Pre-operative Right Heart Echocardiography in Obese Chronic Obstructive Pulmonary Disease Patients Presenting for General Anesthesia: A Case Series on the Role of Ventriculo-Arterial Coupling

INTRODUCTION

Risk stratification in patients presenting for non-cardiac surgery under general anesthesia (GA), can often be challenging, given its’ multifaceted nature, encompassing the patient-related, anesthesia-related, and procedure-related dimensions.^[1] Herein, the importance of baseline evaluation of the ventriculo-arterial coupling at the level of the right heart with echocardiography is recently gaining increased attention from the perioperative fraternity.^[2] The Tricuspid Annular Plane Systolic Excursion/Pulmonary Artery Systolic Pressure or the TAPSE/PASP ratio, in mm/mmHg, serves as an important non-invasive metric in this regard.^[2-4]

CASE SERIES

We report the perioperative course of ten obese patients with chronic obstructive pulmonary disease (COPD) in whom the pre-operative PASP numerically exceeded the TAPSE, to imply a TAPSE/PASP ratio of <1. Obesity was defined by a body mass index (BMI) ≥30 Kg/m², in accordance with the World Health Organization (WHO) criterion.^[5] All the patients had spirometry-confirmed COPD with the forced expiratory volume in 1s (FEV₁) divided by the forced vital capacity below 70%. All the patients had moderate disease severity with the FEV₁ ranging from 50 to 80% of the predicted values, in accordance with the Global Initiative for Chronic Obstructive Lung disease (GOLD) classification system.^[6]

As for the computation of pre-induction TAPSE/PASP, a transthoracic echocardiographic (TTE) examination was performed by a practicing cardiac anesthesiologist in the holding area, employing the Philips Epiq 7 machine (Bothell, WA) fitted with a S5-1 probe. Illustrated in Figure 1, TAPSE was measured by placing M-mode cursor along the tricuspid annulus in the apical-4 chamber view on TTE, to amount for the resultant longitudinal movement in the peak systole.^[7] On the other hand, continuous wave Doppler was utilized in the echocardiographic view to interrogate the tricuspid regurgitation (TR) jet, to provide for the PASP [Figure 1]. This calculation was based on the simplified Bernoulli equation: Right ventricle systolic pressure (RVSP) = 4 (Vmax_TR)² + right atrial pressure (RAP), where the RVSP equates with PASP in the absence of the right ventricle (RV) outflow tract obstruction (Vmax_TR representing the maximum TR velocity).^[8,9] Meanwhile, RAP was non-invasively measured using the inferior vena cava diameter and the corresponding collapsibility ratio,^[10] one may assume the pre-operative RAP as 10 mmHg for the sake of simplicity in the PASP estimation, especially when Vmax_TR happens to be numerically squared in the Bernoulli equation. Moreover, the TAPSE values factor in as independent numerators in the ratio of interest, that is, the TAPSE/PASP.^[2,4] The echocardiographic values were, nonetheless, carefully averaged over at least three consecutive cardiac cycles in normal sinus rhythm and poor-quality apical-4 chamber images were not utilized for computational purposes given the technical challenges posed by obesity to echocardiographic imaging.

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Figure 1:

TTE image panel acquired with the Philips Epiq 7 machine (Bothell, WA) with a S5-1 probe, depicting the computation of TAPSE/PASP in mm/mmHg, where the image on the left shows TAPSE estimation (in mm) on M-mode, in the apical-4 chamber view, with the image on the right utilizing the maximum TR velocity or the VmaxTR, on the continuous wave Doppler, to estimate PASP (in mmHg) by the simplified Bernoulli equation. TTE: Transthoracic echocardiography; TAPSE/PASP: Tricuspid annular plane systolic excursion/pulmonary artery systolic pressure, TR: Tricuspid regurgitation, RVSP: Right ventricle systolic pressure.

