Indian Journal of Anaesthesia

: 2008  |  Volume : 52  |  Issue : 2  |  Page : 217--220

Laparoscopic Cholecystectomy with Pulmonary Hypertension: Anaesthetic Challenges - A Case Report

TVSP Murthy1, Pratyush Gupta2,  
1 Prof and Senior Adviser, Neuroanaesthesiologist & Intensivist, Department of Anesthesiology, Army Hospital (R&R), New Delhi, India
2 Senior Resident, Department of Anesthesiology, All India Institute of Medical, Sciences, New Delhi, India

Correspondence Address:
TVSP Murthy
Neuroanaesthesiology, Army Hospital (R&R), Delhi Cantt-110010


A 38-year-old lady posted for laparoscopic cholecystectomy in a peripheral hospital met with a near fatal cardiac arrest when subjected to anaesthetic induction for the surgery. She was resuscitated, surgery deferred and later referred to our hospital. Here we describe the anaesthetic management of a case of pulmonary hypertension for laparoscopic cholecystectomy in a middle-aged lady.

How to cite this article:
Murthy T, Gupta P. Laparoscopic Cholecystectomy with Pulmonary Hypertension: Anaesthetic Challenges - A Case Report.Indian J Anaesth 2008;52:217-220

How to cite this URL:
Murthy T, Gupta P. Laparoscopic Cholecystectomy with Pulmonary Hypertension: Anaesthetic Challenges - A Case Report. Indian J Anaesth [serial online] 2008 [cited 2020 Dec 3 ];52:217-220
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Full Text


Primary pulmonary hypertension (PPH) is an un­common disorder of unknown etiology, characterized by a progressive increase in pulmonary artery pressure and pulmonary vascular resistance, often leading to right heart failure and death. The most common clinical signs of pulmonary hypertension are dyspnoea and fatigue. These patients are considered high risk for anaesthesia due to increased risk of peri-operative cardiovascular compli­cations. Anaesthetic management for a safe and suc­cessful outcome requires invasive cardiovascular moni­toring and maintenance of stable pulmonary and sys­temic haemodynamics[1] .

 Case report

A 38-yr-old, 154cm, 53kg lady with history of pul­monary hypertension and cholelithiasis presented for laparoscopic cholecystectomy. Her medical history was significant for borderline hypertension (150/90 mm Hg), hypercholesterolemia, and a 6-month history of progres­sive dyspnoea on exertion.

On examination she was slim, not obviously cy­anosed and showed no clubbing. She had no signs of increased jugular venous pressure. Her heart rate was 76 beats.min -1 and arterial pressure measured 154/86 mm Hg. There was a right ventricular lift, and auscultation revealed a grade II systolic murmur with a loud second sound. The lungs were clinically clear. A preoperative echocardiogram showed hypertrophied right ventricle with good function, a septum consistent with right ven­tricular pressure overload, moderate tricuspid regurgi­tation, and an estimated pulmonary artery (PA) systolic pressure of 65 mm Hg and an ejection fraction of 48%. The electrocardiogram showed right axis deviation, with right ventricular strain and occasional ventricular ec­topic beats. Preoperative chest x-ray was normal. Analysis of blood gases on room air (fraction of inspired oxygen 0.21) revealed a PaO 2 of 59 mm Hg, PaCO 2 of 48 mm Hg, and pH of 7.38. Her pulmonary function tests revealed a forced expiratory volume in 1 s 0.90 L, forced vital capacity 0.91 L and a total lung capacity 1.86 L.

Immunologic studies were negative for any cause. Her oral medications included furosemide 40 mg OD, ranitidine 150 mg OD, and nifedipine 20 mg TDS. In­vestigative work up revealed her to have cholelithisasis for which laparoscopic cholecystectomy was planned. Preoperative anaesthetic work up was otherwise satis­factory. Her documents revealed a history of being treated for a near cardiac arrest in a peripheral hospital when subjected for anaesthetic induction for the same surgery from which he was revived, surgery was post­poned and referred to our hospital. She was accepted for laparoscopic cholecystectomy under general anaes­thesia. Premedication with benzodiazepine was avoided to prevent respiratory depression, hypoventilation and hypoxia which might have precipitated a crisis.

