key: cord-0860487-01jodk3p authors: Feldheim, Terrence F.; Denham, Margot; Popescu, Wanda M. title: COVID 19: A Stressor for both the patient and the anesthesiologist date: 2021-02-11 journal: J Cardiothorac Vasc Anesth DOI: 10.1053/j.jvca.2021.02.022 sha: d3e6a99b87f995658218584b56eae02e13ba2238 doc_id: 860487 cord_uid: 01jodk3p The COVID-19 pandemic has created not only widespread morbidity and mortality, but a myriad of social, financial and psychological stressors. In this setting, the medical community has seen a substantial increase in the incidence of cardiac morbidity and mortality and therefore, anesthesiologists should expect a higher incidence in the perioperative period. In this E-Challenge, we present a case in which an acute cardiac decompensation occurred secondary to an unanticipated difficult intubation with an unexpected echocardiographic finding. The COVID-19 pandemic has created not only widespread morbidity and mortality, but a myriad of social, financial and psychological stressors. In this setting, the medical community has seen a substantial increase in the incidence of cardiac morbidity and mortality and therefore, anesthesiologists should expect a higher incidence in the perioperative period. In this E-Challenge, we present a case in which an acute cardiac decompensation occurred secondary to an unanticipated difficult intubation with an unexpected echocardiographic finding. The impact that coronavirus disease 2019 (COVID-19) has had on the medical community is incalculable. The pandemic has presented new challenges daily, not only medically, but economically, socially, and psychologically. As the understanding of this novel disease evolves, new insights into medical management as well as both short-and long-term repercussions continue to be discovered. The medical sequelae are not limited to those who have contracted the COVID-19 virus--those living in the new world of a global pandemic have been affected in surprising ways. In this E-Challenge we present a case of an unanticipated medical consequence in the setting of the COVID-19 pandemic. A 74-year-old male, 104 kg and 172 cm, presented in June 2020 for a scheduled right carotid endarterectomy for high grade (90%) internal carotid artery stenosis which was asymptomatic. Surgery had been postponed since March 2020 as a result of the COVID-19 pandemic. The past medical history was significant for hypertension, hyperlipidemia, type II diabetes mellitus, and obesity. The National Surgical Quality Improvement Program (NSQIP) surgical risk calculator identified the patient at a 1.2% risk for cardiovascular complications. A preoperative transthoracic echocardiogram, performed three months prior, revealed a completely normal exam (Video 1). Electrocardiogram (ECG) showed normal sinus rhythm (NSR) with left axis deviation and poor R wave progression. The patient endorsed an exercise tolerance greater than four metabolic equivalents. Preoperative COVID-19 testing was negative. On the day of surgery, the pre-operative airway exam was notable for Mallampati class III, thyromental distance of 3 cm, large thick neck with redundant tissue, and facial hair. The rest of the physical exam and review of symptoms were unremarkable. The patient denied any new onset chest pain, shortness of breath or other concerning symptoms. The patient was brought to the operating room and placed in a ramped position on the procedure table. Standard ASA monitors were applied. After thorough preoxygenation, induction of anesthesia was performed with 100 mcg fentanyl, 100 mg lidocaine, 150 mg propofol and 80 mg rocuronium. The patient required two-handed mask ventilation with an oral airway. Intubation was initially attempted using a video laryngoscope with a size 4 blade. Upon entry into the oropharynx, no identifiable anatomy was noted, but rather extensive redundant tissue. In order to establish a controlled airway, the patient required multiple intubation attempts, utilizing various airway management devices. During this time, the patient became significantly tachycardic and hypertensive, requiring multiple propofol, fentanyl and esmolol boluses. Throughout the intubation attempts, several episodes of non-sustained ventricular tachycardia were noted, which subsequently progressed to a supraventricular tachycardia, with heart rates between 120 and 150 beats per minute. An intraoperative 12-lead ECG identified new onset atrial fibrillation, with no ST-segment changes. Incremental doses of metoprolol were administered in an attempt to reduce the heart rate and convert the patient to NSR. To evaluate the patient's intra-operative cardiovascular status, a transesophageal echocardiographic examination (TEE) was performed (Videos 