Rhythm Nation: July 2017 Answer

Not a lot of takers on this tough ECG. Here’s some insight.

Initial ECG: Sinus tachycardia, LAD, 1st degree AVB, RBBB

Repeat ECG: NSR, LAD, 1st degree AVB, RBBB, TWI in V4-V6

A Closer Look At The Case

Our patient presented with a worsening headache with associated altered mental status. Vitals were notable for hypertension, and his initial neurologic examination showed sluggishly reactive pupils. His mental status progressively worsened, and imaging showed a posterior mass with an accompanying bleed.

What Was Up With That ECG?

Our patient developed T wave inversion (TWI) in V4-V6 during his clinical course. Given his presentation, these were likely neurogenic, commonly referred to as “cerebral T waves”. They are one of the characteristic ECG changes caused by increased intracranial pressure (ICP). Additional, neurogenic ECG features may include QT prolongation. The vital signs may reflect hypertension (as in our patient) often with associated bradycardia (the Cushing Reflex).

Weird. My Head Affects My Heart?

Subarachnoid hemorrhage (SAH) is well known for its cardiac electrophysiologic manifestations. In the largest case series11 to date, the changes most frequently encountered were U waves, T-wave abnormalities, R-wave abnormalities, and non-specific ST-T changes. It was also associated with sinus dysrhythmias including sinus tachycardia and bradycardia, as well as life-threatening ventricular dysrhythmias, sinoatrial blocks, supraventricular dysrhythmias, and arrest rhythms. Additionally, QT prolongation is associated with hemorrhage in the posterior fossa.

At a basic level, most medical students can rattle off the Cushing Reflex as hypertension from the initial sympathetic surge of increased ICP that leads to bradycardia through the vagal and aortic arch baroreceptor response to increased blood pressure.

How Might It Do That?

There is substantial neurology and cardiology literature discussing neurogenic cardiovascular changes. Early animal studies revealed that blood in the subarachnoid space of rats produced bradycardia, tachycardia, and dysrhythmias.8 Hypothalamic stimulation has also been linked to cardiac sympathetic tone. Rogers et al,10 changed the T wave amplitude in cats by stimulating the right and left sides of the hypothalamus and stellate ganglia.

Recent studies have focused on the insular cortex, an area correlated with our ability to feel our own heartbeat and known to control heart rate during exercise. Stimulating this cortex in rats is known to change blood pressure and heart rate, and ischemia of this region are correlated with dysrhythmias and cardiac arrest.14

Though there is clearly a link between hypothalamic stimulation and autonomic dysfunction, causation is yet to be definitively proven. This remains an active area of neurology and cardiology research and is useful for EM physicians to understand further as well.

What Is Happening In The Heart?

Echocardiograms have documented transient wall motion abnormalities in the hearts of patients with SAH.7 Furthermore, autopsies have shown myocardial contraction band lesions with similar histology to hearts injected with norepinephrine or those in a sympathetic state.

Initially this was attributed to high systemic catecholamine levels in a stressed state, but subsequent studies showed that ECG changes are not linked to such elevated levels. This finding, coupled with the location of the damaged heart suggests a role for intramyocardial nerve endings. Additionally, recent evidence points to the asymmetric innervation of the heart (parasympathetics control the SA and AV nodes and sympathetics control the ventricles) as a causative factor in neurogenic cardiovascular changes. Though unclear, it is possible that QT prolongation can lead to an R on T phenomenon, though other mechanisms have been proposed.

Though long term effects remain unclear at present (ST-elevations often resolve, TWI can persist for months), ECG abnormalities preclude expired SAH patients from heart donation in the United States due to concern for possible cardiac abnormalities.

So How Does This Affect Management?

This patient’s neurogenic ECG abnormalities and clinical course are concerning for increased ICP with risk of herniation. Cardiac events will be managed as usual in the ED, and at present anticoagulation is not indicated. This patient will need intubation given the expected clinical course and admission to a neurologic critical care unit. In the ED, we can facilitate intubation, monitoring and blood pressure control during their time in the department.

As for all our acute CVA patients, it is prudent to raise the head of the bed (HOB) to 30 degrees, consider hypertonic saline, and perform intubation (also at HOB 30 degrees) with good blood pressure control to preserve brain tissue. For the team on this case, this meant pre-oxygenation and nicardipine for blood pressure control prior to intubation. They opted for pre-treatment with fentanyl to lower the sympathetic surge associated with intubation (once a good neurologic exam was documented of course).

The patient was intubated with video laryngoscopy (to lower airway manipulation and sympathetic surges) with PRN push-dose epinephrine (for low BP) and esmolol (for BP spikes) at bedside. He was then started on fentanyl and propofol post-intubation with arterial catheterization for blood pressure monitoring. Optic nerve ultrasonography confirmed increased ICP with a diameter >5 mm, and our neurosurgery and neurology colleagues were consulted for neurologic critical care unit admission and consideration of further management of ICP with ventriculostomy or decompressive craniectomy. Just another day for The Original Kings of County.

