Pulmonary vascular resistance and right ventricular function in morbid obesity in relation to gastric bypass surgery

ELSEVIER

Pulmonary Vascular Resistance and Right Ventricular Function in Morbid Obesity in Relation to Gastric Bypass Surgery Mitsuru Nakatsuka, MD* Department of Anesthesiology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia Study Objective: To inuestigatp right ventricular function (Rw) during gastric Dypass surg9 in morbidly obese patients. To study thr injluencv of obstructiur slerp apnea syndromr on hemodynamirs and Rw as a preoperative rvaluation in morbidly 00~s~ paticxts. Design: Prosprrtive study. Setting: Surgical patients at a univwsity hospital. Patients: 14 morbidly obesepatients undrrgoing gusttic bypass surgery. Interventions: Hemodynamir chan,gesand RVF were investigated using a thermodilution q’ertion fraction volumettic rathetPr and the RXF-1 computer. Measurements and Main Results: Hpmodynamir paramrtws and RVF werp measured: (1) before induction qf anesthesia, awake, (2) after induction of anesthcGa, (3) uftw opening the abdomm, and (4) after closing thP abdomen. Esophagpnl prpssure was measured in thr midesophaLgus qfter induction of anesthesia with a (amino cath&r and its device. Morbidly obesepatients with obstructivr sleep apnua syndrome had sipijicant~ lower PaO,, higher PaCO,, and highw pulmonaqj avte? (PA) pres.yurp and pulmorq vascular r&stance (PI/R) comfiarud with patients without S&I apnea (p < 0.05). Ho~urzq thrrp WPTPno siffn~jirant diff prpnrfs in heart rat?, mPan blood ppssure, pulmona? capillaq wpdgp pressure (PCWT), tight umtricular Pjrction frartion (RVTF), an,d right v&rirular Pntl-diastolic volume. During gastric bypass prorrdurp, PA @ssurp, PCWP, and PVR drrymsed si~pificantly after opening thP abdomen (p c 0.05). Thprr 7um no s&n@ant rhanges in RVEF and rardiac indtx dum’ng cgastric bypass prorpdure. Conclusion: The prrspnrr of chronic hy@xpmia and hyp~rcarbin in our morbidly obps_(p patirnts with obstrurtive SIPQ~ apncz .syndromPwhile awake, rausrs .signijir‘ant inrrmsrs in PA prpssun and PVR. WQ (~1.~0dPmonstratrd that RVKF did not change .si~qnifirantly during gastrir bypass proradurr despitr sicpifit.ant drrrmsccs in PA pssurr, PCWP, and PVR aftu opning thP abdomm. This drcrpasr in PA fjrcssurp and PVR may bp cnusrd tjy dpcrmsrs in @urn1 prpssurp [email protected] by a ronromitant drrrm.rr in Psophagtal f)rrs.sur~.

+Associate Professor Address reprint requests to Dr. Nakatsuka at the Department of Anesthrsiolo
Keywords: Esophageal pressure; gastric bypass surgery; hypercarbia; hypoxemia; morbid obesity; obstructive sleep apnea syndrome; pulmonary hypertension; right ventricular function.

Introduction Morbid obesity can be defined as being over twice the ideal weight or a body mass index over 35. Morbid obesity is often associated with increased left ventricular end-diastolic volume (LVEDV) and pressure.’ Left ventricular dilatation

Journal of Clinical Anesthesia 8205-209, 1996 0 1996 by Elsevirr Science Inc. 65.5 Avenw of the Americas, New York, NY 10010

