what are the major compensatory responses to blood loss?

• Journal List
• J Vis Exp
• (117); 2016
• PMC5226259

J Vis Exp. 2016; (117): 54737.

Integrated Compensatory Responses in a Human Model of Hemorrhage

Victor A. Convertino

ⁱⁱU.Due south. Army Found of Surgical Research, JBSA Fort Sam Houston

³U.South. Army Medical Enquiry and Materiel Command, JBSA Fort Sam Houston

Carmen Hinojosa-Laborde

^oneTactical Gainsay Casualty Care Inquiry, JBSA Fort Sam Houston

²U.S. Army Institute of Surgical Inquiry, JBSA Fort Sam Houston

Gary W. Muniz

¹Tactical Gainsay Prey Care Research, JBSA Fort Sam Houston

²U.Southward. Regular army Establish of Surgical Research, JBSA Fort Sam Houston

Robert Carter,, Three

^aneTactical Combat Prey Care Research, JBSA Fort Sam Houston

ⁱⁱU.South. Ground forces Institute of Surgical Research, JBSA Fort Sam Houston

Abstruse

Hemorrhage is the leading cause of trauma-related deaths, partly considering early diagnosis of the severity of blood loss is hard. Assessment of hemorrhaging patients is hard because electric current clinical tools provide measures of vital signs that remain stable during the early on stages of bleeding due to compensatory mechanisms. Consequently, at that place is a need to empathize and measure out the total integration of mechanisms that recoup for reduced circulating blood book and how they change during ongoing progressive hemorrhage. The body's reserve to compensate for reduced circulating blood volume is chosen the 'compensatory reserve'. The compensatory reserve tin exist accurately evaluated with real-time measurements of changes in the features of the arterial waveform measured with the use of a high-powered computer. Lower Body Negative Pressure (LBNP) has been shown to simulate many of the physiological responses in humans associated with hemorrhage, and is used to study the compensatory response to hemorrhage. The purpose of this report is to demonstrate how compensatory reserve is assessed during progressive reductions in key blood volume with LBNP equally a simulation of hemorrhage.

Keywords: Medicine, Issue 117, hemorrhage, homo, blood pressure regulation, centre rate, stroke volume, arterial waveform features, resuscitation, compensatory reserve

Introduction

The most important office of the cardiovascular organisation is the command of adequate perfusion (blood flow and oxygen delivery) to all tissues of the body through homeostatic regulation of arterial claret pressure. Various mechanisms of compensation (e.g., autonomic nervous system activity, cardiac rate and contractility, venous return, vasoconstriction, respiration) contribute to maintain normal physiological levels of oxygen in the tissues.¹ Reductions in circulating blood volume such equally those caused by hemorrhage can compromise the ability of cardiovascular compensatory mechanisms and ultimately lead to low arterial blood pressure, serious tissue hypoxia, and circulatory shock that can be fatal.

Circulatory shock caused by severe haemorrhage (i.e., hemorrhagic daze) is a leading cause of death due to trauma.^two One of the most challenging aspects of preventing a patient from developing shock is our inability to recognize its early onset. Early and accurate assessment of the progression toward the development of shock is currently limited in the clinical setting by technologies (i.e., medical monitors) that provide measurements of vital signs that alter very little in the early on stages of blood loss because of the body's numerous compensatory mechanisms for regulating blood pressure level.^{iii-half dozen} As such, the adequacy to measure the sum total of the body'south reserve to recoup for blood loss represents the most accurate reflection of tissue perfusion land and the take a chance of developing shock.ⁱ This reserve is chosen the compensatory reserve which tin exist accurately assessed by real-time measurements of changes in features of the arterial waveform.ⁱ Depletion of the compensatory reserve replicates the terminal cardiovascular instability observed in critically sick patients with sudden onset of hypotension; a condition known as hemodynamic decompensation.⁷