Until next time, faithful bloggers.

Yours Truly,
Rhythm Nation

 

  1. Baroldi G. Pathologic evidence of myocardial damage following acute brain injuries. In: Di Pasquale G, Pinelli G, eds. Heart-Brain Interactions. New York, NY: Springer-Verlag; 1992:43-47

 

  1. Chatterjee s, ECG Changes in Subarachnoid Haemorrhage: A Synopsis, Neth Heart J. 2011 Jan; 19(1): 31–34

 

  1. Doshi R, Neil-Dwyer G. Hypothalamic and myocardial lesions after subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry. 1977;40:821-826.

 

  1. Elrifai AM, Bailes JE, Shih SR, Dianzumba S, Brillman J. Characterization of the cardiac effects of acute subarachnoid hemorrhage in dogs. Stroke. 1996;27:737-742.

 

  1. Gregory, T. Cardiovascular complications of brain injury. Contin Educ Anaesth Crit Care Pain (2012) 12 (2): 67-71

 

  1. Jachuck, SJ. Electrocardiographic abnormalities associated with raised intracranial pressure. Br Med J. 1975 Feb 1; 1(5952): 242–244.

 

  1. Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol. 1994;24:636-640

 

  1. Lorenzo et al., The Relationship of the Subarachnoid Injection of Blood and Blood Fractions with Cardiac Rate Change and Arrythmias, Journal of the neurological sciences, 127(2), 1994, pp. 134-142

 

  1. Oppenheimer SM, Cechetto DF, Hachinski VC. Cerebrogenic cardiac arrhythmias. Arch Neurol. 1990;47:513-519

 

  1. Rogers MC, Abildskov JA, Preston JB. Neurogenic ECG changes in critically ill patients: an experimental model. Crit Care Med. 1973;1:192-196

 

  1. Rudehill A, Olsson GL, Sundqvist K, Gordon E. ECG abnormalities in patients with subarachnoid haemorrhage and intracranial tumours. J Neurol Neurosurg Psychiatry. 1987 Oct;50(10):1375-81.

 

  1. Sommargren CE. Electrocardiographic abnormalities in patients with subarachnoid hemorrhage. Am J Critical Care. 2002;11:48–56.

 

  1. Svigelj V, Grad A, Tekavcˇicˇ I, Kiauta T. Cardiac arrhythmia associated with reversible damage to insula in a patient with subarachnoid hemorrhage. Stroke. 1994;25:1053-1055.

 

  1. Tokgozoglu SL, Batur MK, Topçuoglu MA, Saribas O, Kes S, Oto A. Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke. 1999; 30: 1307–1311

 

  1. Weinberg SJ, Fuster JM. Electrocardiographic changes produced by localized hypothalamic stimulations. Ann Intern Med. 1960

 

  1. Yuki K, Kodama Y, Onda J, Emoto K, Morimoto T, Uozumi T. Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium: a case report. J Neurosurg. 1991;75:308-311.
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4 comments for “Rhythm Nation: July 2017 Answer

  1. Ian deSouza
    September 3, 2017 at 2:01 pm

    The rhythm in the repeat ECG may actually be atrial flutter or atrial tachycardia with fixed AV conduction at 3:1. Note the difference in p axis and morphology when compared to the initial tracing.

    • Anonymous
      September 11, 2017 at 7:16 pm

      that’s actually what i thought it was too. and if you don’t buy the atrial tachycardia, its a RBBB + LAFB + 1st degree av block = incomplete trifascicular block as well

      • Anonymous
        September 12, 2017 at 5:13 pm

        Nice thought…I considered this, but wonder if this strictly meets LAFB criteria. Specifically, I wonder if it meets the following criteria from LITFL:

        “Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL
        Small R waves with deep S waves (= ‘rS complexes’) in leads II, III, aVF”

        While I see tall R in I and deep S in aVF, I am not sure i see the Q wave in I or the small r in aVF.

        Does anyone disagree? Is this criteria an absolute criteria?

        • Ian deSouza
          October 8, 2017 at 11:56 am

          According to Medrano and coworkers who studied this is the 1970s, the two current criteria for diagnosis of left anterior fascicular block (LAFB) are “marked left axis deviation (LAD) AND a delay in the time of inscription of the intrinsicoid deflection (ID) in lead aVL asynchronous to V6.”

          Medrano GA, Brenes PC, de Micheli A, et al : Clinical and electrocardiographic diagnosis of the left anterior subdivision block isolated or associated with RBBB. Am Heart J 83:44i-458, 19i2

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