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Risk Factors Involved in Central-to-Radial Arterial Pressure Gradient During Cardiac Surgery

Fuda, Giuseppe MD; Denault, André MD, PhD; Deschamps, Alain MD, PhD; Bouchard, Denis MD; Fortier, Annik MSc; Lambert, Jean PhD; Couture, Pierre MD

doi: 10.1213/ANE.0000000000001096
Cardiovascular Anesthesiology: Research Report
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BACKGROUND: A central-to-radial arterial pressure gradient may occur after cardiopulmonary bypass (CPB), which, in some patients, may last for a prolonged time after CPB. Whenever there is a pressure gradient, the radial artery pressure measure may underestimate a more centrally measured systemic pressure, which may result in a misguided therapeutic strategy. It is clinically important to identify the risk factors that may predict the appearance of a central-to-radial pressure gradient, because more central sites of measurements might then be considered to monitor systemic arterial pressure in high-risk patients. The objective of this study was to assess preoperative and intraoperative risk factors for central-to-radial pressure gradient.

METHODS: Seventy-three patients undergoing cardiac surgery using CPB were included in this prospective observational study. A significant central-to-radial arterial pressure gradient was defined as a difference of 25 mm Hg in systolic pressure or 10 mm Hg in mean arterial pressure for a minimum of 5 minutes. Preoperative data included demographics, presence of comorbidities, and medications. Intraoperative data included type of surgery, CPB and aortic clamping time, use of inotropic drugs, and vasodilators or vasopressors agents. The diameter of the radial and femoral artery was measured before the induction of anesthesia using B-mode ultrasonography.

RESULTS: Thirty-three patients developed a central-to-radial arterial pressure gradient (45%). Patients with a significant pressure gradient had a smaller weight (71.0 ± 16.9 vs 79.3 ± 17.3 kg, P = 0.041), a smaller height (162.0 ± 9.6 vs 166.3 ± 8.6 cm, P = 0.047), a smaller radial artery diameter (0.24 ± 0.03 vs 0.29 ± 0.05 cm, P < 0.001), and were at a higher risk as determined by the Parsonnet score (30.3 ± 24.9 vs 17.0 ± 10.9, P = 0.007). In addition, a longer aortic clamping time (85.8 ± 51.0 vs 64.2 ± 29.3 minutes, P = 0.036), mitral and complex surgery (P = 0.007 and P = 0.017, respectively), and administration of vasopressin (P = 0.039) were identified as potential independent predictors of a central-to-radial pressure gradient. By using multivariate logistic regression analysis, the following independent risk factors were identified: Parsonnet score (odds ratio [OR], 1.076; 95% confidence interval [CI], 1.027–1.127, P = 0.002), aortic clamping time >90 minutes (OR, 8.521; 95% CI, 1.917–37.870, P = 0.005), and patient height (OR, 0.933, 95% CI, 0.876–0.993, P = 0.029). The relative risk (RR) estimates remained statistically significant for the Parsonnet score and the aortic clamping time ≥90 minutes (RR, 1.010; 95% CI, 1.003–1.018, P = 0.009 and RR, 2.253; 95% CI, 1.475–3.443, P < 0.001 respectively) while showing a trend for patient height (RR, 0.974; 95% CI, 0.948–1.001, P = 0.058).

CONCLUSIONS: Central-to-radial gradients are common in cardiac surgery. The threshold for using a central site for blood pressure monitoring should be low in small, high-risk patients undergoing longer surgical interventions to avoid inappropriate administration of vasopressors and/or inotropic agents.

Published ahead of print November 23, 2015

From the Departments of *Anesthesiology and Cardiac Surgery, Montreal Heart Institute, Université de Montréal, Montreal, Quebec, Canada; Coordinating Center, Montreal Heart Institute, Montreal, Quebec, Canada; and §Department of Preventive and Social Medicine, Université de Montréal, Montreal, Quebec, Canada.

Accepted for publication September 20, 2015.

