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).



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.










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

Neurogenic Stress Cardiomyopathy

Proposed Mechanism for HCP causing Takotsubo:

Sympathetic control of the heart is mediated by hypothalamic nuclei that abut the walls of the third ventricle.  Specifically, dysfunction of PVN and DMN has been linked to catecholamine-induced myocardial necrosis.  Hydrocephalus may disrupt these centers, although intracranial hypertension may not be necessary for this to occur.




*Paraventricular nucleus (PVN):   TRH release, CRH relesase, oxytocin release, vasopressin release, somatostatin release

**Dorsomedial nucleus (DMN): BP, HR, GI stimulation



Gharaibeh, Kamel, Jackie Scott, and Nicholas A. Morris. “Neurogenic Stress Cardiomyopathy Precipitated By Acute Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage.” Neurocritical Care (2017): n. pag. Web. 14 Aug. 2017.

“Hypothalamus.” En.wikipedia.org. N.p., 2017. Web. 14 Aug. 2017.

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%




Most common EKG morphologic abnormalities associated with SAH:



Arrythmias associated with SAH:



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



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

NOVA Score

bedside clinical score for prediction of endocarditis in enterococcal bacteremia


  • number of positive blood cultures [3/3 or the majority if more than 3], 5 points
  • unknown origin of bacteremia, 4 points
  • prior heart valve disease, 2 points
  • auscultation of a heart murmur, 1 point

cutoff score <4 points suggested a very low risk for enterococcal IE

useful for avoiding unnecessary TEE in enterococcal bacteremia

Uptodate.  http://www.uptodate.com/contents/treatment-of-enterococcal-infections?source=search_result&search=ENTEROCOCCUS+FAECALIS%5C&selectedTitle=1~37#H10055572.  Accessed 06/22/2016






VF or hemodynamically unstable VT:

  • Oral: 800 to 1600 mg daily in 1 to 2 doses x 1-3 weeks,
  • then 600 to 800 mg daily in 1 to 2 doses x 1 month;
  • then maintenance: 400 mg daily

Pulseless VT or VF :

  • IV push, I.O.: Initial: 300 mg rapid bolus; if pulseless VT or VF continues after subsequent defibrillation attempt or recurs, administer supplemental dose of 150 mg.
  • ROSC –> 1 mg/minute x 6 hours, then 0.5 mg/minute for 18 hours .

Stable VT:

  • IV: 150 mg over 10 minutes, then 1 mg/minute x 6 hours, then 0.5 mg/minute; x 18 hours
  • Breakthrough stable VT: 150 mg supplemental doses in 100 mL D5W or NS over 10 minutes



Atrial fibrillation:

Pharmacologic cardioversion (off-label):

  • Oral: 600 to 800 mg daily in divided doses until 10 g total,
  • then 200 mg daily maintenance
  • maintenance 100 mg daily commonly used for elderly or low BMI
  • Other regimens
    • 800 mg daily x 14 days, then 600 mg daily x 14 days, then 300 mg daily x 1 year, then 200 mg daily thereafter
    • 10 mg/kg/day x 14 days, then 300 mg daily x 4 weeks, then maintenance 200 mg daily
  • IV: 150 mg over 10 minutes,
  • then 1 mg/minute x 6 hours,
  • then 0.5 mg/minute x 18 hours or change to oral maintenance dosing (eg, 100 to 200 mg once daily)

Maintenance of sinus rhythm (off-label):

  • Oral: 400 to 600 mg daily in divided doses x 2-4 weeks
  • then maintenance 100 to 200 mg once daily

Prevention of post-op Afib and flutter with cardiothoracic surgery (off-label):

  • Oral: 200 mg TID x 7 days prior to surgery, then 200 mg daily until discharge
  • IV:
    • Preoperative: 150 mg load then 0.4 mg/kg/hour x 3 days prior to surgery and x 5 days postoperative
    • postoperative regimen: Starting at postop recovery, 1000 mg infused x 24 hours for 2 days

Rate control (off-label):

  • IV: 300 mg over 1 hour,
  • then 10 to 50 mg/hour x 24 hours
  • then oral maintenance 100 to 200 mg once daily.


Supraventricular tachycardia (eg, AVNRT, AVRT): 

Pharmacologic cardioversion (off-label):

  • Oral: 600 to 800 mg daily in divided doses until 10 g total,
  • then 200 mg daily as maintenance
  • IV: 150 mg over 10 minutes,
  • then 1 mg/minute x 6 hours,
  • then 0.5 mg/minute x 18 hours or change to oral


PDF file for Amiodarone table

Doc file for Amiodarone table


Uptodate: Amiodarone: Drug information.  Accessed 1/13/2016.

New Classification Scheme for AMI

new classn of MI

  • Type 1 is due to plaque rupture with thrombosis
  • Type 2 is secondary to an imbalance between myocardial oxygen demand and supply with fixed atherosclerotic obstruction, vasospasm, or endothelial dysfunction playing a permissive role
  • Type 3 includes patients with sudden death having fatal MI even though cardiac biomarker evidence is lacking.
  • Types 4 and 5 include patients with MI associated with PCI and
    CABG, respectively.

REFERENCE:  J Intensive Care Med May 2015 vol. 30 no. 4 186-200

Precocious ACS

Risk factors for Precocious ACS:

1.  dyslipidemia  (63%)

2.  smoker          (60%)

3.  obese            (49%)

4.  hypertension (46.7%)

5.  FMH              (43.6%)

6.  DM                (21%)

7.  cocaine         (10.7%)

8.  CKD             (8.9%)

9.  autoimmune (6.5%)

10. PE/DVT       (5.7%)