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doi:10.1378/chest.06-1768
(Chest. 2007; 131:1301-1307)
© 2007 American College of Chest Physicians
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Radial Artery Pulse Pressure Variation Correlates With Brachial Artery Peak Velocity Variation in Ventilated Subjects When Measured by Internal Medicine Residents Using Hand-Carried Ultrasound Devices*

J. Matthew Brennan, MD; John E. A. Blair, MD; Chetan Hampole, MD; Sascha Goonewardena, MD; Samip Vasaiwala, MD; Dipak Shah, MD; Kirk T. Spencer, MD and Gregory A. Schmidt, MD, FCCP

* From the Department of Cardiology (Drs. Brennan, Blair, Hampole, Goonewardena, Vasaiwala, Shah, and Spencer), The University of Chicago Hospitals, Chicago, IL; and the Carver College of Medicine (Dr. Schmidt), University of Iowa, Iowa City, IA.

Correspondence to: J. Matthew Brennan, MD, Division of Cardiovascular Diseases, Duke University Medical Center, 2300-2399 Erwin Rd, Durham, NC 27710; e-mail: j.matthew.brennan.98{at}alum.dartmouth.org

Abstract

Background: Rapid prediction of the effect of volume expansion is crucial in unstable patients receiving mechanical ventilation. Both radial artery pulse pressure variation ({Delta}PP) and change of aortic blood flow peak velocity are accurate predictors but may be impractical point-of-care tools.

Purpose: We sought to determine whether respiratory changes in the brachial artery blood flow velocity ({Delta}Vpeak-BA) as measured by internal medicine residents using a hand-carried ultrasound (HCU) device could provide an accurate corollary to {Delta}PP in patients receiving mechanical ventilation.

Methods: Thirty patients passively receiving volume-control ventilation with preexisting radial artery catheters were enrolled. The brachial artery Doppler signal was recorded and analyzed by blinded internal medicine residents using a HCU device. Simultaneous radial artery pulse wave and central venous pressure recordings (when available) were analyzed by a blinded critical care physician.

Results: A Doppler signal was obtained in all 30 subjects. The {Delta}Vpeak-BA correlated well with {Delta}PP (r = 0.84) with excellent agreement (weighted {kappa}, 0.82) and limited intraobserver variability (2.8 ± 2.8%) [mean ± SD]. A {Delta}Vpeak-BA cutoff of 16% was highly predictive of {Delta}PP ≥ 13% (sensitivity, 91%; specificity, 95%). A poor correlation existed between the CVP and both {Delta}Vpeak-BA (r = – 0.21) and {Delta}PP (r = – 0.16).

Conclusions: The HCU Doppler assessment of the {Delta}Vpeak-BA as performed by internal medicine residents is a rapid, noninvasive bedside correlate to {Delta}PP, and a {Delta}Vpeak-BA cutoff of 16% may prove useful as a point-of-care tool for the prediction of volume responsiveness in patients receiving mechanical ventilation.

Key Words: hand-carried ultrasound • mechanical ventilation • pulse pressure variation

Predicting hemodynamic responsiveness to volume expansion (VE) is among the most challenging and important assessments in the acute care setting. In studies123456789101112 designed to measure changes in cardiac index following fluid administration in hypotensive patients receiving mechanical ventilation, 28 to 60% of patients showed no significant change. Fluids may not only be ineffective but harmful as well, as suggested by the results of the ARDS Network Fluid and Catheter Treatment Trial.13 Ideally, one could predict in advance whether fluids will augment perfusion so that the treatment focus could shift more rapidly to vasoactive therapy in those who will not respond to fluids. How best to judge fluid responsiveness in the clinical setting is evolving.

Physical examination has been shown to be grossly inadequate in the assessment of volume status,1415161718 and limitations specific to the critical care setting increase the level of error. Traditional markers such as interstitial and pulmonary edema are of limited utility in many disease processes, including sepsis. Limitations to proper patient positioning and the presence of devices designed to secure endotracheal tubes prevent the accurate assessment of the jugular venous pressure.1920

While potentially helpful in other clinical scenarios, both right atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP) have been shown to be poorly predictive of volume responsiveness. Recently, the safety and utility of right-heart catheterization (RHC) have been questioned,1321222324 limiting its availability in some ICU settings.

