively noninvasive means to assess direct changes in right ventricular preload.
Heart rate variability (HRV) decreases during hemorrhage, and has been proposed as a new vital sign to assess cardiovascular stability in trauma patients. The purpose of this study was to determine if any of the HRV metrics could accurately distinguish between individuals with different tolerance to simulated hemorrhage. Specifically, we hypothesized that (1) HRV would be similar in low tolerant (LT) and high tolerant (HT) subjects at presyncope when both groups are on the verge of hemodynamic collapse; and (2) HRV could distinguish LT subjects at presyncope from hemodynamically stable HT subjects (i.e., at a submaximal level of hypovolemia). Lower body negative pressure (LBNP) was used as a model of hemorrhage in healthy human subjects, eliciting central hypovolemia to the point of presyncopal symptoms (onset of hemodynamic collapse). Subjects were classified as LT if presyncopal symptoms occurred during the −15 to −60 mmHg levels of LBNP, and HT if symptoms occurred after LBNP of −60 mmHg. A total of 20 HRV metrics were derived from R–R interval measurements at the time of presyncope, and at one level prior to presyncope (submax) in LT and HT groups. Only four HRV metrics (Long-range Detrended Fluctuation Analysis, Forbidden Words, Poincaré Plot Descriptor Ratio, and Fractal Dimensions by Curve Length) supported both hypotheses. These four HRV metrics were evaluated further for their ability to identify individual LT subjects at presyncope when compared to HT subjects at submax. Variability in individual LT and HT responses was so high that LT responses overlapped with HT responses by 85–97%. The sensitivity of these HRV metrics to distinguish between individual LT from HT subjects was 6–33%, and positive predictive values were 40–73%. These results indicate that while a small number of HRV metrics can accurately distinguish between LT and HT subjects using group mean data, individual HRV values are poor indicators of tolerance to hypovolemia.
lower body negative pressure; hypovolemia; hemorrhage; heart rate variability; heart period variability
Melatonin has been shown to attenuate the reflex sympathetic increases that arise in response to orthostatic challenges. We tested the hypothesis that the attenuated sympathetic increase induced by melatonin premedication may weaken the arterial blood pressure (ABP) preserving the capability during acute hypotension, thereby altering dynamic cerebral autoregulation and causing a further decrease in cerebral blood flow (CBF).
Acute hypotension was induced in 12 healthy subjects by releasing bilateral thigh cuffs before and after an oral dose of melatonin (0.2 mg/kg). Heart rate (HR), arterial blood pressure (ABP), Modelflow estimate of cardiac output (CO), total peripheral resistance (TPR) and cerebral blood flow velocity (CBFV) by transcranial Doppler were measured.
Steady state HR, the mean arterial pressure and CBFV were not altered 60 minutes after melatonin ingestion. Reduced systolic arterial pressure (ΔSAP), changes in HR (ΔHR), CO (ΔCO), and TPR (ΔTPR), ΔHR/ΔSAP and percentage restoration of SAP were not affected after a temporal decrease in ABP induced by thigh cuff release. In the cerebral circulation, melatonin did not affect changes in CBFV, cerebrovascular resistance index, the rate of regulation and percentage restoration of CBFV following a sudden decrease in ABP.
Contrary to our hypothesis, melatonin did not affect the rapid vasodilatory and recovery responses of cardiovascular and dynamic cerebral autoregulation. These results suggest that melatonin premedication may not impair ABP and CBF preserving capability induced by sudden postural changes or hemorrhage.
Blood pressure; Cerebrovascular circulation; Melatonin
OBJECTIVE—To characterise cardiopulmonary baroreflex responses and examine the effects of a 45 minute cycling bout late after successful repair of coarctation of the aorta.
SUBJECTS—10 young adults (mean (SEM) age 18.1 (2.6 years)) operated on for coarctation of the aorta 12.7 (3.5) years earlier, and 10 healthy controls.