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The patients were kept nil per oral, with a minimal fasting of 2h for clear fluids, as per the American Society of Anesthesiologists (ASA) fasting guidelines.^[11] Pre-operative hypertension was well controlled in the patients, alongside other optimizations as mandated in an elective surgical setting, such as a pre-operative hemoglobin ≥10 g/dL. The antihypertensives were continued as per regime, except for the diuretics and angiotensin converting enzyme inhibitors, which were withheld on the morning of surgery. Following the administration of 5 mL/Kg crystalloid, GA was induced with Inj. Fentanyl 2 µg/Kg, Etomidate 0.3 mg/Kg, Rocuronium 0.6 mg/Kg, and then Inj. Xylocard 1.5 mg/Kg 90s before tracheal intubation to blunt the laryngoscopy response. GA was maintained with an inhalational agent to achieve the target mean alveolar concentration and bispectral index of 40–60 alongside standard ASA monitoring. The patients were subjected to volume-controlled positive pressure ventilation with 6–8 mL/Kg of tidal volume with the fractional inspired oxygen concentration and positive end-expiratory pressure titrated to maintain an oxygen saturation of >95%. A balanced crystalloid infusion at 5–10 mL/Kg/h was employed across all the patients, carefully adjusted to the surgical losses.

With the blood pressure non-invasively monitored with oscillometry q1 min at GA induction, q2 min up to 10 min post-induction and then q5 min; arterial hypotension was defined by a decline in the systemic pressure of >30% from the baseline or an absolute mean arterial pressure (MAP) <60 mmHg. The lowest MAP value up to 10 min post-GA induction was employed to compute the maximum % MAP decrement, in reference to the corresponding baseline MAP value. Hypotension, occurring at anesthetic induction or intraoperatively, was treated with intravenous 0.1 mg/Kg ephedrine (Ep) or 50 µg phenylephrine (PE) boluses, with the requirement of the number of vasopressor boluses recorded for every patient, specifically capturing those requiring Ep/PE boluses on 3 or more occasions. The need for blood transfusion was additionally documented and the patients were followed up for post-operative acute kidney injury (AKI), diagnosed and staged as per the Kidney Disease: Improving Global Outcomes or the KDIGO criteria.^[12] Table 1 enlists the baseline characteristics of the patients. As for the pre-operative TAPSE/PASP values of <1 in this cohort of obese surgical patients with diagnosed COPD, hypotension at GA induction transpired in a total of 9 out of the 10 patients, as enlisted in Table 2. Of note, the highest values of maximum % MAP decline of 49.02% and 47.22%, happened to be recorded for the patients who displayed comparatively reduced TAPSE/PASP values of 0.49 and 0.51 mm/mmHg, respectively, on the pre-operative TTE examination. Herein, five out of the ten patients required ≥3 Ep/PE boluses for the maintenance of an adequate intraoperative hemodynamic status [Table 2]. None of the patients required vasopressor infusion. The patient with the lowest pre-induction TAPSE/PASP ratio of 0.49 mm/mmHg landed up in KDIGO stage 1 post-operative AKI, alongside happening to be one of the two patients requiring intraoperative blood transfusion [Table 2]. This patient, nonetheless, demonstrated normal pre-operative renal function, as outlined in Table 1.

DISCUSSION

The above-mentioned case series suggests a potential role of assessing the right ventricle-pulmonary artery or the RV-pulmonary artery (RV-PA) coupling in predilected general surgical patient population who are expected to have prevailing PASP elevation, at presentation. Ahead of the literature associating pulmonary hypertension (PH) and right heart changes in patients with COPD, independent researchers attribute PASP elevation up to 0.4 mmHg for every Kg/m² increment in the BMI.^[13,14] Obesity hypoventilation syndrome or obstructive sleep apnea are expected here to compound the clinical situation furthermore.^[15] Even in the general sense of the matter, Verberne et al. impress on the implications of obesity in patients with COPD.^[6] Talking specifically of PASP though, Liu et al. reveal a significant association between the mean MAP during GA with the pre-induction PASP (r = −0.532 on Spearman correlation analysis; P < 0.05), in a cohort of 75 elderly surgical patients.^[16]