Over the past 5 years, several new tools have emerged to increase the accuracy of the hemodynamic assessment.4891125 These methods rely on the physiologic interplay between respiration and circulation seen during passive ventilation. Mechanical lung inflation raises pleural pressure, transiently impeding venous return and diminishing right-heart and, subsequently, left-heart stroke volume with each inspiratory cycle. The respirophasic changes in stroke volume reveal themselves in changes in the arterial pulse pressure and the aortic peak flow velocity. What makes this particular cardiopulmonary interaction interesting is its dependence on the dynamics of the patient’s individual cardiac output curve. The magnitude of the cyclic variation in stroke volume depends mostly on whether the patient is operating on the steep or the flat portion of the Frank-Starling curve; that is, whether the heart is preload responsive or not.26

Respirophasic radial artery pulse pressure variation ({Delta}PP) has been shown to predict volume responsiveness in hemodynamically unstable patients receiving mechanical ventilation with a positive predictive value (PPV) and a negative predictive value (NPV) of 94% and 96%, respectively.11 {Delta}PP is clearly superior to RAP and PCWP as a predictor of volume responsiveness in patients receiving passive mechanical ventilation. However, like the RAP and PCWP, measurement of the {Delta}PP requires invasive monitoring with a peripheral arterial catheter, which has been associated with a risk of both infectious and embolic complications.27 In addition, measurement of the {Delta}PP requires a specialized monitoring setup that is unavailable in many point-of-care settings where initial patient stabilization occurs.

Ultrasound technology has been used to address the specific limitations of indwelling arterial and venous catheters. Measurement of the respirophasic aortic blood flow peak velocity variation ({Delta}Vpeak-Ao) has been shown to be highly predictive of the response of cardiac output to VE in patients receiving mechanical ventilation, with PPV of 91% and NPV of 100%.25 The technical expertise and expense involved in obtaining this measurement, however, make it impractical in most ICU settings.

Over the past several years, the utility of hand-carried ultrasound (HCU) technology in the ICU setting has undergone rapid expansion.282930 The sharp learning curve involved with the operation of these machines as well as their portability and affordability have led to the increasing availability of this technology in many acute care settings. The HCU assessment of volume status in spontaneously breathing subjects using the inferior vena cava collapsibility index has been validated.31 However, the absolute inferior vena cava dimensions have limited utility in the prediction of RAPs in patients receiving mechanical ventilation.32

Newer-generation HCUs have incorporated Doppler technology and vascular probes as standard features, making the noninvasive bedside measurement of respirophasic variation of peak blood flow velocity ({Delta}Vpeak) in peripheral arteries possible. In this study, we sought to determine whether a peripherally measured {Delta}Vpeak could substitute as an accurate, noninvasive point-of-care surrogate for {Delta}PP in patients receiving mechanical ventilation.

Materials and Methods

The research protocol was approved by the institutional review board for human subjects at the University of Chicago Hospitals. Written informed proxy consent was obtained from each subject’s next of kin.

Patients
We studied 30 patients receiving passive mechanical ventilation with clinically indicated peripheral arterial catheters. The patients were enrolled without regard to their body habitus or clinical situation. Exclusion criteria included the absence of sinus rhythm, presence of a ventricular assist device, a contraindication to the prespecified ventilatory parameters (a period of passive ventilation at tidal volume [VT] ≥ 8 mL/kg of predicted body weight and positive end-expiratory pressure [PEEP] of 5 to 10 mm Hg). A medical student performed an initial patient screening and collected subject demographics and clinical history for each patient prior to the collection of peak velocity and pulse pressure data.

Brachial Peak Velocity Measurement
A SonoSite Titan HCU (SonoSite; Bothell, WA) device with a 5-MHz broadband linear array transducer weighing 7.7 lb at a cost of approximately $40,000 was used to obtain each of the measurements. Two internal medicine residents with minimal exposure to ultrasound techniques were given approximately 30 min of formal instruction in the operation of the HCU and the proper technique for obtaining Doppler measurements from the brachial artery. Ten supervised patient examinations were performed prior to the beginning of the study.

Arterial blood flow velocities were measured from the brachial artery just proximal to the antecubital fossa in the arm contralateral to the arterial catheter over 30 s (Fig 1 ). Residents obtaining ultrasound images were blinded to the results of the arterial pulse pressure variations that were collected independently by a medical student. All image angles were corrected up to 15° for the best signal and stored for immediate review following each measurement. The total period of data acquisition lasted from 2 to 5 min per patient, during which time a 30-s loop of images was obtained. Each 30-s loop was divided into two equal segments for purposes of on-line data analysis. The maximum and minimum peak velocity was recorded from each of the 15-s segments by the medical residents. Velocity variation was calculated for each segment, and the results were averaged to arrive at the mean peak velocity variation for the study interval. Mean intraobserver brachial artery blood flow velocity variation (Vpeak-BA) measurements calculated across the 30 study subjects was 2.8 ± 2.8% [mean ± SD]. Vpeak-BA was calculated using the standard formula25: {Delta}Vpeak-BA (%) = 100 x (peak velocity maximum – peak velocity minimum)/[(peak velocity maximum + peak velocity minimum)/2].


