CHEST PAIN

Approach

Obtain & review an ECG w/i 10 min of pt arrival & compare w/ prior if available. If pain persists, repeat q15–20min; consider R-sided & posterior leads if high probability w/ initially nl appearing ECG.

•  Intervene early w/ IV, O₂, & cardiac monitoring

•  CXR for all nontrivial CP

•  Give ASA 325 mg if considering a cardiac etiology & you do not suspect aortic dissection

•  Give NTG for pain

•  Obtain PQRST of pain & recheck after pain medication is given

•  Obtain CAD hx: Prior MI, CABG, catheterization, stress test, angina

Risk stratify: Age >50, HTN, DM, HL, +FH, smoking, cocaine; use of risk stratification models such as TIMI, GRACE, or PURSUIT can be useful to assist in decision making w/ regard to tx options in pts w/ suspected ACS.

•  Always consider immediately life-threatening causes of CP

ACUTE CORONARY SYNDROME (OVERVIEW)

Approach

•  See Approach above

Definitions

•  ACS: Represents a clinical spectrum ranging from UA through NSTEMI & STEMI

ACS develops when a vulnerable or high-risk plaque undergoes disruption of the fibrous cap which is a stimulus for thrombogenesis w/ ultimate imbalance b/w myocardial O₂ supply & demand

•  UA (subtotal coronary thrombosis, angina that is new onset, crescendo, OR at rest, usually <30 min, ±ST depression &/or TWI)

•  Rest angina: Angina occurring at rest & prolonged, usually >20 min

•  New-onset angina: New-onset angina of at least CCS class III severity

•  Increasing angina: Previously diagnosed angina that has become distinctly more frequent longer in duration, or lower in threshold (ie, increase by 1 or more CCS class)

•  NSTEMI (same as UA but w/ +troponin)

•  STEMI (total coronary thrombosis, angina usually at rest >30 min, ST elevations, +troponin)

•  Note: Most troponin elevations in ED are not due to primary ACS, but demand ischemia

History (NEJM 2005;294:2623)

•  Typical sxs

•  Angina (substernal pressure/pain/tightness, radiation to neck/jaw/arms, precipitated by exertion/relieved w/ rest or NTG); w/ ACS, new onset, crescendo, or at rest

•  Associated sxs: Dyspnea diaphoresis, N/V, palpitations, LH; ∼23% MIs lack typical sxs (AJC 1973;32:1)

Physical Exam

•  Usually unremarkable exam

Evaluation

•  ECG: ST change (up or down), TWI, LBBB that is new. Q wave or PRWP suggests prior MI → CAD. Always check ECG w/i 10 min, w/ changes in sxs, at 6–12 h & c/w baseline. If pain persists, repeat q15–30min.

•  It is reasonable to obtain supplemental ECG leads V7–V9 in pts whose initial

ECG is nondiagnostic to r/o MI due to L circumflex occlusion

•  Sgarbossa’s criteria: In setting of old LBBB, STEMI Dx requires ≥1 mm STE concordant w/ QRS (sens 73%, spec 92%) or ≥5 mm discordant (sens 31%, spec 92%) any lead (NEJM 1996;334:481).

Cardiac Biomarkers

•  Requires serial testing at 6 & 12 h after sx onset. It is reasonable to remeasure positive biomarkers at 6- to 8-h intervals 2–3 times or until levels have peaked, as an index of infarct size & dynamics of necrosis.

•  Troponin (I or T) is most sens & spec. Also seen in myocarditis, CMP, severe CHF, cardiac trauma, cardioversion, sepsis, ICH, renal failure.

•  Cardiac index, CI = (CK – MB/CK) × 100. CI <3 suggests skeletal source, CI 3–5 → indeterminate, CI >5 suggests cardiac source

•  Other labs: Chem 7, CBC, coags, T/S (if intervention planned), tox (if cocaine suspected)

•  CXR: Check for cardiomegaly, pulmonary edema

•  Echo: If ECG is not interpretable (prior LBBB, paced) & suspicion for ACS is high, can obtain echo to evaluate for regional wall abnlty.

