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Print version ISSN 0034-7094
On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.57 no.6 Campinas Nov./Dec. 2007
Evaluation of the aorta-to-radial artery pressure gradient in patients undergoing surgery with cardiopulmonary bypass*
Evaluación del gradiente presórico aorto-radial en pacientes sometidos a la intervención quirúrgica con circulación extracorpórea
Maria José Carvalho Carmona, TSAI; Luiz Carlos de Melo Barboza JúniorII; Roberto Yara BuscattiIII; Fábio Antônio GaiottoIV; Alexandre Ciappina HuebV; Luiz Marcelo Sá Malbouisson, TSAVI
Livre-Docente Associada da Disciplina de Anestesiologia da FMUSP; Diretora da
Divisão de Anestesia do Instituto Central do HC-FMUSP
IIAluno da Graduação da FMUSP; Bolsista de Iniciação Científica da FAPESP (Projeto FAPESP 99/11900-3)
IIIBolsista Fundação Zerbini Especialização em Anestesia e Pós-operatório de Cirurgia Cardíaca e Torácica do Instituto do Coração do HC-FMUSP
IVCirurgião Cardíaco; Pós-Graduando do Programa de Pós-graduação em Cirurgia Torácica e Cardiovascular da FMUSP
VDoutor em Ciências pela USP; Médico Assistente da Divisão de Cirurgia do InCor HC-FMUSP
VIDoutor em Ciências pela USP; Especialista em Medicina Intensiva AMIB; Médico Supervisor da UTI-Anestesia do Instituto Central do HC-FMUSP
OBJECTIVES: Several studies have demonstrated a significant difference between
the aortic and radial artery pressures in patients on cardiopulmonary bypass
(CPB). The objectives of this study were to evaluate the behavior of the aorta-to-radial
artery pressure gradient during myocardial revascularization (MR) with CPB and
its correlation with the systemic vascular resistance.
METHODS: After approval by the Ethics Committee of the hospital, 16 patients undergoing MR with hypothermic CPB were studied. Systolic, diastolic and mean blood pressures were obtained at the root of the aorta and in the radial artery by using specific catheters. The cardiac output was obtained using a pulmonary artery catheter or from the CPB equipment, and the systemic vascular resistance index (SVRI) pre-CPB, at the beginning of CPB, after the last MR, at the end of the CPB, and post-CPB was calculated. Statistical analysis was done with Analysis of Variance for repeated measurements and Spearman correlation, and a level of significance of 0.05 was established.
RESULTS: After beginning CPB, the radial artery pressure was systematically lower than the aortic pressure by 3 to 5 mmHg. A significant correlation between the mean aorta-to-radial artery pressure gradient and SVRI was observed only in the last MR, corresponding to the rewarming of the patient (Rho = 0.67, p = 0.009).
CONCLUSIONS: Measurement of the radial artery pressure underestimated, systematically, the arterial pressure at the root of the aorta after CPB and the SVRI did not provide an accurate estimate of the magnitude of the aorta-to-radial artery pressure gradient.
Key Words: MONITORING: aorta-to-radial artery pressure gradient, systemic vascular resistance; SURGERY, Cardiac: cardiopulmonary bypass, myocardial revascularization.
Y OBJETIVOS: Diversos estudios han demostrado diferencia significativa entre
la presión aórtica y la presión radial en pacientes sometidos
a la circulación extracorpórea (CEC). Los objetivos de este estudio
fueron evaluar el comportamiento de la diferencia entre presión arterial
radial y la presión aórtica durante revascularización del
miocardio (RM) con CEC y su correlación con la resistencia vascular sistémica.
MÉTODO: Después de la aprobación por el Comité de Ética hospitalaria, 16 pacientes sometidos a la RM con CEC hipotérmica fueron estudiados. Presiones sistólica, diastólica y media fueron obtenidas en la raíz de la aorta y en la arteria radial, a través de catéteres específicos. Débito cardíaco se obtuvo usando catéter de arteria pulmonar o directamente de la máquina de CEC y Resistencia Vascular Sistémica indexada (RVSi) fue calculada en los momentos pre-CEC, inicio de la CEC, después de la última RM, al final de la CEC y pos-CEC. El análisis estadístico se realizó a través de Análisis de Variancia para medidas repetidas y correlación de orden de Spearman y el nivel de significancia se estableció en 0,05.