DESIGN—Forearm blood flow (venous occlusion plethysmography) and vascular resistance, left ventricular internal diastolic diameter, and central venous pressure estimated from an antecubital vein were measured in the supine position at baseline and during five minute applications of lower body negative pressure (LBNP) at −15 mm Hg (LBNP−15) and −40 mm Hg (LBNP−40). Venous samples were obtained at baseline and during LBNP−40 for noradrenaline (norepinephrine), adrenaline (epinephrine), renin activity, and aldosterone. The tests were repeated after 45 minutes of moderate exercise.
RESULTS—Baseline heart rate (78 (9) v 64 (6) beats/min), echocardiographic cardiac output (6.9 (1.1) v 5.0 (0.2) l/min), shortening fraction (41.7 (1.8)% v 33.3 (1.3)%), and forearm blood flow (3.4 (0.4) v 2.3 (0.3) ml/100 g/min) were higher in the coarctation group than in the controls (p < 0.05). Changes in forearm blood flow and forearm vascular resistance from baseline to LBNP−40 were similar in both groups, but the relation between forearm vascular resistance and estimated central venous pressure or left ventricular internal diastolic diameter was shifted downward in the coarctation group. Plasma adrenaline was increased in the coarctation group (baseline: 3.2 (0.6) v 2.4 (0.3) pmol/l in controls; LBNP−40: 687 (151) v 332 (42) pmol/l) (p < 0.05). Both groups showed a similar downward displacement of forearm vascular resistance (p < 0.05) after exercise.
CONCLUSIONS—There appears to be resetting of the cardiopulmonary baroreflex to a lower forearm vascular resistance in young adults operated on for coarctation of the aorta, associated with hyperdynamic left ventricular function. Raised circulating adrenaline could contribute to the lower forearm vascular resistance.
Keywords: coarctation of aorta; cardiopulmonary baroreflex; forearm vascular resistance; circulating catecholamines
Cardiovascular deconditioning after long duration spaceflight is especially challenging in women who have a lower orthostatic tolerance (OT) compared with men. We hypothesized that an exercise prescription, combining supine aerobic treadmill exercise in a Lower Body Negative Pressure (LBNP) chamber followed by 10 min of resting LBNP, 3 to 4 times a week, and flywheel resistive training every third day would maintain orthostatic tolerance (OT) in women during a 60-day head-down-tilt bed rest (HDBR). Sixteen women were assigned to two groups (exercise, control). Pre and post HDBR OT was assessed with a tilt/LBNP test until presyncope. OT time (mean ± SE) decreased from 17.5±1.0 min to 9.1±1.5 min (−50±6%) in control group (p<0.001) and from 19.3 ±1.3 min to 13.0 ± 1.9 min (−35±7%) in exercise group (p<0.001), with no significant difference in OT time between the two groups after HDBR (p=0.13). Nevertheless compared with controls post HDBR, exercisers had a lower heart rate (mean±SE) during supine rest (71±3 versus 85±4, p<0.01), a slower increase in heart rate and a slower decrease in stroke volume over the course of tilt/LBNP test (p<0.05). Blood volume (mean±SE) decreased in controls (−9±2%, p<0.01) but was maintained in exercisers (−4±3%, p=0.17).
Our results suggest that the combined exercise countermeasure fails to protect OT but improves cardiovascular response to subtolerance levels of orthostatic stress.
Bed Rest; Dizziness; prevention & control; Exercise; physiology; Exercise Tolerance; physiology; Female; Head-Down Tilt; physiology; Heart Rate; physiology; Humans; Lower Body Negative Pressure; Stroke Volume; physiology; Tilt-Table Test; Time Factors; Weightlessness Simulation; simulated microgravity; cardiovascular deconditioning; exercise countermeasure; lower body negative pressure; WISE 2005
The aim of this article is to identify non-invasive, inexpensive, highly sensitive and accurate techniques for evaluating and diagnosing gastric diseases. In the case of the stomach, there are highly sensitive and specific methods for assessing gastric motility and emptying (GME). However, these methods are invasive, expensive and/or not technically feasible for all clinicians and patients. We present a summary of the most relevant international information on non-invasive methods and techniques for clinically evaluating GME. We particularly emphasize the potential of gastric electrical bioimpedance (EBI). EBI was initially used mainly in gastric emptying studies and was essentially abandoned in favor of techniques such as electrogastrography and the gold standard, scintigraphy. The current research evaluating the utility of gastric EBI either combines this technique with other frequently used techniques or uses new methods for gastric EBI signal analysis. In this context, we discuss our results and those of other researchers who have worked with gastric EBI. In this review article, we present the following topics: (1) a description of the oldest methods and procedures for evaluating GME; (2) an explanation of the methods currently used to evaluate gastric activity; and (3) a perspective on the newest trends and techniques in clinical and research GME methods. We conclude that gastric EBI is a highly effective non-invasive, easy to use and inexpensive technique for assessing GME.