Figure 1
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  		Figure 1. Correlating simultaneous brachial artery image (left, A), brachial artery Doppler recording (top right, B), and pulse pressure recording (bottom right, C).

 
{Delta}Vpeak-Ao
Arterial pressure and telemetry tracings were recorded over a 30-s interval simultaneously with the ultrasound measurement of the Vpeak-BA collected by a medical student, and analyzed by a boarded critical care physician blinded to the ultrasound results. Systolic and diastolic pressures were measured on a beat-to-beat basis, and pulse pressure was calculated as systolic – diastolic pressure. The maximum pulse pressure (PPmax) and minimum pulse pressure (PPmin) values were determined across the 30-s cycle, and the {Delta}PP was calculated using the following standard formula11: {Delta}PP (%) = 100 x (PPmax – PPmin)/[(PPmax + PPmin)/2].

Central Venous Pressure Measurement
In the 17 subjects in whom central venous catheters were present, the central venous pressure (CVP) was measured at end-expiration in the standard fashion by a medical student immediately prior to the study interval.

Study Protocol
Each of the 30 patients was sedated and received mechanical ventilation using volume-control settings with a mean VT of 9 ± 2 mL/kg and PEEP of 7 ± 2 cm H2O. All patients received passive mechanical ventilation as judged by ventilator and CVP waveforms (when available), as well as clinical observations made to exclude the recruitment of abdominal muscles. Patients who could not be made passive on the ventilator were excluded from the study, and none received paralytic medications during the trial period.

Statistical Analysis
Pearson correlation coefficients were calculated as a means of comparing {Delta}PP with {Delta}Vpeak-BA and CVP measurements. Using the established {Delta}PP cutoff of 13%, patients were designated as either predicted responders ({Delta}PP ≥ 13%) or nonresponders ({Delta}PP < 13%). Based on this grouping, a receiver operating characteristic curve was developed to establish the most accurate {Delta}Vpeak-BA cutoff. Based on this cutoff, test performance parameters were determined, including sensitivity, specificity, PPV, NPV, prevalence, and positive and negative likelihood ratios.

A Bland-Altman plot33 was constructed to assess the level of agreement between {Delta}PP and {Delta}Vpeak-BA. Weighted {kappa} values were calculated using contingency tables with {Delta}PP groupings of 5% (0 to 5%, 5 to 10%, 10 to 15%, 15 to 20%, 20 to 25%, and > 25%) as the "gold standard."

Results

The 30 patients included in our study were evenly split between male and female genders, with mean age and body mass index of 60 ± 15 years and 29 ± 8 k/m2, respectively (Table 1 ). Twenty of the 30 subjects received IV vasoactive medications, and all but one of the subjects were considered hemodynamically stable (with no change in vasoactive medications, or heart rate or BP changes > 10% in the 15-min period before starting the protocol) at the time of investigation. The average mean arterial pressure and heart rate were 78 ± 15 mm Hg and 101 ± 18 beats/min, respectively (Table 2 ).


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  		Table 1. Subject Demographics*

 

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  		Table 2. Baseline Hemodynamic Parameters

 
The average respirophasic {Delta}Vpeak-BA and {Delta}PP were 13 ± 8% and 11 ± 7%, respectively. A tight, linear positive correlation (r = 0.84, Fig 2 ) was observed between the {Delta}Vpeak-BA and {Delta}PP. Using a {Delta}PP cutoff of 13% to predict response to a fluid challenge (Fig 3 ), an optimal {Delta}Vpeak-BA cutoff of 16% was established (area under the receiver operator characteristic curve, 0.947). Test parameters were calculated (Table 3 ), including sensitivity and specificity of 91% and 95%, respectively.


Figure 2
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  		Figure 2. Comparison of pulse pressure variation with bracheal artery peak blood velocity variation.

 

Figure 3
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  		Figure 3. Predicting fluid responsiveness. Predicted favorable response to an IV challenge ("responders") is based on the {Delta}PP cutoff of 13%. Patients with {Delta}PP ≥ 13% were predicted most accurately using a cutoff for {Delta}Vpeak-BA ≥16%, as shown above.

