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A 50-Year-Old Woman With a History of Hypertension and Tobacco Use Presenting With Hypoxia FREE TO VIEW

Hangyul M. Chung-esaki, MD; Sara Nikravan, MD
Author and Funding Information

Dr Chung-esaki is currently at Queen’s Medical Center (Honolulu, HI).

Stanford University Hospital and Clinics, Palo Alto, CA

CORRESPONDENCE TO: Sara Nikravan, MD, Stanford University Hospital and Clinics, 300 Pasteur Dr, Room H3583, MC 5640, Palo Alto, CA 94305


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(3):e73-e76. doi:10.1016/j.chest.2015.12.045
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Published online

A 50-year-old woman with a history of hypertension and tobacco use was brought in by ambulance after sudden loss of consciousness with persistent coma. She was intubated in the field for airway protection and was profoundly hypertensive on presentation to the emergency department. On arrival, she underwent CT imaging of the brain, which revealed a Hunt and Hess grade 5, Fisher grade 3 subarachnoid hemorrhage (SAH) (Fig 1), with a 5-mm anterior communicating artery aneurysm (Fig 2).

Figure Jump LinkFigure 1 Head CT scan showing diffuse subarachnoid hemorrhage.Grahic Jump Location

Figure Jump LinkFigure 2 Head CT angiography showing a 5-mm anterior communicating artery aneurysm.Grahic Jump Location

After head imaging had been performed, she developed severe hypoxia requiring 100% inspired oxygen. A chest radiograph demonstrated patchy bilateral infiltrates (Fig 3).

Figure Jump LinkFigure 3 Portable chest radiograph showing bilateral patchy infiltrates. Calipers were used to measure endotracheal tube position.Grahic Jump Location

Given her SAH, hypoxia, and severe hypertension, she was admitted to the ICU for blood pressure control and neurologic monitoring. A few hours after admission, she became hypotensive despite cessation of nitroprusside infusion. Point-of-care transthoracic echocardiography (TTE) was performed to investigate the cause of her hypoxia and new-onset hypotension (Videos 1, 2).

Question: On the basis of Videos 1 and 2, and the patient’s clinical presentation, what is the most likely diagnosis?

Answer: Neurogenic stress cardiomyopathy

Focused point-of-care TTE was done in this case (see Video 3) to investigate the etiology of the patient’s hypoxia and new-onset hypotension. The TTE immediately revealed left ventricular (LV) dysfunction. With further careful investigation, regional wall motion abnormalities (RWMAs) were noted in the parasternal short-axis view of the left ventricle at the mid-papillary level. Although the parasternal short-axis view of the left ventricle showed septal, inferior, and lateral wall motion abnormalities, the apex was not visualized in this view. Point-of-care TTE, while focused, should allow for full visualization of both ventricles during the investigation of unexplained hypotension and hypoxia. Preserved LV apical function was noted only after obtaining the subcostal four-chamber view, one that allows for visualization of the apex. Collectively, Videos 1 and 2 revealed a dilated inferior vena cava, depressed LV function with RWMAs, and apical sparing. There were no ST-T segment changes seen on the ECG, but troponin I was elevated to 8.9 ng/mL. Initiation of epinephrine infusion rapidly improved her hypotension, hypoxia, and cardiac function. Follow-up troponin I levels were down-trending. Formal TTE on day 2 confirmed reduced LV systolic function, with an estimated ejection fraction of 45% and inferior, lateral, and septal wall motion abnormalities. The patient received a diagnosis of neurogenic stress cardiomyopathy (NSCM) and continued receiving supportive measures with mechanical ventilation and ionotropic support. After aneurysm coiling, the patient continued to improve, with an increased ejection fraction to 54% on day 3. By day 5, she was weaned off epinephrine, following commands, and extubated with minimal oxygen requirements.

NSCM is seen in 17 to 40% of patients following aneurysmal SAH (aSAH), resulting in increased morbidity and mortality. LV dysfunction usually occurs within 2 days of ictus without coronary artery occlusion, and tends to improve spontaneously over days to weeks. This phenomenon is thought to be caused by excessive catecholamine release in the sympathetic nerve terminals, due to acute stress and stimulation of the medullary autonomic center, similar to other stress-related cardiomyopathies (eg, takotsubo syndrome, pheochromocytoma-related cardiomyopathy, and cardiac dysfunction in critical illness).

Diagnosis of NSCM requires the presence of cardiac dysfunction with a predisposing neurologic condition (eg, aSAH, ischemic stroke, severe head trauma). Clinically, patients may be asymptomatic or present with cardiogenic shock, with 10% of patients developing pulmonary edema. Abnormalities on the ECG are found in 25 to 75% of patients and may include sinus bradycardia, ST segment changes, inverted T waves, and QT prolongation. An elevation in troponin I is seen in 20 to 30% of patients with aSAH and is associated with higher Hunt and Hess grades, early LV dysfunction, RWMAs, and ventricular arrhythmias.