Gastrointestinal motility; Gastric emptying; Bioimpedance technique; Diagnostic techniques; Digestive system
Cardiac output measured by thermodilution in 25 patients within 24 hours of acute myocardial infarction was compared with cardiac output measured by Doppler echocardiography (24 patients) and electrical bioimpedance (25 patients). The mean (range) cardiac outputs measured by Doppler (4.03 (2.2-6.0) 1/min) and electrical bioimpedance (3.79 (1.1-6.2) 1/min) were similar to the mean thermodilution value (3.95 (2.1-6.2) 1/min). Both non-invasive techniques agreed closely with thermodilution in most patients. None the less, three results with each method disagreed with thermodilution by more than 1 1/min. Both non-invasive techniques were reproducible and accurate in most patients with acute myocardial infarction. Doppler echocardiography was time consuming and technically demanding. Electrical bioimpedance was simple to use and had the additional advantage of allowing continuous monitoring of the cardiac output.
The purpose of this study was to evaluate the use of the conjunctival oxygen tension (PCJO2) monitor during the early assessment of injured patients in the A&E Department of a large District General Hospital. The conjunctival oxygen sensor provides a non-invasive continuous monitor of tissue oxygenation in the palpebral conjunctiva and has been shown to detect early hypovolaemia in animal and human studies. For this preliminary report PCJO2 was recorded with initial clinical findings, standard cardiorespiratory parameters (pulse rate, blood pressure, respiratory rate, Glasgow Coma Score) and final diagnosis. Low PCJO2 (less than 45 mmHg) was associated with hypovolaemia, reduced cardiac output and chest injury. Normal PCJO2 in patients with severe head injury requiring transfer to the Regional Neurosurgical Centre or patients from multivictim road traffic accidents (RTAs) indicated no early occult cardiorespiratory compromise and this was subsequently confirmed. Monitoring PCJO2 seems to provide a valuable adjunct in the initial assessment of the injured patient.
Laryngoscopy and tracheal intubation (LTI) increase blood pressure and heart rate (HR). Intensity of these changes is influenced by the anaesthetic depth assessed by the bispectral index (BIS). We determined the effect of phenytoin on anaesthetic depth and its influence on haemodynamics following LTI. Fifty patients of ASA grades I and II on oral phenytoin 200 to 300mg per day for more than one week were compared with 48 control patients. Standard anaesthesia technique was followed. BIS, non invasive mean blood pressure (MBP) and HR were recorded 30, 60, 90 and 120 sec after LTI. Phenytoin group needed lesser thiopentone for induction, 5 mg (1.1) vs. 4.3 mg (0.7) [p=0.036]. BIS was significantly lower in the phenytoin group vs. the control 30, 60, 90 and 120 sec after LTI [43.1 (16.0) vs. 48.9 (14.9), p=0.068, 56.3 (16.7) vs. 64.3 (14.4), p=0.013, 59.8 (15.8) vs. 67.5 (12.1), p=0.008, 62.6 (14) vs. 68.9 (11.2), p=0.017, and 64.2 (11.3) vs. 69 (11.7), p=0.033], respectively. MBP was also lower in the phenytoin group 30, 60, 90 and 120 sec after LTI [112.8 mmHg (13.8), vs. 117.9 mmHg (18) p=0.013, 108.6 (12.8) vs. 117.5 (16) p=0.003, 106.1 mmHg (14.1) vs. 113.2 mmHg (14.9), p=0.017, 101.8 mmHg (13.8) vs. 109.5 mmHg (14.1), p=0.007], respectively. HR was lower in phenytoin group at 30 sec. (p=0.027), 60 sec (p=0.219), and again at 120 sec (p=0.022). Oral phenytoin therapy for over a week results in greater anaesthetic depth as observed using BIS, which also attenuated haemodynamic response of LTI.