Published ahead of print November 23, 2015

Funding: Montreal Heart Institute Foundation.

The authors declare no conflicts of interest.

Reprints will not be available from the authors.

Address correspondence to Pierre Couture, MD, Department of Anesthesiology, Montreal Heart Institute, 5000 Bélanger St., Montreal, QC, Canada H1T 1C8. Address e-mail to pierre.couture@icm-mhi.org.

Direct intraradial arterial pressure monitoring is routinely used in cardiac surgery; however, a central-to-radial arterial pressure gradient may occur after cardiopulmonary bypass (CPB), which, in some patients, may last for a prolonged period, varying from 10 minutes after discontinuation of CPB1 to sternal closure.2 Whenever there is a pressure gradient, the radial artery pressure measure may underestimate a more centrally measured systemic pressure, which may result in a misguided therapeutic strategy.1

Since the first mention of this phenomenon by Stern et al.,1 numerous reports have described a central-to-radial arterial pressure gradient, and the reported incidence varies from 10% to 72%, depending on the definition used.1–22 Although the etiology leading to central-to-radial artery pressure gradient has been studied extensively, its exact mechanism is still controversial and is probably multifactorial.1–3,6,8,17,20

Despite the many studies published on the subject, the data investigating the risk factors that may predict the appearance of a central-to-radial pressure gradient are few. In addition, the natural intraoperative evolution of the gradient is unknown. This is clinically important because the insertion of a femoral artery catheter to monitor systemic arterial pressure may be considered in patients found to be at high risk of developing a central-to-radial arterial pressure gradient. We hypothesized that several risk factors could be identified in cardiac surgery patients who develop central-to-radial arterial pressure gradient during the intraoperative period.

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METHODS

This prospective observational study was approved by the IRB and Research Ethics Committee and conducted in accordance with the Declaration of Helsinki. Seventy-three patients undergoing coronary artery bypass graft surgery (CABG), valve surgery, or both procedures were included in the study that took place between March 2007 and April 2008. No prestudy power analysis was performed. After 13 months, the department elected to terminate this exploratory study and analyze the data. Only patients in whom a radial artery catheter and a femoral artery catheter were simultaneously placed for systemic pressure monitoring were included. The decision to use radial artery and femoral artery pressure monitoring was left to the clinical judgment of the anesthesiologist and cardiac surgeon; this decision generally depends on the complexity of the surgical intervention, the health status of the patient, and the anticipated length of CPB and aortic clamping. More than half of the anesthesiologists in our institution routinely use simultaneous radial and femoral artery pressure monitoring. Informed consent was waived because of the observational nature of the study.

Preoperative data were collected immediately after the decision to use both radial and femoral catheters and included demographics (age, gender, weight, height, body surface area [BSA], and body mass index), presence of comorbidities (left ventricular dilation, left ventricular hypertrophy, hypertension, diabetes, unstable angina, previous myocardial infarction, and peripheral vascular disease), Parsonnet score, and concurrent medications. The following intraoperative data were collected: type of surgery (CABG), valvular surgery, or complex surgery (combined CABG and valve surgery, or >1 valve surgery with or without CABG), CPB time, aortic clamping time, use of inotropic drugs, and use of vasodilators or vasopressor agents. Values of pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), and cardiac output (CO) were collected before and after CPB. Central temperature was recorded at each time period. We routinely measure hemoglobin and lactate levels before CPB, 20 minutes after the beginning of CPB, 10 minutes after the end of CPB, and at sternal closure; these data were collected.

