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 Table of Contents  
Year : 2019  |  Volume : 4  |  Issue : 1  |  Page : 47-49

Anesthetic management of a patient with acute pulmonary hypertension for laparoscopic low anterior resection

Consultant Anaesthesia, Prince Sultan Military Medical City, Riyadh, KSA

Date of Submission17-Jun-2018
Date of Acceptance18-Jun-2018
Date of Web Publication26-Sep-2019

Correspondence Address:
Dr. Sadaf Malik
Prince Sultan Military Medical City, Riyadh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/SJL.SJL_8_18

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Anesthetic management of patients with acute pulmonary hypertension (PH) for noncardiac surgery has received little attention in the literature. We present a case of acute PH due to pulmonary embolism for laparoscopic low anterior resection. A thorough preoperative assessment followed by invasive hemodynamic monitoring was done. Factors precipitating pulmonary vasoconstriction were avoided, and intravenous nitroglycerine infusion was used to control PH perioperatively. The problems encountered were increased airway pressure caused by pneumoperitoneum and Trendelenburg position.

Keywords: Acute pulmonary hypertension, laparoscopic low anterior resection, pulmonary embolism

How to cite this article:
Malik S. Anesthetic management of a patient with acute pulmonary hypertension for laparoscopic low anterior resection. Saudi J Laparosc 2019;4:47-9

How to cite this URL:
Malik S. Anesthetic management of a patient with acute pulmonary hypertension for laparoscopic low anterior resection. Saudi J Laparosc [serial online] 2019 [cited 2023 Jun 9];4:47-9. Available from: https://www.saudijl.org/text.asp?2019/4/1/47/267862

  Introduction Top

Acute pulmonary hypertension (PH) is distinctive because it differs in clinical presentation, diagnostic findings, and response to treatment from chronic PH. These patients are considered high risk for anesthesia due to increased risk of perioperative cardiovascular complications. Anesthetic management for a safe and successful outcome requires invasive cardiovascular monitoring and maintenance of stable pulmonary and systemic hemodynamics.

  Case Report Top

A 79-year-old female, known diabetic and hypertensive, was presented for laparoscopic low anterior resection for rectal CA. She was diagnosed to have pulmonary embolism (PE) causing acute severe PH (pulmonary artery pressure [PAP] 70 mmHg) with right ventricular (RV) strain (mild pleural effusion and upper abdominal ascites) 20 days before the procedure. She was managed with diuretic therapy and therapeutic anticoagulation was started with enoxaparin. On examination, she had a pulse of 69 beats/min, blood pressure was 129/65 mmHg, and saturation of 98% on room air. There were few basal crackles, no pedal or sacral edema, and no nocturnal dyspnea. The heart auscultation was normal, and the jugular venous pressure was not raised. After assessment of the perioperative risk involved, the patient was classified as the American Society of Anesthesiologists 3 and was taken high-risk consent, and risk of the laparoscopic procedure was informed to the patient and the surgeon. In the operating theater baseline, monitors were applied, slow iv induction was done with fentanyl 100 ug with etomidate 16 mg. Intubation was done 3 min after cisatracurium 10 mg and lidocaine 100 mg was given to attenuate the intubation response. The right radial arterial line and ultrasound-guided right internal jugular line were placed under aseptic technique. The Flo Trac sensor was connected, and continuous monitoring of cardiac output (CO), cardiac index (CI), stroke volume (SV), and SV variation (SVV) was started. The patient was ventilated at 6–7 ml/kg tidal volume with pressure limiting to 28 mmHg and arterial carbon dioxide (CO2) targeted 35 mmHg with FiO2 of 0.6. Anesthesia was maintained with sevoflurane 2% along with fentanyl 2ug/kg/hour with cisatracurium 2 mg repeated every hour. Urinary catheter and oral temperature probe were inserted. Temperature was maintained between 36 C and 37 C and lower body Bair hugger was used. The initiation of pneumoperitoneum and Trendelenburg position caused an increase in CVP and a decrease in CO and CI. This was managed by the initiation of nitroglycerine infusion at a rate of 0.25–1 ug/kg/min. CO returned to baseline after initiation of nitroglycerine infusion. The fluid status was monitored and managed by SVV%. The ABG was repeated every 1 h with target pH of 7.35–7.45. Increase in end-tidal and arterial CO2 was managed by a compensatory increase in respiratory rate. The intra-abdominal pressure was kept below 14 mmHg. Nitroglycerine infusion was tapered off by the end of the procedure. The patient was extubated after reversal with glycopyrrolate and neostigmine and transferred to Intensive Care Unit for postoperative monitoring as scheduled.

