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Table of Contents
Year : 2011  |  Volume : 14  |  Issue : 2  |  Page : 156-158
Post-extubation pulmonary edema after open cholecystectomy: Significance of diastolic cardiac dysfunction

Department of Anaesthesia and Intensive Care, PGIMER, Chandigarh, India

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Date of Web Publication25-May-2011

How to cite this article:
Sethi S, Arya VK, Chauhan S. Post-extubation pulmonary edema after open cholecystectomy: Significance of diastolic cardiac dysfunction. Ann Card Anaesth 2011;14:156-8

How to cite this URL:
Sethi S, Arya VK, Chauhan S. Post-extubation pulmonary edema after open cholecystectomy: Significance of diastolic cardiac dysfunction. Ann Card Anaesth [serial online] 2011 [cited 2021 Jan 25];14:156-8. Available from:

The Editor,

Pulmonary edema after tracheal extubation due to diastolic cardiac dysfunction in anesthetized patients is not common to find in the literature. A considerable number of patients undergoing noncardiac surgery have diastolic cardiac function that may lead to diastolic heart failure (DHF), which can complicate their perioperative course. This form of failure occurs more commonly in patients with hypertensive or valvular heart disease, diabetes mellitus, myocardial ischemia, as well as in hypertrophic or restrictive cardiomyopathy, and is more prevalent in the elderly. [1] Despite diastolic dysfunction being increasingly recognized as a cause of heart failure, its presence in the perioperative period remains insignificant for most of anesthesiologists. We report a case of acute post-extubation pulmonary edema because of aggravation in preexisting diastolic cardiac dysfunction.

A 55-year-old female patient was scheduled for elective open cholecystectomy. She had well controlled hypertension and diabetes for the past 10 years. All preoperative investigations were unremarkable except for borderline left ventricular (LV) hypertrophy (LV posterior wall thickness, 9 mm) and mild LV diastolic dysfunction (E=A; isovolumic relaxation time (IVRT), 112 ms) on echo and prominent bronchovascular markings on chest x-ray. Her physical examination and airway assessment were unremarkable.

Anesthesia was administered with intravenous morphine 0.1 mg/kg, inj. propofol 2 mg/kg and inj. vecuronium 0.1 mg/kg. Trachea was intubated by a trainee, and was associated with increase in blood pressure (186/106 mm Hg). The anesthesia was maintained with 50% nitrous oxide and oxygen mixture with isoflurane concentration titrated to achieve a combined mean alveolar concentration value between 1 and 1.5. Intraoperative course in the first hour was uneventful, during which 1 L of normal saline was infused. At the end of the surgery, neuromuscular blockade was antagonized with intravenous glycopyrrolate 0.4 mg and neostigmine 2.5 mg. During extubation, BP again increased to 186/110 mm Hg; and it gradually settled down after extubation. Approximately 15 minutes following this, the patient became drowsy, unresponsive and had airway obstruction, which was relieved with jaw lift. Despite this, saturation dropped to 87% and was administered 100% oxygen with facemask while breathing spontaneously. SpO 2 improved to 95%-96% on 100% oxygen, and she started obeying commands. She had stable vitals at this time and was pain free. However, she was desaturating below 90% on removing oxygen supplementation. She was shifted to post-operative care unit. Chest auscultation revealed bilateral basal coarse inspiratory crepitations. Arterial blood gas analysis (ABG) showed pH of 7.30; PaO 2 , 56.8 mm Hg; PaCO 2 , 51.4 mm Hg; bicarbonate 0 24.9 mmol/L; base excess, -2.1 mmol/L; and SpO 2 , 86%. chest X-ray showed bilateral infiltrates. by now the patient was conscious, hemodynamically stable and breathing normally. Continuous positive airway pressure (CPAP) of 6 cm H 2 O with FiO 2 of 0.6, and intravenous furosemide 40 mg was administered. electrocardiogram was normal during this episode. Enquiring qithe patient again revealed prior hospital admissions for breathlessness and pedal edema associated with high blood pressure. Troponin T test after 4 hours was normal; however, transthoraic echocardiography revealed moderate diastolic dysfunction (A>E; A deceleration time, 96 ms; and E deceleration time, 258 ms; [Figure 1]a and b) with normal systolic function and inferior vena cava collapse. The patient recovered in 24 hours with noninvasive ventilation (NIV) CPAP and intravenous boluses of furosemide 40 mg 8 th hourly. She remained hemodynamically stable thereafter, and the diastolic function improved to mild diastolic dysfunction (E=A; IVRT, 115 ms) postoperatively after 48 hours.
Figure 1: Transthoracic echo images - (a) A>E; A deceleration time, 96 ms; (b) A>E; E deceleration time, 258 ms, suggestive of diastolic dysfunction