2, 3, 4). Based on your interpretation of the TEE videos what is the most likely etiology for this patient's cardiovascular decompensation? What about the time period of the COVID-19 pandemic makes this finding more likely? A rescue, time-constrained, intra-operative TEE examination was performed and therefore the ECG is absent in Videos 3 and 4. The echocardiographic examination revealed markedly reduced left ventricular (LV) systolic function with a visually estimated ejection fraction (EF) of 15-20%. Despite the LV foreshortening seen in Video 3, the apex is notably akinetic while the basal segments appear more contractile and the left atrium appears dilated. Figure 1 illustrates the LV in end-systole in the midesophageal two-chamber view. The arrows indicate the classic sign of "apical ballooning" observed in Takotsubo cardiomyopathy (TC) patients. Given the acute changes in LV function and the new onset of atrial fibrillation with a high ventricular rate, the decision was made amongst the anesthesiology team, the surgical team, and a cardiology consultant to cancel the planned procedure. The patient was kept intubated and transferred to the intensive care unit (ICU) on a propofol infusion for sedation. The ICU team, in concert with cardiology, felt that the patient's presentation merited non-urgent evaluation for a coronary syndrome, and scheduled a cardiac catheterization the next morning. While awaiting this, his ICU course was remarkable for a spontaneous conversion to NSR. A transthoracic echocardiogram at that time revealed, despite conversion to NSR, only a mild improvement in his EF to 30% with persistent apical akinesia and hyperdynamic basal segments (Video 5). Troponins T were trended and they peaked at 0.530 ng/ml on post-operative day 0 and then returned to normal. On post-operative day 1, the left heart catheterization identified only non-obstructive coronary artery disease. Given the patient's severely reduced EF with regional wall motion abnormalities (RWMA) consistent with apical ballooning (Figure 1) , mildly elevated troponin levels, and non-obstructive coronary disease, the patient was indeed diagnosed with stress-induced (Takotsubo) cardiomyopathy. The patient was started on heparin infusion, aspirin and a combination of sacubitril (neprilysin inhibitor) and valsartan (angiotensin II receptor blocker). He was discharged home within 48 hours of admission. A repeat echocardiogram four weeks after discharge was notable for a full recovery of the EF to 60% and normalization of all RWMA (Video 6). Six weeks later, the patient underwent an uneventful transcarotid artery revascularization under general anesthesia. For this procedure the airway was secured via an awake bronchoscopic intubation. Takotsubo cardiomyopathy is a rare syndrome of acute, reversible heart failure in patients presenting with symptoms suggestive of acute coronary syndrome (ACS). It is typically described in post-menopausal women and triggered by major stressor events. TC remains a diagnosis of exclusion and each patient warrants a timely and thorough work-up for coronary ischemia. Takotsubo Syndrome (1). Echocardiographic examination represents a cornerstone of the diagnosis. The classic feature of "apical ballooning" consists of transient hypokinesis, akinesis, or dyskinesis of the LV, usually involving the apical and mid segments (2) . Rare cases of basal ballooning have been described and termed "reverse Takotsubo" (3). Additionally, in very rare instances, a midventricular form of TC and a focal form, mostly involving the anterolateral wall, have been described (4) . Right ventricular involvement is characterized by dilation with hypo-or akinesia of the free wall and the apex (5). Generally, RWMAs cross multiple coronary perfusion territories (1). In patients with a prominent septal bulge, due to the hypercontractile basal segments, left ventricular outflow tract (LVOT) obstruction and systolic anterior motion of the mitral valve leaflets with subsequent mitral regurgitation are observed. However, mitral regurgitation can also be present due to the leaflet tethering related to papillary muscle dysfunction. Severe obstructive coronary pathology or acute plaque rupture are not identified during cardiac catheterization. However, often patients with TC carry a concomitant diagnosis of coronary artery disease (6) . Speckle-tracking echocardiography may be helpful in distinguishing the global aspect of TC versus a more regional distribution found with coronary artery occlusion (7) . Patients with TC evaluated with speckle-tracking echocardiography present with a typical "circular" systolic dysfunction. A paradoxical positive longitudinal systolic strain of biventricular mid-apical