  Discussion Top

PH is defined as a mean PAP >25 mmHg at rest or >30 mmHg with exercise.[1]

Acute PH is distinctive because they differ in their clinical presentation, diagnostic findings, and response to treatment from chronic PH. Significant pathophysiologic differences exist between acute and chronic PH. Therapy of acute PH should generally be aimed at acutely relieving RV pressure overload and preventing RV dysfunction. Increased RV afterload leads to RV dilatation in most acute cases of PH when there is not enough time for adaptive mechanisms (e.g., RV hypertrophy) to develop. Acute PH can be caused by sepsis, acute lung injury, PE, cardiac surgery, and drug induced.[2]

Acute PH in PE is characterized by mechanical obstruction by thrombus with subsequent vasoconstriction causing an increase in pulmonary vascular resistance. The normal RV can acutely adapt to high flow but is not able to tolerate any but very short acute high-pressure load.[3] The normal RV cannot acutely increase and sustain mean PAP >40 mmHg for more than a brief period.[4] RV systolic dysfunction, severe tricuspid regurgitation, arrhythmias, and the left ventricular dysfunction caused by ventricular interdependence may contribute to low CO and hypotension in patients with PH. Regardless of the underlying cause of PH, the final common pathway for hemodynamic deterioration and death is cor pulmonale and RV failure. Thus, the monitoring of RV function is of great importance. The assessment of PVR plays an important role in the diagnosis and management of PH.[5]

Our patient had developed acute PH few days before surgery, and the aim of this management was to prevent any further increase in PVR to prevent acute RV failure secondary to acute high-pressure load as there are no compensatory mechanisms (hypertrophy) developed in acute PH.

Anesthetic management of patients with PH undergoing noncardiac surgery has received little attention in the literature. Successful anesthesia and surgery require accurate preoperative assessment and invasive hemodynamic to guide fluid, inotropes, and vasodilator therapy.[6] Factors that may further increase PH or decrease ventricular function such as relative hypovolemia, depressant anesthetic agents, hypoxia, acidosis, hypothermia, arrhythmias, stress, and pain should be avoided. It is, therefore, essential to select a method of anesthesia that will have minimum effects on myocardial contractility, systemic vascular resistance (SVR), pulmonary vascular resistance, and venous return. Both regional and general anesthesia have risks.[7]

For the acute PH, conventional therapy includes the right fluid management, ventilation management, and nonspecific drugs (oxygen, warfarin, and diuretics). In acute PH associated with decreased cardiac contractility and/or SVR, the use of vasopressors with or without pulmonary vasodilators is necessary to maintain coronary and end-organ perfusion. Progression of RV failure should be always considered in the management plan. The choice of vasopressor and inotropes in patients with acute PH should take into consideration their effects on PVR and CO when used alone or in combinations with other agents and should be individualized based on the individual patient response.[6]

We used nitroglycerine infusion to decrease the PVR triggered by the position and pneumoperitoneum. The fluid status was monitored and managed by the SVV%. We had planned to use a small dose of phenylephrine in case of decrease in MAP; however, fortunately, the patient did not require it.

Problems associated with anesthesia for laparoscopic procedures pose a higher risk in these patients. Insufflation of peritoneal cavity with CO2 causes an increase in end-tidal CO2. 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 intra-abdominal pressures. This results in an increase in the pulmonary vascular resistance further. The situation could be made worse if the Trendelenburg position is adopted.[6] The other possible complications associated with this case include pneumothorax and gas embolism. All these patients should be aimed at on-table extubation as the prolonged positive pressure ventilation carries deleterious effects.[7]

The most serious concerns about general anesthesia are that if laryngoscopy and intubation is performed under light anesthesia, it can further increase pulmonary artery pressure. Controlled ventilation can reduce venous return and can cause a severe fall in the CO and subsequent hypotension.[8]

Thiopentone and propofol decrease SVR, whereas etomidate maintains a stable hemodynamics. Atracurium and vecuronium have been recommended for muscle relaxation for the same reason. Isoflurane and oxygen-enriched compressed air (FiO2 of 0.4) and supplemental doses of fentanyl as per the requirement seemed to be ideal during maintenance intraoperatively.[9] The value of a pulmonary floatation catheter in the management is controversial. Transesophageal 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.[7]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Rodriguez RM, Pearl RG. Pulmonary hypertension and major surgery. Anesth Analg 1998;87:812-5.  Back to cited text no. 1
McGoon MD, Kane GC. Pulmonary hypertension: Diagnosis and management. Mayo Clin Proc 2009;84:191-207.  Back to cited text no. 2
Blaise G, Langleben D, Hubert B. Pulmonary arterial hypertension: Pathophysiology and anesthetic approach. Anesthesiology 2003;99:1415-32.  Back to cited text no. 3
Chin KM, Kim NH, Rubin LJ. The right ventricle in pulmonary hypertension. Coron Artery Dis 2005;16:13-8.  Back to cited text no. 4
Via G, Braschi A. Pathophysiology of severe pulmonary hypertension in the critically ill patient. Minerva Anestesiol 2004;70:233-7.  Back to cited text no. 5
Fischer LG, Van Aken H, Bürkle H. Management of pulmonary hypertension: Physiological and pharmacological considerations for anesthesiologists. Anesth Analg 2003;96:1603-16.  Back to cited text no. 6
Hoeper MM, Galiè N, Simonneau G, Rubin LJ. New treatments for pulmonary arterial hypertension. Am J Respir Crit Care Med 2002;165:1209-16.  Back to cited text no. 7
Sammut MS, Paes ML. Anaesthesia for laparoscopic cholecystectomy in a patient with Eisenmenger's syndrome. Br J Anaesth 1997;79:810-2.  Back to cited text no. 8
Cheng DC, Edelist G. Isoflurane and primary pulmonary hypertension. Anaesthesia 1988; 43:22-4.  Back to cited text no. 9


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