09.52-8 180/96/q 15.00 SSDI OI).‘,‘L-8180(95)00231-6

Original Contkbutions

and eccentric hypertrophy may develop in morbidly obese patients.’ Changes in intrapleural pressure by intermittent positive pressure ventilation (IPPV), particularly with positive end-expiratory pressure (PEEP) as well as release of intraabdominal pressure in morbidly obese patients, may influence left and particularly right ventricular function (RVF) .= Since an impaired right ventricle is more dependent on optimal afterload and preload, the right ventricular performance may depend on the baseline RVF.4 If an impaired right ventricle encounters an acute increase in pulmonary artery (PA) pressure due to a sudden onset of severe hypoxemia and/or hypercarbia, this impaired right ventricle may start to fail.&” During induction of anesthesia for morbidly obese patients, a hypoxemic episode may be encountered not only due to a much shorter safe duration of apnea, but also due to possible difficult airway and intubation.7 Obese patients with obstructive sleep apnea syndrome (OSAS) may develop pulmonary hypertension and eventually right ventricular failure.“” To my knowledge, right ventricular response to sustained hypoxemia and hypercarbia in awake morbidly obese patients has not been documented. There is also no information available on RVF and hemodynamic data during gastric bypass surgery in morbidly obese patients. Currently, measurement of RVF by the thermodilution method has become available with the use of an ejection fraction volumetric PA catheter. However, the presence of tricuspid regurgitation may interfere with accurate estimation of right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume (RVEDV) . I investigated changes in RVF and hemodynamics during gastric bypass procedure in morbidly obese patients using this modified PA catheter. I also investigated the effects of OSAS on hemodynamics and RVF in morbidly obese patients as a part of preoperative assessment in the holding area prior to entering the operating room (OR).

Materials

and Methods

Patient Selection Following approval of the Institutional Review Board of the Medical College of Virginia, and after obtaining written informed consent, 14 patients scheduled for elective gastric bypass procedure were studied. Preoperatively, assessment, these 14 patients were divided into two groups: (1) 8 morbidly obese patients without OSAS (aged 27 to 47 years), and (2) 6 morbidly obese patients with OSAS (aged 32 to 48 years). Morbidly obese patients with a history of heavy snoring and excessive daytime sleepiness were defined as patients with OSAS. All our patients with OSAS were studied in the sleep disorder laboratory with apnea-hypopnea index greater than five per hour. Obstructive sleep apnea was defined as absence of air flow for more than 10 seconds. Mean age of these patients was 34 years. Of the 14 patients, 5 were male and 9 were female. 206

J. Clin. Anesth., vol. 8, May 1996

Protocol In each patient, a radial artery catheter and a fast response thermodilution ejection fraction catheter (American Edwards Laboratories, Santa Ana, CA) were inserted prior to induction of anesthesia with local anesthesia without any premeditation. Preoperative assessment of RVF and hemodynamic data was initially performed in both groups of morbidly obese patients in the preoperative holding area. Anesthesia was induced with thiopental 2 to 3 mg/kg, sufentanil 50 to 100 pg, and succinylcholine 1 to 1.5 mg/ kg. Maintenance of anesthesia was with oxygen/air (FiO, = 0.6), isoflurane 0.5% to l%, and sufentanil 0.1 to 0.2 pg/kg/hr. Vecuronium was used for muscle relaxation. Hemodynamic changes and RVF were measured in the following stages during gastric bypass procedure in the supine position: (1) before induction of anesthesia, (2) after induction of anesthesia, (3) after opening the abdomen, and (4) after closing the abdomen. Each patient was monitored with pulse oximetry, ECG, capnography, and a nerve stimulator for neuromuscular blockade. After induction of anesthesia, esophageal pressure was also measured in midesophagus with a camino catheter and its device. This camino catheter has a transducer in its tip. This esophageal pressure was used as a substitute of intrapleural pressure, because changes in esophageal pressure accurately reflect changes in intrapleural pressure swings in either direction.“‘z”

Measurements Arterial blood gas tensions were measured with the standard gas analyzer in each patient for the preoperative evaluation. The fast-response thermodilator catheter can estimate RVEF, cardiac output (CO), and heart rate (HR) . Right ventricular end-diastolic volume is derived as stroke volume divided by RVEF. There was a statistical correlation of RVEF values between this thermodilution method and other methods such as echocardiography, cineventriculography, and radionuclide angiography.“~‘” Cardiac output and RVF were determined at least in triplicate by injecting 10 ml of iced saline using this catheter and a bedside microprocessor (REF-1 computer, American Edwards Laboratories, Santa Ana, CA). The injectate port was placed within the right atrium 1 to 2 cm above the tricuspid valve. Hemodynamic data and RVF were measured in each stage as described in the protocol: HR, mean arterial pressure (MAP), central venous pressure (CVP) , mean pulmonary artery pressure (MPAP) , pulmonary capillary wedge pressure (PCWP), cardiac index (CI), pulmonary vascular resistance index (PVRI), RVEDVI, RVEF, and esophageal pressure.

