Left coronary artery: divides into left circumflex and left anterior descending.
LAD does anterior aspect around the inferior margin and connects with posterior diagonal branch of RCA. Main blood supply to anterior and septal portions of heart.
Circumflex: goes from AV sulcus to connect with RCA. Supplies anterior and large portion of lateral wall.
RCA: runs around AV sulcus between right atrium/ventricle. Has marginal branch near lower aspect of heart and ends at right posterior descending artery. Supplies right side of heart and perfuses inferior aspect of left ventricle through posterior descending. AV conduction system receives blood flow by AV branch of RCA and septal branch of LAD. The RBB and left posterior division contain dual blood supply from LAD and RCA.
Discomfort rather than pain. Pressure/heaviness/fullness/squeezing. Less commonly knife-like, sharp, stabbing. Usually retrosternal or left sided. Radiation into arm/neck/jaw. Chest wall pain not uncommon due to pericardium being inflamed.
Angina typically is < 10 minutes, improves within 2-5 minutes after rest. Easy fatiguability can be prominent symptom for ACS, particularly with women.
Cardiac RF are poor predictors of risk for MI/ACS in the ED.
Bradycardia: MC in inferior wall (RCA). BP not predictive (HTN with sympathetic response/anxiety; hypotension with pump failure).
Presence/absence of noted heart sounds is not usually helpful in the ED.
ECG within 10 minutes of presentation.
Inferior wall MI shoulder have right sided V4 (V4R) because V4R elevation suggest RV infarction.
Within persistent pain, repeat ECGs in 15-30 minutes.
Reciprocal ST changes predict larger infarction, increased severity, more severe pump failure, higher likelihood of complications, increased mortality. More elevated ST segment, the more extensive the injury as well.
Inferior wall MI can result from LCA and RCA. STE in lateral lead (V5,V6, VL) with isoelectric STE in lead I is likely LCA. STE Lead III>Lead II predicts RCA. If ST in V1 or V4R, likely proximal RCA with RV infarction.
Only recommended addition to standard 12lead would be right sided precordial leads in acute inferior MI for detecting RV involvement.
LBBB: Look for: 1) ST elevation 1mm or greater and concordant (same direction as main deflection) – odds ratio 25; St depression 1mm or greater in V1-V3, St elevation 5mm or greater and discordant (opposite direction). New LBBB not used for cath lab activation any further. Needs concordance or extreme disconcordance (25% ratio).
Troponin: single troponin elevation of only 39% in acute MI. Serial samplings increased sensivitiy to 90-100%.
Elevated troponin in renal failure patients can be false positive though they do predict worse outcome.
STEMI: repercussion by PCI within 90 minutes of ED arrival, or fibrinolysis within 30 minutes of ED arrival if PCI cannot be accomplished within 90 minutes.
Oxygen: only required if <90%. 2L NC reasonable, though not required. High flow can be detrimental.
Coronary angioplasty ballooning: can cause small arterial dissection or aneurysmal expansion. Laser therapy to extract atherosclerotic tissue is available as well. Stenting are expanded like balloon to provide scaffolding. When adding GPIIb/IIIa inhibitor and plavix, lower adverse effect at 6 months compared to those without the medication.
The longer the duration of symptoms, the better PCI is over fibrinolytic.
NSTEMI – PCI within 24-48hrs reduces rate of debt, MI, recurrent ACS. Early invasive approach to NSTEMI with refractory angina, hemodynamic instability.
Fibrinolytics: plasminogen activators. Indicated for STEMI if time to treatment is <6 hours to 12 hours and ECG has at least 1mm STE in 2 or more leads. 5% experience an allergic reaction, though usually resolves with antihistamine. Hypotension during infusion responds to decreasing infusion rate and volume expansion. Streptokinase has half life of 23 minutes but produces fibrinolytic state for 24 hours. Absolute contraindications: prior ICH, known structural CV lesion, brain neoplasm, ischemic stroke within last 3mo, active internal bleeding (excluding menses), suspected aortic dissection/pericarditis. Relative CI: SBP > 180/110, hx/o prior ischemic stroke >3mo, INR > 2, recent trauma (past 2 week), prolonged CPR > 10min, major surgery <3 week, recent internal bleeding <2-4weeks), patients previously tx with streptokinase should not receive it again. Other fibrinoltyics: tPa, reteplase, tenecteplase. no benefit added with doing fibrinolytic + PCI compared to PCI alone.
Rescue PCI (after failed fibrinolytic) if: cariogenic shock < 75yo, severe heart failure or pulmonary edema, patients with hemodynamically compromising vtach/vfib, failed fibrinolytic with moderate/large area of myocardium at risk.
Earlier the better when it comes to PCI. “Early” PCI for NSTEMI/UA still considered less than 48 hours, though patients presenting weekends/evenings have been shown to do worse.
Antiplatelets: GPIIb/IIIa antagonists are stronger than aspirin.