•  CTCA: May be useful for evaluating pts w/ intermed & low PreTP for CAD w/ nl serial ECGs/biomarkers (Circulation 2006;114:1761; JACC 2006;48:1475; NEJM 2012;366(15):393; NEJM 2012;367(4):299)

Treatment

•  See STEMI & UA/STEMI for details

Disposition

•  If hx & initial ECG/biomarkers are non-Dx: Repeat ECG/biomarkers at 3 & 6 h from 1st set & if suspicion for ACS is low, may monitor for recurrent sx. If no ACS, can evaluate for inducible ischemia via stress test.

•  Stress testing may be done as an outpt if low risk (age <70, no prior CAD, CVD, PAD; no rest angina) at 72 h (0% mortality, <0.5% MI, [Ann Emerg Med 2006;47:427])

•  If STEMI or UA/NSTEMI: Admit (see below)

Pearls

•  Give ASA if you suspect ACS & there are no CIs. It provides the greatest morbidity/mortality benefit of any tx in the ED for ACS (50–70% drop D/MI for UA/NSTEMI, NEJM 1988;319:1105; 23% drop death in STEMI, ISIS-2, Lancet 1988;ii:349).

•  Women, diabetics, & elderly pts often present w/o CP; anginal equivalents: SOB, fatigue, weakness

STEMI

Definition

•  Total coronary thrombosis, angina usually at rest >30 min, ST elevations, +troponin

Evaluation

•  ≥0.2 mV precordial leads, ≥0.1 mV limb leads, & ≥0.5 mV in R-sided & posterior leads in at least 2 contiguous leads

Treatment

•  Decide whether the pt will receive lysis or PCI as soon as possible

•  If PCI is to be performed, call cardiology/PCI lab (if one is available) as early as possible (potentially even before the pt arrives in the ED – if reliable prenotification of STEMI via EMS)

•  If pt will be transferred for PCI, call for transfer early, & ensure their door-to-balloon time is <90 min

•  Antithrombotic/adjunctive therapy, should not delay transfer for PCI

Routine Medical Therapies “MONAB”

•  Morphine: Drug of choice for pain relief in pts w/ STEMI; typical dose 0.05–0.1 mg/kg IV

•  O₂: Appropriate only in hypoxic pts w/ O₂ saturation <90%, as routine O₂ use may cause higher risk of death for pts w/ confirmed AMI

•  Nitrates: No mortality benefit, but may ameliorate sxs; typical dose 0.4 mg SL q5min × 3 doses; CI w/ hypotension, RV infarct, concomitant PD inhibitor use w/i 24–48 h.

•  Aspirin: 23% ↓ in death (ISIS-2, Lancet 1988;2:349); typical dose 162–325 mg PO

•  Beta-blockers: Oral BB should be administered w/i 24 h of STEMI w/o CIs. Routine IV should not be used & recommended in those w/o CIs or w/ ongoing ischemia. Increased risk of cardiogenic shock in those >70 y/o, SBP <120 mmHg, HR >110 bpm (COMMIT/CCS-2, Lancet 2005;366:1622); when used, typical dose Metoprolol tartate 5 mg IV

•  Other: Often started as inpts include oral BBs, statins, ACE inhibitors/ARBs

Fibrinolysis

•  Fibrinolytic therapy should be given to pts w/ STEMI & onset of sxs w/i previous 12 h when it is anticipated that primary PCI cannot be performed w/i 120 min of 1st medical contact

•  Indications: Sx <12 h & either STE ≥1 mm in ≥2 contig. Leads or LBBB not known to be old; benefit if sx >12 h less clear; reasonable if persistent up to 24 h sx & STE.

