The implications of ECG in patients with SAH

  ECG abnormalities may be seen in approximately 50% of patients with SAH.

  In most of the surviving patients, abnormal ECG reverts to normal within 2 weeks.

      In some patients, ECG abnormalities may partially resolve or may even persist.

  Clinically significant arrhythmias (
atrial tachyarrhythmia, ventricular tachycardia) after SAH

      are associated with a high mortality rate, and serious cardiac and neurological comorbidity.

  Myocardial dysfunction without coronary involvement may be seen in acute cerebral diseases (Takotsubo

      cardiomyopathy, etc.).

  ST segment elevation during SAH may mimick acute myocardial infarction.

      Mild elevation of cardiac enzymes may be seen during SAH, too. Together these findings may result in

      inappropriate administration of anticoagulant and thrombolytic therapy. This may further deteriorate the

      clinical status of a with patient SAH.

  Documented ECG abnormalities in a patient with SAH who has brain death mean the heart is not accepted

      as a donor organ because of the possibility of cardiac abnormalities.




ECG abnormalities during SAH

  QT interval prolongation

  Sinus bradycardia and sinus tachycardia

  Sinus arrhythmia

  Clinically significant arrhythmias (atrial tachyarrhythmia, ventricular tachycardia) are seen

      in only 1-4% of SAH patients.

  ST segment elevation or depression

  Q waves

  T wave inversion (may be extensive)

  Negative and/or prominent U wave.

  J-wave-associated ventricular fibrillation.




Why do ECG abnormalities develop in SAH?

  Hypothalamic stimulation causes autonomic neural stimulation which in turn causes

      a hyperdynamic cardiovascular state.

 
Increased levels of circulating catecholamine pathologically leads to subendocardial band necrosis

      in the myocardium.

  Elevated catecholamine levels have been correlated with QT-interval prolongation and myocardial damage.




ECG and prognosis in SAH

  QT prolongation (corrected QT interval >410 ms) and tachycardia (heart rate >100 beats/minute) on ECG

      were reported to be independently associated with angiographic vasospasm after aneurysmal SAH.

  Tachycardia and nonspecific ST-segment changes are also significantly associated with poor outcome.




References

  Stroke 2012;43:2102-2107.

  Postgrad Med J 1981;57:294-296.

  J Cerebrovasc Endovasc Neurosurg 2012;14:90-94.

  Europace 2012;14:1063-1064.

  BMJ Case Rep 2012 Mar 27; doi: 10.1136/bcr.11.2011.5134.

  BMJ Case Rep 2011 Feb 17; doi: 10.1136/bcr.08.2010.3253.

  Am J Crit Care 2002;11:48-56.

  J Electrocardiol 2002;35 Suppl:257-262.





ECG 1a. The ECG above is from a 46 years-old man who had sudden loss of consciousness. He had no known heart disease.
Extensive SAH and cerebral edema was detected. The rhythm is atrial fibrillation with 3 VPCs.
Leads V3 to V6 show ST segment depression.

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ECG 1b. Above is his ECG which was recorded one hour after ECG 1a. The rhythm is now sinus. No VPCs are seen.
Leads V3 and V4 show "upsloping" ST segment depression while leads V5 to V6 show horizontal ST segment depression.

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ECG 1c. Above is his ECG which was recorded 5 hours after ECG 1a.
ST segment depression is not seen anymore. QT interval iis prolonged.
The rhythm is atrial fibrillation with a high ventricular rate.
Atrial tachyarrhythmias after SAH are associated with a high mortality rate, and serious cardiac and neurological comorbidity.
The patient died next day.

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ECG 2a. The ECG above is from a 56 years-old man with subarachnoid hemorrhage.
The rhythm is ectopic atrial rhythm.
Negative T waves are seen in anterior and inferior leads.
Troponin I level was not elevated. He had no known coronary artery disease.
Precordial leads were recorded at a calibration of 5 mm/mV.

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ECG 2b. Above is his 6-channel precordial rhythm tracing which was recorded 30 minutes after the ECG 2a.
Now the precordial leads were recorded at a calibration of 10 mm/mV.
Negative T waves are seen in leads V3 to V6.

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