Aspirin: 325mg ASAP with STEMI, NSTEMI/UA. Prevents formation of thromboxane A2, lasts 8-12 days. In STEMI, aspirin alone reduces risk of mortality by 23%. Doses >162mg cause immediate complete inhibition. Smaller doses provide prophylaxis but not to same effect as larger dose.
Clopidogrel/ticlopidine: inhibit platelet aggregation. Plavix > ticlopidine due to rapid inhibition and less side effects. FDA warned patients on omeprazole had 50% decreased reduction rate of plavix effect and recommended ranitidine, famotidine, nizatidine. Plavix also increases risk of bleeding in CABG and recommended being withheld 5 days prior to CABG if possible. 5-20% of UA/NSTEMI will receive CABG – guidelines do not recommend withholding.
GP IIb/IIa: abciximab / eptifibatide / tirofiban – all require IV infusion to show benefit. Recommended in patients with positive troponins, likely to receive PCI.
Unfractioned Heparin: reduces risk of AMI and death during acute phase of UA. Weight adjusted bolus (60unit/kg, max 4000 per AHA).
LMWH: no monitoring. If patient is going to CABG, LMWH should be held and UFH can be used 12-24 hrs prior to surgery.
Nitrates: IV nitroglycerin should be used to titrate SBP (30% reduction in MAP with HTN and 10% reductio in normotensive pts) rather than treating to pain. ACC/AHA recommend IV nitro for first 24-48hrs after patients with STEMI and recurrent ischemia/CHF/HTN. Do not use with RV infarction – 1/3 of inferior wall MIs involve RV. Treat hypotension with fluids. Do not give with patient on sildenafil (last 24hrs) or tadalafil (48 hrs).
Beta-Blockers: anti-arrythmic, anti-ischemic, anti-HTN properties. They diminish myocardial O2 demand by decreasing HR, BP, contractility. Recent trials have shown no benefit for early B-blocker therapy. ACC/AHA recommend start PO, not IV in STEMI/NSTEMI within 24 hrs.
ACE: reduce LV dysfunction and LV dilation and slow CHF development. Oral recommended due to increased risk of hypotension. Recommended within 24 hours but not necessarily in the ED.
Magnesium: systemic/coronary vasodilation, antiplatelet effects. No support for it at this time.
CCB: antianginal, vasodilatory, antiHTN properties. Do not reduce mortality rate of AMI and may be harmful with some patients with CV disease.
Dysrhythmias: sinus bradycardia (35-40%), sinus tachycardia (30-35%, common in anterior MI), accelerated idioventricular rhythm (50-70%), ventricular tachycardia non sustained (60-69%). Afib can occur in first 24 hours and is transient. Mobitz I (Wenckebach) occurs within AV node, narrow complex and results from ischemic injury. MC in inferior than anterior. Mobitz II is wide complex, usually anterior and does progress to complete heart block. PVCs are common, but don’t have any prognostic ability.
Possible pacemaker placement: unresponsive symptomatic bradycardia, mobitz II or higher AV block, new LBBB/RBBB with first degree block, LBBB and bifasicular block.
New RBBB in 2% of AMI, usually due to anteroseptal AMI, has increased mortality. New LBBB occurs in 5% of AMI and has increased mortality.
Cardiac Failure – 15-20% of AMI have CHF.
Sudden decompensation of stable patient with MI should raise concern for tissue rupture/tear. Free wall rupture usually 1-5 days after infarction. Rupture of OV leads to pericardial tamponade and death. Interventricular septal rupture presents with chest pain, SOB, murmur. Usually from anterior MI. Tx is surgical. Papillary muscle rupture occurs in 1% and usually inferior MI usually 3-5 days after AMI. Tx surgical.
Pericarditis – 10-20% of patients. Occurs 2-4 days post MI. Dressler syndrome occurs 2-10 weeks post MI and has chest pain, fever, pleuropericarditis – no NSAIDs.
RV infarction – can cause shock. Tx by maintaining preload, reducing RV after load. Start with NS bolus. If no improvement, consider dobutamine.
Cocaine-induced MI: beta blockers are contra-indicated. Tx with aspirin, nitrates and benzodiazepines. Still tx with PCI.
References / Resources
Tintinalli, Seventh Edition, Chapter 53
Whats New in Emergency Cardiology: 2017 Literature Update, Amal Mattu, AAM Scientific Assembly
Attorney would like a specific diagnosis at the end rather than just ‘chest pain’ or ‘abdominal pain.’
History is important. Characterizing the pain is the most important over associated symptoms/risk factors (Lee and Goldman, 2000).
Highest negative predictive values: sharp, pleuritic, positional, chest wall tenderness, normal EKG. (Panju, JAMA 1998).
EKG: write your interpretation, address improper computer dxs.
Troponin: HEART Score, emcreg.org, Mayo Clinic (Hess).
Full history, no shortcuts. Read EMS/RN notes, address abnormal VS.
If sending someone home, probably shouldn’t have long differential diagnosis. If you have a trop and are sending home, you will need to explain why.
Advanced Documentation: Acute Coronary Syndrome, Larry Weiss, The Crashing Patient Conference 2015