graph TD
A[Acute Chest Pain<br>ED Evaluation] --> B(12-lead ECG)
B --> C[Normal/ST-T changes, but No STE]
B --> D[ST Elevation]
D --> E(Active STEMI Protocol)
C --> F(Tn-<br>Unstable Angina)
C --> G(Tn+<br>NSTEMI)
19 Acute Coronary Syndrome
19.1 Note
19.1.1 UA/NSTEMI
*** UA/NSTEMI
- BMP, CBC
- A1c
- Lipids
- TSH w/ reflex
- Treatment
- ASA 162/325 (if indicated)
- Heparin gtt (per ACS protocol)
- BB
- Nitrates (SLN, paste?)
- Other anti-anginal: CCB (if unable to tolerate BB), nitrates (long-acting if refractory to BB), ranolazine (adjunct to BB)
- Anti-platelet: ASA +/- clopidogrel
- Statin
- Optimize BP control, e.g. ACEi/ARB
- Optimize glycemic control in pts w/ DM
- Nicotine replacement therapy (if indicated)
- Lifestyle modifications
- Smoking cessation
- Exercise
- Weight loss
- Supplemental O2 PRN
- Diet: low fat, low cholesterol19.1.2 STEMI
TODO
19.2 Definitions
- UA is angina that is either:
- new (< 2 months)
- increased in severity or frequency
- occurs at rest
- The difference between unstable angina (UA) and NSTEMI is the absence or presence of cardiac enzymes, respectively.
19.3 MI Subtypes based on etiology
- Type 1: Spontaneous MI due to a primary coronary event
- Type 2: MI secondary to ischemia due to either increased oxygen demand or decreased supply, eg, coronary artery spasm, anemia, or arrhythmias
- Type 3: Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia
- Type 4: MI associated with PCI or stent thrombosis
- Type 5: MI associated with CABG
19.4 Clinical Presentation
- Pts presenting with NSTE-ACS, 1/3 will have a normal ECG!
- Repeat in 15-30 mins (esp if hx raises suspicion for ACS)
- Consider add’l leads, i.e. posterior, RV
- Telemetry
💡Response to nitroglycerin should not be used as a diagnostic test in the evaluation of chest pain.
Assuming a base rate of 15%, i.e. pre-test probability of 15%.
| Feature or Finding | LR+ | Post-test Probability |
|---|---|---|
| Radiation to both arms | 9.7 | 63% |
| Radiation to right arm | 7.3 | 56% |
| Third heart sound | 3.2 | 36% |
| Hypotension | 3.1 | 35% |
| Radiation to left arm | 2.2 | 28% |
| Radiation to right shoulder | 2.2 | 28% |
| Crackles | 2.1 | 27% |
| Diaphoresis | 2.0 | 26% |
| Nausea and vomiting | 1.9 | 25% |
19.4.1 Factors that increase likelihood of ACS (per ACC/AHA)
- Chest or left arm pain that reproduces prior angina
- History of CHD
- Transient mitral regurgitation murmur
- hypOtension
- diaphoresis
- pulmonary edema
- crackles
19.4.2 Mimics
- Prinzmetal (vasospastic) angina; can be diagnosed in cath lab with ergonovine infusion
- Tx: CCBs, nitrates
- Clue: ischemia-Sx that occur at about the same time each day; EKG w/ transient ST elevation during pain episode.
- See non-cardiac causes of chest pain
19.4.3 Likelihood of MI based on ECG findings
- New ST elevation > 1 mm, LR+ = 5.7–53
- New Q wave, LR+ = 5.3–24.8
- Any ST elevation, LR+ = 11.2
- New Q or ST elevation, LR+ = 11
- Any ECG abnormality, LR- = 0.04
19.4.4 Likelihood of MI based on Troponin
Warning
Patients with kidney disease often have elevated troponin levels raising the risk of false-positive tests for MI.
- sensitivity, 95%; specificity, 98%; LR+, 48; LR–, 0.05
19.5 Inferior MI
- Inferior MI may present with acute severe epigastric pain, anorexia, n/v and diaphoresis
- Why? ↑ vagal tone and irritation of the diaphragm by adjacent infarcted inferior wall
- Every pt presenting with a suspected acute inferior MI should get a right-sided EKG
- R-sided EKG will show ≥ 1 mm ST elevation in leads RV4-RV6
- If a pt presenting with inferior MI + hypOtension → get a R-sided EKG
- Right ventricular infarction is almost always due to occlusion of the right coronary artery (RCA)
- Clinical triad of right ventricular infarction
- hypOtension
- clear lung fields
- ↑ JVP
- In acute inferior MI and PA catheter shows ↓ PCWP, ↑ RA pressure: give fluids until BP normalizes
- What’s going on? RV infarct → RV failure, so the RV is unable to fill the L side of the heart
- Management of RV infarction differs from mgmt of LV infarction in the following ways:
- avoid nitrates and other agents that ↓ preload in RVI
- give fluids if RVI + hypOtensive
- Cardiac complications more common with inferior MIs (compared to anterior MIs):
- bradycardia
- AV block
- Why these complications with inferior MIs? Due to ↑ vagal tone and AV nodal ischemia associated w/ inferior infarcts
Although AV block is more common with inferior MIs. If it does occur with anterior MI, it is due to destruction of a large amount of myocardium in the interventricular septum. ∴ AV block in setting of an anterior MI is associated with higher mortality than AV block in setting of inferior MI (transiet, no ppm required). AV block due to anterior MI requires pacemaker placement.