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Protocol

The monitoring used included a 5-lead electrocardiogram, pulse oximeter, a radial arterial line (Angiocath 20 GA, 1.1 × 48 mm, Becton Dickinson, Sandy, UT), a central venous 15-cm 3-lumen catheter (CS-12703, Arrow International Inc., Reading, CA), and a pulmonary artery catheter (Swan-Ganz catheter 7.5 Fr; Baxter Healthcare Corporation, Irvine, CA). Before the insertion of the radial arterial line, the radial artery diameter was measured using B-mode ultrasonography with a 12-MHz probe (Vivid 7, GE Healthcare System, Milwaukee, WI) and based on an inner edge to inner edge measurement. The femoral artery catheter (4F, 11 cm, Cordis Corporation, Miami Lakes, FL) was placed after the induction of general anesthesia under ultrasonography with a 12-MHz probe (Vivid 7, GE Healthcare System), as is routinely done in our institution. The diameter of the femoral artery was also measured by ultrasonography. The radial and femoral arterial pressures were measured with a disposable pressure transducer (Edwards Lifesciences, Irvine, CA) and a 72-inch fluid filled low compliant tubing. The mid-axillary level was used as the zero point. The dynamic characteristics of the catheter–transducer system were determined by using the fast-flush technique.23

Anesthesia was induced with 0.04 mg/kg midazolam and 1 μg/kg sufentanil, and muscle relaxation was achieved with rocuronium. After tracheal intubation, anesthesia was maintained with 1 μg/kg/h sufentanil, 0.04 mg/kg/h midazolam, and 30–50 μg/kg/min propofol. Isoflurane was administered in every patient, and the concentration used was left to the discretion of the attending anesthesiologist. The lungs were ventilated by intermittent positive-pressure ventilation with a 0.8 inspired oxygen fraction by use of an Ohmeda volume-cycled ventilator (Ohmeda, Helsinki, Finland), with a respiratory rate of 8 breaths/min, a tidal volume of 7 to 8 mL/kg, and an inspiratory/expiratory ratio of 1:2. Fluid and medications were administered as needed according to the patient’s clinical status. A 5.0-MHz TEE omniplane probe (Vivid 7, GE Healthcare System) was inserted after induction of general anesthesia.

On insertion and before removal of the aortic cannula, the central aortic pressure was noted. Blood cardioplegia was used in all patients. Induction and maintenance of cardioplegia were at the same temperature as the CPB perfusate (32°C –34°C). The blood to crystalloid ratio was 4:1. The crystalloid cardioplegic solution consisted of lactated Ringer’s solution containing either 80 mmol (high) or 32 mmol (low) of potassium. The pump flow was adjusted to obtain an output of 2.2 L/min/m2 of BSA and was reduced to 0.5 L/min/m2 for aortic clamping and unclamping. SIII (Stockert, Munich, Germany) roller pumps were used in all patients. The oxygenator was Sorin Monolyth (Mirandola, Italy). Each valvular procedure was done with temperatures of 32°C to 34°C. For CABG procedures, temperature was allowed to drift to 34°. Weaning from CPB was attempted after systemic temperature (central and bladder) reached 36°.

Different definitions of central-to-radial pressure gradient have been used in the literature, varying from 5 to 10 mm Hg for mean arterial pressure or 10 mm Hg for systolic arterial pressure.4,6,14,17–19 In our study, clinically significant central-to-radial arterial pressure gradient was defined as a difference of 25 mm Hg for systolic pressure or 10 mm Hg for mean arterial pressure between femoral and radial artery pressures for a minimum duration of 5 minutes at any point before, during, and after CPB. We used this criterion because we considered this pressure gradient to be more clinically significant, which may lead to a change in therapeutic management. The same investigator measured radial-femoral pressure gradients after anesthetic induction, immediately before and immediately after CPB was initiated, at 5, 10, 20, and 40 minutes after beginning CPB, immediately after separation from CPB, at 5, 10, 20, and 40 minutes after discontinuation of CPB, and after sternal closure. An automated anesthesia information management system was not used at the time of the study.

