|Year : 2017 | Volume
| Issue : 1 | Page : 19-22
Anesthetic management of a patient with heart failure and reduced ejection fraction for radical cholecystectomy with liver resection surgery
Amit Kumar Mittal1, Itee Chowdhury1, Manisha Arora1, Chamound Rai Jain2
1 Department of Anaesthesiology, Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, India
2 Department of Cardiology, Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, India
|Date of Web Publication||27-Jun-2017|
Amit Kumar Mittal
A-3/225, Sector-5; Rohini, New Delhi - 110 085
Source of Support: None, Conflict of Interest: None
We report a case focusing on achieving an optimum cardiac output (CO) in a patient with heart failure with severely reduced ejection fraction using EV1000 monitor to obtain various dynamic parameters such as stroke volume (SV), SV variation (SVV), systemic vascular resistance (SVR), and CO. We optimized preload by SVV-guided intraoperative goal-directed fluid transfusion and modulated SVR using multipronged anesthetic techniques to decrease afterload and increase forward flow to improve CO in a patient undergoing radical cholecystectomy with wedge liver resection.
Keywords: Cardiac output, EV1000 clinical platform, heart failure with reduced ejection fraction, liver resection surgery, systemic vascular resistance
|How to cite this article:|
Mittal AK, Chowdhury I, Arora M, Jain CR. Anesthetic management of a patient with heart failure and reduced ejection fraction for radical cholecystectomy with liver resection surgery. Indian Anaesth Forum 2017;18:19-22
|How to cite this URL:|
Mittal AK, Chowdhury I, Arora M, Jain CR. Anesthetic management of a patient with heart failure and reduced ejection fraction for radical cholecystectomy with liver resection surgery. Indian Anaesth Forum [serial online] 2017 [cited 2020 Jun 6];18:19-22. Available from: http://www.theiaforum.org/text.asp?2017/18/1/19/208969
| Introduction|| |
Better medical facilities and increase in life span have resulted in a considerable rise in the number of patients presenting for major abdominal surgery having heart failure with reduced ejection fraction (HFrEF) and moderate-to-severe diastolic dysfunction. Nearly 15.2% of such elderly patients undergoing noncardiac surgeries  are associated with considerable perioperative morbidity and mortality due to increased risk of cardiac arrhythmias, rapid decompensation of heart failure, and sudden cardiac arrest and death.
The goals of anesthetic management in these patients for major surgery include optimization of preload, maximize forward flow, maintain stable hemodynamics, and prevent complications such as arrhythmias and precipitation of heart failure. We present a case report highlighting the skillful selection of anesthetic agents and techniques, monitoring dynamic parameters (stroke volume variation [SVV], stroke volume index, and systemic vascular resistance [SVR]) by EV1000 clinical platform (Flo Trac/EV1000 setups, Edward Lifesciences Corporation, Irvine, CA, USA), and continuous modulation of dynamic indices aiming to bring down SVR to help increase forward flow, decrease central venous pressure (CVP), improve heart–lung interaction, liver decongestion, and increase CO.
| Case Report|| |
A 72-year-old elderly diabetic male, weighing 54 kg, with long-standing coronary artery disease, having carcinoma gall bladder with liver infiltration, was posted for radical cholecystectomy with wedge resection of liver at our institute. The patient had undergone coronary artery bypass grafting 20 years back, followed by angioplasty 15 years later. There was a history of progressive exertional dyspnea (New York Heart Association Grade II) for 2 years, his present medical treatment included β-blockers, angiotensin-converting enzyme inhibitors, diuretics, and oral hypoglycemic. On examination, the patient had bilateral fine basal crepitation, and preoperative lung ultrasound (LUS) revealed B-lines. Echocardiography (ECHO) showed dilated atrium and ventricle, severe global hypokinesia, paradoxical septal wall motion abnormality with left ventricular ejection fraction (LVEF) of 29%, Grade II diastolic dysfunction, and mild-to-moderate mitral regurgitation. Stress ECHO was positive for provocable ischemia at 85% target heart rate. Laboratory investigations were normal except for Hb - 9 g%. Inside operation theater, intravenous (IV) access was secured, routine monitors were attached, epidural catheter (T10–T11) was placed, and internal jugular vein and radial artery were cannulated, which were later connected to the EV1000 monitor through FloTrac transducer. After placing bispectral