•  Door-to-needle time should be ≤30 min

•  ∼20% ↓ mortality in anterior MI or new LBBB; 10% ↓ mortality in IMI

•  ∼1% risk of ICH; high-risk groups include elderly (∼2% if >75 yr), women, low weight

•  Fibrin-specific lytic (front-loaded tPA) 14% ↓ mortality c/w SK (1% abs Δ; GUSTO, NEJM 1993;329:673) although ↑ ICH (0.7% vs. 0.5%); 3rd-generation bolus lytics easier to administer, but no more safe or efficacious

•  Fibrinolytic agents:

Tenecteplase (TNK-tPA): Single IV weight-based bolus

30 mg for weight <60 kg

35 mg for 60–69 kg

40 mg for 70–79 kg

45 mg for 80–89 kg

50 mg for ≥90 kg

Reteplase (rPA): 10 U + 10 U IV bolus given 30 min apart

Alteplase (tPA): Bolus 15 mg, infusion 0.75 mg/kg for 30 min (max 50 mg), then 0.5 mg/kg (max 35 mg) over 60 min; total dose not to exceed 100 mg

Adjunctive Antithrombotic Therapy for Fibrinolytic Therapy

•  ASA (162–325 mg PO) & Clopidogrel (300 mg LD for pts ≤75 y/o, 75 mg for pts >75 y/o) should be administered to pts w/ STEMI who receive fibrinolytic therapy (ISIS-2, Lancet 1988;2:349; CLARITY-TIMI 28, NEJM 2005;352:1179; COMMIT, Lancet 2005;366:1607)

•  Pts w/ STEMI undergoing reperfusion w/ fibrinolytic therapy should receive anticoagulation therapy for minimum of 48 h, w/ recommended regimens:

UFH weight-based infusion w/ IV bolus 60 U/kg (max 4000 U) followed by infusion of 12 U/kg/h (max 1000 U) to maintain aPTT ∼50–75 s for 48 h or until revascularization

Enoxaparin: If <75 y/o, 30 mg IV bolus, then 15 min later, 1 mg/kg SC q12h; if >75 y/o; no bolus, 0.75 mg/kg SC q12h; if CrCl <30 mL/min, 1 mg/kg q24h

Fondaparinux: Initial 2.5 mg IV, then 2.5 mg SC the following day, CI in CrCl <30

Indications for Transfer for Angiography After Fibrinolysis

•  Immediate transfer for cardiogenic shock or severe acute HF irrespective of time delay from MI onset

•  Urgent transfer for failed reperfusion or reocclusion

•  As part of an invasive strategy in stable pts w/ PCI b/w 3 & 24 h after successful fibrinolysis

Primary PCI (NEJM 2007;356:47)

•  Should be performed w/i 90 min of arrival by skilled operator at high-volume center

•  Superior to lysis: 27% ↓ death, 65% ↓ re-MI, 54% ↓ stroke, 95% ↓ ICH (Lancet 2003;361:13)

•  Transfer to center for 1° PCI may also be superior to lysis (DANAMI-2, NEJM 2003;349:733) if can achieve acceptable door-to-balloon times (as above)

Adjunctive Antithrombotic Therapy for Primary PCI

•  ASA 162–325 mg PO (crushed/chewed) should be given before primary PCI (Circulation 1987;76:125; Eur Heart J. 2009;30:900; NEJM 2010;363:930)

•  A loading dose of a P2Y₁₂ receptor inhibitor should be given as early as possible or at the time of primary PCI in pts w/ STEMI:

•  Clopidogrel 600 mg PO (NEJM 2010;363:930; ARMYDA-6 MI, J Am Coll Cardiol 2011;58:1592; CURRENT-OASIS 7, Lancet 2010;376:1233)

•  Prasugrel 60 mg PO (NEJM 2007;357:2001; TRITON-TIMI, Lancet 2009;373:732); should not be used in pts w/ a prior h/o stroke or TIA