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Statistical Analysis

Continuous variables are presented as mean ± SD, and categorical variables are presented as frequency (percentages). Analyses were performed to determine whether there were significant differences between the presence or absence of significant femoral-radial arterial pressure gradient groups in terms of baseline characteristics, preoperative and post-CPB medication, and intraoperative variables. These differences were tested using Student t test for continuous variables; χ2 test and Fisher exact test were used for categorical parameters. The value of these differences and their 95% confidence intervals are also presented. Repeated measures analysis of variance modeling was used to compare the 2 groups regarding the evolution of systolic and mean radial-femoral pressure gradient values during the intraoperative period (model effects: group, time, group × time interaction; time as repeated factor). This type of analysis was also used to study the difference between aortic and femoral pressure (systolic and mean) in the 2 groups (model effects: group, artery, group × artery interaction; artery as repeated factor) and to compare the 2 groups with respect to the evolution of PCWP, CVP, and CO from pre-CPB to post-CPB (model effects: group, time, group × time interaction; time as repeated factor). We also sought to identify the predictors of presence of a significant gradient using univariate and multivariate logistic regressions. Because of the small number of patients in each of the 2 groups (absence/presence of gradient), only parameters with P < 0.05 in univariate logistic regression were selected to be used in the multivariate model. Backward selection process was used to determine which variables would stay in the final multivariate model, and forward selection process was used as sensitivity analysis. When linearity between independent variables and logit was not satisfied, transformation or categorization of independent variables was done. For aortic clamping time, dichotomic categories were used; clamping time <90 minutes and clamping time ≥90 minutes. More than 90 minutes was considered clinically significant for prolonged aortic clamping time. Given that the incidence of the outcome exceeds 10%, relative risks were calculated using a modified Poisson regression model with robust error variance to better estimate, comparing with odds ratio, the effect of the independent predictors. Finally, logistic regression model validation was done using the jackknife variance estimation method. For all tests, a P < 0.05 was considered statistically significant. According to the exploratory/observational nature of this study, no correction was used to account for the multiple statistical tests. Statistical analysis was performed using SAS 9.3 (SAS Institute Inc., Cary, NC).

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RESULTS

Patients were classified according to the presence or absence of a significant femoral-radial arterial pressure gradient at any time during the intraoperative period.

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Patient Characteristics

Table 1

Table 1

Table 2

Table 2

Of the 73 patients studied, 33 developed a femoral-radial arterial pressure gradient in the intraoperative period (45%). Of these 33 patients, a femoral-radial arterial pressure gradient was first observed immediately before CPB in 3 patients, during CPB in 22 patients, and after separation from CPB in 8 patients. Thirty-one patients (42%) had CABG or single-valve surgery, and 42 patients (58%) underwent a complex procedure (CABG and valve surgery or >1 valve surgery). Patients with a significant radial-femoral pressure gradient had a smaller weight (P = 0.041), a smaller height (P = 0.047), a smaller BSA (P = 0.025; Table 1) and were at higher risk as determined by their Parsonnet score (P = 0.007; Table 1). Furthermore, patients with a significant gradient had a smaller radial artery diameter before anesthetic induction as measured using B-mode ultrasonography (P < 0.001; Table 1). The height of the patient was positively correlated with the radial artery diameter (r = 0.289, P = 0.013). No difference in preoperative medication was found between the 2 groups (Table 2).

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Intraoperative Data

Table 3

Table 3

Intraoperative factors associated with a radial-femoral artery pressure gradient include a longer duration of aortic cross-clamping (P = 0.036) and the type of surgery (mitral surgery and complex surgery, P = 0.007 and P = 0.017, respectively; Table 3). More patients with a radial-femoral gradient received IV vasopressin during the intraoperative period (P = 0.039; Table 3).

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Predictors of a Significant Central-to-Radial Arterial Pressure Gradient

Table 4

Table 4

Table 5

Table 5

A multivariate logistic regression analysis identified the Parsonnet score (P = 0.002), duration of aortic clamping (P = 0.005), and patient height (P = 0.029) as independent risk factors for the development of radial-femoral pressure gradient (Table 4). Because the incidence of the outcome (radial-femoral pressure gradient) exceeds 10%, the relative risk estimates are also provided in Table 4. The relative risk estimates remained statistically significant for the Parsonnet score and the aortic clamping time (P = 0.009 and P < 0.001, respectively), whereas the relative risk estimate of height, although showing a trend (P = 0.058), did not reach the statistical significance level. These findings were supported by the results of the multivariate logistic regression model validation using jackknife variance estimation method. This model validation identified the Parsonnet score (P = 0.012) and the duration of aortic clamping (P = 0.008) as independent risk factors and concluded that height was no longer statistically significant, although it was close (P = 0.051). Predictors of the presence of a significant gradient are summarized in Table 4, and model validation data are presented in Table 5.

