Troponin in Critical Illness


  • Troponin abnormality is set at the 99th percentile in the healthy population
  • As the tests become more and more sensitive, the absolute cutoff value for “abnormal” has become lower and lower and the test has become less specific for myocardial infarction
  • From 1995 to 2007, the limit of troponin detection fell from 0.5 ng/mL to 0.006 ng/mL
  • often raised in the critically unwell (medical ICU, surgical ICU, trauma ICU, sepsis and septic shock, hypovolaemic shock)


  • cardiac TNI and TNT are regulatory proteins that control the calcium-mediated interaction of actin and myosin, producing myocardial contraction
  • myocardial injury, including but not limited to ischemia, causes release of these proteins into blood


Myocardial infarction

  • Type 1 (due to atheromatous plaque rupture)
  • Type 2 (due to other precipitant, e.g. hypotension, anaemia, vasospasm)

Other cardiac causes

  • Acute and chronic heart failure
  • Myocarditis
  • Cardiac contusion from trauma
  • Cardioversion
  • Endomyocardial biopsy
  • Aortic dissection
  • Hypertrophic cardiomyopathy
  • Aortic valve disease (aortic stenosis or regurgitation)
  • Cardiotoxic drugs
  • Tachyarrhythmia (SVT, V-tach, atrial fibrillation)
  • Bradyarrhythmia or heart block
  • Cardiac surgery
  • Cardioversion
  • Tako-tsubo cardiomyopathy
  • Rhabdomyolysis
  • Stenting or angioplasty (percutaneous coronary intervention/PCI)
  • Irukandji syndrome

Non-cardiac causes

  • Renal failure
  • Pulmonary embolism
  • Severe pulmonary hypertension
  • Sepsis
  • Severe critical illness
  • Burns
  • Extreme exertion
  • Amyloidosis or other infiltrative diseases
  • Stroke
  • Subarachnoid hemorrhage


Myocardial infarction

  • distinct rise and fall
  • typically rise 4-8 hours post onset of symptoms in MI
  • peaks at 18-24 hours
  • levels stay elevated for 10 days (allows late diagnosis of MI, may detect re-infarction with serial testing)


  • length of stay: associated with increased LOS
  • mortality: increased
  • in ACS: increased mortality


  • greater specificity than CK-MB as this is also found in skeletal muscle, gut, and uterus



  • widely available
  • high familiarity
  • rises over 4-8 hours, peaks at 10-24 hours, declines over 10 days
  • can be used to detect re-infarction
  • predicts outcome/ mortality (if negative, then low risk 30 day outcomes)
  • area under the curve of troponin elevation correlates with infarct size
  • new assays are highly sensitive


  • low specificity: multiple causes of raised troponin other than infarction e.g. PE and RV strain (see above)
  • different reference ranges for different assays
  • elevated baseline troponin in renal failure
  • diagnosis of infarction often requires repeated tests leading to a delay in diagnosis
  • ‘washout’ occurs after reperfusion
  • unclear significance of raised troponin post-cardiac surgery


  • History
  • ECG — Specific (97%) but not sensitivity (28%)
  • Lower sensitivity troponin requires at least 6 hours between time of initial lab and repeat troponin to see a conclusive increase to rule in AMI
  • Serial sampling of high sensitivity tropinin at 0 and 2 hours can safely rule-out of AMI (can be discharged if TIMI 0 or 1, and normal ECG)

References and Links


Journal articles

  • Cullen, L et al. Validation of high-sensitivity troponin I in a 2-h diagnostic strategy to assess 30-day outcomes in emergency-department patients with possible acute coronary syndrome. Journal of the American College of Cardiology, 2013. PMID: 23583250
  • Korff S, Katus HA, Giannitsis E. Differential diagnosis of elevated troponins. Heart. 2006 Jul;92(7):987-93. PMC1860726.
  • Shah ASV, Newby DE, Mills NL. High-sensitivity troponin assays and the early rule-out of acute myocardial infarction. Heart (British Cardiac Society) 2013. PMID: 23955806

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

One comment

  1. I’ve seen a TNT hs of 27 in an anxious hyperventilating panic attack this week ECG N aged 59 smoker no other risks
    Feeling perfectly well now
    Should I admit for another at 3 hours , 12 or just ignore it ?

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