The relationship between the utilization of the compensatory reserve and regulation of blood pressure during ongoing blood loss in humans tin can be demonstrated in the laboratory using a comprehensive gear up of physiological measurements (e.m., blood pressures, heart rate, arterial blood oxygen saturation, stroke volume, cardiac output, vascular resistance, respiration rate, pulse character, mental status, finish-tidal CO₂, tissue oxygen) provided past standard physiological monitoring during continuous progressive reductions in central claret volume similar to those that occur during hemorrhage. Lowered central claret volume can be induced noninvasively with progressive increases in Lower Torso Negative Force per unit area (LBNP).⁸ Using this combination of physiological measurements and LBNP, the conceptual understanding of how to assess the body'due south ability to compensate for reduced central blood book can easily exist demonstrated. This study depicts the prelab preparation, the sit-in of compensatory response in relation to other physiological responses during imitation hemorrhage, and the postlab evaluation of results. The experimental techniques necessary for making measurements of compensatory reserve are demonstrated in a human volunteer.

Protocol

Prior to any man procedure, the institutional review lath (IRB) must corroborate the protocol. The protocol used in this study was approved by the US Army Medical Research and Materiel Control IRB. The protocol is designed to demonstrate the physiological responses of compensation to a progressive reduction in fundamental blood volume similar to that experienced by individuals during ongoing hemorrhage in a controlled and reproducible laboratory setting. The laboratory room temperature is controlled at 23 - 25 ˚C.

1. Equipment Training

1. Turn on equipment and devices requiring warm-upward and calibration. Annotation: Equipment and devices include a data conquering organisation to tape data at 1 Hz; two dissever devices that provide noninvasive, continuous measurements of brachial artery blood pressure level and arterial oxygen saturation (SpO₂) using ii split up infrared finger photoplethysmography cuff sensors^9-11; a capnograph for measurement of terminate-tidal CO_ii and respiratory charge per unit; and a finger pulse oximeter to acquire peripheral pulsatile arterial waveforms for measuring Compensatory Reserve.

2. Synchronize all of the instruments with internal clocks past adjusting the time stamp on each instrument to match a laboratory main clock that will be used to mark time during the experiment.

ii. Subject Training

1. Instruct the subject to avoid caffeine, alcohol, and strenuous practise 24 h prior to testing, and to avert eating at to the lowest degree ii h prior to the protocol in the event that hemodynamic decompensation induces nausea.

2. Prior to initiation of the protocol, accept the physician perform a medical screening exam to ensure the subject meets minimal health requirements, and ensures the absence of exclusion criteria (nicotine utilise, hypertension, autonomic dysfunction, or history of syncopal episodes). Since pregnancy is an exclusion criterion for participation, require female participants to take a standard urine pregnancy test on the day of the study. NOTE: For the condom of the bailiwick, the study physician is certified in advanced life support, and is present during the study. A fully-equipped 'crash cart' is immediately available to back up the subject's airway, respiration, and circulation in the event of loss of consciousness or an acute cardiac arrhythmia taking place during the LBNP process.

3. Inform the subject about the procedure, and obtain written consent to participate in the study. Annotation: Explain to the subject that the goal of the written report is to utilize LBNP until the onset of cardiovascular decompensation (presyncope). Explain that at that place are cardiovascular parameters that define this indicate, and LBNP will be terminated when these cardiovascular parameters are observed. Inform the subject field that they may also experience symptoms typically associated with presyncope during the LBNP procedure. Instruct the subject to notify the investigator if these symptoms occur and LBNP will immediately be terminated.

4. Identify the neoprene LBNP skirt on the subject. Ensure that the skirt is snug effectually the waist and torso in guild to create an air-tight seal.