index (BIS) sensor on the patient's forehead, induction of anesthesia was done with fentanyl 2 mcg/kg, etomidate 0.2 mg/kg, and muscle relaxation was achieved by atracurium 0.5 mg/kg. Using 8 F endotracheal tube, intubation was facilitated with C-Mac video laryngoscope and controlled ventilation with positive-end expiratory pressure (5 cmH2O). Keeping BIS value of 40–60, anesthesia was maintained by oxygen/air (50:50) with isoflurane (0.6–1.0 Mac) and propofol infusion (25–100 mcg/kg/min). Analgesia was supplemented with boluses of IV morphine 6 mg initially followed by aliquots of fentanyl (50 mcg) and epidural infusion of 0.125% bupivacaine infusion at 4–8 ml/h, titrated according to SVR values. Intraoperative lactate-free crystalloid was used at 1 ml/kg as the maintenance fluid and additional 50 ml boluses were transfused to maintain SVV in the range of 4–10. Hemodynamic parameters were obtained by the EV1000 clinical platform for monitoring, management, and intervention under anesthesia [Table 1] and [Figure 1]. Throughout the surgery, total fluid transfused over 4 h was 1100 ml (one packed cell and 700 ml crystalloid), blood loss was 350 ml, and urine output was 400 ml. At the conclusion of surgery, before extubation, no B-lines were detected on repeat LUS, and arterial blood gas revealed normal lactate levels (0.7 mmol/cc). Postoperatively, the patient was monitored for mean arterial pressure (MAP), CVP, and urine output, and analgesia was managed with patient-controlled analgesia morphine infusion and patient-controlled epidural analgesia 0.125% bupivacaine infusion till the next 48 h, rest of the course was uneventful.
|Table 1: Intraoperative hemodynamic (dynamic and static) parameters as obtained by EV1000 monitor at 30 min interval|
Click here to view
|Figure 1: Dynamic parameters (vertical down solid arrows) and static parameters (horizontal solid arrows) displayed on EV1000 monitor|
Click here to view
| Discussion|| |
Patients with HFrEF have elevated left ventricular end-diastolic pressure (LVEDP), left atrial pressure (LAP), and CVP due to impaired relaxation and contraction in the enlarged and noncompliant ventricles. Preoperatively, our patient had elevated LVEDP and LAP with raised transpulmonary venous and capillary pressure gradient (TPG), which along with lesser absorptive capabilities of alveolar capillaries  led to pulmonary congestion. The elevated TPG and higher right ventricle (RV) afterload further resulted in an elevated CVP and raised hepatic venous pressure (HVP), leading to liver congestion.
The major concerns in anesthetic management of this patient were as follows:
- Improve CO and prevent cardiac decompensation
- Improve oxygenation and heart–lung interaction by reducing alveolar–interstitial edema and TPG
- Keep a low CVP and HVP to decongest liver during wedge liver resection.
In HFrEF, ventricular filling depends directly on atrial contraction and indirectly on the pressure gradient between the left atrium and left ventricle (LV), so marginal drop in preload causes rapid fall in stroke volume (SV), and hypovolemia is poorly tolerated, while minimal volume transfusion or rise in afterload can cause rapid decompensation of the heart due to raised LVEDP and TPG. A fine balance between preload and afterload is mandatory for obtaining better outcome and to avoid perioperative morbidity.
Soon after induction, these patients have hypotension, which we avoided to an extent [Table 1] using etomidate as an induction agent (transient hypertension produced due to activation of alpha-2 adrenergic receptors) and by passive leg raising instead of using vasopressors and rapid fluid transfusion. Clinical studies revealed that, in more than 50% of hypotensive patients, fluid boluses failed to increase CO, instead causing futile resuscitation and functional cardiac impairment, vasopressors on the other hand can help in marginal rise of MAP but at the cost of increasing afterload. Use of vasopressors and conditions causing sympathetic stimulation leads to increased SVR, left ventricular end-diastolic pressure (LVDEP) and TPG, increased myocardial work, and oxygen demand with decreased myocardial performance and CO. The anesthetics which were supposed to decrease CO by their cardiodepressant action actually helped to improve the CO by reducing SVR and suppressing baroreceptor reflex-induced tachycardia. In addition, HFrEF patients have adaptation for low pressure-dependent autoregulation and perfusion in microcirculatory vessels of vital organs, so in spite of few episodes of low MAP, we avoided vasopressors and over-zealous fluid transfusion.