Phenytoin sodium; Anaesthetic requirement; Bispectral index; Intubation response
Computational models of integrative physiology may serve as a framework for understanding the complex adaptive responses essential for homeostasis in critical illness and resuscitation and may provide insights for design of diagnostics and therapeutics. In this study a computer model of human physiology was compared to results obtained from experiments using Lower Body Negative Pressure (LBNP) analog model of human hemorrhage. LBNP has been demonstrated to produce physiologic changes in humans consistent with hemorrhage. The computer model contains over 4000 parameters that describe the detailed integration of physiology based upon basic physical principles and established biologic interactions. The LBNP protocol consisted of a 5 min rest period (0 mmHg) followed by 5 min of chamber decompression of the lower body to −15, −30, −45, and −60 mmHg and additional increments of −10 mmHg every 5 min until the onset of hemodynamic decompensation (n = 20). Physiologic parameters recorded include mean arterial pressure (MAP), cardiac output (CO), and venous oxygen saturation (SVO2; from peripheral venous blood), during the last 30 s at each LBNP level. The computer model analytic procedure recreates the investigational protocol for a virtual individual in an In Silico environment. After baseline normalization, the model predicted measurements for MAP, CO, and SVO2 were compared to those observed through the entire range of LBNP. Differences were evaluated using standard statistical performance error measurements (median performance error (PE) <5%). The simulation results closely tracked the average changes observed during LBNP. The predicted MAP fell outside the standard error measurement for the experimental data at only LBNP −30 mmHg while CO was more variable. The predicted SVO2 fell outside the standard error measurement for the experimental data only during the post-LBNP recovery point. However, the statistical median PE measurement was found to be within the 5% objective error measure (1.3% for MAP, −3.5% for CO, and 3.95% for SVO2). The computer model was found to accurately predict the experimental results observed using LBNP. The model should be explored as a platform for studying concepts and physiologic mechanisms of hemorrhage including its diagnosis and treatment.
Systems analysis; Validation; Hemorrhagic shock
In this paper a new non-invasive, operator-free, continuous ventricular stroke volume monitoring device (Hemodynamic Cardiac Profiler, HCP) is presented, that measures the average stroke volume (SV) for each period of 20 seconds, as well as ventricular volume-time curves for each cardiac cycle, using a new electric method (Ventricular Field Recognition) with six independent electrode pairs distributed over the frontal thoracic skin. In contrast to existing non-invasive electric methods, our method does not use the algorithms of impedance or bioreactance cardiography. Instead, our method is based on specific 2D spatial patterns on the thoracic skin, representing the distribution, over the thorax, of changes in the applied current field caused by cardiac volume changes during the cardiac cycle. Since total heart volume variation during the cardiac cycle is a poor indicator for ventricular stroke volume, our HCP separates atrial filling effects from ventricular filling effects, and retrieves the volume changes of only the ventricles.
ex-vivo experiments on a post-mortem human heart have been performed to measure the effects of increasing the blood volume inside the ventricles in isolation, leaving the atrial volume invariant (which can not be done in-vivo). These effects have been measured as a specific 2D pattern of voltage changes on the thoracic skin. Furthermore, a working prototype of the HCP has been developed that uses these ex-vivo results in an algorithm to decompose voltage changes, that were measured in-vivo by the HCP on the thoracic skin of a human volunteer, into an atrial component and a ventricular component, in almost real-time (with a delay of maximally 39 seconds). The HCP prototype has been tested in-vivo on 7 human volunteers, using G-suit inflation and deflation to provoke stroke volume changes, and LVot Doppler as a reference technique.