5. Instruct the subject to lay supine on the bed of the LBNP bedroom while straddling a stationary mail service to secure the torso in place during LBNP. Instruct the subject area to relax the lower body during LBNP exposure. Secure the bailiwick into the LBNP bedchamber by sliding the bed into the chamber and attaching the neoprene skirt to the chamber opening to create an air-tight seal. Note: The LBNP chamber provides the capability of accurately (within 0.1 mmHg) controlling the internal pressure from 0 to -100 mmHg either manually or with a computerized profile. The bedroom includes an adjustable saddle to secure the subject field's body position. Clear plexiglass windows let for visualization of the bailiwick's legs. An adaptable aluminum waist lath allows for an air-tight seal to be created by a neoprene skirt worn by the subject and the LBNP bedroom at the level of the iliac crest (Figure one).

6. Place electrocardiogram (ECG) electrodes on the right and left humoral-clavicular joints, and on the right and left lower ribs (total of iv) in a modified lead 2 configuration (Figure 1) for continuous measurement of eye rate.

7. Position the subject field's artillery on the arm rests, adjusted and so that the easily are supported at centre level. Using appropriate size finger cuffs, place an infrared finger photoplethysmographydevice on the left and right middle fingers for continuous noninvasive crush-to-crush measurement of blood pressure.

8. Attach the finger cuffs to the pressure monitors. Calibrate the devices and record blood pressure according to the manufacturer instructions.¹² Enter field of study information (age, sex, tiptop, and weight) to enable the appropriate assumptions for calculation (estimation) of stroke volume, cardiac output and peripheral vascular resistance by the Modelflow algorithm if desired.^13,xiv

9. Identify the finger pulse oximeter on the right index finger for continuous measurement of compensatory reserve^i,12 (Figure ii).

10. Place a nasal cannula on the discipline and instruct the subject to breathe through the nose to assure sensitive reflections in inspiration and expiration. Nasal air sampling volition let the subject to talk freely for self-reporting of developing symptoms. Connect the nasal cannula to the capnograph for the continuous measurement of respiration and end tidal CO₂.

three. Performing the LBNP Protocol

1. Start data recording by clicking the "Kickoff" button on the data conquering organization. Tape baseline data for 5 min. Initiate the beginning level of primal hypovolemia by turning on the vacuum motor and setting negative pressure level to -fifteen mmHg, and concord this pressure for 5 min. Effigy 3 outlines the protocol.

2. Increase the LBNP to -xxx mmHg, and hold this pressure for 5 min.

3. Increase the LBNP to -45 mmHg, and agree this pressure for v min.

4. Increase the LBNP to -60 mmHg, and hold this pressure for 5 min.

5. Increment the LBNP to -seventy mmHg, and hold this force per unit area for 5 min.

6. Go along to increase LBNP levels by -ten mmHg every 5 min until the end of the protocol (5 min at -100 mmHg LBNP) or the point of hemodynamic decompensation. Terminate the LBNP by pressing the pressure release push on the LBNP sleeping accommodation. NOTE: Hemodynamic decompensation is identified past a abrupt fall in systolic arterial force per unit area below 80 mmHg, or the subject reporting presyncopal symptoms such as gray-out (loss of color vision), tunnel vision, sweating, nausea or dizziness (Figure four).

7. Continue recording data on the data acquisition organisation during 10 min afterwards the cessation of LBNP (postLBNP recovery).

8. Finish recording information at the end of the 10-min recovery period by clicking the "Finish" push button on the data acquisition system.

9. Detach all instrumentation from the subject and remove the bailiwick from the LBNP chamber. Enquire the subject field to sit after stepping down from the LBNP platform to ensure they are symptom-free before leaving the laboratory. The study is at present complete.

10. Download data files from the acquisition arrangement for extraction of the Compensatory Reserve Index (CRI), Mean Arterial Pressure (MAP), heart rate, and SpO_ii values. ^i,15,sixteen

Representative Results

The LBNP process causes a reduction in air pressure level around the lower torso and legs. As this vacuum is progressively increased, blood book shifts from the head and upper trunk to the lower torso to create a state of central hypovolemia. The progressive reduction in central blood book (i.e., LBNP) produces significant alterations in the features of the arterial waveform measured with the infrared finger photoplethysmograph (Effigy 5). The Compensatory Reserve Alphabetize (CRI) is calculated from the recorded arterial pulse wave using a unique machine learning algorithm which analyzes changes in moving ridge grade characteristics to summate an estimated compensatory reserve (Figure half-dozen).^1,15,16 Each continuous noninvasive photoplethysmograph waveform (represented as the monitored 'Patient'south Arterial Waveform') is the input to calculate an estimate of an individual's compensatory reserve (represented every bit the 'CRI Guess') based on comparison to a large 'library' of reference waveforms (represented equally the 'Algorithm Waveform Library') generated from progressive levels of central hypovolemia.