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Diastolic heart failure is an underestimated pathology with a high risk of acute decompensation throughout the perioperative period during the periods of stress. Any increase in venous and/ or arterial tone, as during periods of catecholamine surges due to inadequate anesthetic depth or exaggerated stress response in association with a relatively small increase in central blood volume can produce a substantial increase in left ventricular diastolic and pulmonary venous pressures, resulting in pulmonary edema. The worsening of diastolic dysfunction the earliest harbinger of myocardial ischemia; further worsening relaxing properties and aggravating diastolic dysfunction. Vasan and Lewy [2] proposed diagnostic criteria for DHF and divided it into definite, probable and possible DHF. Echocardiographically, moderate diastolic dysfunction is diagnosed with impaired relaxation indicated by mitral inflow parameter A wave > E wave with prolonged deceleration of E wave > 240 ms. [3]

Many risk factors, including female gender, uncontrolled hypertension, atrial fibrillation, myocardial ischemia, diabetes mellitus, renal insufficiency and echo findings (left ventricular hypertrophy, impairment of diastolic dysfunction, preserved left ventricular ejection fraction (LVEF), [3] may precipitate overt systolic and diastolic heart failure. [4],[5] However, uncontrolled hypertension is involved in more than 50% of cases of acute DHF.

In the above context, our patient fulfilled the criteria for possible diagnosis of DHF as a consequence of hemodynamic instability due to exaggerated stress response at the time of intubation and extubation. Also preoperative history of hospital admission suggestive of previous DHF and additional risk factors such as diabetes mellitus, female gender and old age could have accentuated perioperative decompensation.

The primary alternative diagnosis in our case could be flash pulmonary edema (FPE), which is characterized by sudden and recurrent episodes of breathlessness at rest resulting from acute pulmonary congestion in the presence of normal or well-preserved left ventricular systolic function and is often precipitated by acute myocardial infarction, acute mitral and aortic regurgitation, accelerated hypertension or almost by any cause of elevated left ventricular filling pressures. This is mostly nocturnal and occurs suddenly and is often associated with renovascular disease, but the reported patient had neither renovascular disease nor dyspnea was not nocturnal. The pulmonary edema occurred immediately after extubation, not at rest.

Aspiration leading to pulmonary edema seems unlikely in this case as there was no evidence for it (regurgitation or vomits), and typical chest X-ray of aspiration appeared within 1 hour.

Negative pressure pulmonary edema is less likely because airway obstruction was partial, very brief and not sustained enough to explain development of markedly negative intrapleural pressures.

In conclusion, it is time for anesthetists to be aware of diastolic dysfunction of the heart.

   References Top

1.Alsaddique AA, Royse AG, Royse CF, Fouda MA. Management of diastolic heart failure following cardiac surgery. Eur J Cardiothorac Surg 2009;35:241-9.  Back to cited text no. 1
2.Vasan RS, Levy D. Defining diastolic heart failure: A call for standardized diagnostic criteria. Circulation 2000;101:2118-21.  Back to cited text no. 2
3.Pirracchio R, Cholley B, De Hert S, Solal AC, Mebazaa A. Diastolic heart failure in anaesthesia and critical care. Br J Anaesth 2007;98:707-21.  Back to cited text no. 3
4.Tsuyuki RT, McKelvie RS, Arnold JM, Avezum A Jr, Barretto AC, Carvalho AC, et al. Acute precipitants of congestive heart failure exacerbations. Arch Intern Med 2001;161:2337-42.  Back to cited text no. 4
5.Zannad F, Mebazaa A, Juillière Y, Cohen-Solal A, Guize L, Alla F, et al. Clinical profile, contemporary management and one-year mortality in patients with severe acute heart failure syndromes: The EFICA study. Eur J Heart Fail 2006;8:697-705.  Back to cited text no. 5

Correspondence Address:
Sameer Sethi
Department of Anaesthesia,PGIMER, Sector 12, Chandigarh - 160 012
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.81576

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