1. Causes of A-fib:
-Structural heart changes: MI, acute mitral valve failure, myocarditis, pericarditis
-Pulmonary: PE, acute onset pulmonary disease leading to vasoconstriction
-Endo: hyperthyroid,
-Iatrogenic: cardiac/thoracic surgery (postop a-fib very common)
-Alcohol intake "holiday heart syndrome"
-Electrocution
2. Mechanisms of Cerebral ischemia: 
-Embolic: from heart (afib) or carotids
-Thrombotic: native cerebral vessel thromboses (85% of CVA are this)
-Cardiogenic: acute onset heart failure (arrhythmia, MI, acute valve failure)
-Hemorrhagic: brain bleed.
-Hematologic: hyperviscosity (polycythemia, myeloproliferative), hypercoagulable (coag factor mutations, lupus, etc), sickle cell
-Vascular: vasculitis, extrinsic vessel compression/kinking, vasospasm (c-o-c-a-i-n-e, migraine)
3. TIA predictive of stroke risk: 
-TIA symptoms => 8-12% risk of stroke within a week
-11-15% risk of stroke within a month.
4. CI to tPA for stroke:
-Recent history of heparin or warfarin administration
-Unknown history of anticoagulation
-Clinical suspicion of bleeding risk/thromobcytopenia
5. Workup for stroke, before initiation of tPA
-Noncontrast head CT
-BMP: lytes, renal function
-EKG/cardiac enzymes: to look for concomitant heart disease (very common). Everyone should get a cardiac workup within 24 hours of a suspected stroke.
-CBC/Coags: tells you about bleeding risk, also infection risk, hypoxia 2/2 severe anemia.
-O2 sat
-Blood glucose
-Other tests per clinical suspicion (i.e. drugs, hepatic, seizures)
6. Cardiac Biomarkers:
-Troponin=marker of choice for the diagnosis MI, more specific than CK-MB. They rise 4-6 hours after MI, and remain up for ~10 days so can be hard to time injury.
-CK-MB rises 4 to 12 hours after the event, remains elevated for only 36 to 48 hours. An elevated serum CK-MB can help confirm the timing of an acute myocardial infarction; in addition, repeat elevations may indicate recurrent myocardial injury.
-Don't use total CK or LDH to diagnose MI.
-Myoglobin is small and rapidly released from damaged cells; sensitivity approx = CK-MB. Myoglobin and LDH are nonspecific for heart. Injury to skeletal mm can cause elevation, as can cocaine use in people with compromised renal function (decreased clearance)
-B-type Natriuretic Peptide (BNP) is 32-amino-acid polypeptide secreted by the ventricles 2/2 pressure overload. BNP elevation can indicate ventricular dysfunction (including from PE!), levels correlate with both severity of symptoms & prognosis.
7. Standard approach for diagnosing MI with cardiac enzymes: 
-Serum troponin-T (cTnT) or troponin-I (cTnI) is measured at first presentation.
-If the troponin WNL, repeat at 6-9 hours, or earlier if if you think they are still having NSTEMI. Repeat again at 12-24 hrs if the first 2 came back neg but there is strong clinical suspicion of MI.
-CK-MB if you can't get troponin, or if you suspect MI within 2 weeks of a previous, known MI.
8. Management of A-fib with RVR: first, rate control
-Rate control until you can do the maneuvers for rhythm control
-Goal is to block the AV node (so class II/IV antiarrhythmics)
-If there is no evidence of heart failure, use B-blockers or non-dihydropyridine CCB (ditiazem drip, verapamil)
-if there is evidence of heart failure, use amiodarone or digoxin.
9. Management of A-fib with RVR: second, anticoagulation 
-Start heparin drip (goal PTT 45-60), or lovenox subQ (don't need to monitor)
-Low risk: heparin drip, cardiovert soon after, then aspirin
-High risk: heparin drip, transition to warfarin, continue warfarin to goal of INR 2-3.
10. Management of A-fib with RVR: third, rhythm control. 
-Cardioversion can temporarily increase the risk of thromboembolic events and stroke, so you don't want to cardiovert someone if you think there is a good chance they will embolize something.
-If someone is low risk for having an embolization (<48 hours since onset of a-fib, TEE shows no thrombus) then you can cardiovert once you start the heparin drip.
-If someone is high risk for embolization, or you saw a thrombus on TEE, wait until they are therapeutically, stably anticoagulated for 3-4 weeks on warfarin to cardiovert.
-Cardioversion can occur with direct-current under anaesthesia
-Cardioversion can also occur pharmacologically: use Class IC antiarrythmics (flecanide, propafenone) work better than Class III antiarrhythmics (ibutilide, amiodarone). Be careful as you can push the rate too fast or slow with these drugs.