In this experiment, a subject was exposed to LBNP until the onset of hemodynamic decompensation which occurs when the trunk is no longer able to compensate for the hypovolemia. The values for mean arterial pressure level, eye rate, SpO_ii, and CRI plotted against time (i.east., progressive reductions in central blood volume caused by increasing levels of LBNP) are shown in Figure 7. The results of the experiment show that changes in hateful arterial pressure level, eye rate, and SpO₂ occur during the later phases of hemorrhage (i.e., >15 min into the protocol for heart rate and >25 min for mean arterial pressure and SpO_two) while CRI decreases early and progressively throughout the multiple steps of LBNP.

Tolerance to reduced central blood volume is defined as the fourth dimension from the beginning of the experiment to decompensation. In this example, tolerance was approximately 27.5 min at a level of -70 mmHg LBNP. Based on previous experiments that were designed to equate the magnitude of actual claret loss with LBNP,^eight the equivalent blood loss that our subject area was able to tolerate was estimated at approximately ane.2 L.

Figure 1: LBNP Bedchamber. A subject is shown in a supine position on the bed of the LBNP chamber. The neoprene brim around the subject'south waist is used to create an airtight seal inside the LBNP bedroom. Previously published in Cooke et al. ¹⁷Please click here to view a larger version of this effigy.

Effigy 2: Compensatory Reserve Monitoring Device. The device consists of a noninvasive finger pulse oximeter that transmits pulse oximeter and waveform information via a USB connectedness to a compensatory reserve monitor. The monitor unit contains an algorithm which calculates a value for compensatory reserve known as the Compensatory Reserve Index (CRI)^1,12. Data are recorded at each centre beat and displayed on the monitor and stored on a retention card. Please click here to view a larger version of this figure.

Figure 3. Stepwise Changes in LBNP During Experiment. During the experimental protocol, LBNP (mmHg) is adjusted in a stepwise style (5 min/level) to induce progressive key hypovolemia. This diagram shows LBNP increasing from 0 to -100 mmHg during 40 min of an experimental protocol. Modified from Convertino et al. ^eighteen Please click hither to view a larger version of this figure.

Figure 4: Hemodynamic Decompensation. Sample blood pressure (mm Hg, yellow tracing) and lower body negative pressure level (mmHg, white tracing) recordings are shown from a bailiwick at the point of hemodynamic decompensation. At the point of decompensation, claret pressure is 78/55 mmHg, and lower body negative pressure is -lx mmHg. Blood pressure returns to normal after abeyance of lower torso negative pressure level. Modified from Convertino et al. ^ane Please click hither to view a larger version of this figure.

Figure 5. Arterial Waveforms During LBNP. Sample recordings of arterial pressure waveforms are shown during baseline (upper tracing) and during -threescore mmHg lower body negative pressure (LBNP, lower tracing). The changes in the characteristic features of the arterial waveforms are evaluated to gauge compensatory reserve. Please click here to view a larger version of this figure.

Figure six: How the CRI is Calculated. Diagram illustrating the process of the compensatory reserve alphabetize (CRI) algorithm that compares beat-to-shell arterial claret pressure waveform tracings over an interval of thirty heartbeats (A) to a 'library' of waveforms (B) collected from humans exposed to progressive reductions in central blood volume for generation of an estimated CRI value (C). Reproduced from Convertino et al. ¹⁵ Please click hither to view a larger version of this figure.

