Risk Score to Predict QTc Prolongation in Hospitalized Patients

For patients with COVID-19, we are using drugs that prolong QT-interval.  The risk of life-threatening arrhythmias from QT prolongation may be higher.  This article reports a scoring system to identify patients that are at risk for QT prolongation.

The study found that the following factors predicted QTc prolongation:  female, sepsi, LV dysfunction, administration of QT-prolong drug, >= 2 QT prolonging drugs, loop-diuretic, age >68, serum K <3.5, admitting ATc >450ms.

A risk score was developed.  Risk was classified as low (score of 0-6), moderate (7-10) and high (11-21).

 

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A high risk score >11 was associated with 74% Sn and 77% Sp (PPV 79% NPV 76) for predicting QTc prolongation.  Incidence of QTc prolongation 15% in low risk, 37% in moderate risk and 73% in high risk.

 

 

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Reference:

Tisdale, J., Jaynes, H., Kingery, J., Mourad, N., Trujillo, T., Overholser, B., & Kovacs, R. (2013). Development and Validation of a Risk Score to Predict QT Interval Prolongation in Hospitalized Patients. Circulation: Cardiovascular Quality And Outcomes, 6(4), 479-487. doi: 10.1161/circoutcomes.113.000152

EKG findings in CNS Disorders

What is the relationship between acute CNS events and cardiovascular abnormalities? 

CNS events can induce cardiac abnormalities in EKG morphology and rhythm.  Most commonly, these abnormalities involve the T wave (diffuse, deep inversions).  Minor ST segment elevation have also been reported in leads with abnormal T waves.  T wave asymmetric, characteristic outward bulge in the ascending portion.  ST elevation usually less noticeable, and <3mm in most instances.    T inversions are more pronounce din midprecordial and lateral precordial leads.  May be found to a lesser extent in limb leads. Other EKG features in acute CNS injury include prominent U waves and QT prolongation.

Explanation for EKG findings – may involve CNS-mediated increases in sympathetic adn vagal tone, as well as actual myocardial damaage termed contraction band necrosi.

EKG changes with these disease processes can include ST segment depression, T wave inversion, PR shortening, QT prolongation, accentuation of U wave, bradyarrhythmia, and tachyarrhythmia (both ventricular and supraventricular). Derangement of autonomic nervous system activity may be responsible for these.

 

CNS modulates cardiac function via two pathways:

  1. indirect effect via humoral mediators (E and NE)
  2. direct effect via afferent and efferent connections with SNS and pSNS

Damage to hypothalamus may be the primary cause of autonomic dysfunction.

Hypothalamic dysfunction –> excessive humoral catecholamine production and autonomic tone –> HTN, inc cardiac O2 demand, vasospasm, ??direct toxic insult to cells –> subendocardial ischemia, microhemorrahges, focal myonecrosis –>  EKG changes / enzymologic and histopathologic changes

 

Classic EKG changes with SAH

  • first described by Byer (1947)
  • symmetric, deep T-wave inversion with QT prolongation
  • EKG changes seen in 72% of SAH
  • arrhythmias in 91% of cases, 41% of which were serious
  • subendocardial damage with myocytolysis, myofibrillar degeneration, fuchsinophilic degeneration
  • CPK elevations in 40-50%
  • focal or global wall motion abnormalities in ~50%

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Most common EKG morphologic abnormalities associated with SAH:

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Arrythmias associated with SAH:

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EKG changes with acute thromboembolic stroke

  • morphologic changes
    • QT interval prolongation
    • ST segment, and T wave abnormalities
    • prominent U waves
  • Rhythm abnormalities
    • atrial fibrillation
    • sinus tachycardia
    • premature ventricular contractions
    • premature atrial contractions

 

Cushing response

  • sinus bradycardia + increased SBP + widened pulse pressure
  • EKG changes include prominent U waves, ST segment changes, notched T waves, and prolongation of the QT interval
  • result of compressive forces on the brainstem and diencephalic structures –> induces vagal and sympathetic discharges that can trigger either bradycardias or supravent / ventricular tachy-dysrhythmias

 

Reference:

Perron, Andrew D., and William J. Brady. “Electrocardiographic Manifestations Of CNS Events”. The American Journal of Emergency Medicine 18.6 (2000): 715-720. Web.