segments is also identified (8) . Electrocardiographic changes, such as ST-segment elevation or depression, nonspecific T-wave inversions, QT prolongation or low QRS voltage, are common findings in TC (9) . A moderate elevation in serum cardiac troponin and creatinine kinase and a more profound increase in plasma beta-natriuretic peptide levels is seen. Nevertheless, the increase in serum myocardial necrosis biomarkers is disproportionally low compared to the severity of the RWMA, suggesting a reversible nature of injury (10) . Cardiac MRI identifies the presence of cardiac edema and the absence of late gadolinium enhancement. The presence of infectious myocarditis excludes the diagnosis of TC (1). Interestingly, TC has recently been described in COVID-19 positive patients. The pathophysiology of TC in this context, appears to be related to the direct "toxic" effect of cytokines on the cardiomyocyte (11). The incidence of TC among patients with symptoms of ACS has generally been 1-2% (12) . However, a recent large retrospective cohort study showed an increased incidence of TC during the COVID-19 pandemic. In this study, patients presenting for ACS during March and April 2020 had a 7.8% incidence of TC as diagnosed by echocardiographic features in the context of non-obstructive coronary disease observed during cardiac catheterization (13) . It is important to note that in this study all patients diagnosed with TC tested negative for COVID-19. Therefore, the authors suggested that the social, financial and psychological stressors posed by the COVID-19 pandemic itself have created the perfect milieu for the development of TC. Analysis of the etiology of TC has shown physical stress (35-55%) is more often cited than emotional stress (20-39%) as an inducing event (14) . In the setting of this global pandemic, we suspect that there may be a two-hit phenomenon contributing to the increased incidence of TC. The social, psychological and economic strife facing many patients may lead to an increased baseline catecholamine state and ultimately lower the threshold for additional insults (physical or psychological in nature) to incite the debut of TC (15) . In our case, for a patient whose important surgery was delayed for months due to the COVID-19 pandemic, the unanticipated difficult intubation served as a "second hit" to trigger intraoperative stress-induced cardiomyopathy. The management of stress-induced cardiomyopathy consists of primarily providing supportive care until recovery of ventricular function. In patients with none or mild signs of heart failure, initiation of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARB) and beta blockers (BBs) is recommended (16) . However, in patients exhibiting signs of heart failure, diuretics and nitroglycerine could be added to the therapeutic regimen provided that LVOT obstruction is not present (16) . Patients presenting with hypotension or cardiogenic shock should be initially evaluated for the presence of LVOT obstruction. In patients with LVOT obstruction, gentle hydration with intravenous fluid as well as the cautious use of short acting BBs can be considered. Patients in cardiogenic shock may require temporary circulatory support (16) . An important consideration for perioperative physicians is that, in all patients with TC, the use of inotropic medications should be avoided, as they may worsen the cardiomyopathy due to the high catecholamine state seen in the disease process (16) . Anticoagulant therapy can be considered in patients with decreased EF or arrhythmias (16) . The overall prognosis of TC is good, with 96% of patients exhibiting a full cardiac recovery (17) . However, TC is not a completely benign disease process, incurring a mortality of 1-2%. Heart failure and pulmonary edema are the most common complications (16) . Recurrence involves 5-10 % of patients and is typically seen within the first month of the initial event (18) . In conclusion, given the new data pertaining to the increased risk of developing stress-induced cardiomyopathy during this unprecedented period, we believe that it is of critical importance to alert perioperative clinicians to consider this diagnosis when assessing patients with unexplained perioperative hemodynamic instability. Use of echocardiography proves to be an invaluable asset in the diagnostic process. If a diagnosis of TC is entertained, it is important to abstain from utilizing inotropic therapy, which could further aggravate the cardiomyopathy. The white arrows identify the left ventricular apex with a semi-sphere (or balloon) shape rather than its traditional conical shape. 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Popescu) have any conflict of interest to disclose.