On arrival in the operation theatre, her peripheral oxygen saturation was 90% on room air and 99% on 3 liters of oxygen by mask. After securing an IV cannula, monitoring was established which included ECG, pulse oximetry, invasive blood pressure under local analgesia (Lt radial artery), temperature (nasopharyngeal), cen­tral venous pressure line and pulmonary artery pressure (PA catheter) were introduced after giving midazolam 2mg and local analgesia. PA pressure measured 67/24 mm Hg with a mean of 38 mm Hg. The arterial pressure measured between 134/86 to 122/70 mmHg and Central venous pressure registered around 12 -14 mmHg.

Prior to induction a noradrenaline infusion was started, at the rate of 0.05 µ -1 min -1, to avoid any sudden hypotension during induction which could pre­cipitate a crisis. General anaesthesia was induced with oxygen (3-4 liters.min -1 ), fentanyl(2 µ -1 ) and midazolam i/v(2 mg) and propofol (2 -1 ) slowly. Trachea was intubated using vecuronium( -1 ). An infusion of nitroglycerin was kept ready to deal with any hypertensive episodes. (especially pulmonary) Ana­esthesia was maintained with midazolam (1-2 mg ), 0.6% to 0.8% isoflurane and oxygen enriched compressed air (FiO2 of 0.4) and supplemental doses of fentanyl ( 0.5 - 1 µ -1 ) as per the requirement. Neuromuscular block was achieved with vecuronium. No nitrous oxide was used so as to avoid any chance of increased pulmonary vascular resistance as well as diffusion hypoxia in the intra or immediate postoperative period, which could pre­cipitate a haemodynamic crisis.

Intraoperatively, noradrenaline infusion (4­10µg.min -1 ) was adjusted to maintain systemic pressure between 130/70- 110/80 mmHg. Her oxygen saturation was always maintained above 95%. Pulmonary artery pressures remained satisfactory and were maintained between 40 -50/20-25 mmHg with a low dose of nitro­glycerine infusion( 5 µg.min -1 and increased to 5 - 10 µg.min -1 ). The increase in the end tidal CO2 after pneu­moperitoneum was managed by increasing the ventila­tion rate rather than tidal volume. Intra abdominal pres­sure was maintained at less than 12 mm Hg. The intra­operative monitoring - ECG( within normal range with no ST/T changes or ectopics), peak airway pressure( within the range of 18 - 26 mmHg), temperature (35 -36 degrees centigrade)(nasopharyngeal), arterial pressure( 110/70 - 136/80 mmHg), pulmonary artery pressures(40 -50/20-25 mmHg) , pulse oximetry(95% - 97%), EtCO 2 (38-42 mmHg), arterial blood gas analysis ( pH 7.32, PaO 2 108mmHg, PaCO 2 43 mmHg, HCO 3 24 mEq.L -1 and a base excess of -4), urine output maintained at 2-4 -1 .h -1 and fluid balance ( using lactated Ringer and normal saline , 4 -1 .h -1 ) were essentially within nor­mal limits. The fluctuations of both systemic and pulmo­nary pressures were with in the range of 15 - 20/8-10 mmHg from the base line during induction, intubation and during pneumoperitoneum.

Surgery was uneventful and lasted for 75 minutes, and on completion of the procedure, neuromuscular blocking agent was antagonized with neostigmine and glycopyrrolate in conventional doses. The patient was extubated and sent to intensive care unit as planned for postoperative monitoring. The noradrenaline and nitro­glycerine drips were later weaned and stopped within 6 hrs. She was shifted out to general ward next day. Post­operative analgesia was provided by diclofenac 75 mg intramuscular on day one and later with a tablet of paracetamol as per the requirement. She had an unevent­ful recovery.


The corner stone in the anaesthetic management of patients with pulmonary hypertension is maintenance of perioperative systemic vascular resistance [1]. The pathogenesis of pulmonary hypertension involves a com­plex and multifactorial process. Endothelial dysfunction seems to play an integral role in mediating the structural changes [2] . These patients require optimum work up be­fore being subjected for surgery. The medical therapy for pulmonary arterial hypertension included use of cal­cium channel antagonists, oral anticoagulants, continu­ous intravenous administration of epoprostenol [3] in severe cases and recently the use of thromboxane inhibitors and endothelin receptor antagonists. Phophodiesterase inhibi­tors (milrinone /amrinone) have also been used success­fully in patients with pulmonary hypertension [4] .