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Intraoperative Evolution of the Central-to-Radial Arterial Pressure Gradient

The changes in systolic and mean radial-femoral gradient during the intraoperative period are shown in Figures 1 and 2. For the 2 types of pressure, the interaction term of the repeated measures analysis of variance models showed that the change in gradient during the intraoperative period did not follow the same pattern in the 2 groups (systolic: P < 0.001; mean: P = 0.008). There was no significant difference in systolic and mean radial-femoral pressure immediately after the induction of anesthesia. However, significant radial-femoral systolic and mean pressure gradients were already present immediately before the beginning of CPB (P = 0.008 and P = 0.003, respectively). These gradients increased after the beginning of CPB, reaching a maximal value 40 minutes after the beginning of CPB for the mean radial-femoral gradient and 5 minutes after the end of CPB for the systolic gradient. Thereafter, both mean and systolic radial-femoral pressure gradients decreased until sternal closure but remained significantly high. In the group with a pressure gradient, 12 patients (14%) still had a systolic radial-femoral pressure gradient >25 mm Hg or a mean gradient >10 mm Hg at sternal closure. Table 6 shows the values of systolic and mean central aortic and femoral pressures at the beginning and immediately after the end of CPB. There was no difference between central aortic and femoral systolic pressures between groups (interaction term: P = 0.97) before CPB and immediately after the end of CPB. This pattern was also observed for the central aortic and femoral mean pressures.

Table 6

Table 6

Figure 1

Figure 1

Figure 2

Figure 2

Table 7

Table 7

Table 8

Table 8

There was no difference between PCWP, CVP, and CO in the 2 groups before and after CPB (Table 7), and no difference was found in the number of patients receiving inotropic agents or vasopressors at CPB separation except for vasopressin (Table 8). There was no significant difference in central temperature in patients with or without radial-femoral gradient during the intraoperative period (interaction term: P = 0.953). There were also no significant differences in hemoglobin or lactate levels between patients with or without radial-femoral gradient (interaction term: P = 0.958 and 0.209, respectively).

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DISCUSSION

A significant central-to-radial arterial pressure gradient was common in our population, occurring in 45% of patients during the intraoperative period. The gradient’s appearance is dynamic, which might explain why intermittent measurement may lead to such variability in the reported prevalence. In patients who developed a gradient, none was observed after the induction of anesthesia, but a small gradient appeared immediately before CPB, increased after the beginning of CPB, reaching maximal values near its end for the mean gradient and 5 minutes after its end for systolic gradients. Although decreasing thereafter, the radial-femoral pressure gradient remained statistically greater in the group with a gradient compared with the group without a gradient. In the group with a pressure gradient, 12 patients (14%) still had a systolic radial-femoral pressure gradient >25 mm Hg or a mean gradient >10 mm Hg at sternal closure. In these patients, the measurement of radial artery pressure often underestimates the more centrally measured systemic pressure, which may result in a misguided vasoactive treatment.1 Consequently, it is important to identify the risk factors to predict the occurrence of a central-to-radial pressure gradient.

In our study, we found that smaller patients were predisposed to develop a radial-femoral pressure gradient. Another variable associated with the appearance of a pressure gradient was a higher Parsonnet score, a scoring system for predicting risk in cardiac surgery,24 suggesting a multifactorial etiology for the development of pressure gradients, increasing with the severity of patient- and surgery-related factors. Furthermore, a longer duration of aortic cross-clamping was also associated with the appearance of the gradient. In the validation model, we found that Parsonnet score and aortic clamping time remained significant predictors of a central-to-radial arterial pressure gradient. Although the height was not an independent predictor of a pressure gradient in the test set, it was close to reaching statistical significance.

