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Utility of Bedside Cardiac POCUS in Identification and Management of a Patient With Subarachnoid Hemorrhage and Takotsubo Cardiomyopathy

By Currents Editor posted 10-19-2021 07:29


Jennifer Mears, PA, Weill Cornell Medicine/New York-Presbyterian Hospital

Judy Ch’ang, MD, Weill Cornell Medicine/New York-Presbyterian Hospital


 The incidence of subarachnoid hemorrhage (SAH) patients who develop Takotsubo cardiomyopathy (TCM) is approximately 4-15%.1 Vasospasm is another common complication of SAH. Treatments of vasospasm can compromise cardiac function.2 This case report suggests cardiac point of care ultrasound (cPOCUS) may be assistive in frequent monitoring of cardiac status and management adjustments in complex SAH patients.

In aneurysmal SAH patients, euvolemia is targeted in order to prevent delayed cerebral ischemia (DCI) and irreversible neurological damage.3 Treatment for DCI and vasospasm includes maintaining euvolemia and utilizing vasopressors to preserve cerebral blood flow. However, these management techniques can be very difficult to achieve if the patient also has severe cardiac dysfunction. Takotsubo cardiomyopathy (TCM) is an acute cardiac condition of diminished cardiac contractility caused by sympathetic nervous stimulation and catecholamine surge which can be due to acute neurological injury.4,5  It is seen in approximately 4-15% of SAH patients. TCM may result in sudden onset heart failure, independent of any cardiac issues preceding the neurologic injury. The pathognomonic echocardiogram pattern for TCM is hypercontractile basal segments and apical hypokinesis leading to “apical ballooning,” giving it the appearance of a Japanese octopus trap. TCM is considered to be a reversible cause of acute heart failure, with a majority of patients expected to have a complete cardiac recovery.4

Case & Discussion 

A 71-year-old female presented with a Hunt Hess 4, Modified Fisher 4 SAH from a ruptured right posterior communicating aneurysm. Her course was complicated by early, severe vasospasm in her right internal carotid artery, right middle cerebral artery, and bilateral anterior cerebral arteries with correlating transient motor deficits. On post bleed day 2, she was noted to have supraventricular tachycardia on telemetry, a type II NSTEMI with troponin leak, BNP 1700, and anterior-inferior acute ischemic changes on EKG with diffuse T wave inversions (Figure 1). Our bedside cPOCUS revealed the classic TCM pattern with left ventricular (LV) apical hypokinesis, and with our ultrasound’s auto-EF function the EF was calculated to be approximately 30%. Cardiology recommended administering a beta-blocker and ACE inhibitor; however, this could not be tolerated from a neurologic standpoint. At this time, she was requiring moderate doses of vasopressors to improve cerebral perfusion with improvement in her neurologic exam. 

Cardiac POCUS on post bleed day 4 was performed in the setting of worsening oxygenation and neurological fluctuations concerning for worsening vasospasm. It re-demonstrated depressed left ventricle ejection fraction and apical hypokinesis. The overall assessment including physical exam, chest x-ray, straight leg raise and inferior vena cava (IVC) collapsibility determined that the etiology of her hypoxia was related to being fluid overloaded in the setting of her depressed ejection fraction and aggressive fluid resuscitation. As her cardiac biomarkers were downtrending, the decision was made to prioritize using vasopressors over further fluid resuscitation, in addition to diuresis. Other less cardiotoxic methods, such as cerebral intra-arterial verapamil, angioplasty, and stellate ganglion blocks, were used frequently throughout her severe vasospasm window.  

Repeated cardiac POCUS studies helped guide management decisions by revealing gradual resolution of the apical hypokinesis and improvement in systolic function. This was confirmed by repeat official transthoracic echocardiogram on post bleed day 32, which revealed an EF of 38% with decreased inter-segmental variation in wall motion dysfunction. After a month in the ICU, she was discharged to the stepdown unit. She required a tracheostomy, PEG tube, and ventriculoperitoneal shunt, and was discharged to acute rehabilitation. Her cardiac function subsequently improved as expected, requiring no further work up. 