 

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  		Table 3. Test Performance Using {Delta}Vpeak-BA ≥ 16% for the Prediction of Patients With {Delta}PP ≥ 13%

 
The Bland-Altman plot of variance showed excellent agreement between the two parameters (mean difference, – 2.1 ± 4.1%; Fig 4 ) and contingency tables constructed to further analyze the level of agreement between {Delta}Vpeak-BA and {Delta}PP validated this finding (weighted {kappa}, 0.82).


Figure 4
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  		Figure 4. Bland-Altman plot.

 
CVP measurements were available in 17 of the 30 patients (57%), with an average measurement of 10 ± 6 mm Hg. A poor, negative correlation existed between CVP and both {Delta}Vpeak-BA (r = – 0.21) and {Delta}PP (r = – 0.16).

Discussion

Traditional static measures of right- or left-sided cardiac pressures are poorly predictive of changes in cardiac output that occur with VE in patients receiving passive mechanical ventilation.37113435 Studies481112 have demonstrated excellent accuracy for the prediction of fluid responsiveness when using dynamic parameters such as {Delta}PP and {Delta}Vpeak-Ao. However, the acquisition of these parameters has limitations that may be addressed by measuring {Delta}Vpeak-BA with an HCU device.

Traditionally, static measures of preload obtained through a central venous catheter or RHC have been used as guides to fluid resuscitation in hypotensive patients. However, a large number of studies111321222324 in patients with trauma, burns, sepsis, or following cardiac surgery, and even in normal volunteers, show that CVP and pulmonary artery occlusion pressure are no better than a coin toss in predicting fluid responsiveness in patients receiving passive ventilation. Keeping with these observations, CVP correlated poorly with {Delta}PP (r = – 0.16) in our study. This finding reaffirms the disconnect between static and dynamic parameters and re-emphasizes the importance of using dynamic parameters (eg, {Delta}PP or {Delta}Vpeak) to assess fluid responsiveness.

Respirophasic pulse pressure and aortic root velocity variations have been shown to be highly accurate indicators of fluid responsiveness in patients receiving passive mechanical ventilation.1112 Unfortunately, the acquisition of both {Delta}PP and {Delta}Vpeak-Ao has serious limitations. {Delta}PP relies on an indwelling peripheral arterial catheter, which has been associated with infectious and embolic risk.27 In addition, the measurement of {Delta}PP requires a calibrated pressure transducer that is often unavailable in point-of-care settings, including many military trauma units, emergency departments, and initial ICU evaluations. Likewise, aortic velocity variation requires esophageal intubation with an echocardiographic transducer, an invasive and time-consuming intervention. Indwelling probes that measure variations in aortic blood flow have addressed many of the limitations of this technique and allow for continuous monitoring36; however, the utility of these probes is limited by the need for specialized equipment and software to analyze both aortic diameter and blood velocity. In addition, the variation intrinsic to the measurement of both aortic diameter and blood velocity are compounded by this method and may lead to an unnecessary level of error when predicting volume responsiveness.

The use of HCU devices to measure {Delta}Vpeak-BA provides a practical solution to the limitations of both {Delta}PP and {Delta}Vpeak-Ao. Our results demonstrate an excellent correlation and a high level of agreement between the invasively measured {Delta}PP and noninvasively measured {Delta}Vpeak-BA using an HCU device. As we have shown, the learning curve for this technique is sufficiently steep to allow its application by clinicians with only minimal exposure and training in the field. The technique takes advantage of the rapidly expanding field of HCU technology, and offers a new utility for an increasingly useful tool in the field of acute care medicine.

The tight correlation that we have shown between the HCU {Delta}Vpeak-BA and {Delta}PP suggests that the ultrasonographic technique may represent an accurate substitute for the more invasive parameter. A {Delta}Vpeak-BA ≥ 16% is highly predictive of a {Delta}PP ≥ 13%, the well-established cutoff for predicting fluid responsiveness in hypotensive patients receiving passive mechanical ventilation. However, the Bland-Altman analysis has shown that clinically meaningful variation does exist between the two techniques, necessitating the validation of the cutoffs for this technique in a study designed to follow changes in cardiac output with VE.

