1. Angina equivalent or atypical angina: dyspnea, dizziness, syncope, fatigue, diaphoresis, nausea, epigastric pain
2. Right sided MI
- ST elevation in V4-R is the most predictive finding
- Treat hypotension with fluid first (to increase preload). If that fails, go to inotropes-- inotropes will increase myocardial O2 demand and possibly extend the infarction so it's not first-line
3. Second degree AV block
- Mobitz I: can occur in the absence of structural heart disease- in athletes or old people. It can also occur in conjunction with ischemic heart disease, and with AV nodal blocking agents (b-blockers, ca-channel blockers, digoxin). Only treat if you get symptomatic bradycardia resulting in decreased cerebral or cardiac perfusion. Start treatment by stopping things that slow conduction through AV node (the drugs), fix any increased vagal tone (i.e. 2/2 vomiting or pain), fix ischemia.
- Mobitz II: often occurs in conjunction with other conduction disease (bundle, fasicular block). Needs a pacemaker, because this suddenly and unpredictably progresses to complete heart block.
-Second degree AV block in conjunction with any other conduction disease (bundle or fascicular block) buys you a pacemaker, even asymptomatic wenckebach's.
4. Management of chronic stable angina:
- Anti-anginal agents: PRN nitrate (can increase to long acting if frequently using PRN), beta-blocker (20% decrease mortality), calcium channel blocker
- Vasculoprotecive agents: ACE (17-23% reduction in cardiovascular mortality), statin (25-30% reduction cardiovascular events), aspirin (33% decrease MI/stroke/sudden death). Plavix has no role in management of chronic stable angina- increases bleed risk.
- If someone is hypertensive or tachycardic, increase B-blocker - should titrate to resting HR of 55-60 and 75% of the heart rate that produces angina on exertion.
- Ranolazine new antianginal agent (affects Na-dependent Ca channels? prevents Ca overload? Shifts to carbohydrate-focused metabolism rather than less efficient fatty acid metabolism?). Add on when optimal medical therapy, including long-acting nitrate and max-dose b-blocker and ca-channel blocker, have failed.
- If still have angina despite max medical therapy, PCI is warranted.
5. Stress test: 
- Indication: CHD risk score 10-90% based on symptoms age and gender (see below), complete RBBB or <1mm ST depression at rest

- Exercise stress test is preferred to chemical, as it tells you how much work is possible before you get angina, hemodynamic response and exercise tolerance are both predictive of outcomes (if you're not healthy enough to do the treadmill test, that's a really bad sign). Exercise to goal of 85% of ideal HR = 0.85 (220-age)
- Limitations of exercise stress- it's EKG based, so abnormal EKG @ baseline = should pick a different test.
6. Adenosine nuclear perfusion 
- Contraindicated in patients with significant bronchospastic disease (since adenosine may stimulate A2B receptors, which lead to bronchospasm), significant hypotension, sick sinus or high degree block as it may worsen block.
- Theophylline and caffeine should be avoided for 48 & 12 hours beforehand as they may blunt the response to vasodilation
7. Dobutamine stress echo 
- Used when patients have a contraindication to vasodilators, have taken theophylline within last 48 hrs or caffeine within last 12.
- Contraindications: hypertension (systolic at rest >180), hemodynamically significant LV outflow obstruction, aortic disseection, sustained ventricular arrhythmias
8. CAD workup
- Framingham risk score <10: nothing, go home
- Risk 10-20: coronary calcium scoring
- When to go to coronary angiography? Lifestyle limiting angina despite optimal medical therapy, markedly positive stress test, resuscitation from sudden cardiac death, documented vtach, complete r/o of CAD in someone with chest pain
- When to place a stent? Angina despite medical therapy, large area of at-risk myocardium on stress test, high-risk obstructions like left main disease or 3-vessel disease, significant CAD with decreased LV systolic function.
9. Tachycardias
- Idioventricular tachycardia/slow ventricular tachycardia: wide QRS, HR 60-100
- MAT: 3+ p-wave morphologies, often occurs in chronic lung disease.
10. Complications of acute MI:
- Acute mitral regurg from papillary muscle rupture -- occurs several days after the MI, more common after inferior MI -- treat with balloon pump as a bridge to surgery
- Ventricular free wall rupture- occurs 1-4 days after MI, presents as tamponade, PEA, sudden death
- LV aneurysm: late complication. presents as intractable v-tach, systemic emboli, heart failure
- Ventricular septal defect: 2-7 days after MI, presents as sudden onset dyspnea, hypotension, new systolic murmur