Physiological and Medical Monitoring for En Route Care of Combat Casualties

Convertino, Víctor A.; Ryan, Kathy L.; Rickards, Caroline A.; Salinas, José; McManus, John; Cooke, William H.; Holcomb, John B.

doi:10.1097/ta.0b013e31816c82f4

Cited by 99 publications

(79 citation statements)

References 27 publications

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“…[1][2][3][4][5][6] LBNP is an excellent model for acute haemorrhage and hypovolaemic circulatory stress by inducing central hypovolaemia and unloading of baroreceptors and sympathetic activation. 8,9 The pooling of blood in the calf during LBNP was reduced in a stepwise manner in relation to diabetes severity. The degree of blood pooling in the lower limb is linked to venous compliance, 20,24 and reduced venous compliance has been found in diabetes patients.…”

Section: Discussionmentioning

confidence: 99%

“…LBNP is an established technique causing well-defined circulatory stress by pooling blood in the lower part of the body, with reduction in central blood volume and unloading of central baroreceptors. 8,9,13,20,21 After at least 45 min of supine rest, LBNP of 30 cm H 2 O was instituted and maintained for 8 min.…”

Section: Methodsmentioning

confidence: 99%

“…4,5,7 Lower body negative pressure (LBNP) is an excellent model for acute haemorrhage and hypovolaemic circulatory stress. 8,9 Orthostatic hypotension is more common in diabetes patients, 3,4 but also diabetes patients with no or only mild neuropathy have increased risk of orthostatic hypotension, signalling other contributory factors. 3 Two important and rapid mechanisms to maintain cardiovascular homeostasis during acute hypovolaemic stress are mobilisation of venous capacitance blood from peripheral tissues to the central circulation (capacitance response) and net capillary fluid absorption from extra-to intravascular space.…”

Section: Introductionmentioning

confidence: 99%

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Impaired compensatory response to hypovolaemic circulatory stress in type 1 diabetes mellitus

Lindenberger

Olsen

Länne

2011

Diabetes and Vascular Disease Research

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Diabetes mellitus is associated with decreased haemodynamic stability and reduced tolerance to hypovolaemia. Compensatory haemodynamic responses during experimental hypovolaemia in type 1 diabetes patients with (DMR+) and without (DMR-) retinopathy as well as healthy controls (C) were studied. Lower body negative pressure created hypovolaemic circulatory stress. Volumetric techniques were used to assess the compensatory capacitance response (redistribution of peripheral venous blood to the central circulation) and to assess capillary fluid absorption from tissue to blood. The compensatory capacitance response was 1/3 lower in DMR+ compared with C (p = 0.002) and DMR-(p = 0.01). Net capillary fluid absorption was reduced by one-third in DMR-and DMR+ compared with C (each p < 0.05). Type 1 diabetes patients with retinopathy demonstrate reduced mobilisation of peripheral venous blood to the central circulation. Furthermore, type 1 diabetes patients present with impaired capillary fluid absorption, which in combination with potentially decreased sympathetic vasoconstriction impedes cardiovascular homeostasis during acute hypovolaemic stress.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impaired compensatory response to hypovolaemic circulatory stress in type 1 diabetes mellitus

Lindenberger

Olsen

Länne

2011

Diabetes and Vascular Disease Research

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“…Existing, deidentified physiological data from humans subjected to a LBNP protocol were analyzed. The data collection procedures were approved by the Institutional Review Board of the Brooke Army Medical Center (Fort Sam Houston, TX) and are described in detail in several recent publications (7,20).…”

Section: Methodsmentioning

confidence: 99%

Improved pulse transit time estimation by system identification analysis of proximal and distal arterial waveforms