19.6 ECG Criteria
19.6.1 STEMI ECG Criteria
- New ST elevation at the J point in 2 contiguous leads > 1 mm (0.1 mV) in all leads except V2–V3
- New ST elevation V2–V3 of >= 2 mm in men younger than 40 years or >= 1.5 mm in women
- New, or presumed new, left bundle branch block
Posterior MI may be a STEMI, but appear as ST-depression on a routine 12-lead EKG. Confirm STEMI by obtaining a R-sided EKG.
19.7 Management of ACS
| Management | Indications |
|---|---|
| Cath lab ASAP | STEMI NSTEMI unstable/cardiogenic shock severe LV dysfunction recurrent/persistent angina at rest despite intensive medical therapy new/worsening MR or VSD sustained ventricular arrhythmia |
| Cath lab within 24 hrs | NSTEMI/UA TIMI: intermediate (3-4) or high (5-7) risk |
| Cath lab prior to discharge | NSTEMI/UA TIMI: low (1-2) risk and (+) EKG changes or ↑ Troponin |
| Medical management | NSTEMI/UA Stable and TIMI: low (1-2) risk |
- First med to give to a pt presenting with chest pain and concern for ACS: non-enteric coated ASA 162/325 mg bite and chew x1
- Within the first 10 minutes of the encounter for a pt w/ suspected ACS, do the following:
- Give ASA
- Obtain EKG, troponin
- Obtain H&P
- Labs
- Troponin
- first elevated 4 hrs after an MI
- peaks 44 hrs after MI
- Troponin
- For pts presenting with UA/NSTEMI, calculate the TIMI score (Fig Figure 19.1) to determine if and when patient should go to the cath lab.
- TIMI ≥ 3 → Cath lab w/in 24 hrs
- Patients with ACS who need to go to Cath lab ASAP
- STEMI
- NSTEMI
- unstable or cardiogenic shock
- severe LV dysfunction
- recurrent/persistent angina at rest despite intensive medical therapy
- new/worsening mitral regurgitation or VSD (See @ref(mi-complications))
- sustained ventricular arrhythmia
Historically, a “new” left bundle branch block (LBBB) in the setting of chest pain was to be treated like a STEMI. Recent studies demonstrate that most patients with chest pain and a “new” LBBB do not have a STEMI (Jain et al., 2011; Kontos et al., 2011). (Source)
If a patient has taken a PDE-5 inhibitor, e.g. viagra, you should wait 24 hrs before giving nitroglycerin
- Exception: tadalafil (Cialias), where you should wait 48 hrs
19.7.1 Revascularization in STEMI
Complete revascularization is superior to culprit-only revac for the primary endpoint of CV death and MI.(Mehta et al. 2019) Of note, these patients were NOT in shock.
Revascularization of the non-culprit lesions need not occur at the time as primary PCI (revascularization of the culprit lesion(s)). In other words, can use a staged revascularization strategy.
Optimal timing of staged procedure unclear
- Pre-discharge or within 30 days resulted in same outcome
In the COMPLETE trial, complete revascularization was not performed at index Primary PCI
For patients who present in cardiogenic shock (See Chapter 42), mortality was lower among those who had culprit-only PCI rather than immediate (not staged) multivessel PCI. (Thiele et al. 2017)
Any potential advantage of multivessel PCI is outweighed by mortality hazard of the initial longer procedure.
Main proven goal in shock is rapid and complete reperfusion of culprit vessel
19.7.2 STEMI at non-PCI hospital
If expecting delay, i.e. first medical contact to primary PCI >120 min
Pharmaco-invasive strategy
Full dose lysis, heparin, clopidogrel (loading dose) and
- Clopidogrel 300 mg (or 75 mg if > 75 yo)
Send to PCI-capable hospital for routine PCI
Outcomes equivalent to and safe as primary PCI
CAPTIM (Bonnefoy et al. 2009; Steg et al. 2003)
WEST (P. W. Armstrong 2006)
Fast MI registry (Danchin et al. 2008)
STREAM (Paul W. Armstrong et al. 2013)
Look for evidence of successful reperfusion after 90-120 mins of getting lytics
looking for STE resolution, specifically >50% resolution in initial ECG of lead with maximum STE
If no STE resolution, considered to have failed lytic therapy → go urgently to cath lab
If STE resolution, then responded to lytics → go to cath lab 3-24 hrs after getting lytics for revasc
- Avoid routine immediate coronary angiography d/t higher risk of stent thrombosis and CVA
19.7.3 Conservative (medical) management of acute UA/NSTEMI
- anticoagulation: heparin, enoxaparin
- DAPT: ASA + clopidogrel or ticagrelor
19.7.4 Indications for temporary pacing at time of MI
Sx bradyarrythmia refractory to meds
asystole or sinus arrest
complete (3rd degree) AV block
Mobitz type 2 (2nd degree) AV block
19.7.5 Medications with mortality benefit in MI
antiplatelet therapy
high-intensity statin
β-blockers (if LVEF < 40% or prior MI)
- all MI pts should be started on a BB after an MI for at least 3 yrs. Continue indefinitely if LVEF < 40% or prior MI.
ACEi
- only indicated post-MI if LVEF < 40%, DM, HTN or CKD
Order an Echo after a STEMI to evaluate for cardiac function (e.g. EF) and mechanical complications
The most important prognostic factor in pts w/ CAD is the degree of LV dysfunction
19.7.6 Indications for coronary artery bypass graft (CABG)
Left main CAD w/ > 50% stenosis
3-vessel CAD with > 70% stenosis in each vessel
significant (> 70% stenosis) in 2-vessels with 1 of these 2 vessels being the proximal LAD [Left main equivalent]
CABG vessel patency at 10 yrs:
internal mammary artery (IMA) graft: 90% are patent at 10 yrs
saphenous vein: 50% are patent at 10 yrs