Statistical

Analysis

All values are expressed as means * standard deviation (SD). For each parameter, a Friedman two-way analysis of variance was performed over measurements and a paired t-test was used comparing data during gastric bypass pro-

Table

1.

Hemodynamic

Patients Without OSAS With OSAS

Data in Both Groups

of Morbidly

HR (beats per min)

MAP 6nmI-w

SO? 13 go+ 19

112*18 lOSkY

Obese Patients

Note: Data are presented as mean + SD. *p < 0.05. HR = heart rate; MAP = mean arterial pressure; C\T = central venous pressure; PCMT = pulmona~ pulmonary artery pressure; CI = cardiac index; OSAS = obstructive sleep apnea syndrome.

cedure. A p-value less than 0.05 indicated statistical significance. The confidence intervals for the variables of the results that reach statistical significance are such that mean differences of those variables are within 95% confidence limits.

3.3 k 0.6 3.2 + 0.7

32 * 6 46?8*

21*6 23* 13

18+5 20 f 8

CI (L/min/m’)

MPAP (mHg)

PCWP (WI-W

CVP (mm%)

capillav

wedge pressure; MPAP = mean

PCWP, and RVEDV were considered elevated or in the higher end of normal values in the preoperative stage among morbidly obese patients.

Discussion Results Among 14 morbidly obese patients, 8 patients without OSAS had a mean weight of 354 + 29 lbs (161 * 13 kg), with ages ranging from 29 to 47 years. Six patients with OSAS had a mean weight of 358 t 46 lbs (162 f 21 kg), with ages ranging from 32 to 47 years. The preoperative assessment of hemodynamic parameters including RVF is summarized according to two groups (morbidly obese patients with and without OSAS) in Tables 1 and 2. Morbidly obese patients with OSAS had significantly lower PaO, and higher PaCO, than patients without OSAS in the preoperative resting condition with room air (59.1 k 9.7 mmHg vs. 89 + 9.6 mmHg in PaO,; 54.2 + 9.6 mmHg vs. 37 + 4 mmHg in PaCO,) (p < 0.05). There were no significant differences in HR, MAP, CVP, PCWP, CI, RVEDV, and RVEF among these groups. Changes in RVF and hemodynamics in each stage of gastric bypass procedure in the 14 patients are summarized in Table 3. MPAP, PCWP and PVRI significantly decreased (p < 0.05) after opening the abdomen and later increased after closing the abdomen (p < 0.05)) with concomitant changes in esophageal pressure in the same direction (p < 0.01). RVEDV tended to be inversely proportional to changes in esophageal pressure (p = 0.07). Despite these changes, the CVP, CI, and RVEF were not significantly altered in each stage of gastric bypass surgery. The CVP, MPAP,

Table

2.

Morbid obesity can alter cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increasing circulating blood volume and CO seen in morbidly obese patients may cause ventricular dilatation and ultimately eccentric hypertrophy of the left ventricle.’ In fact, abnormalities of left ventricular diastolic function occur frequently in asymptomatic morbidly obese patients and may present as obesity cardiomyopathy.‘4 Left ventricular systolic function also may be determined by left ventricular loading conditions in morbidly obese patients. In other words, in obese patients, left ventricular functional shortening varies inversely with left ventricular internal dimension in diastole, left ventricular end-systolic wall stress, and systolic blood pressure (SBP) .I5 OSAS and/or obesity hypoventilation syndrome are not infrequently seen in morbidly obese patients.‘“.t7 Morbidly obese patients with a history of OSAS are reported to have a high risk of sudden cardiovascular death, despite the absence of other risk factors.” Obese patients with OSAS were also reported to have a high incidence of right ventricular hypertrophy.‘” Obstructive sleep apnea seems to contribute to the development of pulmonary hypertension and right ventricular dysfunction, primarily due to pulmonary vasoconstriction caused by hypoxia. However, intermittent apnearelated hypoxia may not be sufficient to cause pulmonary

Right Ventricular Function in Both Groups of Morbidly Obese Patients RVEF (%)

Without OSAS With OSAS

47 i 6 41 f 7

Note: Data are mrans i SD. *p < 0.05. RVEF = right ventricular ejection fraction; RVEDVI = right ventricular OSAS = obstructive sleep apnea syndrome.