•  Ticagrelor 180 mg PO (PLATO, Circulation 2010;122:2131)

*(Consider deferring decision regarding timing of P2Y₁₂ receptor inhibitor use to cardiology, given potential need for CABG)

•  It is reasonable to begin tx w/ an IV GPIIb/IIIa receptor antagonist in the precatheter setting to pts w/ STEMI for whom primary PCI is intended (JAMA 2004;292:362; RELAx-AMI, J Am Coll Cardiol 2007;49:1517)

•  Abciximab: 0.25 mg/kg bolus, then 0.125 mcg/kg/min (max 10 mcg/min)

•  Tirofiban (high-bolus dose): 25 mcg/kg IV bolus, then 0.15 mcg/kg/min; ↓ by 50% in CKD

•  Eptifibatide: (double bolus): 180 mcg/kg IV bolus, then 2 mcg/kg/min; a 2nd 180 mcg/kg bolus given 10 min after 1st bolus; ↓ by 50% in CKD, avoid in dialysis pts

•  For pts undergoing primary PCI, the following anticoagulant regimens are recommended:

•  UFH w/ GP IIb/IIIa inhibitor: 50–70 U/kg bolus to achieve therapeutic ACT

•  UFH w/o GP IIb/IIIa inhibitor: 70–100 U/kg bolus to achieve therapeutic ACT

•  Bivalirudin: 0.75 mg/kg IV bolus, then 1.75 mg/kg/h infusion w/ or w/o UFH; preferred over UFH w/ GP IIb/IIIa inhibitor in pts at high risk of bleeding

Nonprimary PCI

•  Facilitated PCI: Lytic before PCI harmful (Lancet 2006;367:569; Lancet 2006;367:579), & partial dose lytic no better than no lytic (FINESSE, NEJM 2008;358:2205); upstream GPI also shows increased mortality

•  Rescue PCI (after full dose lytics & persistent STEMI or cx): Beneficial if <50% ST segment resolution by 90 min (NEJM 2005;353:2758)

•  Routine angio ± PCI w/i 24 h of successful lysis: ↓ D/MI/Revasc (Lancet 2004;364:1045)

•  Late PCI (median day 8) of occluded infarct-related artery: No benefit (NEJM 2006;355:2395)

Disposition

•  Admit to cardiology → cath lab → CCU

Pearls

•  Mortality 6% w/ reperfusion tx (PCI or lytic), ∼20% w/o

•  Predictors of mortality: Age, time to therapy, anterior MI, LBBB, heart failure (Circulation 2000;102:2031)

Guideline: O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of STEMI: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):e78–e140.

UA/NSTEMI

Definition

•  UA (subtotal coronary thrombosis, angina that is new onset, crescendo, OR at rest, usually <30 min, ±ST depression &/or TWI); see above for CCS classification

• Rest angina: Angina occurring at rest & prolonged, usually >20 min

• New-onset angina: New-onset angina of at least CCS class III severity

• Increasing angina: Previously diagnosed angina that has become distinctly more frequent longer in duration, or lower in threshold (ie, increase by 1 or more CCS class)

•  NSTEMI (same as UA but w/ +troponin)

•  Consider calling cardiology for +Tn, ongoing CP

Routine Medical Therapies “MONAB”

•  Morphine: Reasonable to use if there is uncontrolled ischemic CP despite NTG; typical dose 0.05–0.1 mg/kg IV

•  O₂: Supplemental O₂ should be administered to pts w/ UA/NSTEMI w/ an arterial satura_tion less that 90%, respiratory distress, or other high risk features for hypoxia

•  Nitrates: Pts w/ ongoing ischemia should receive NTG SL (0.4 mg) q5min for a total of 3 doses, after which assessment should be made about need for IV NTG if no CIs (CI w/ hypotension, RV infarct, concomitant PD inhibitor use w/i 24–48 h)

•  Aspirin: 23% ↓ in death (ISIS-2, Lancet 1988;2:349); typical dose 162–325 mg PO

•  Beta-blockers: Oral BB should be administered w/i 24 h of NSTEMI w/o CIs. Routine IV should not be used. It is reasonable to administer IV BBs to UA/NSTEMI pts who do not have 1 or more of the following: (1) signs of HF, (2) e/o low-output state, (3) increased risk of cardiogenic shock, (4) other CIs to BB therapy (RAD, heart block, etc.).