Soubrier et al37 reported the successful use of {Delta}PP as a predictor of volume responsiveness in spontaneously breathing ICU patients (area under the receiver operating characteristic curve, 0.81). Although the study was limited by a relatively small patient population (n = 32) and reported sensitivity and specificity based on a {Delta}PP of 12% (rather than the established 13% cutoff), the results are promising. The major limitation for the application of this technique to spontaneously breathing patients involves the difficulty of standardizing pleural pressure changes given the potential variation in breath size from patient to patient. Based on the reported results, however, further testing of our method in the spontaneously breathing patient population would be warranted.

Limitations
This study did not evaluate the utility of {Delta}Vpeak-BA as a direct predictor of volume responsiveness, as judged by serial cardiac output evaluations using RHC or serial transthoracic echocardiograms. Serial transthoracic echocardiographic evaluations have accuracy limitations, and publications regarding the utility of indwelling RHC have severely limited its use in our patient population, reducing the pool of eligible patients with RHC for enrollment in studies like this. Instead, we chose to compare our technique with {Delta}PP. Given the excellent performance of this parameter for the prediction of volume responsiveness (PPV, 94%; NPV, 96%), a {Delta}PP ≥ 13% was set as the "gold standard" for predicting which patients could be expected to respond to an IV fluid challenge with an increase in cardiac output ≥ 15%.

Several points must also be made regarding the application of any technique that takes advantage of the respirophasic variations in pulse pressure or blood flow velocity to predict volume responsiveness (eg, {Delta}PP, {Delta}Vpeak-Ao, {Delta}Vpeak-BA). First, these methods are not applicable when there are significant arrhythmias. Since varying respiratory rate intervals affect stroke volume, the impact of the ventilator cannot easily be distinguished from that of the arrhythmia. In addition, the accuracy of these techniques in patients receiving mechanical ventilation has been shown to be dependant on an exaggerated change in pleural pressures resulting from VTs > 8 mL/kg of predicted body weight and PEEP settings from 5 to 10 mm Hg.38 Since many patients receiving mechanical ventilation have acute lung injury and should be receive a VT of 6 mL/kg of predicted body weight, using any of these methods requires a brief ventilator manipulation to temporarily raise the VT. It is important also to ensure that patients receiving mechanical ventilation receive passive ventilation for the period of evaluation, since a standardized inspiratory increment in pleural pressure underlies the physiologic basis for the method. Any active ventilatory effort will alter the resulting pleural pressure change and may affect the accuracy of the test. In the modern era of sedative interruption, lung-protective ventilation, and avoidance of paralytic drugs, most patients are active no matter the ventilatory mode. Until further testing is available to judge the accuracy of this method in the spontaneously breathing patient, care must be taken to ensure that the patient is passive by paying careful attention to the patient, the ventilator waveform display, and any intrathoracic vascular catheter tracings.

Conclusions

Our results have shown that {Delta}Vpeak-BA is an accurate point-of-care correlate to {Delta}PP in patients receiving mechanical ventilation, while CVP is not. In our patient population, {Delta}Vpeak-BA ≥ 16% was highly predictive of a {Delta}PP ≥ 13%, the well-established cutoff for predicting volume responsiveness in patients receiving passive ventilation. In addition, this parameter can be measured by clinicians with limited ultrasound expertise using HCU technology after only a brief period of formal training. The use of this technique as a point-of-care tool for the prediction of fluid responsiveness in those critically ill patients in whom {Delta}PP is either contraindicated or impractical will allow for the more judicious use of IV fluid boluses and potentially a more timely move toward inotropic and vasopressor medications in critically ill patients receiving passive ventilation. Future studies are needed to validate our {Delta}Vpeak-BA cutoff in patients receiving passive ventilation and test the accuracy of this method for the prediction of volume responsiveness in spontaneously breathing, critically ill patients.

Footnotes

Abbreviations: CVP = central venous pressure; HCU = hand-carried ultrasound; NPV = negative predictive value; PCWP = pulmonary capillary wedge pressure; PEEP = positive end-expiratory pressure; PPmax = pulse pressure maximum; PPmin = pulse pressure minimum; PPV = positive predictive value; {Delta}PP = radial artery pulse pressure variation; RAP = right atrial pressure; RHC = right-heart catheterization; VE = volume expansion; {Delta}Vpeak = peak blood flow velocity; {Delta}Vpeak-Ao = aortic blood flow peak velocity variation; {Delta}Vpeak-BA = brachial artery blood flow velocity variation; VT = tidal volume

The authors have no conflicts of interest to disclose.

Received for publication July 15, 2006. Accepted for publication December 14, 2006.

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