Acute Reversible Left Ventricular Dysfunction  Following General Anesthesia

A Anjaneyulu, V Koti Reddy, P Krishnam Raju, A Rajagopalaraju, 
A Sreenivas Kumar, R Ravichandra
 Departments of Cardiology and Cardiac Anesthesia, Care Hospital, Hyderabad

Acute reversible left ventricular dysfunction due to myocardial stunning is a known phenomenon during acute  myocardial infarction, coronary angiography, coronary angioplasty or after coronary artery bypass surgery. We  report a rare case of acute reversible dysfunction of the myocardium as a complication of general anesthesia in  a patient with normal coronary arteries. This is a potentially fatal complication unless recognized early and  treated aggressively. (Indian Heart J 2001; 53: 508–510)

 Key Words: Myocardial stunning, Complications, Anesthesia   

Cardiogenic shock as a complication of general  anesthesia is usually secondary to a myocardial  infarction (MI) in patients with underlying coronary artery  disease (CAD). When this complication occurs in patients  without pre-existing CAD, it could be due to severe coronary  spasm. This may result in an infarct or stunning of the  myocardium leading to left ventricular (LV) dysfunction. A  transmural infarct may heal with scarring and  thereby residual LV dysfunction, whereas a stunned  myocardium can regain its normal contractility. Bedside  echocardiography helps in recognizing this complication  early, and aggressive management to support the  dysfunctional myocardium by inotropic drugs, intra-aortic  balloon pump (IABP) or LV assist devices could restore the  LV function to normal. We report a case of stunned  myocardium following endotracheal intubation. 

Case Report

A 45-year-old woman, mildly hypertensive with no other  coronary risk factor and with a normal resting  echocardiogram, was taken up for nasal polypectomy under  general anesthesia. She was premedicated with 75 mg of  pethidine intravenously (i.v.). General anesthesia was  induced with i.v. pentothal sodium and vecuronium was  used as a muscle relaxant. Endotracheal intubation was  difficult and required three attempts which took about 2–3  minutes. Oxygen saturation ranged between 85% and 90%  during this period. Soon after intubation, she had an episode  of ventricular tachycardia which was converted to sinus  rhythm with a bolus of 60 mg i.v. lignocaine. Within the  next 5 minutes, she developed sinus tachycardia of 160  beats/min with an S3 gallop and hypertension (blood  pressure 180/120 mmHg). She developed pulmonary  edema, with frothy fluid gushing out of the endotracheal  tube. There was a fall in systemic arterial oxygen saturation  (SaO 2 78%). Initially her oxygen saturation improved to  85% with 60 mg i.v. furosemide and a nitroglycerine drip at  a rate of 5 µg/min. The systemic pressure fell to 70 mmHg  systolic within 10 minutes of starting the nitroglycerine  drip and she was put on inotropic support (dopamine 10  µg/kg/min and dobutamine 7.5 µg/kg/min). The  electrocardiogram (ECG) taken within 15 minutes of the  episode showed sinus tachycardia with no ST- or T-wave  changes. Arterial blood gas (ABG) levels deteriorated and  were: PaO2 54 mmHg; PaCO2 38 mmHg; and the pH was  7.210. At this stage, an echocardiogram revealed severe LV dysfunction (LVend-systolicdimension[LVESD]:3.4cm,and  LVend-diastolicdiastolic dimension [LVEDD]: 4cm)withan  akinetic anterior wall and dyskinetic interventricular  septum. The left ventricular ejection fraction (LVEF) was  25% and there was mild mitral regurgitation (Fig. 1). She  was shifted to the ICCU and a central venous pressure (CVP)  line as well as an arterial line for pressure monitoring were  established along with continued ventilatory and inotropic  support. Her CVP was 10 mmHg. An ABG analysis after 3  hours of support showed improvement (PaO2 108 mmHg;  PaCO2 32 mmHg; pH 7.350). Metabolic acidosis was corrected by i.v. sodium bicarbonate. The systemic  blood pressure was 96/50 mmHg and the urine output  40 ml/hour. The patient was put on L-carnitine. After 12  hours, she developed another bout of pulmonary edema  while on maximal inotropic (dobutamine 15 µg/kg/min  and dopamine 15 µg/kg/min) and ventilatory support. The  systemic blood pressure was 60 mmHg (systolic), ABG  measurements were: PaO 2 64 mmHg; PCO 2 40 mmHg and  the pH 7.345. A repeat echocardiogram showed severe LV  dysfunction involving all the segments with an LVESD of  3.5 cm; LVEDD of 3.9 cm and EF of 15%. At this stage,  IABP support was initiated. She became hemodynamically  stable with a mean arterial pressure of 82 mmHg and an  augmented pressure of 106 mmHg. The ABG levels  improved over the next 6 hours—PaO2 124 mmHg, PCO2  28 mmHg at an FIO2 of 80%. Cardiac enzyme levels were  mildly elevated (CK 640 IU, CK-MB 32 IU) on the first day.  Serial CK and CK-MB readings over the next two days were  CK 210 IU and 146 IU, CK-MB 20 IU and 18 IU, respectively.  Repeat echocardiograms over the next 4 days showed  progressive improvement in LV contractility with more  segments regaining normal contractility. Serial ECGs did  not show any evolving changes of transmural MI. Small  daily doses of 3.125 mg carvedilol and 0.25 mg of digoxin  were added on the third day. She maintained stable arterial  pressure and good urine output (50–60 ml/hour). By the  fifth day, the LVEF improved to 45% (LVESD 3 cm, LVEDD  4.1 cm). Chest X-ray showed no evidence of pulmonary edema and she was weaned away from IABP support. By  the seventh day, she was weaned away from the ventilator  and inotropic support. At this time, the echocardiagram  showed a normal-sized LV (ESD 2.8 cm; EDD 4 cm) with an  EF of 50%. There was hypokinesia of the lateral wall and  distal part of the septum. The ECG at this stage showed ST  coving with T-wave inversion in leads I and aVL. The patient  was fully ambulant with no cardiac symptoms by the tenth  day. Her echocardiogram showed normal LV function with  no regional wall motion abnormality (Fig. 2). A diagnosis  of pheochromocytoma was ruled out by the estimation of  urinary vanillylmandelic acid (VMA) and metanephrine,  and a negative abdominal ultrasound for adrenal and para-aortic  masses. Coronary angiography done after an interval  of 3 weeks revealed normal epicardial coronary arteries.  She was discharged on diltiazem and was doing well at 6  months follow-up with a normal ECG and echocardiogram. 