It has been proved by various studies that SVV helps to predict cardiac preload and fluid responsiveness in patients with poor cardiac reserve. Hence using SVV as a guide, we transfused a total of 700 ml crystalloid including the maintenance fluid and additional boluses, which could have been otherwise more with conventional monitoring indices. Whenever SVV rose above 10, we observed hypotension and fall in CO (as shown by increase in SVR and fall in SV, [Table 1], sr. no. 5), which was corrected by transfusing additional 50 ml aliquots of fluid. Total blood loss was 350 ml (130 ml during surgical dissection and 220 ml during liver resection); one packed red blood cell was transfused to compensate blood loss to ensure optimal oxygen delivery to the tissues. Decreasing SVR (600–850 dyne-s/cm 5) using vasodilatory properties of anesthetic agents (titrating the propofol infusions, additional morphine and fentanyl boluses, and increasing isoflurane dial concentration) and epidural bupivacaine infusion helped to maintain CVP in the range of 2–3 cmH2O during liver resection, which along with the use of Cavitron ultrasonic aspirator (by surgeons) during liver resection helped to limit blood losses.
A low SVR helps to increase the forward flow from LV and reduces LVDEP, resulting in the following changes in cardiopulmonary mechanics:
- Improvement of myocardial performance by reducing wall tension (p = LVDEP, r = radius of LV, and h = LV wall thickness), thus improving subendocardial perfusion and reduced myocardial oxygen demand
- Reduced LAP and TPG, resulting in shifting of excessive alveolar and interstitial fluid to pulmonary circulation, thus reducing the RV afterload and pulmonary congestion. This redistribution of fluid is due to the fact that TPG is a flow-dependent interface which exhibits remarkable pliability being able to refurbish its integrity after normalization of LAP and LV afterload 
- As a consequence of reduced RV afterload, right-sided heart pressure falls and lowers the CVP (0–5 mmHg) and HVP resulting in hepatic decongestion, limiting surgical blood loss and fluid shifts, decreasing liver resection time, and providing hemodynamic stability during liver resection.
We used EV1000 clinical platform for managing this case, as it provides both continuous and intermittent real-time physiological status of the patient, it also supports the perioperative goal-directed fluid therapy and enables one to choose the desired parameter for modulation. Modulating SVR resulted in better forward flow, improved myocardial performance, and reduced pulmonary congestion with improved heart–lung mechanics.
| Conclusion|| |
Patients with very low LVEF undergoing major abdominal surgery including liver resection pose various challenges to the anesthesiologist. The key to successful anesthetic management of these very high-risk patients includes detailed knowledge of pathophysiological changes, precise and beat-to-beat monitoring, intervention and intraoperative modulation of various hemodynamic parameters using EV1000 clinical platform.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Phillip B, Pastor D, Bellows W, Leung JM. The prevalence of preoperative diastolic filling abnormalities in geriatric surgical patients. Anesth Analg 2003;97:1214-21.
van Diepen S, Bakal JA, McAlister FA, Ezekowitz JA. Mortality and readmission of patients with heart failure, atrial fibrillation, or coronary artery disease undergoing noncardiac surgery: An analysis of 38 047 patients. Circulation 2011;124:289-96.
Borlaug BA, Paulus WJ. Heart failure with preserved ejection fraction: Pathophysiology, diagnosis, and treatment. Eur Heart J 2011;32:670-9.
Guazzi MD, Agostoni P, Perego B, Lauri G, Salvioni A, Giraldi F, et al.
Apparent paradox of neurohumoral axis inhibition after body fluid volume depletion in patients with chronic congestive heart failure and water retention. Br Heart J 1994;72:534-9.
Murray RH, Thompson LJ, Bowers JA, Steinmetz EF, Albright CD. Hemodynamic effects of hypovolemia in normal subjects and patients with congestive heart failure. Circulation 1969;39:55-63.
Vasan RS. Diastolic heart failure: The condition exists and needs to be recognized, prevented, and treated. BMJ 2003;327:1181-2.
Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: A systematic review of the literature. Crit Care Med 2009;37:2642-7.
Wan Z, Ristagno G, Sun S, Li Y, Weil MH, Tang W. Preserved cerebral microcirculation during cardiogenic shock. Crit Care Med 2009;37:2333-7.
Preisman S, Kogan S, Berkenstadt H, Perel A. Predicting fluid responsiveness in patients undergoing cardiac surgery: Functional haemodynamic parameters including the respiratory systolic variation test and static preload indicators. Br J Anaesth 2005;95:746-55.
Elliott AR, Fu Z, Tsukimoto K, Prediletto R, Mathieu-Costello O, West JB. Short-term reversibility of ultrastructural changes in pulmonary capillaries caused by stress failure. J Appl Physiol 992;73:1150-8.