The ex-vivo measurements showed that ventricular filling caused a pattern over the thorax quite distinct from that of atrial filling. The in-vivo tests of the HCP with LVot Doppler resulted in a Pearson’s correlation of R = 0.892, and Bland-Altman plotting of SV yielded a mean bias of -1.6 ml and 2SD =14.8 ml.
The results indicate that the HCP was able to track the changes in ventricular stroke volume reliably. Furthermore, the HCP produced ventricular volume-time curves that were consistent with the literature, and may be a diagnostic tool as well.
OBJECTIVE: To determine, using an animal model of blood loss, (1) if stroke distance, derived non-invasively from the time integral of the maximum velocity of red cells in the aorta, changed to a greater extent than heart rate and mean arterial pressure (MAP), which are recognised to be unreliable indicators of blood loss; (2) if changes in stroke distance reflected changes in stroke volume derived from thermodilution cardiac output measurements. METHODS: Eight anaesthetised swine had baseline measurements of heart rate, MAP, stroke volume, and stroke distance and were then exsanguinated at a rate of 1 ml/kg/min. Percentage changes from baseline of heart rate, MAP, stroke volume, and stroke distance were compared after 10, 20, and 30 ml/kg blood loss. The animal's blood was then reinfused at the rate of 2 ml/kg/min for 15 min, followed by normal saline 1 ml/kg/min. Percentage changes from baseline measurement of stroke volume and stroke distance over the whole experiment were evaluated by regression analysis. RESULTS: Heart rate, MAP, and stroke distance changed +7.9%, -22.5%, and -18.1% respectively (from baseline values) after 10 ml/kg blood loss; +23.2%, -44.0%, and -47.4% after 20 ml/kg blood loss; and +55.7%, -62.0%, and -69.8% after 30 ml/kg blood loss. Regression analysis of percentage changes in stroke volume and stroke distance from their baseline values at experimental time zero is stroke volume = 1.014 x stroke distance -2.156, r = 0.92, n = 54, P < 0.0001. CONCLUSIONS: (1) At maximal blood loss, stroke distance changes to a greater extent than heart rate and MAP. (2) Changes in stroke distance reflected changes in stroke volume but with less variability at lower values. Stroke distance may be a more useful measure of blood loss than heart rate and MAP.
During carotid endarterectomy (CEA), hemodynamic stability and adequate fluid management are crucial to prevent perioperative cerebral stroke, myocardial infarction and hyperperfusion syndrome. Both pulse pressure variation (PPV) and stroke volume variation (SVV), dynamic preload indices derived from the arterial waveform, are increasingly advocated as predictors of fluid responsiveness in mechanically ventilated patients. The aim of this study was to evaluate the accuracy of PPV and SVV for predicting fluid responsiveness in patients undergoing CEA.
Twenty seven patients undergoing CEA were enrolled in this study. PPV, SVV and cardiac output (CO) were measured before and after fluid loading of 500 ml of hydroxyethyl starch solution. Fluid responsiveness was defined as an increase in CO ≥ 15%. The ability of PPV and SVV to predict fluid responsiveness was assessed using receiver operating characteristic (ROC) analysis.
Both PPV and SVV measured before fluid loading are associated with changes in CO caused by fluid expansion. The ROC analysis showed that PPV and SVV predicted response to volume loading (area under the ROC curve = 0.854 and 0.841, respectively, P < 0.05). A PPV ≥ 9.5% identified responders (Rs) with a sensitivity of 71.4% and a specificity of 90.9%, and a SVV ≥ 7.5% identified Rs with a sensitivity of 92.9% and a specificity of 63.6%.
Both PPV and SVV values before volume loading are associated with increased CO in response to volume expansion. Therefore, PPV and SVV are useful predictors of fluid responsiveness in patients undergoing CEA.
