Year : 2009  |  Volume : 12  |  Issue : 1  |  Page : 49--52

Induced mild hypothermia in post-cardiopulmonary bypass vasoplegia syndrome


Mukesh Tripathi, Prabhat Kumar Singh, Naresh Kumar, Kailash Chandra Pant 
 Department of Anaesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Correspondence Address:
Mukesh Tripathi
Department of Anaesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014
India

Abstract

The state of vasoplegia in immediate post-cardiopulmonary bypass period is characterized by severe hypotension, supranormal cardiac output, low systemic vascular resistance (SVR), and resistance to vasoconstrictors. We could successfully use induced mild hypothermia to increase SVR, and could avoid very high doses of nor-epinephrine (>0.3 mcg/kg/min) in the background of severe pulmonary hypertension (systolic pulmonary pressure >90mmHg). Its effects such as decreased oxygen demand, positive inotropy and better right ventricle performance probably helped to improve oxygenation in presence of pulmonary oedema.



How to cite this article:
Tripathi M, Singh PK, Kumar N, Pant KC. Induced mild hypothermia in post-cardiopulmonary bypass vasoplegia syndrome.Ann Card Anaesth 2009;12:49-52


How to cite this URL:
Tripathi M, Singh PK, Kumar N, Pant KC. Induced mild hypothermia in post-cardiopulmonary bypass vasoplegia syndrome. Ann Card Anaesth [serial online] 2009 [cited 2019 Sep 16 ];12:49-52
Available from: http://www.annals.in/text.asp?2009/12/1/49/45013


Full Text

 Introduction



Cardiopulmonary bypass (CPB) technique used for open-heart surgery exposes patients to numerous adverse effects. Vasoplegia syndrome (VS) is one such, reported in the early postoperative period of CPB in cardiac surgery. It commonly presents with generalized profound vasodilatation resulting in the decreased systemic vascular resistance (SVR) and hypotension despite adequate cardiac output (CO). [1] There is decreased arteriolar reactivity towards vasoconstrictors, increased need for filling volume and vasopressor agents. A release of proinflammatory cytokines leading to inflammatory response is the major contributing factor. [2],[3] The authors wish to share the use of mild hypothermia in the management of post-CPB vasoplegia.

 Case Report



A 39-year-old male patient weighing 49 kg had undergone closed mitral valvotomy 8 years ago and presented with progressive worsening of dyspnoea (class III) and orthopnoea in last one year. On examination, patient had congestive cardiac failure (CCF) - engorged neck veins, enlarged liver (two fingers below the costal margin), pedal oedema and bilateral crepitations on chest. The patient was taking oral digoxin (0.25 mg/day), enalepril (2.5 mg twice a day), frusemide (40 mg/day) and intravenous heparin. His echocardiography revealed calcified stenotic mitral valve (area: 0.6 cm 2 ) with vegetations on the anterior and posterior mitral leaflet, large left atrium (56 mm), moderate tricuspid regurgitation, severe pulmonary arterial hypertension (PAH) (right ventricular systolic pressure - 72 mmHg) and normal ventricular contractility (ejection fraction - 70%). ECG showed atrial fibrillation with a heart rate of 96 beats/min. The final diagnosis was rheumatic heart disease with post-commissurotomy mitral valve stenosis, severe PAH, and the congestive cardiac failure. Mitral valve replacement was planned in this patient.

Premedication, night before surgery included tab lorazepam (2 mg) and tab ranitidine (150 mg) and repeated on the morning of surgery. Patient shifted to operation room with oxygen inhalation by face-mask. Radial artery and the right internal jugular vein cannulation were performed under local anaesthesia and continuous cardiac output (CCO) catheter (Baxter India Ltd.) was monitored during surgery. Base line values were recorded as radial artery pressure (109/56 mmHg), central venous pressure (CVP) (16 mmHg), pulmonary artery pressure (82/32 mmHg), pulmonary artery wedge pressure (PAWP) (32 mmHg), cardiac output (1.8 l/min), pulmonary vascular resistance (PVR) (533 dynes/scm 5 /m 2 ) and SVR (2400 dynes/scm 5 /m 2 ).