•  Other: Often started as inpts include oral BBs, statins, ACE inhibitors/ARBs

Conservative vs. Early Invasive Strategy (JACC 2002;40:166)

•  Conservative approach = selective angiography

•  Medical tx w/ pre-d/c stress test

•  Angio only if recurrent ischemia or strongly +ETT

•  Early invasive approach = routine angiography w/i 24–48 h

•  25% ↓ MI, 34% ↓ rehospitalization for ACS & nonsignificant 8% ↓ death c/w cons (JAMA 2005;353:1095), but results dominated by peri-PCI MI; post-d/c benefits of INV c/w prior data

•  No benefit to PCI w/i 24 h compared to PCI w/i 72 h (N Engl J Med 2009;360:2165)

•  General tx approach

•  If low-risk pt (–Tn, no ST ↓, & TRS 0–2)

•  If ↓ EF, recent PCI, prior CABG then → INV strategy

•  If not, then → CONS strategy (stress test once stabilized, before d/c)

•  If high-risk pt (+Tn, ST ↓ >0.5 mm, or TRS ≥3) → INV strategy

•  In those where an initial conservative strategy is selected, if recurrent sxs/ischemia, HF, or serious arrhythmias appear, then diagnostic angiography should be performed

Antiplatelet Therapy

•  ASA 162–325 mg PO (crushed/chewed) should be given as early as possible in pts w/ UA/NSTEMI (VA Cooperative Study, NEJM 1983;309:396; NEJM 1988;319(17):1105)

If ASA allergy: Clopidogrel (300–600 mg LD followed by daily maintenance dose) should be administered

•  Early invasive strategy

•  Before PCI:

•  Clopidogrel (NEJM 2001;345:494; PCI-CURE, Lancet 2001;358:527); or

•  Ticagrelor (PLATO, NEJM 2009;391:1045); or

•  An IV GP IIb/IIIa inhibitor, where eptifibatide & tirofiban are preferred

•  At the time of PCI:

•  Clopidogrel if not started before PCI; or

•  Prasugrel (TRITON-TIMI, NEJM 2007;357:2001); or

•  Ticagrelor (PLATO, NEJM 2009;391:1045); or

•  An IV GP IIb/IIIa inhibitor, where eptifibatide & tirofiban are preferred

•  Initial conservative strategy is selected, clopidogrel (300–600 mg LD) or ticagrelor (180 mg LD) should be added to ASA & anticoagulation therapy as soon as possible after admission

A loading dose of a P2Y₁₂ receptor inhibitor is recommended for UA/NSTEMI pts for whom PCI is planned. One of the following regimens is used:

a.  Clopidogrel 600 mg PO (J Am Coll Cardiol 2006;48:1339; CURRENT-OASIS 7, Lancet 2010;376:1233)

b.  Prasugrel 60 mg PO (TIMI, Lancet 2009;373:732); should not be used in pts w/ a prior h/o stroke or TIA

c.  Ticagrelor 180 mg PO (PLATO, Circulation 2010;122:2131)

•  In those where an initial conservative strategy is selected, it may be reasonable to add eptifibatide or tirofiban to anticoagulant & oral antiplatelet therapy

•  Tirofiban: 0.4 mcg/kg IV bolus over 30 min, then 0.15 mcg/kg/min; ↓ by 50% in CKD (PRISM-PLUS; NEJM 1998;338:1488)