RESULTADOS: Después del inicio de la CEC, la presión arterial radial fue sistemáticamente menor que la presión aórtica en 3 a 5 mmHg. Se observó correlación significativa entre el gradiente medio de presión aorto-radial y la RVSi solamente después de la ultima RM, correspondiendo al calentamiento del paciente (Rho = 0,67, p = 0,009).
CONCLUSIONES: La medida de presión en la arterial radial subestimó sistemáticamente la presión arterial en la raíz de la aorta después de la CEC y la RVSi no suministró estimación puntual de la magnitud del gradiente de presión aorto-radial.
Several studies have identified differences between the arterial pressure measured at the root of the aorta and in the radial artery in patients undergoing cardiac surgery, particularly during and after cardiopulmonary bypass (CPB). The etiology of the difference, although controversial, has been attributed to an association between the state of contractility of the peripheral arteries and arterioles, hypothermia and the blood volume of the patient. Some authors have suggested that a reduction in vascular resistance in the upper limb or in the hand, secondary to vasodilation, could be responsible for the aorta-to-radial artery pressure gradient 1-3. On the other hand, Baba et al. and Nakayama et al. reported that the mechanism responsible for the pressure gradient between the aorta and radial artery could be the vasoconstriction/vasospasm related with the cardiopulmonary bypass or vasopressors 4,5. To support this hypothesis, Rich et al. and De Hert et al. observed that the development of this pressure gradient was associated with the beginning of the cardiopulmonary bypass 6,7.
This difference between the pressure measured at the root of the aorta, which determines the perfusion pressure of the body, and the pressure in the radial artery can result in inadequate adjustments in the hemodynamic parameters of patients with compromised cardiovascular function, leading to hypoperfusion and unnecessary increases in myocardial oxygen consumption that could lead to myocardial ischemia. Measurement of the systemic vascular resistance provides an indirect estimate of the arterial and arteriolar vasoconstriction that could be related to the aorta-to-radial artery pressure gradient and, therefore, contribute for a better accommodation of hemodynamic parameters after removal of CPB, minimizing the risk.
The objectives of this study were to evaluate the behavior of the pressure gradient between the radial artery and the root of the aorta before, during, and after hypothermic CPB in patients undergoing surgical myocardial revascularization (MR) and its correlation with the systemic vascular resistance at each moment,
The size of the study population, 16 patients, was determined considering a test power of 95% and a level of significance of 5%. After approval of the research project by the Scientific Commission of the Instituto do Coração and by the Medical Ethics Commission of the Hospital das Clínicas da Faculdade de Medicina da USP, 16 patients undergoing myocardial revascularization with cardiopulmonary bypass were enrolled. Inclusion criteria were: 1) first myocardial revascularization; 2) elective surgery; and 3) absence of peripheral artery disease. Exclusion criteria included: 1) associated surgeries, such as revascularization and change of valve in the same surgery; 2) dissection or prior puncture of the radial artery that supposed to be catheterized during the surgery; 3) presence of aneurysm of the left ventricle; 4) electrocardiographic evidence of important right ventricular dysfunction; 5) infarct-related mechanical complications, such as mitral regurgitation or rupture of the interventricular septum; 6) presence of associated organic dysfunction: 7) left ventricular dysfunction with ejection fraction < 0.35; 8) blunted arterial pressure curve on the monitor or early occlusion of the catheter; and 9) need of mechanical circulatory support with aortic balloon counterpulsation.