Effigy seven. Sample Results of an LBNP Experiment. Values of Mean Arterial Pressure (MAP, mmHg), Heart Rate (Hr, beats/min), arterial oxygen saturation (SpO_two, %), Compensatory Reserve Index (CRI) and Lower Body Negative Pressure (LBNP, mmHg) are shown for one discipline during an LBNP experiment. The dashed line represents the onset of cardiovascular decompensation, Please click here to view a larger version of this effigy.

Figure 8: Characteristic Features of the Arterial Waveform. Two wave forms are shown that demonstrate the characteristic features of the arterial ejected and reflected waveforms during normovolemia and hypovolemia. The red line indicates the integrated waveform that is recorded and observed in a tracing. Previously published in Convertino et al. ^one Delight click here to view a larger version of this figure.

Discussion

Using LBNP to cause progressive and continuous reductions in central blood volume, we were able to induce a typical response of hemodynamic decompensation in the discipline, characterized by a sudden onset of hypotension and bradycardia (Effigy 7). It is important to empathise that the integrated compensatory response to hemorrhage is very complex,¹⁹ resulting in pregnant individual variability in the tolerance to blood loss.¹ Every bit such, some individuals have relatively responsive compensatory mechanisms while others exercise not compensate every bit effectively. Therefore, a disquisitional stride in the protocol is to comport the experiment to the point of the onset of cardiovascular decompensation so that tolerance to hypovolemia can be accurately assessed. Premature termination of the experiment will not provide tolerance data. The experiments on more than than 250 humans immune us to classify individuals into two full general populations^1,15,20-23 — those with relatively high tolerance (completion of the -lx mmHg level of the LBNP protocol) to reduced central blood volume (i.east., proficient compensators) and those with low tolerance (poor compensators who failed to complete the -60 mmHg level of the LBNP protocol). 1 tertiary (33%) of the humans we have tested has low tolerance, and two thirds (67%) of the subjects have high tolerance to hypovolemia. The discipline tested in the presentation (Figure 7) would exist classified as having loftier tolerance since he completed the -lx mmHg LBNP level.

LBNP is a well-established technique in the report of hypovolemia in humans, and troubleshooting is rarely necessary. Notwithstanding, using LBNP to appraise TOLERANCE to hypovolemia requires that the experiment be conducted to the betoken of presyncope. A key factor in this experiment is maintaining a minimal adventure of an agin event (syncope) for the bailiwick. As a issue, all experiments are conducted in the presence of a study dr.. In addition, all experiments are terminated immediately upon request of the subject or when systolic arterial pressure falls below 80 mmHg. The cessation of LBNP immediately redistributes claret book to vital organs such every bit the encephalon and heart, subsequently restoring hemodynamic stability (Figure 4).

As can be expected, the airtight seal around the waist of the discipline is a critical requirement to allow the progressive increases in negative pressure in the chamber. Occasionally, especially at college LBNP levels, the closed seal tin be compromised. At this bespeak, modifications tin be made to reinforce the seal by tightening the laces on the neoprene skirt or placing foam pads betwixt the discipline'south waist and LBNP table. The LBNP vacuum device tin adapt minor leaks in the seal without affecting the pressure level in the chamber.

The hemodynamic responses to LBNP have been shown to mimic those observed during hemorrhage.^8,17,24,25 We accept used LBNP to report the compensatory responses to progressive bleeding in an endeavor to evaluate the body's integrative effort to maintain cardiovascular stability during blood loss (compensatory reserve) and to provide a measurement of compensatory reserve. While LBNP is a valid model for studying the compensatory responses to hemorrhage in humans, a limitation of this technique is the absence of other factors unremarkably associated with hemorrhage such as trauma and pain. Clearly, the effects of these factors on the hemodynamic responses to hemorrhage cannot be assessed by LBNP induced hypovolemia in man volunteers.