Discussion  

This 45-year-old woman with no significant coronary risk  factor developed cardiogenic shock following endotracheal  intubation for general anesthesia. This case was  characterized by acute severe LV dysfunction in a previously  normal heart with normal LV function. She developed  transient hypertension and extreme sinus tachycardia  followed by hypotension and pulmonary edema. The ECGs  did not show any acute MI pattern (ST elevation) and there was no significant elevation of cardiac enzyme levels, thus  ruling out an acute transmural MI. The fact that the  myocardial contractility improved slowly with inotropic  support shows that the myocardium was metabolically  active. 

Stunned myocardium is characterized by reversible  contractile dysfunction, when the myocardial blood flow is  fully or almost fully restored. In this condition, no metabolic  deterioration occurs during inotropic stimulation. If  myocardial stunning is severe, involving large parts of the  LV and thus impairing global LV function, it can be reversed  with inotropic agents and procedures. Our patient required  IABP support. 

What is the trigger for acute LV dysfunction in these  cases? In our case, no surgical procedure had been started;  only endotracheal intubation was done which was preceded  by the administration of pentothal sodium and vecuronium.  However, intubation was not easy and required multiple  attempts. A number of agents used during general  anesthesia may have negative effects on myocardial  contractility.1 Halothane and enflurane have mild negative  inotropic effects, especially in pre-existing LV dysfunction.  However, our patient did not receive any of these agents.  Intravenous thiopental and methohexital may also depress  myocardial contractility in patients with impaired LV  function or elderly subjects. Though our patient received  i.v. pentothal, it is unlikely that this would have contributed  to the LV dysfunction because prior LV function was normal.  In the absence of a specific myocardial depressant and as  the patient had persistent sinus tachycardia with an initial  elevation of blood pressure, we postulate that an acute  hyperadrenergic state developed following endotracheal  intubation. This could have produced transient severe  coronary spasm2 resulting in global LV dysfunction and  cardiogenic shock. 