Each patient was medicated with oral midazolam, 0.1 to 0.2 mg.kg-1 30 minutes before the surgery. After admission to the operating room, patients were monitored with a cardioscope (DII and V5 derivations) and pulse oximetry with a multiparametric Siemens monitor model SC7000 (Siemens Medical, Berlin, Germany). Venipuncture with a 16G teflon catheter in every patient. To monitor the mean arterial pressure a 20G teflon catheter was introduced in the right radial artery. After confirmation of the proper positioning by the backflow of blood through the catheter, the arterial line was connected to a disposable Edwards TRUWAVE pressure transducer (Edwards Lifesciences, Irvine, CA, USA) with precision of ± 1 mmHg. Calibration was done at ambient pressure, and at the level of the middle axillary line. Induction of anesthesia was accomplished with midazolam, 0.3 to 0.5 mg.kg-1, 20 to 30 µg.kg-1 of fentanyl and 0.1 mg.kg-1 of pancuronium. Anesthesia was maintained with variable concentrations of inhalational isoflurane and supplementary doses of fentanyl. During the CPB, supplementary doses of midazolam and neuromuscular blocker were administered to maintain hypnosis and muscular relaxation. After induction, a pulmonary artery catheter (CCO/SvO2/VIPTM TD catheter, Edwards Healthcare Co., Irvine, CA, USA) was introduced in the right internal jugular vein. An esophageal thermometer and bladder catheter were also introduced after anesthetic induction. Tidal volume was set between 6 and 8 mL.kg-1 and respiratory rate between 10 and 14 inspirations per minute to maintain PaCO2 between 30 and 40 mmHg. Inspiration was set as 33% of the respiratory cycle. Positive end-expiratory pressure was set between 3 and 5 cm H2O to avoid hindering visualization of the surgical field.
After thoracotomy and administration of 500 IU.kg-1 of heparin, an arterial cannula with a lateral luer-lock connection at the proximal end was inserted in the ascending aorta and venous cannulas were introduced in the superior and inferior vena cava. Cardiopulmonary bypass was performed with a non-pulsatile flow under moderate hypothermia using a membrane oxygenator OXI Master Century (Braile, São José do Rio Preto, SP, Brazil), the circuit was filled with Ringer's lactate and 50 g of 20% mannitol. After starting the CPB, the core temperature of the patient was reduced and maintained between 32° and 34°C. The programmed flow of the CPB was 100 mL.kg-1 and was checked directly from the flow meter of the cardiopulmonary bypass equipment corresponding indirectly to the cardiac output of the patient. After the end of the anastomosis, the core temperature of the patient was elevated to 37°C and the cardiocirculatory assistance of the cardiopulmonary bypass equipment was gradually reduced until full return of the physiological circulation. Variable doses of vasoactive and vasodilator drugs were infused to facilitate removal of the CPB. After the end of the surgery, patients were transported to the intensive care unit.
To investigate the impact of the cardiopulmonary bypass and hypothermia on the temporal behavior of the aorta-to-radial artery pressure gradient, immediately after insertion of the cannula in the root of the aorta, the surgeon connected a pressure monitoring device to the lateral connection of the aortic cannula. To collect hemodynamic data, the transducers of radial and aortic pressures, arterial pulmonary pressure, and right atrial pressure were calibrated simultaneously. Hemodynamic data were recorded at the following times: 1) after placement of the aortic catheter, before beginning CPB; 2) before occlusion of the aorta, after cooling the patient to 32°C; 3) after the last anastomosis, with core temperature at 32°C; 4) at the end of CPB, after rewarming the patient to 37°C and before removing the CPB; and 5) 10 minutes after removal of the CPB, after the patient had resumed spontaneous circulation, and after the administration of protamine.
Besides measurement of radial artery and aortic pressures, the systemic vascular resistance index (SVRI) was evaluated. To calculate the SVRI the cardiac index was determined as the mean of three injections of D5W at room temperature (around 21°C) by thermodilution 8,9 pre- and post-CPB. During CPB, the cardiac index was determined from the total flow provided by the CPB equipment. Venous drainage was adjusted in order to obtain a pressure of zero in the right atrium (RAP). The systemic vascular resistance index was calculated according to the following formula:
The normal distribution of the hemodynamic data gathered was determined with the Kolmogorov-Smirnov test. Comparison of the difference of mean and systolic blood pressure, and of the systemic vascular resistance throughout the study was done by Analysis of Variance for repeated measurements. Concordance of the temporal behavior of the aorta-to-radial artery pressure gradient and systemic vascular resistance index was evaluated by the presence of interaction in the two-way analysis of repeated measurements. For this purpose, only the interaction analysis, and not the analysis of intergroup factors (between SVR and aorta-to-radial artery pressure gradient) and intragroup (time), was considered. If interaction were present, i.e., the absence of concordance in the temporal behavior of the parameters, correlation tests among the parameters at different moments were conducted using the Spearman test. The level of significance was set at 0.05 and the correlations were considered significant when the Rho coefficient was greater than 0.5. Data are presented as mean ± SD.