This study does not provide a physiologic explanation for the inverse relationship between the height of the patient and the central-to-radial pressure gradient. Normally, radial systolic arterial pressure is higher than aortic systolic pressure in awake patients.20,25 This central-to-radial pulse amplification has been attributed to pressure wave transmission and peripheral wave reflection and depends on the gradual stiffening of the central elastic toward the peripheral muscular arteries. Hashimoto and Ito25 observed a reversed stiffness pattern in hypertensive patients and attributed it to an increase in aortic stiffness in shorter patients with smaller femoral artery diameters. Kanazawa et al.20 also documented a reverse stiffness pattern in patients developing an aortic-radial pressure gradient after CPB. We speculate that a short stature with smaller arteries may be a predisposing factor for developing a central-to-radial pressure gradient through an exacerbation of the reverse stiffness pattern between the aorta and the peripheral artery.

A higher Parsonnet score was an independent factor associated with the appearance of a significant central-to-radial pressure gradient. The Parsonnet score is a multifactorial scoring system24 combining patient- and surgery-related factors, and this score indicated here that sicker patients undergoing valvular or complex surgery were at more risk of developing a pressure gradient. Many patient-related factors included in the Parsonnet score,24 such as the presence of diabetes, hypertension, and age, may contribute to a change in aortic stiffness, which may in turn have an additive effect to short stature for the development of pressure gradient during CPB.

We also found that prolonged aortic clamping time was an independent predictor for the development of a central-to-radial pressure gradient. Our finding that femoral-radial pressure gradients reached their maximal values at the end of CPB is in agreement with this association. In contrast, de Hert et al.11 did not find such an association with aortic clamping time; however, they studied patients undergoing CABG with only short CPB and aortic cross-clamping times.

Previous studies have suggested various mechanisms to explain the appearance of central-radial pressure gradients.1–22 The hemodilution and decrease in viscosity associated with the initiation of CPB might be expected to lead to a reduction in peripheral resistance arteries and could decrease the radial arterial pressure.11,26 A decrease in hand vascular resistance and/or forearm vascular resistance1,6 has also been proposed to explain the aortic-radial pressure gradient and may be triggered by the initiation of CPB and hemodilution. Baba et al.2 suggested radial vasoconstriction2 as the etiology for central-radial pressure gradient. Our finding that patients with a significant gradient received more vasopressin is in favor of a contributing role for arterial vasoconstriction in some patients. The administration of vasodilators has also been found to intensify the magnitude and duration of the pressure gradient,8 although we did not observe such an association. Taken together, these explanations suggest a multifactorial etiology for central-to-radial pressure gradient. A given patient may present predisposing factors, resulting in a pressure gradient induced by the initiation of CPB, increasing with the duration of aortic clamping, with a possible effect of rewarming14 and which may be influenced by the administration of vasoconstrictor agents.

There are alternative methods that can be used to detect a central-to-radial arterial pressure, including the direct measure of aortic pressure using a 22-gauge needle when the sternum is open. A standard blood pressure cuff on the arm or leg may also be used, but its value compared with a central arterial pressure measurement has not been determined. In patients presenting with mitral regurgitation documented by transesophageal echocardiography, and in whom a pulmonary artery is also used, the central systolic arterial pressure should be approximated by adding the PCWP to the pressure gradient value between the left atrium and the left ventricle (measured with a continuous Doppler of the mitral regurgitation).27 If a pressure gradient is documented, a femoral catheter can be then inserted during the surgery.