Consequent with previously reported observations^1,15,16 we used the LBNP model of hemorrhage to demonstrate that measurement of the compensatory reserve identifies a trajectory to hemodynamic instability (decompensation) well in advance of clinically significant changes in currently available vital signs. This is an important bespeak to understand since earlier recognition of clinical urgency is critical to improving patient outcomes, especially in the emergency medical setting.^26-34 Existing methods for predicting cardiovascular decompensation rely on traditional vital signs that do not change until the onset of decompensation. The ability of the CRI algorithm to assess continuous changes in features of the arterial waveform allows automobile-learning of the clinical status of the individual patient. In this regard, continuous real-time measurement of the compensatory reserve provides the most sensitive and specific technique to appraise the tolerance of each individual to blood loss, and represents a significant improvement over existing methods for predicting hemorrhagic stupor in the clinical setting.

It is important to recognize the CRI algorithm output as reflecting the integration of all physiological compensatory mechanisms involved in the compensation for a relative deficit in circulating claret volume. This notion is logical since the arterial waveform is fabricated up of 2 distinct waves — the ejected wave (caused by wrinkle of the eye) and the reflected wave (acquired by the arterial wave that reflects back from the arterial vasculature). All compensatory mechanisms that impact cardiac output (e.one thousand., autonomic nerve activity, cardiac filling, respiration, cardiac medications, etc.) are independent within features of the ejected wave while all compensatory mechanisms that affect vascular resistance (e.g., sympathetic nerve activity, circulating catecholamines, arterial pH or CO₂, arterial elasticity, muscle contractions, etc.) are represented by features of the reflected wave.ⁱ As illustrated in Figure eight, the characteristic features alter distinctly from an apparent single moving ridge with a pocket-sized notch in a normovolemic land (left panel) to two separated waves with smaller magnitudes of height and width in conditions of reduced central blood volume (right console) such as occurs during hemorrhage. Every bit such, changes in features of the arterial waveform in response to hemorrhage give a unique individual-specific predictive capability to assess one's chapters to recoup adequately for claret loss. Each individual's compensatory reserve is correctly estimated in real time considering the machine-learning adequacy of the CRI algorithm accounts for compromised circulating blood book as it "learns" and "normalizes" the totality of compensatory mechanisms based on the individual's arterial waveform features.^one In this regard, the compensatory reserve is a superior measure out of the physiological status of a bleeding patient than any one or combination of vital signs.

CRI has also been estimated in case reports across the standard LBNP laboratory surroundings. Compensatory reserve measurements were obtained from humans with conditions of compromised tissue perfusion acquired by controlled hemorrhage ^xvi, trauma ^one, trauma followed by sepsis ³⁵, astute appendicitis ³⁵, burn injury ³⁵, massive hematemesis ³⁵, childbirth ³⁵, cardiac abort ³⁵, postural orthostatic tachycardia ³⁵, progressive hypovolemia with heat stress ³⁵, and Dengue hemorrhagic fever. ¹ These results indicate that the measurement of compensatory reserve using the CRI algorithm has provided accurate patient diagnosis in clinical weather condition of compromised tissue perfusion associated with pain and tissue injury, and in varying environmental challenges.

The ability to measure the compensatory changes associated with blood loss is critical to providing acute care in emergency situations in both military and civilian scenarios. The LBNP technique volition continue to be used as a valid model of human being hemorrhage to provide information for creating, testing and refining time to come algorithms and devices to measure Compensatory Reserve.

Disclosures

The authors declare that they have no competing financial interests. The views expressed herein are the individual views of the authors and are not to exist construed as representing those of the US Department of the Ground forces or the United states Section of Defence force.

Acknowledgments

This work is supported by funding from the United States Army, Medical Research and Materiel Command, Combat Casualty Intendance Plan. We thank LTC Kevin S. Akers, Doctor and Ms. Kristen R. Lye for their help in making the video.