RVEDVI

(ml/m*)

208 * 42 225 t 33

end-diastolic

PVRI (dynes.

sec/cm-5/m2)

264 f 156 615?237*

lzolume index; PVRI = prrlmonan vascrrlar resistance in&x;

,J. Clin. Anesth., vol. 8, May 1996

207

Original

Contributions

Table 3.

Changes in Hemodynamic

Parameters

and Right Ventricular

18 35 21 369

7.4 9.6 9.9 234

(ml/m’)

After Opening the Abdomen 18 * 5.9 26 + 8.3* 19 f 6.6” 203 + 132* 8.1 + 2.Ot 3.3 f 0.6 43 5 7.8 247 k 59

Note: Data are means + SD. *p < 0.05. tp < 0.01. CVP = central venous pressure; MPAP = mean pulmonary artery pressure; PCWP = pulmonary vascular resistance index; EP = esophageal pressure; CI = cardiac index; RVEF = right ventricular end-diastolic volume index. L

Y

1

hypertension and right ventricular failure. Sustained pulmonary hypertension seems to be associated with sustained hypoxia as seen in morbidly obese patients with OSAS who often have hypoxia while awake.’ OSAS may further contribute to impaired left ventricular function in these morbidly obese patients.” Morbidly obese patients have significantly shorter safe duration of apnea and are more susceptible to severe hypoxemia during difficult airway management and intubation, partly due to a decreased functional residual capacity and increased oxygen consumption.’ Sudden increase in PVR, due to severe hypoxemia may significantly elevate right ventricular afterload sufficiently to precipitate right ventricular failure, since the right ventricle may not tolerate an acute increase in SBP much above 35 mmHg.lz4 There is little information on RVF in morbidly obese patients, especially with OSAS and RVF during the course of gastric bypass surgery. In the study, preoperative assessment demonstrated that morbidly obese patients with OSAS had significantly increased MPAP (46 ? 8 mmHg) and PVRI (615 + 237 dynes) compared with patients without OSAS (MPAP: 32 k 6 mmHg; PVRI: 264 * 156 dynes) (p < 0.05). This might be due to significant chronic hypoxemia and hypercarbia seen in my patients with OSAS (p < 0.05).

However,

there

were

no significant

differences

in

HR, MAP, CVP, PCWP, CI, and RVEF between these patients. I also demonstrated that RVEF and CI did not change significantly during gastric bypass procedure in morbidly obese patients. However, MPAP, PCWP, PVRI, and esophageal pressure decreased significantly following the opening of the abdomen. Right ventricular afterload (MPAP, PVRI) significantly decreased and RVEDV tended to increase with decreases in intrapleural pressure estimated by esophageal pressure during gastric bypass procedure, as changes in esophageal pressure accurately reflect pleural pressure swings in either direction. In summary,

morbidly

obese

patients

with

OSAS

fre-

quently have hypoxemia and hypercarbia while awake, significantly increasing MPAP and PVRI despite normal 208

J. Clin. Anesth., vol. 8, May 1996

Gastric Bypass Procedure

19 f 4.2 31 f 7.9 23 f 5.2 274 f 184 16 + 3.9 2.8 f 0.8 42 + 8.8 216?56

3.2 + 0.6 46 k 6.7 211*40

RVEF (%) RVEDVI

f k f f

During

After Induction

Preinduction CVP (mmHg) MPAP (mmHg) PCWP (mmHg) PVIU (dynes. set/cm-“/m’) EP (mmHg) CI (L/min/m’)

Function

RVEF.

During

After Closing the Abdomen 21 34 23 351 14 2.7 40 215

f 5.1 f 7.7* + 5.5” f 199* f 1.6t k 0.5 k 6.5 f 66

capillary wedge pressure; PVRl = pulmonary ejection fraction; RVEDVI = right ventricular

induction

and

maintenance

of anesthesia

for morbidly obese patients, especially with OSAS, further hypoxemia and hypercarbia should be carefully avoided to prevent augmentation of elevated MPAP and PVRI and inducing right ventricular dysfunction. Also, high PEEP and large tidal volume should be avoided to ventilate morbidly obese patients with OSAS who already have increased PVRI. During gastric bypass procedure, further increase in intrapleural pressure by the high airway pressure due to the high positive pressure ventilation and by Trendelenburg position should be carefully managed, particularly when the abdomen is closed, since this can cause more increases in MPAP and PVRI.

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