The case series adds to the only and a very recent, that is, a 2025 prospective observational study by Gülaştı et al. which delineates pre-operative TAPSE/PASP as a non-invasive predictor of post-GA hypotension.^[2] The authors discovered a TAPSE/PASP cutoff of ≤1.98 to predict hypotension following GA induction, with a sensitivity and specificity of 72.5% and 64.1%, respectively (Area under the curve: 0.733, 95% Confidence Interval: 0.621–0.826, P < 0.001). Meanwhile, they included 79 patients with no known heart disease, as high as 54.43% of their study patients happened to be ASA I.^[2] In contrast, our case series focused a predisposed subset as far as RV-PA dynamics are concerned, although with preserved left ventricular ejection fraction and again, with no known structural or valvular heart disease. The merit of the former is nested in the fact that our patients demonstrated much lower pre-operative TAPSE/PASP values when compared to the Gülaştı et al. ASA I patients, where ahead of systemic arterial hypotension, the need for vasopressors and morbid organ outcomes like AKI, were additionally taken note of.^[2] Meanwhile, a heterogenous surgical subset featured in the case series, the fact remains to be reiterated that hypotension manifesting around the induction of GA, especially the maximum % MAP decrement up to 10 min post-GA induction, is expected to be more reflective of the patient-specific characteristics, rather than the nature and extent of the surgical intervention. Moreover, couple of these patients with TAPSE/PASP values lower than 0.55 mm/mmHg, wherein RV-PA uncoupling is believed to set in, as per the literature in the subject, demonstrated the maximum % MAP decrement.^[4] As for the 2022 European Society of Cardiology and European Respiratory Society Guidelines on PH, lower TAPSE/PASP cutoffs like 0.32 mm/ mmHg have been used to denote more severe forms of RVPA uncoupling.^[3,4]

The underpinning pathophysiology relating to anesthetic induction and ventriculo-arterial coupling at the level of the right heart classifies as interesting. Price et al., while discussing the perioperative management in patients with PH, highlight as to how the induction of GA and cessation of spontaneous ventilation predispose to accentuated pulmonary vascular resistance (PVR), especially in backdrop of sympathetic stimulation, hypoxia-hypercapnia, and elevated airway pressures.^[17] Indeed, Bellotti et al. associate a reduced risk of post-induction hypotension with the preservation of spontaneous ventilation (Odds Ratio: 0.925, P = 0.012).^[18] The influence of an elevated PVR on the RV function cannot be overemphasized, where the latter might not be able to tolerate acute afterload elevations due to its’ anatomical-physiological peculiarities.^[17] It also remains to be buttressed that in a biventricular circulation connected in a series arrangement, the output of the RV constitutes the input of the left ventricle, which if compromised, can lead to a decreased systemic cardiac output, let alone the effect of the ventricular interdependence.^[19] Although none of our patients had any features suggestive of autonomic neuropathy, the role of a decreased systemic vascular resistance (SVR) is difficult to overlook, wherein we chose to induce GA with etomidate, unlike the use of propofol by Gülaştı et al., given that it may reduce SVR to result in arterial hypotension.^[2,20] For defining obesity, we relied on BMI, in isolation, while adhering to the WHO-laid criterion where the ethnic associations of BMI can have their part to play in precise patient characterization.^[5,21] Finally, the relationship between the right heart dynamics and post-operative AKI makes for an equally valuable investigation.^[12]

CONCLUSION

While the case series furthers the evolving role of RV-PA (un) coupling in predisposed patients receiving GA for routine non-cardiac surgery, it concurrently motivates dedicated future research in the subject involving a wider frame of clinically relevant patient outcomes.