1. Localization of ischemia: 
- ST elevation and q-waves are localizing. T-wave depression and ST depression are NOT localizing-- just because they are in leads of a certain distribution means nothing.
- Seeing reciprocal ST depressions in the opposite territory increases likelihood of MI, vs something like pericarditis which can have a similar clinical presentation and ST-elevation on EKG.
- Anterior: V1-V4 = LAD
- Lateral: I, aVL, V5, V6 = Lateral circumflex
- Inferior (meaning inferior part of septum): II, III, aVF = R coronary, lateral circumflex
- Posterior: see large R in V1, ST depression V1 and V2 = R coronary
2. Coronary anatomy 

- R acute marginal (labeled here as R marginal)- comes off RCA, supplies RV free wall. Thus if you clot off the RCA high enough, you will infarct out the RV as well as the posteroinferior part of the septum

- Posterior descending - comes off RCA in 80-90% of people. So inferior MIs are generally RCA infarcts. In the rest of the people, it comes off the circumflex from the LAD. 

- LAD - gives off septal branch that supplies the septum, and diagonal branches & obtuse marginals (labeled here as L marginals) that supply the lateral wall. 

3. When you see inverted T-waves, ST-elevations, and Q waves all at the same time on the same EKG- think resolving MI (~24 hours out). When the MI starts to resolve, T-waves start flipping back. 

4. If you suspect R side MI: 

- Put the leads on the R side of the chest, V1 in the center V6 on the lateral R. If you see ST elevation in V4, that is very characteristic of R MI. 

- Do NOT give nitroglycerin-- because the R side will be preload-dependent, if you give nitro (venodilator), blood will pool in the legs and you will have decreased preload and they will lose their pressure. 

- On the contrary, in L side MI, blood backs into the lungs as the L side fails, so venodilation will be good because it pulls blood out of the lungs. Probably still drops preload but in this case the cost-benefit is a little different. 

5. Things that mimic an MI: 

- Repolarization changes (benign early repolarization/BER) can cause ST elevation (usually concave up): common in young, healthy males. If your suspicion for MI is low, you can walk the patient. Changes in HR will often make the repolarization pattern change, often the ST elevation will disappear. If you have reason to suspect someone is actually having a STEMI, don't walk them. 

- Pericarditis: will see concomitant PR depression and ST elevation. ST elevation will often be diffuse, and there will be no reciprocal ST depressions. Also, PR elevation & ST depression in aVR are both very characteristic of pericarditis and are a rarely seen in MI or BER. 

- Dig toxicity: will cause rounded ST depression 

6. Electrolytes

- High K: peaked T, flattened P, eventually torsades 

- Low K: U-waves

- Hypercalcemia: short QT

- Hypocalcemia: long QT 

- Common causes of hypocalcemia: giant transfusions, as the citrate in the transfused blood chelates off all the Calcium. Watch out in MICU patients who get admitted for GI bleeds and get a lot of transfusions. Can also occur after parathyroidectomy. 

7. PE

- Most common EKG change? Sinus tach #trickquestion

- Can also see S1Q3T3: s-wave in I, Q wave in III, T wave inversion in III. 

8. Other EKG findings;: 

- Osborne wave: tiny peak after narrow QRS = hypothermia 

- Delta wave: WPW. Often accompanied by a short PR interval (the electrical signal bypasses) 

9. Pacemakers

- Looks like a LBB pattern, because they typically pace from RV apex

- Most modern pacemakers are dual chamber pacing and sensing; if they sense no P, they will give an atrial pace, await QRS; if they sense no QRS, they will give a ventricular pace. If they sense an intact P or QRS, they will allow the natural rhythm to occur. 

- Bi-ventricular pacemakers will have narrow-complex QRS because they are pacing bilaterally. 

10. Phosphate replenishing

- K-Phos: don't use if your K is >4.5 as it raises your K by around 0.2

- NaPhs: current national shortage.