•  Eptifibatide: 180 mcg/kg IV bolus, then 2 mcg/kg/min; ↓ by 50% in CKD, avoid in dialysis pts (PURSUIT, NEJM 1998;339(7):436)

Anticoagulant Therapy

•  Anticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI pts as soon as possible after presentation

•  For pts undergoing invasive strategy, the following anticoagulant regimens are recommended:

•  UFH w/ GP IIb/IIIa inhibitor: 50–70 U/kg bolus to achieve therapeutic ACT

•  UFH w/o GP IIb/IIIa inhibitor: 70–100 U/kg bolus to achieve therapeutic ACT

•  Bivalrudin: 0.75 mg/kg IV bolus, then 1.75 mg/kg/h infusion w/ or w/o UFH; preferred over UFH w/ GP IIb/IIIa inhibitor in pts at high risk of bleeding

•  For pts in whom a conservative strategy is selected, regimens using either enoxaparin, UFH, or fondaparinux are recommended:

•  UFH weight-based infusion w/ IV bolus 60 U/kg (max 4000 U) followed by infusion of 12 U/kg/h (max 1000 U) to maintain aPTT ∼50–75 s for 48 h or until revascularization

•  Enoxaparin: If <75 y/o, 30 mg IV bolus, then 15 min later, 1 mg/kg SC q12h; If >75 y/o; no bolus, 0.75 mg/kg SC q12h; If CrCl <30 mL/min, 1 mg/kg q24h

•  Fondaparinux: Initial 2.5 mg IV, then 2.5 mg SC the following day, CI in CrCl <30

Disposition

•  Admission to CCU, step-down unit, or ward bed, depending on risk & whether conservative or early invasive approach is chosen

•  Consider admitting to a CP/observation unit if pt deemed low risk, –Tn, & nondiagnostic ECG. Reconsider/admit pts w/ recurrent sxs, ECG changes, +Tn.

Guideline: Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with UA/NSTEMI: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2007;50(7):e1–e157.

Guideline: Anderson JL, Adams CD, Antman EM, et al. 2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with UA/NSTEMI: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(23):e179–e347.

PRINZMETAL’S (VARIANT) ANGINA

Definition

•  Distinct syndrome of ischemic CP classically occurring at rest & associated transient STE as a result of coronary artery spasm

•  Although VA results from focal coronary spasm, the exact etiology is unknown

History

•  Usually younger pts (35–50 y/o), smokers, F>M; often occurs in the AM, precipitated by hyperventilation or cold, but not exertion

•  No known cardiac hx & may have had a negative coronary angiogram

•  Associations: EtOH use, family h/o migraine, Raynaud’s syndrome, pericarditis, & primary MV prolapse

•  Sxs include substernal pressure that radiates to jaw & arm, usually in morning hours awakening from sleep; pain is typically responsive to NTG

Evaluation

•  EKG reveals transient STE in a distribution of a sp coronary artery & reciprocal STΔs; these episodes may induce a variety of conduction disturbances or arrhythmias

•  Stress testing may induce no STΔs, STDs, or STEs; STEs may be seen during recovery phase of stress testing

•  Angiography → nonobstructive CAD; intracoronary acetylcholine injection (90% sens)

•  Provocative testing w/ ergonovine or hyperventilation (not performed in ED)

Treatment

•  High-dose CCB (nifedipine, verapamil, diltiazem), nitrates (SL prn); d/c smoking

Disposition

•  Admit, given risk of MI & arrhythmia during acute episodes

COCAINE-INDUCED ANGINA

Definition

•  Cocaine-induced angina is caused by multiple cardiovascular effects of cocaine, including increased HR, BP, contractility, & end-systolic wall stress (from sympathomimetic effects) which all lead to increased myocardial demands as well as cocaine-induced coronary arterial vasoconstriction resulting in decreased O₂ supply

•  Acute thrombosis of coronary arteries after cocaine use can also occur & use has been a/w premature coronary atherosclerosis