Table I shows the data regarding gender, age, weight, height, and body surface area. Figure 1 shows the behavior of the blood pressure at the different moments of the experiment. As can be observed there was a significant reduction in mean arterial pressure, both at the root of the aorta and in the radial artery, immediately after starting CPB, returning to normal afterwards. As it was expected, there was a significant reduction in body temperature from 35.1 ± 0.8°C to 33 ± 1°C after the institution of the CPB (p < 0.001); temperature brought to normal values (36.6 ± 0.7°C) at the end of CPB, which was maintained after discontinuation of CPB. The mean arterial pressure at the root of the aorta was smaller than in the radial artery in all moments of the study except immediately after the initiation of the CPB (Figure 2). The temporal behavior of the systemic vascular resistance was opposite of the cardiac index (Figure 3). On the other hand, the systemic vascular resistance index showed variations in accordance with the variation of the mean aorta-to-radial artery pressure gradient, except for the final moment, after discontinuation of CPB. However, only after the last anastomosis in the myocardium a significant correlation between the systemic vascular resistance index and the aorta-to-radial artery pressure gradient was observed (Rho = 0.67, p = 0.009) (Figure 4).
The main results of this study were: 1) the mean arterial pressure in the radial artery underestimates the arterial pressure at the aortic root after beginning the CPB; however, this difference is approximately 3 to 5 mmHg; 2) a consistent correlation between the aorta-to-radial artery pressure gradient and the vascular systemic resistance index after beginning cardiopulmonary bypass was not observed.
Invasive monitoring of the radial artery pressure is routinely done in patients undergoing cardiac surgery with cardiopulmonary bypass, due to the need of real-time control of the perfusion pressure, the catheter is easily inserted and the incidence of complications is low. Based on the radial artery pressure, vasopressors or vasodilators are prescribed to adjust the systemic vascular resistance and to maintain adequate balance between the greater cardiac output possible and the perfusion pressure. In this specific population of patients undergoing cardiac surgery with hypothermic cardiopulmonary bypass, several studies have demonstrated a discrepancy between the radial artery pressure and the pressure at the aortic root 6,10-12, which could contribute for the inadequate hemodynamic management; this can lead to an inappropriate increase in myocardial oxygen consumption when the radial pressure underestimates the aortic pressure or tissue hypoperfusion in patients whose radial artery pressure is greater than the aortic pressure 6,11. In this study, it was observed that, after beginning CPB, the mean arterial pressure at the root of the aorta was smaller than in the radial artery by a mean of 1.2 mmHg. This gradient was inverted in posterior moments, in which the mean aortic pressure was 3 to 5 mmHg greater than the mean radial artery pressure. In situations in which high concentrations of vasopressors are needed, this gradient might be even greater.
Due to the lack of accuracy of the pressure measured in the radial artery to reflect the pressure at the root of the aorta, other indices, such as systemic vascular resistance could, in theory, provide estimates of the degree of difference between the aortic and radial artery pressures during and after the hypothermic phase of the CPB and provide more adequate evaluations for the hemodynamic adjustments necessary. Despite the temporal behavior of the SVRI being in agreement with the aorta-to-radial artery pressure gradient in most moments, as can be observed in figure 3, the correlation between the systemic vascular resistance and the aorta-to-radial artery pressure gradient was observed only after the last anastomosis in the myocardium, when the patient was being rewarmed and receiving vasoactive drugs. The systemic vascular resistance calculated through invasive hemodynamic measurements at the bedside with intravascular catheters is computed as the ratio between the radial artery-to-right atrium pressure gradient and the systemic flow, reflecting mainly the impedance promoted by the arteriolar microcirculation and the venous bed to the blood flow. The absence of correlation suggests that other factors besides the resistive arteriolar and venous components might contribute to the genesis of the aorta-to-radial artery pressure gradient. However, besides this resistive microvascular circulatory component after beginning CPB, other factors also seem to be related with the modulation of pressure transmission in the arteries, which does not allow interferences from the magnitude of the aorta-to-radial artery pressure gradient from the SVRI.