References

• Convertino VA, Wirt MD, Glenn JP, Lein BC. The compensatory reserve for early and accurate prediction of hemodynamic compromise: a review of the underlying physiology. Shock. 2016;45(6):580–590. [PubMed] [Google Scholar]
• Eastridge BJ, et al. Expiry on the battlefield (2001-2011): Implications for the future of combat casualty care. Journal of Trauma and Acute Intendance Surgery. 2012;73(6):S431–S437. [PubMed] [Google Scholar]
• Orlinsky M, Shoemaker W, Reis ED, Kerstein Doctor. Electric current controversies in shock and resuscitation. Surg. Clin. North Am. 2001;81(6):1217–1262. [PubMed] [Google Scholar]
• Wo CCJ, et al. Unreliability of blood pressure and centre charge per unit to evaluate cardiac output in emergency resuscitation and critical illness. Crit Care Med. 1993;21:218–223. [PubMed] [Google Scholar]
• Bruijns SR, Guly Hour, Bouamra O, Lecky F, Lee WA. The value of traditional vital signs, daze index, and historic period-based markers in predicting trauma mortality. J Trauma Acute Intendance Surg. 2013;74(6):1432–1437. [PubMed] [Google Scholar]
• Parks JK, Elliott Air conditioning, Gentilello LM, Shafi South. Systemic hypotension is a late mark of shock after trauma: a validation study of Advanced Trauma Life Back up principles in a large national sample. Am. J. Surg. 2006;192(six):727–731. [PubMed] [Google Scholar]
• Brunauer A, et al. The arterial blood pressure level associated with last cardiovascular collapse in critically ill patients: a retrospective cohort study. Crit Care. 2014;18(half dozen):719. [PMC complimentary article] [PubMed] [Google Scholar]
• Hinojosa-Laborde C, et al. Validation of lower trunk negative pressure as an experiomental model of hemorrhage. J. Appl. Physiol. 2014;116:406–415. [PMC gratuitous commodity] [PubMed] [Google Scholar]
• Martina JR, et al. Noninvasive continuous arterial claret force per unit area monitoring with Nexfin(R) Anesthesiology. 2012;116(5):1092–1103. [PubMed] [Google Scholar]
• Imholz BP, Wieling Due west, Langewouters GJ, van Montfrans GA. Continuous finger arterial pressure: utility in the cardiovascular laboratory. Clin. Auton. Res. 1991;ane(one):43–53. [PubMed] [Google Scholar]
• Imholz BPM, Wieling Westward, van Montfrans GA, Wesseling KH. Fifteen years experience with finger arterial pressure monitoring: assessment of technology. Cardiovasc. Res. 1998;38:605–616. [PubMed] [Google Scholar]
• Roelandt R. Finger pressure reference guide. Finapres Medical Systems BV; 2005. [Google Scholar]
• Harms MPM, et al. Continuous stroke volume monitoring past modelling flow from not-invasive measurement of arterial pressure in humans under orthostatic stress. Clin. Sci. 1999;97:291–301. [PubMed] [Google Scholar]
• Leonetti P, et al. Stroke volume monitored past modeling flow from finger arterial pressure waves mirrors blood volume withdrawn past phlebotomy. Clin. Auton. Res. 2004;14(3):176–181. [PubMed] [Google Scholar]
• Convertino VA, Grudic Chiliad, Mulligan J, Moulton Due south. Estimation of individual-specific progression to impending cardiovascular instability using arterial waveforms. J. Appl. Physiol(Bethesda, Md :1985) 2013;115(8):1196–1202. [PubMed] [Google Scholar]
• Convertino VA, et al. Individual-specific, beat out-to-beat trending of significant human blood loss: the compensatory reserve. Shock. 2015;44(Supplement one):27–32. [PubMed] [Google Scholar]
• Cooke WH, Ryan KL, Convertino VA. Lower torso negative pressure as a model to written report progression to acute hemorrhagic shock in humans. J. Appl. Physiol. 2004;96:1249–1261. [PubMed] [Google Scholar]