Arterial blood pressure; Cardiac output; Carotid endarterectomy; Fluid therapy; Stroke volume
Stroke volume (SV) is a parameter that is being recognized as an endpoint in fluid resuscitation algorithms. Its role is now being realized as an important variable in hemodynamic assessment in various clinical scenarios such as septic and cardiogenic shocks. Direct measurement of stroke volume (SV) and its novel corollary, stroke volume variation (SVV) derived by proprietary software, are preferred over mean cardiac output (CO) measurements because they render a more accurate reflection of hemodynamic status independent of heart rate. Flotrac-Vigileo monitor (FTV) (Edwards Lifesciences, Irvine, CA, USA) is a system that uses a complex algorithm analyzing arterial waveform to calculate SV, SVV, and CO. We assessed the feasibility of obtaining SV measurements with a portable echocardiogram and validated its accuracy with the FTV system in mechanically ventilated patients in our intensive care unit (ICU). Furthermore, we emphasized the importance of hemodynamic measurements and familiarity with critical care echocardiography for the intensivists.
Ten patients who were on mechanical ventilation were studied. A femoral arterial line was connected to the FTV system monitoring SV and CO. A portable echocardiogram (M-Turbo; Sonosite, Bothell, WA) was used to measure SV. CO was calculated by multiplying SV by heart rate. No patient had arrhythmia. We used biplane Simpson’s method of discs to calculate SV in which subtraction of end-systolic volume from end-diastolic volume yields the SV.
The comparison of simultaneous SV and CO measurements by echocardiography with FTV showed a strong correlation between the 2. (For SV, y = 0.9545x + 3.3, R2 = 0.98 and for CO, y = 0.9104x + 7.7074, R2 = 0.97).
In our small cohort, the SV and CO measured by a portable echocardiogram (Sonosite M-Turbo) appears to be closely correlated with their respective values measured by FTV. Portable echocardiography is a reliable noninvasive tool for the hemodynamic assessment of the critically ill. Its results need further validation with gold standard measures in a larger cohort of patients. However, our results suggest portable echocardiography could be an attractive tool in assessment of different hemodynamic scenarios in the critically ill.
noninvasive hemodynamics; cardiac output; monitoring; stroke volume variation
During hypotension induced by tilt-table testing, low presyncopal blood pressure (BP) usually recovers within 1 min after tilt back. However, in some patients prolonged post faint hypotension (PPFH) is observed. We assessed the hemodynamics underlying PPFH in a retrospective study.
Seven patients (2 females, aged 31–72 years) experiencing PPFH were studied. PPFH was defined as a systolic BP below 85 mmHg for at least 2 min after tilt back. In 6 out of 7 presyncope was provoked by 0.4 mg sublingual NTG, administered in the 60° head-up tilt position following head-up tilt for 20 min. Continuous BP was monitored and stroke volume (SV) was computed from pressure pulsations. Cardiac output (CO) was calculated from SV × heart rate (HR); and total peripheral resistance (TPR) from mean BP/CO. Left ventricular contractility was estimated by dP/dtmax of finger pressure pulse.
Systolic BP (SYS), diastolic BP (DIAS) and HR during PPFH were lower compared to baseline: SYS 75 ± 14 versus 121 ± 18 mmHg, DIAS 49 ± 9 versus 71 ± 9 mmHg and HR 52 ± 14 versus 67 ± 12 beats/min (p < 0.05). Marked hypotension was associated with a 47% fall in CO 3.1 ± 0.6 versus 5.9 ± 1.3 L/min (p < 0.05) and decreases in dP/dt, 277 ± 77 versus 759 ± 160 mmHg/s (p < 0.05). The difference in TPR was not significant 1.1 ± 0.3 versus 1.0 ± 0.3 MU (p = 0.229). In four patients, we attempted to treat PPFH by 30° head-down tilt. This intervention increased SYS only slightly (to 89 ± 12 mmHg).
PPFH seems to be mediated by severe cardiac depression.
Hypotension; Syncope; Cardiac output; Continuous hemodynamics; Ventricular contractility; Total peripheral resistance
Cardiac output after burn injury has been measured by the non-invasive method of impedance plethysmography. An initial study of 143 normal subjects was undertaken in order to investigate variations in cardiac output with age. Fifteen patients were monitored during resuscitation after extensive burns. Fourteen patients showed a depression of stroke volume below the lower limits of the normal range, derived from the initial study on normal people.