Saturday, 17 June 2017

Myocardial Infarction

Definition
ST Elevation 1mm in limb leads
ST elevation 2mm in chest leads
New LBBB
Posterior MI - Tall R waves in V1-V3 ST depression +/- T wave inversion
 plus CP within 10 hours

Features
Diaphoresis is the strongest predictor of AMI, as is nausea and vomiting, and radiating to both shoulders.
Severity of pain is not associated with the likelihood of MI.

ECG Diagnosis

 II, III, aVF = inferior leads
   V1-V2 = septal leads (not V3, V4 as seen in some texts (see Zipes et al, 2004))
   V1-V6 = anterior leads

   I, aVL, V6 = lateral leads


Treatment
Aspirin - inhibits platelet aggregation by inhibiting cyclo-oxygenase, and thus formation of thromboxane A2.

Clopidogrel - promotes formation of platelet c-AMP, lowering platelet calcium, and reducing platelet aggregation.

Ticagrelor - anti-platelet agent that is a useful alternative to clopidogrel.


Fondaparinux - factor Xa inhibitor that has less associated bleeding complications.

Right Ventricular Infarction
In 50% of patients with inferior myocardial infarction, the clinical triad of high central venous pressure, clear lung fields, and hypotension combined with right sided ECG changes is strongly suggestive of right ventricular infarction. Look for this carefully using a V4R which may confirm ST elevation, and do an echo.
This is treated by maintaining right ventricular preload, so drugs that reduce preload (nitrates and opiates) should be avoided. Fluid challenge is important, with careful monitoring.

Troponin
A protein, involved in muscle contraction. Very cardiospecific, with little crossover into skeletal muscle. In renal failure, troponin just isn't cleared as quickly, so can be falsely high. With a roche or abbot high sensitivity troponin - normal at arrival and three hours = rule out ischaemia.
Troponin peaks within 12 - 24 hours, and remains elevated for about two weeks.

Remember troponin is normal in unstable angina

Cocaine Associated
Cocaine causes a sympathomimetic response, with increase in heart rate and blood pressure. It can cause acute thrombosis of the coronary artery - this is probably due to more than an increase in platelet count and activation.
Make sure you rule out aortic dissection as well, and “crack lung,” -  hypoxemia, hemoptysis,
respiratory failure, and diffuse pulmonary infiltrates. Also, think about MI if patient presents with dyspnoea or diaphoresis.

Troponin is still very useful, and about two thirds of MI events occurred within 3 hours of cocaine ingestion. ECGs are abnormal in 56 - 84% of patients, although this may be early repolarisation mis-interpreted.

Treat as per normal ACS, but make sure you give early benzodiazepines. GTN might still help. Beta blockers are probably safe.



References
http://circ.ahajournals.org/content/117/14/1897
http://calgaryguide.ucalgary.ca/wp-content/uploads/image.php?img=2015/04/MI-Findings-on-Investigations.jpg
https://www.rcemlearning.co.uk/modules/chest-pain-syndromes/
https://www.aliem.com/2013/03/chest-pain-value-of-good-history/
https://www.rcemlearning.co.uk/modules/management-of-stemi-and-its-complications/ 
https://www.rcemlearning.co.uk/modules/unstable-angina-and-non-stemi-risk-assessment-and-management/ 
https://www.aliem.com/2010/11/paucis-verbis-sgarbossas-criteria-with-lbbb/
https://www.aliem.com/2013/05/pv-card-early-repolarization-vs-stemi-on-ekg/

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