Induction of general anaesthesia was done with fentanyl (150 g), propofol (40 mg) and pancuronium bromide (8 mg). Just after orotracheal intubation, patient developed fast atrial fibrillation (heart rate - 150 to 160 bpm). Systolic pulmonary pressure increased to 88 mmHg as against the systolic arterial pressure of 82 mmHg. Cardiac output decreased to 1.4 l/min. Anaesthesia was maintained on FiO 2 (0.5) in air, isoflurane, fentanyl, and vecuronium chloride. Heparin (3 mg/kg) was given to establish the anticoagulation before aortic cannulation. The CPB was started after superior and inferior vena cava cannulations. Single-dose blood cardioplegia (1000 ml) was given through the aortic root after aortic cross-clamp and mitral valve replaced using Sorin mitral valve (size: 29 mm). The total aortic cross clamp time lasted 23 min, and the total CPB time was 80 min. Before the removal of the aortic cross clamp, milrinone (50 g/kg) and amiodarone (3 mg/kg) was added to the pump followed by the infusion of the milrinone (0.5 mcg/kg/min) and the amiodarone (0.6 mg/kg/h). Immediately after de-aeration of heart chambers and removal of the aortic cross clamp sinus rhythm returned spontaneously. Nitroglycerine (0.1 g/kg/min) and epinephrine (0.15 mcg/kg/min) infusions were started during the rewarming of the patient to 36.5C.

On routine protocol of endotracheal suction before ventilation and off CPB, we noticed pink frothy secretions in endotracheal tube. Considering the development of pulmonary oedema, frusemide (40 mg) intravenously was given. CPB was terminated at systemic arterial pressure of 79/46 mmHg and pulmonary artery pressure (68/32 mmHg). Lung ventilation was resumed with FiO 2 (1.00) and PEEP (8 cm H 2 O). Protamine was slowly given to neutralize the heparin-induced anticoagulation.

Post-CPB haemodynamic (heart rate, arterial pressure, CVP, SVR, PVR) and arterial blood gas parameters are presented in the graphic form to appreciate the trend of events which followed till the point of extubation [Figure 1]. After 15 min off CPB, the CCO measured high CO (10.8 l/min) with very low SVR (469 dynes/scm 5 /m 2 ) and PVR (212 dynes/scm 5 /m 2 ). Heart rate was 140/min and PaO 2 was 79 mmHg at 100% FiO 2 . In view of very low measured SVR, milrinone and nitroglycerine infusion were discontinued and the norepinephrine (0.15 g/kg/min) infusion was started and increased up to 0.3 g/kg/min.

For the next 30 min, the haemodynamic parameters remained the same. The diagnosis of post-CPB vasoplegia was considered on the basis of clinical picture of the patient. Due to tachycardia and high pulmonary pressure, further increase in nor-epinephrine associated with tachycardia was considered more detrimental. Therefore, we decided to induce mild hypothermia (core temp 34C) by surface cooling using hypo-hyperthermia blanket (Gaymar Industries Inc., New York, USA). After 60 min of institution of mild hypothermia, SVR gradually improved along with normalization of cardiac output, decreased heart rate, and increased mean arterial blood pressure.

Nor-epinephrine infusion was gradually titrated down (from 0.15 to 0.05 g/kg/min) and stopped after 4-h use as the haemodynamic parameters returned to normal. We re-warmed the patient gradually in the next 4 h. Arterial blood oxygenation also improved significantly (PaO 2 - 126 mmHg at FiO 2 of 0.5) with the use of hypothermia. Patient was extubated 12 h after mechanical ventilation. Rest of the post-operative period was uneventful and patient was discharged on the 10th post-operative day.