The anaesthetic management of patients with pul­monary hypertension undergoing non-cardiac surgery has received little attention in literature. Successful anaes­thesia and surgery in patients with primary pulmonary hypertension requires accurate pre-operative assessment and invasive haemodynamic monitoring including con­tinuous measurements of both systemic and pulmonary arterial pressures to guide fluid, inotropes and vasodila­tor therapy [5] . Factors that may further increase pulmo­nary hypertension or decrease ventricular function such as relative hypovolaemia, depressant anaesthetic agents, hypoxia, acidosis, hypothermia, arrhythmias, stress and pain should be avoided. It is therefore essential to select a method of anaesthesia that will have minimum effects on myocardial contractility, systemic vascular resistance, pulmonary vascular resistance and venous return. Both regional as well as general anaesthesia have risks [6] .

Bird and Strunin administered a small dose of met­araminol during preoxygenation to avoid a decrease in systemic vascular resistance which lead to hypertension and bradycardia and required atropine administration in their study [7] . Keeping in view of the history of a cardiac arrest during induction at a peripheral hospital, norad­renaline infusion at induction was used to avoid an unex­pected fall in systemic vascular resistance. This option was chosen for easy and accurate control of arterial pressure which was especially important during differ­ent levels of surgical stimulation. Moreover, the overt effects of noradrenaline were counterbalanced by si­multaneous nitroglycerine infusion, which lead to main­tenance of near normal haemodynamics [8] . The uninter­rupted feed back provided by the intra-arterial pressure and pulmonary arterial catheter was essential and re­flected the actual changes both in the pulmonary and the systemic circuits prompting us to take remedial mea­sures either with a vasopressor or a vasodilator to en­sure optimal haemodynamics [8] .

Problems associated with anaesthesia for laparoscopic procedures pose a higher risk in these pa­tients. Insufflation of peritoneal cavity with carbon diox­ide causes an increase in end tidal carbon dioxide. Acido­sis, arrhythmias and hypotension may follow, all of which could be the precipitating causes of a crisis. Equally, ef­forts to maintain normocapnia are often accompanied by increased pulmonary airway pressures, particularly at high intraabdominal pressures. These result in increase in the pulmonary vascular resistance further. The situation could be made worse if the Trendlenburg position is adopted which fortunately was not the case in this patient who required a slight head up tilt [5].

The other possible complications associated with this case include pneumothorax and gas embolism. All these patients should be aimed at on table extubation as prolonged positive pressure ventilation carries deleteri­ous effects. Though best analgesia is provided post op­eratively by opioids we chose to give non steroid anti­inflammatory drug - diclofenac so as to avoid any pos­sible complication of respiratory depression in the early postoperative period. This was further changed to oral paracetamol, which provided adequate pain relief [6] .

The most serious concerns about general anaesthe­sia are that laryngoscopy and intubation performed under light anaesthesia, which can aggravate pulmonary artery pressure and controlled ventilation can reduce venous re­turn causing severe fall in the cardiac output and hypoten­sion [9] . Perhaps, this happened when she was induced at a peripheral hospital for the same surgery..

Ketamine has also been recommended as the drug of choice for induction because it has little effect on pul­monary and systemic vascular resistance; where as thio­pentone and propofol decrease systemic vascular resis­tance (SVR). Atracurium and vecuronium have been recommended for muscle relaxation for the same rea­son. Isoflurane and oxygen enriched compressed air (FiO 2 of 0.4) and supplemental doses of fentanyl as per the requirement seemed to be ideal during maintenance intraoperatively [10] . Pretreatment with phenylephrine to prevent changes in SVR is also recommended [5],[8], though it may cause similar vasoconstriction in both pulmonary and systemic circulations, hence not considered for use in our case. A recent study using sildenafil citrate as therapy for patients with pulmonary hypertension under­going non cardiac surgery has also been described [11] . Studies have shown that administration of xenon anaes­thesia has cardiovascular stability in patients with pul­monary hypertension and Eisenmenger syndrome [12],[13]. Abdominal field block along with epidural analgesia as a sole anaesthetic technique has also been described as safe alternative in these cases [14],[15].

The value of a pulmonary floatation catheter in the management is controversial. Transoesophageal echocardiography is useful and allows monitoring of pos­sible gas embolism during gas insufflation of peritoneal cavity. Monitoring of invasive arterial pressure, allowing continuous measurement of blood gas determinations is generally accepted as a standard monitoring practice [6] .

The case is presented to highlight the potential com­plications which pose a severe risk during administra tion of anaesthesia and to emphasize the importance of inva­sive investigation and monitoring, the absence of which could lead to occurrence and delayed detection of unex­pected complications in the perioperative period.


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