•  Overall incidence of cocaine-associated MI is 0.7–6% of those presenting w/ CP after ingestion (Acad Emerg Med 2000;36:469; COCHPA, Acad Emerg Med 1994;1:330)

History

•  CP (pressure-like) that may be a/w dyspnea, anxiety, palpitations, diaphoresis, dizziness, or nausea

•  Sxs typically occur w/i 3 h of ingestion, but cocaine metabolites may persist up to 24 h to cause delayed or recurrent vasoconstriction

•  RF for cocaine-induced MI: Male gender, current smoker, nonwhite

Evaluation

•  Similar to ACS (see above)

•  Urine toxicology: Usually detects the cocaine metabolite benzoylecgonine which has a urine t1/2 of 6–8 h, & can be detected for up to 24–48 h after use (range 16–66 h)

•  Chronic cocaine users may have cocaine detectable in urine for weeks after last ingestion

Treatment

•  Pts should be treated similarly to possible ACS (see “routine medical therapies” above)

•  IV BZD

•  Antihypertensives: IV NGT, sodium nitroprusside, or phentolamine; avoid BBs as an unopposed α-adrenergic effect can lead to worsening coronary vasoconstriction & BP

•  STEMI: Early PCI

•  Drug-abuse counseling

Disposition

•  EDOU if sxs controlled & cardiac markers negative

•  Admit to cardiac unit if +cardiac markers or ongoing CP

Pearls

•  Cx: Arrhythmia & heart failure (∼90% occur w/i 12 h of presentation)

•  Ventricular tachyarrhythmias immediately after cocaine use result from the local anesthetic (sodium channel) effect on the myocardium & may respond to sodium bicarbonate therapy in addition to standard therapies (ie, lidocaine)

•  Cocaine-associated CP may be caused not only by myocardial ischemia but also by aortic dissection, thus maintain high index of suspicion

Guideline: McCord J, Jneid H, Hollander JE. Management of cocaine-associated chest pain and myocardial infarction: A scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Cardiology. Circulation. 2008;117:1897–1907.

STRESS TESTING

Approach

•  Noninvasive eval for CAD is done in the ED for pts after “r/o MI”

•  It should not be done on pts w/ high-risk ACS, ongoing CP

Indications

•  Dx CAD, assess Δ clinical status in pt w/ known CAD, localize ischemia

Contraindications

•  Absolute: Severe acute illness – AMI w/i 48 h, high-risk UA, PE/aortic dissection/pericarditis, CHF, arrhythmias – or underlying, severe AS

•  Relative: Inability to exercise, high-degree AVB, severe HTN, LM CAD, mod valvular stenosis, HCMP, severe electrolyte abnl

Findings

•  HR: A “diagnostic” exercise test requires minimum 85% of max predicted HR (220 – age)

•  METS (max exercise capacity), also displayed in minutes

•  ECG changes: Downsloping or flat ST ↓ predicts CAD, but does not localize dz; ST ↑ an even better predictor

•  Duke Treadmill Score (NEJM 1991;325:848) = Duration of exercise in minutes – (5 × max ST dev, in mm) – (4 × angina index*)

*Angina index: 0 none, 1 nonlimiting, 2 limiting:

Score >+5 → predicted 4-yr survival 98%; average annual mortality 0.25%

Score –10 to 4 → predicted 4-yr survival 94%; average annual mortality 2–3%

Score <–10 → predicted 4-yr survival 81%; average annual mortality 5%

•  Imaging: Either radionucleotide defect or echo wall motion abnlty; reversible defect → ischemia; fixed defect → infarct

•  Myocardial viability: To find cardiac muscle that can be “saved” by intervention. Can be done w/ multiple modalities: MRI (sens >95%, spec ∼70%), PET (sens ∼90%, spec ∼75%), dobutamine stress echo (sens ∼70%, spec ∼85%), rest redistribution thallium (sens ∼90%, spec ∼55%).