Several mechanisms have been proposed to explain the aorta-to-radial artery pressure gradient in patients undergoing CPB, and hypothermia, hemodynamic instability, change from pulsatile to continuous non-pulsatile blood flow, and the variation in the caliber of the great vessels due to a change in arterial elasticity induced by the CPB or by high doses of vasomodulator drugs are mentioned more often. Immediately after beginning CPB, the radial artery pressure was slightly higher than the pressure in the aortic root. At this moment there is severe hemodilution due to the 2 liters of Ringer's lactate added to the circulation, causing an abrupt reduction in hematocrit and consequent reduction in blood viscosity and systemic vascular resistance 13, which could compensate the vasoconstriction induced by hypothermia and release of inflammatory mediators during CPB 6,7. During the CPB, great part of the crystalloid in the perfusate leaks to the extravascular space as a consequence of the systemic inflammatory reaction induced by the CPB 14, which might increase the hematocrit and blood viscosity, contributing to the increase in vascular resistance in the smaller arteries, which would justify the beginning and maintenance of the aorta-to-radial artery pressure gradient at 3 to 5 mmHg, even after discontinuation of the CPB 16. On the other hand, De Hert et al. did not observe a correlation between the magnitude of the pressure gradient and the changes in the hematocrit and blood temperature in 68 patients 7. Another factor possibly associated with the genesis of the aorta-to-radial artery pressure gradient is the caliber of the large arteries. Studying 12 patients undergoing cardiac surgery with CPB, Kanazawa et al. observed that 7 patients had an aorta-to-radial artery pressure gradient greater than 10 mmHg after CPB 12. This reduction in radial artery pressure in relation to the aortic pressure was associated with a progressive reduction in the velocity of the pulse wave towards the periphery. Using the equation proposed by Moens-Korteweg to calculate the arterial elasticity based on the velocity of the pulse wave16, those authors observed a reduction in elasticity that could lead to a dampening of the pulse wave and of the arterial pressure at the level of the radial artery, thus explaining the aorta-to-radial artery pressure gradient 12. This change in vascular tone could be secondary to the release of vasoactive substances, commonly observed after beginning CPB 14. Finally, anatomical changes, such as arterial atheromas, could contribute to the reduction in radial artery pressure in relation to the aortic pressure. Due to the inversion of the pressure gradient immediately after beginning CPB, suggesting the absence of arterial stenosis, the presence of anatomical alterations does not seem to be an important contributing factor for the genesis of the aorta-to-radial artery pressure gradient in the present study. In cases in which the condition of the radial artery might be an important factor in the genesis of the pressure gradient, monitoring could be done by puncturing the brachial or femoral artery 17.
To conclude, the radial pressure underestimated systematically the pressure at the root of the aorta after the beginning of hypothermic cardiopulmonary bypass in patients undergoing myocardial revascularization and this pressure gradient was between 3 and 5 mmHg. Although small, this difference can lead to inappropriate or even harmful management conducts. Systemic vascular resistance does not provide an accurate estimate of the magnitude of the aorta-to-radial artery pressure gradient, and this difference of 3 to 5 mmHg between the aortic and radial artery pressures should be considered when making therapeutic decisions in patients undergoing myocardial revascularization with hypothermic CPB.
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Dra. Maria José Carvalho Carmona
Divisão de Anestesia do ICHC
Av. Enéas Carvalho de Aguiar, 255, 8° andar Cerqueira César
05403-900 São Paulo, SP
Submitted em 27
de novembro de 2006
Accepted para publicação em 21 de agosto de 2007
* Received from Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP), São Paulo, SP