Figure 1


 POCUS Short Clips

1) Parasternal long axis view

2) Apical 4-chamber view

3) IVC


The parasternal long-axis and apical 4-chamber views demonstrate the classic pattern of wall motion abnormality with apical hypokinesis and basal hypercontractility in the LV. The proposed pathophysiology of the Takotsubo pattern suggests a high concentration of beta adrenoreceptors in the LV apex as opposed to the basilar segments of the LV. In response to neurologic injury, the increased circulating catecholamines therefore stun the apical myocardium, leaving the base to be contractile.4 

The IVC POCUS demonstrates decreased respiratory variability of IVC, measuring over 2mm, concerning for increased volume status. However, it should be noted that while our patient was intubated, she was not paralyzed. IVC measurement in critical care has been shown to be a poor predictive metric for fluid responsiveness in isolation, and should therefore only be regarded as supplemental material for an overall clinical picture.6, 7 


While cardiac POCUS is not yet a highly utilized bedside skill among neurocritical care units, it can provide important information regarding cardiac function and fluid status which can help guide vasospasm and cardiopulmonary management.8 If not caught early enough in a patient’s course, TCM may contribute to worse outcomes and significantly increase mortality in SAH patients. In one study, SAH patients with TCM had a mortality rate of 22% compared to 15% mortality in SAH patients without TCM.9 This must be taken into careful consideration when making management decisions regarding fluid administration, diuresis, vasopressor use, and inducted hypertension goals. Cardiac POCUS can help guide this delicate balance of preserving neurologic and cardiac function. 

Works Cited 

  1. Shimada M, Rose JD. Takotsubo cardiomyopathy secondary to intracranial hemorrhage. Int J Emerg Med. 2014;7:33. Published 2014 Sep 4. doi:10.1186/s12245-014-0033-4
  2. Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown RD Jr, Wijdicks EF. Takotsubo cardiomyopathy in aneurismal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. PMID: 17219832 DOI: 10.3171/jns.2006.105.2.264
  3. Nassar HGE, Ghali AA, Bahnasy WS, Elawady MM. Vasospasm following aneurysmal subarachnoid hemorrhage: prediction, detection, and intervention. Egypt J Neurol Psychiatr Neurosurg. 2019;55(1):3. doi:10.1186/s41983-018-0050-y
  4. Akashi YJ, Goldstein DS, Barbaro G, et al. Takotsubo Cardiomyopathy: A New Form of Acute, Reversible Heart Failure. Circulation. 2008;118:2754-2762. Doi: 10.1161/CIRCULATIONAHA.108.767012 PMID 19106400
  5. Benarroch EE. The central autonomic network: functional organization, dysfunction, and perspective. Mayo Clin Proc. 1993 Oct;68(10):988-1001. doi: 10.1016/s0025-6196(12)62272-1. PMID: 8412366.
  6. Caplan, M., Durand, A, Bortolotti P. et al. Measurement site of inferior vena cava diameter affects the accuracy with which fluid responsiveness can be predicted in spontaneously breathing patients: a post hoc analysis of two prospective cohorts. Ann. Intensive Care. 2020: 10(168). Doi: 10.1186/s13613-020-00786-1.
  7. Orso D, Paoli I, Piani T, et al. Accuracy of Ultrasonographic Measurements of Inferior Vena Cava to Determine Fluid Responsiveness: A Systematic Review and Meta-Analysis. J Intensive Care Med. 2020 April: 35(4):354-363. Doi: 10.1177/0885066617752308. PMID: 29343170.  
  8. Pourmand A, Pyle M, Yamane D, Sumon K, Frasure SE. The utility of point-of-care ultrasound in the assessment of volume status in acute and critically ill patients. World J Emerg Med. 2019;10(4):232-238. doi:10.5847/wjem.j.1920-8642.2019.04.007
  9. Talahma M, Alkhachroum AM, Alyahya M, Manjila S, Xiong W. Takotsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: Institutional experience and literature review. Clin Neurol Neurosurg. 2016 Feb;141:65-70. doi: 10.1016/j.clineuro.2015.12.005. Epub 2015 Dec 17. PMID: 26741878.


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