On echocardiograms, RWMAs are seen in 8 to 13% of patients with SAH. Classically, stress-related cardiomyopathies are associated with “apical ballooning” with hypercontractile basal segments in the left ventricle as seen in takotsubo syndrome.,, The increased contractility of the basal segments may cause dynamic LV outflow tract obstruction due to systolic anterior motion of the anterior mitral leaflets. While this pattern is observed in some cases of NSCM, an “inverse” pattern involving the basal and mid-ventricular segments without apical involvement, as in our case, may be more common with neurologic injury. The cause of this variation in RWMA is unclear, but both patterns appear to involve multiple epicardial coronary vessel territories, distinguishing it from acute myocardial infarction.

Identifying NSCM in aSAH has implications in management. In hemodynamically stable patients, catecholamines should be limited and α and β blockade may be considered. In cardiogenic shock, inotropes such as milrinone may be used to avoid sympathetic activation. However, vasopressors and inotropes may be required to support cerebral perfusion and minimize ischemia in vasospasm. LV dysfunction may also limit “triple H” therapy (hypertension, hypervolemia, hemodilution) for vasospasm. In these cases, aggressive endovascular therapies and other methods of hemodynamic augmentation such as intraaortic balloon pump should be considered. Worsening LV dysfunction can be seen with the development of brain death. However, as LV function may improve with time, NSCM does not preclude cardiac donation after brain death as long as LV function is monitored closely by serial echocardiography.

  • 1.

    Point-of-care TTE can be used as a real-time tool for the evaluation of unexplained hypoxia and hypotension.

  • 2.

    Visualization of the entire left ventricle is critical to rule out the presence of RWMA.

  • 3.

    NSCM should be considered in patients with severe aneurysmal subarachnoid hemorrhage, especially those with ECG changes, elevated troponin, pulmonary edema, and hypotension.

  • 4.

    RWMAs can be seen in NSCM with or without apical ballooning, but usually are not limited to a single epicardial vessel territory.

  • 5.

    Patients with NSCM should be monitored by serial echocardiography, as worsening LV dysfunction is associated with increased mortality and worse outcomes.

Financial/nonfinancial disclosures: None declared.

Author contributions: H. M. C.-e. and S. N. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis, including and especially any adverse effects. H. M. C.-e. helped design the study and write the manuscript; S. N. helped write the manuscript.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Additional information: To analyze this case with the videos, see the online version of this article.

Hravnak M. .Frangiskakis J.M. .Crago E.A. .et al Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage. Stroke. 2009;40:3478-3484 [PubMed]journal. [CrossRef] [PubMed]
 
Banki N. .Kopelnik A. .Tung P. .et al Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15-20 [PubMed]journal. [CrossRef] [PubMed]
 
Lee V.H. .Oh J.K. .Mulvagh S.L. .Wijdicks E.F.M. . Mechanisms in neurogenic stress cardiomyopathy aneurysmal subarachnoid hemorrhage [review]. Neurocrit Care. 2006;5:243-249 [PubMed]journal. [CrossRef] [PubMed]
 
Bybee K.A. .Prasad A. . Stress-related cardiomyopathy syndromes. Circulation. 2008;118:397-409 [PubMed]journal. [CrossRef] [PubMed]
 
Friedman J.A. .Pichelmann M.A. .Piepgras D.G. .et al Pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurosurgery. 2003;52:1025-1031 [PubMed]journal. [CrossRef] [PubMed]
 
Lee J.W. .Kim J.Y. . Stress-induced cardiomyopathy: the role of echocardiography [review]. J Cardiovasc Ultrasound. 2011;19:7-12 [PubMed]journal. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 Head CT scan showing diffuse subarachnoid hemorrhage.Grahic Jump Location
Figure Jump LinkFigure 2 Head CT angiography showing a 5-mm anterior communicating artery aneurysm.Grahic Jump Location
Figure Jump LinkFigure 3 Portable chest radiograph showing bilateral patchy infiltrates. Calipers were used to measure endotracheal tube position.Grahic Jump Location

Tables

References

Hravnak M. .Frangiskakis J.M. .Crago E.A. .et al Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage. Stroke. 2009;40:3478-3484 [PubMed]journal. [CrossRef] [PubMed]
 
Banki N. .Kopelnik A. .Tung P. .et al Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15-20 [PubMed]journal. [CrossRef] [PubMed]
 
Lee V.H. .Oh J.K. .Mulvagh S.L. .Wijdicks E.F.M. . Mechanisms in neurogenic stress cardiomyopathy aneurysmal subarachnoid hemorrhage [review]. Neurocrit Care. 2006;5:243-249 [PubMed]journal. [CrossRef] [PubMed]
 
Bybee K.A. .Prasad A. . Stress-related cardiomyopathy syndromes. Circulation. 2008;118:397-409 [PubMed]journal. [CrossRef] [PubMed]
 
Friedman J.A. .Pichelmann M.A. .Piepgras D.G. .et al Pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurosurgery. 2003;52:1025-1031 [PubMed]journal. [CrossRef] [PubMed]
 
Lee J.W. .Kim J.Y. . Stress-induced cardiomyopathy: the role of echocardiography [review]. J Cardiovasc Ultrasound. 2011;19:7-12 [PubMed]journal. [CrossRef] [PubMed]
 
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