 Discussion



Systemic vascular resistance usually increases after CPB due to a transient rise in several vasoconstrictive hormones including catecholamines, serotonin, [4] arginine and vasopressin. [5],[6] This perhaps forms the basis to use inodilators in early post-CPB period and more so in patients for mitral valve replacement, where the PAH is also a primary concern for failing right ventricle. Inodilators are commonly used for decreasing SVR and increasing CO with minimal changes in the arterial blood pressure.

In contrast, in our patient, the observed low SVR in the immediate post off-CPB period was attributed to the combined effect of milrinone and nitroglycerine; therefore, the infusions were stopped. Only amiodarone was continued to control the heart rate and prevent recurrence of atrial fibrillation, which is more detrimental for the cardiac performance.

Soon, non-responsiveness of the patient towards a high dose of norepinephrine led us to review our diagnosis in favour of post-CPB vasoplegia. Generally, the criteria for the diagnosis of post-CPB vasoplegia included the following: (1) mean arterial pressure less than 60 mmHg despite normal ventricular filling condition; (2) cardiac index more than 3.5 l/m 2 ; (3) calculated SVR -5m -2 ; and (4) sustained increase of mean arterial pressure after administration of 5 to 10 mcg of norepinephrine. [7] Our patient met the first three criteria to confirm the diagnosis. He also had the high-risk factors for post-CPB vasoplegia such as angiotensin-converting enzyme-inhibitor usage, re-operation, CCF and opioid anaesthesia amongst the numerous risk factors related to post-CPB vasoplegia in preserved left ventricular function. [1],[8]

In the presence of severe PAH (almost equal to systemic arterial pressure) with low SVR and high CO, any further increase in the norepinephrine infusion was deferred to avoid worsening of the existing tachycardia and PAH. Other choice could have been the use of the intravenous methylene blue. [8] The methyline blue inhibits guanylate cyclase and thus increases SVR and arterial pressure by avoiding guanosine 3,5 monophosphate (cGMP) mediated vasorelaxant effect of nitric oxide. [9] We did not use methylene blue due to its non-availability at our place and more so in lack to prior experience with the drug. With the result, we decided to use mild hypothermia (34C) by surface cooling. The induced mild hypothermia effectively restored back the SVR and the blood pressure to normal within 4 h without adversely affecting the pulmonary pressure.

Vasoplegia has been correlated with the release of vasodilator inflammatory mediators (cytokines), arginine-vasopressin system impairment, endothelial dysfunction and decreased myogenic reactivity to catecholamine despite enhanced catecholamine release, [10] cytokines like TNF and interleukin-1 targeting the vessel wall with the induction of nitric oxide (NO)-synthetase and increased NO production, resulting in marked relaxation of the vascular smooth muscles. [11]

Higher SVR has been reported in hypothermic CPB than the normothermic CPB, and it has been suggested that this cannot be solely attributed to the neuro-humoral phenomenon but perhaps other factors too. [12] Vasodilatation occurring with warm heart surgery is at least partly mediated by temperature dependent release of cytokines. Hypothermia decreases the release of cytokines and therefore blunts the vasodilatation responses of the normothermic CPB. [13] Furthermore, induced mild hypothermia has been reported in experimental studies to improve the cardiac function by positive inotropic effect, [14] the improved response to epinephrine [15] and norepinephrine. [16] There is also evidence that mild hypothermia reduced pulmonary vascular resistance, [17] and significantly decreased work done by the right ventricle despite an increase in PVR after lung transplantation. [18] These factors together might have helped for the better oxygenation seen in due course of time. Thus, induced mild hypothermia helped in the recovery of our patient from post-CPB vasoplegia.

Although it would not be prudent to conclude from single case management, but it has been suggested that the mild hypothermia may be an effective alternative to treat CPB-induced vasoplegia, especially in presence of severe PAH, where a-adrenergics may be counter productive to right ventricle performance. However, hypothermia-induced cardiac arrhythmia, coagulopathy and related problems will remain a point of concern.

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