Ryan

Rickards

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Xu D, Ryan KL, Rickards CA, Zhang G, Convertino VA, Mukkamala R. Improved pulse transit time estimation by system identification analysis of proximal and distal arterial waveforms. Am J Physiol Heart Circ Physiol 301: H1389 -H1395, 2011. First published July 29, 2011 doi:10.1152/ajpheart.00443.2011.-We investigated the system identification approach for potentially improved estimation of pulse transit time (PTT), a popular arterial stiffness marker. In this approach, proximal and distal arterial waveforms are measured and respectively regarded as the input and output of a system. Next, the system impulse response is identified from all samples of the measured input and output. Finally, the time delay of the impulse response is detected as the PTT estimate. Unlike conventional foot-to-foot detection techniques, this approach is designed to provide an artifact robust estimate of the true PTT in the absence of wave reflection. The approach is also applicable to arbitrary types of arterial waveforms. We specifically applied a parametric system identification technique to noninvasive impedance cardiography (ICG) and peripheral arterial blood pressure waveforms from 15 humans subjected to lower-body negative pressure. We assessed the technique through the correlation coefficient (r) between its 1/PTT estimates and measured diastolic pressure (DP) per subject and the root mean squared error (RMSE) of the DP predicted from these estimates and measured DP. The technique achieved average r and RMSE values of 0.81 Ϯ 0.16 and 4.3 Ϯ 1.3 mmHg. For comparison, the corresponding values were 0.59 Ϯ 0.37 (P Ͻ 0.05) and 5.9 Ϯ 2.5 (P Ͻ 0.01) mmHg for the conventional technique applied to the same waveforms and 0.28 Ϯ 0.40 (P Ͻ 0.001) and 7.2 Ϯ 1.8 (P Ͻ 0.001) mmHg for the conventional technique with the ECG waveform substituted for the ICG waveform. These results demonstrate, perhaps for the first time, that the system identification approach can indeed improve PTT estimation.arterial blood pressure; arterial stiffness; foot-to-foot detection; impulse response; pulse wave velocity ACCORDING TO THE MOENS-KORTEWEG equation, pulse wave velocity (PWV) increases as the arteries stiffen. Indeed, PWV is the most popular index of arterial stiffness because of the ease of its measurement and its proven independent value in predicting cardiovascular events and mortality in hypertensive patients (2,4,12,14). In addition, because arterial stiffness increases with arterial blood pressure (ABP), PWV and ABP often show positive correlation, suggesting that PWV could provide a means to achieve continuous, noninvasive, and cuffless ABP monitoring (18).Conventionally, PWV is determined from the distance and pulse transit time (PTT) between proximal and distal arterial sites (5). PTT is, in turn, estimated by acquiring arterial waveforms from the two sites and then detecting the foot-tofoot time delay between the waveforms. The premise is that the foot of the proximal waveform represents a time before the return of the reflected wave to its measureme...

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“…Standard vital signs for detection of hemorrhage, such as arterial pressure, arterial oxygen saturation, and radial pulse character, are regulated by reflex compensatory mechanisms, so only begin to change with substantial loss of blood volume. [1][2][3] Furthermore, some metrics, such as heart rate (HR), lack specificity to hemorrhage; HR may increase very early due to an underlying hemorrhagic injury, but also due to other stimuli associated with trauma such as pain, anxiety, dehydration, heat or cold stress, physical activity/ movement, and ingestion of exogenous substances. Moreover, in many instances HR will actually decrease with traumatic injury.…”

Section: Introductionmentioning

confidence: 99%

The efficacy of novel anatomical sites for the assessment of muscle oxygenation during central hypovolemia

Sprick

Soller

Rickards

2016

Exp Biol Med (Maywood)

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Muscle tissue oxygenation (SmO 2 ) can track central blood volume loss associated with hemorrhage. Traditional peripheral measurement sites (e.g., forearm) may not be practical due to excessive movement or injury (e.g., amputation). The aim of this study was to evaluate the efficacy of three novel anatomical sites for the assessment of SmO 2 under progressive central hypovolemia. 10 male volunteers were exposed to stepwise prone lower body negative pressure to decrease central blood volume, while SmO 2 was assessed at four sites-the traditional site of the flexor carpi ulnaris (ARM), and three novel sites not previously investigated during lower body negative pressure, the deltoid, latissimus dorsi, and trapezius. SmO 2 at the novel sites was compared to the ARM sensor and to stroke volume responses. A reduction in SmO 2 was detected by the ARM sensor at the first level of lower body negative pressure (À15 mmHg; P ¼ 0.007), and at À30 (the deltoid), À45 (latissimus dorsi), and À60 mmHg lower body negative pressure (trapezius) at the novel sites (P 0.04). SmO 2 responses at all novel sites were correlated with responses at the ARM (R ! 0.89), and tracked the reduction in stroke volume (R ! 0.87); the latissimus dorsi site exhibited the strongest linear correlations (R ! 0.96). Of the novel sensor sites, the latissimus dorsi exhibited the strongest linear associations with SmO 2 at the ARM, and with reductions in central blood volume. These findings have important implications for detection of hemorrhage in austere environments (e.g., combat) when use of a peripheral sensor may not be ideal, and may facilitate incorporation of these sensors into uniforms.

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Physiological and Medical Monitoring for En Route Care of Combat Casualties

Cited by 99 publications

References 27 publications

Impaired compensatory response to hypovolaemic circulatory stress in type 1 diabetes mellitus

Impaired compensatory response to hypovolaemic circulatory stress in type 1 diabetes mellitus

Improved pulse transit time estimation by system identification analysis of proximal and distal arterial waveforms

The efficacy of novel anatomical sites for the assessment of muscle oxygenation during central hypovolemia

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