An increase in plasma adrenaline and noradrenaline  concentrations has been observed following tracheal  intubation and surgery.3 Oral premedication with  metoprolol attenuates the hypertensive response to tracheal  intubation and reduces arrhythmias and operative blood  loss during hysterectomy.3 Post-tachycardia-related  cardiomyopathy was considered a possibility, but the interval  between the tachycardia and LV dysfunction noted by echo-cardiography  was very short (15 minutes). Studies using  ambulatory ECG monitoring4 have also demonstrated  myocardial ischemia during tracheal intubation and  extubation. There have been reports of intraoperative  coronary spasm during noncardiac surgery and one of  these cases required several hours to become  hemodynamically stable.5 Since our patient had a normal coronary angiogram, coronary spasm is a possibility which  might have resulted in acute ischemic LV dysfunction.  Structure-independent epicardial vasospasm can be an  important element in serious cardiac ischemic events,  particularly the focal persistent vasospasms that occur  without plaques or injury.6 There was a case report of a 23-year-old woman without previous CAD developing an acute  non-Q MI and stunned myocardium following topical  lignocaine and phenylephrine used during nasal  septoplasty.7 However, our patient did not receive any topical  nasal medication. The possibility of severe LV systolic  dysfunction secondary to an acute increase in after-load  (severe hypertension) was also considered. In this event,  the systolic dysfunction should resolve within a few hours  of correcting the hypertension. 

Our patient required more than 96 hours of inotropic  and IABP support which would indicate an ischemia-induced  LV dysfunction. Since the majority of LV myocardial  segments were involved in the dysfunction (akinesia,  dyskinesia) and all of them returned to normal contractility,  it would fit in with the phenomenon of “stunned  myocardium”. Although acute MI due to anesthesia-induced  coronary spasm has been reported,8 only a few  cases of stunned myocardium have been reported so far  following noncardiac surgery.9

Correspondence:
Dr Anne Anjaneyulu, 
Department of Cardiology,  
Care Hospital, Road No. 1, 
Banjara Hills, 
Hyderabad 500 034.  
e-mail: anjan_anne@yahoo.com

References 

  1. Mckinney MS, Fee JP, Clarke RS. Cardiovascular effects of isoflurane  and halothane in young and elderly adult patients. Br J Anaesth  1993; 71: 696–701 

  2. Yamasaki F, Sato T, Takata J, Chikamori T, Ozawa T, Sasaki M, et al.  Sympathetic hyperactivity in patients with vasospastic angina. Jpn  Circ J 1996; 60: 10–16 

  3. Jacobsen CJ, Blom L. Effect of perioperative metoprolol on  cardiovascular and catecholamine response and bleeding during  hysterectomy. Eur J Anaesthesiol 1992; 9: 209–215 

  4. Edwards ND, Alford AM, Dobson PM, Peacock JE, Reily CS.  Myocardial ischemia during tracheal intubation and extubation.  Br J Anaesth 1994; 73: 537–539 

  5. Yammanoue T, Horibe M, Izuri H, Tsuchiya T. Intraoperative  coronary spasm: retrospective review of 10 cases. Masui 1990; 39:  376–382 

  6. Homsmeyer K, Miyagawa K, Kelly ST, Rosch J, Hall AS, Axthelm  MK, et al. Reactivity-based coronary vasospasm independent of  atherosclerosis in Rhesus monkeys. J Am Coll Cardiol 1997; 29: 671–  680 

  7. Aschi M, Wiedmann HP, James KB. Cardiac complications from use  of cocaine and phenylephrine in nasal septoplasty. Arch Otolaryngol  Head Neck Surg 1995; 121: 681–684 

  8. Zainea H, Duvernoy WF, Chauhan A, David S, Soto E, Small D. Acute  myocardial infarction in angiographically normal coronary  arteries following induction of general anesthesia. Arch Intern Med  1994; 154: 2495–2498 

  9. Shirakami G, Shingu K, Tamai S, Ando A, Suga S, Nakao K, et al.  Case of stunned myocardium after noncardiac surgery. Anesthesia  Analg 1994; 79: 175–179