Our study has the following limitations. Even though this study was a prospective observational study, we elected to assess only patients in whom a radial artery catheter and femoral artery catheter were simultaneously placed. Moreover, this decision was left to the judgment of the anesthesiologist and surgeon and generally depended on the complexity of the surgical procedure, health status of the patient, and anticipated duration of CPB and aortic clamping. Consequently, there is a bias in the recruitment criteria. However, the development of radial-to-femoral gradient in sicker patients undergoing more complex surgeries has not yet been reported, and this has allowed us to identify new predicting risk factors. These findings may not be generalized to lower risk groups. In addition, given the observational nature of this study, chance association may have occurred. Also, femoral-radial artery pressure gradient was arbitrarily defined as a difference of 25 mm Hg for systolic pressure and 10 mm Hg for mean arterial pressure for a minimum duration of 5 minutes. This pressure gradient definition was higher than in other studies, where it usually varies between 5 and 10 mm Hg for mean arterial pressure or 10 mm Hg for systolic arterial pressure.4,6,14,17–19 We used this criterion because we considered this pressure gradient to be more clinically significant, which may lead to a change in therapeutic management. However, even with our definition, the incidence of central-to-radial pressure gradient is still high in this current population, with an incidence of 45%. It is also worth noting that the observation of gradients of this magnitude also decreases the chance of bias by the investigator. The use of an electronic anesthesia record system would have eliminated any inaccuracy in data collection and improved the documentation of the time course of the gradient; unfortunately, this was unavailable at the time of the study. However, we believe that the risk factors identified for pressure gradients remain valid.

Although we identified many predicting risk factors, we did not investigate the mechanisms responsible for the occurrence of a radial-femoral pressure gradient and can, therefore, only speculate as to the role of the various factors. Moreover, we monitored femoral artery pressure to evaluate a more central systemic blood pressure, because it has a good correlation with aortic pressure during cardiac surgery,4 as we have observed. The risks associated with the placement of a femoral artery catheter are equivalent to radial artery catheter insertion28 and are approximately 1% with the standard palpation technique.29 The complication rate may be reduced with the use of ultrasound-guided puncture of the femoral artery.30 Although the institution of vasopressors or inotropic therapy when not needed can be potentially harmful, there is no evidence in the literature to the effect that the gradient actually poses harm to the patient. Consequently, a risk–benefit analysis of radial/femoral artery catheterization should be performed, particularly for lower risk patients. Finally, we found that an actual cross-clamping time of >90 minutes was an independent predictor for the development of a central-to-radial arterial pressure gradient. However, because this information is not known at the time the decision is made to place a femoral arterial catheter, the anticipated aortic clamping time should be used as a function of surgeon and procedures. This approach has not been well studied for aortic clamping time and deserves further investigation.

In conclusion, the occurrence of a significant central-to-radial arterial pressure gradient is common during cardiac surgery. These gradients are dynamic. They increase after the beginning of CPB, reaching their maximal values at the end of CPB. Smaller patients, as well as those identified as being at higher perioperative risks according to their Parsonnet score, or those undergoing procedures with a long aortic clamping time, were found to be at risk of developing a central-to-radial pressure gradient. Knowing the risk factors for the development of a central-to-radial arterial pressure gradient is important because it may increase the level of suspicion so that more central sites of measurements could be considered, either at the beginning of the surgery or later during the operation.

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DISCLOSURES

Name: Giuseppe Fuda, MD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Giuseppe Fuda approved the final manuscript.

Name: André Denault, MD, PhD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: André Denault attests to the integrity of the original data and the analysis reported in this manuscript and approved the final manuscript.

Name: Alain Deschamps, MD, PhD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Alain Deschamps approved the final manuscript.

Name: Denis Bouchard, MD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Denis Bouchard approved the final manuscript.

Name: Annik Fortier, MSc.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Annik Fortier approved the final manuscript.

Name: Jean Lambert, PhD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Jean Lambert approved the final manuscript.

Name: Pierre Couture, MD.

Contribution: This author helped design the study, conduct the study, collect the data, analyze the data, prepare the manuscript, and is the archival author.

Attestation: Pierre Couture attests to the integrity of the original data and the analysis reported in this manuscript and approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.

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ACKNOWLEDMENTS

The authors thank Denis Babin and Antoinette Paolitto for their help in preparing the manuscript.

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REFERENCES

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