I know the random fact throwing thread is very popular on here and I wanted to start a PCCN/CCRN edition to help those who are planning on taking the PCCN/CCRN study :)
Hyperacute (tall) T waves that are localized in the absence of hyperkalemia could be an early sign of ischemia.
Ischemia: ST depression and/or T wave inversion in >/ 2 contiguous leads
Injury: ST-segment elevation >/ 1mm in >/ 2 contiguous limb or >/ 2mm in precordial leads
Infarction: pathological Q waves (>0.04sec wide, >25% amplitude of the R wave)
NSTEMI: subendocardial damage (doesn't go all the way through). Normal R wave progression, ST-segment depression, normal Q.
STEMI: transmural damage, loss of R wave progression, ST elevation with abnormal Q wave
Anterior MI (LCD, LAD)
- leads V3, V4
- tachycardia, pulmonary edema (dyspnea, orthopnea)
Inferior MI (RCA)
- leads II, III, aVF (these leads are also at the bottom or inferior part on a printed 12-lead EKG which helps me remember)
- bradycardia, hypotension
- **do a right-sided EKG because there is a chance a patient with an inferior MI will have a RVMI.
Lateral MI (LCA, Circumflex)
- Leads V5, V6, I, aVL
- ventricular dysrhythmias, heart failure, AV blocks
Septal MI
- Leads V1, V2
- Tachycardia, atrial fibrillation, septal rupture
Posterior MI (LCA, Circumflex, RCA)
- Pathological R waves in V1-V4
- ST depression in V1, V2
- You need to look through the heart for reciprocal changes
- Bradycardia, junctional rhythms
RVMI
- As mentioned above, you need to do a right-sided EKG in a patient with an inferior MI, incidence is about 40%!
- Lead V4R
- Hypotension, bradycardia, absence of pulmonary edema in a true RVMI (clear lungs!)
Cardiogenic pulmonary edema (more common)
- increase in hydrostatic pressure (push) within the pulmonary-capillary bed due to heart failure. Third-spacing occurs in the INTERSTITIUM.
- bibasilar rales, vascular prominence, bilateral infiltrates
Non-cardiogenic pulmonary edema: third spacing into the ALVEOLI
- ARDS