• Convertino VA, et al. Inspiratory resistance maintains arterial force per unit area during central hypovolemia: implications for treatment of patients with severe hemorrhage. Crit Care Med. 2007;35(4):1145–1152. [PubMed] [Google Scholar]
• Carter R, 3, Hinojosa-Laborde C, Convertino VA. Variability in integration of mechanisms associated with loftier tolerance to progressive reductions in central claret volume: the compensatory reserve. Physiol Reports. 2016;4(1) [PMC complimentary commodity] [PubMed] [Google Scholar]
• Convertino VA, Sather TM. Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans. Clin. Physiol. 2000;20:177–184. [PubMed] [Google Scholar]
• Convertino VA, et al. Utilize of advanced motorcar-learning techniques for noninvasive monitoring of hemorrhage. J. Trauma. 2011;71(one Suppl):S25–S32. [PubMed] [Google Scholar]
• Convertino VA, Rickards CA, Ryan KL. Autonomic mechanisms associated with heart rate and vasoconstrictor reserves. Clin. Auton. Res. 2012;22:123–130. [PubMed] [Google Scholar]
• Rickards CA, Ryan KL, Cooke WH, Convertino VA. Tolerance to central hypovolemia: the influence of oscillations in arterial pressure and cerebral claret velocity. J. Appl. Physiol. 2011;111(iv):1048–1058. [PubMed] [Google Scholar]
• Johnson BD, et al. Reductions in fundamental venous pressure by lower trunk negative pressure of blood loss elicit similar hemodynamic responses. J. Appl. Physiol. 2014;117:131–141. [PMC free commodity] [PubMed] [Google Scholar]
• van Helmond N, et al. Coagulation Changes during Lower Body Negative Pressure and Blood Loss in Humans. Am. J. Physiol. Heart Circ. Physiol. 2015;309:H1591–H1597. [PubMed] [Google Scholar]
• Gerhardt R, Berry J, Blackbourne 50. Analysis of life-saving interventions performed by out-of-hospital gainsay medical personnel. J. Trauma. 2011;71:S109–S113. [PubMed] [Google Scholar]
• Pinsky MR. Hemodynamic evaluation and monitoring in the ICU. Chest. 2007;132(6):2020–2029. [PubMed] [Google Scholar]
• Rivers E, et al. Early goal-directed therapy in the handling of severe sepsis and septic shock. N.Engl.J.Med. 2001. pp. 1368–1377. [PubMed]
• Rivers EP, et al. The influence of early hemodynamic optimization on biomarker patterns of astringent sepsis and septic shock. Crit Care Med. 2007;35(nine):2016–2024. [PubMed] [Google Scholar]
• Rivers EP, Coba V, Whitmill M. Early goal-directed therapy in severe sepsis and septic shock: a contemporary review of the literature. Curr Opin Anaesthesiol. 2008;21(ii):128–140. [PubMed] [Google Scholar]
• Cap AP, Spinella PC, Borgman MA, Blackbourne LH, Perkins JG. Timing and location of blood product transfusion and outcomes in massively transfused combat casualties. J. Trauma. 2012;73:S89–S94. [PubMed] [Google Scholar]
• Spinella PC, Perkins JG, Grathwohl K, Beekley A, Holcomb JB. Warm fresh whole claret is independently associated iwth improved survival for patients with combat-related traumatic injuries. J. Trauma. 2009;66:S69–S76. [PMC gratuitous article] [PubMed] [Google Scholar]
• Kragh J, et al. Survival with emergency tourniquet use to stop bleeding in major limb trauma. Ann Surgery. 2009;249(1):1–7. [PubMed] [Google Scholar]
• Chung KK, et al. Continous renal replacement therapy improves survival in severly burned military casualties with acute kidney injury. J. Trauma. 2008;64:S179–S187. [PubMed] [Google Scholar]
• Stewart CL, et al. The compensatory reserve for early and accurate prediction of hemodynamic compromise: instance studies for clinical utility in acute care and physical performance. J Special Op. Med. 2016;xvi:vi–xiii. [PubMed] [Google Scholar]

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5226259/

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