•  CT/MR coronary angiography

•  Coronary calcium score: Evaluate for CAD & estimate plaque burden based on quantifying coronary artery calcification

•  Can assess significant stenosis w/ sens/spec >85% w/ 64-slice CT, but limited by a large portion of nonevaluable artery segments (as much as 30%); requires relative bradycardia (often βB); b/c high NPV → useful for r/o (1) obstructive CAD in pts w/ anginal sxs, (2) CAD in pts w/ intermed & low pretest probability w/ nl serial ECGs/biomarkers (NEJM 2001;345:1863; JAMA 2006;296:403; JACC 2006;48:1475; Circulation 2006;114:1761).

Disposition

•  For adequate study (HR, METS achieved) & no e/o ECG changes, sxs, or imaging abnormalities, pt may be discharged home w/ PCP/cards f/u. If low pretest probability, & nondiagnostic test, pt may be discharged home w/ close f/u & 2nd testing modality done as outpt.

•  For adequate study w/ high-risk test results, consider coronary angiography, ± admission depending on clinical presentation

Pearl

•  Remember that +stress test indicating CAD in a pt who presented to ED w/ CP does not necessarily mean that CP was caused by CAD. Conversely, most of these tests are poorly sens/spec, so a negative result should not be particularly reassuring, esp in high-risk &/or high-PreTP pts.

CARDIAC CATHETERIZATION

Indications

•  ACS, high-risk stress test result or indeterminate result & high-risk or high PreTP for CAD, s/p cardiac arrest (SCD, VT), suspected nonatherosclerotic cause of ischemia (ie, spasm), systolic dysfxn of unclear etiology, or persistent angina despite tx or w/ systolic dysfxn

Types

•  Balloon angioplasty: Effective but has unique cx: Coronary artery dissection & restenosis from vessel remodeling

•  BMS: ↓ restenosis & repeat revasc (to ∼10% @ 12 mo) c/w balloon angioplasty but requires lifelong ASA & clopidogrel for at least 4 wk

•  DES (NEJM 2006;354:483): ↓ restenosis (by ∼75%) & repeat revasc (by ∼50%); to <5% (by 12 mo); no Δ D/MI over 1 yr c/w BMS; requires lifelong ASA & clopidogrel for at least 1 yr (Circulation 2007;115:813)

POST-PCI COMPLICATIONS

Approach

•  Ask about h/o back pain, noncompliance/recent d/c of antiplt Rx, √ access site (groin), distal pulses, ECG, CBC, Cr, CK-MB

Treatment

•  Bleeding (femoral access site, retroperitoneal)

If hematoma/active bleeding @ groin, apply pressure, reverse/stop anticoag

If retroperitoneal bleed, may c/o back pain, ± Hct drop, ↓ BP, ↑ HR; obtain abd/pelvic CT (I–), reverse/stop anticoag, consult IR/surgery

•  Vascular damage

Pseudoaneurysm: Pain, expanding mass, systolic bruit; obtain US; tx w/ manual compression, ± thrombin injection/surgery

•  AV fistula

Continuous bruit; obtain US; tx w/ surgery ↓ perfusion to LE (from embolization, dissection, thrombus): ↓ distal pulses; obtain angiogram; consult card &/or surgery for repair (either percutaneous or operative)

•  Renal failure

2° contrast, usually w/i 24 h, peaks 3–5 d

•  Stent thrombosis

P/w acute CP & STE. Consult cards/cath lab, for urgent catheterization. Common causes include underexpanded stent, dissection, or d/c antiplt Rx (JAMA 2005;293:2126).

Late stent stenosis DES > BMS (JACC 2006;48:2584)

•  Stent stenosis

P/w more chronic return of prior anginal sx, months after PCI (10% p/w ACS). Occurs 2° postprocedure remodeling, not atherosclerosis. Frequency: Balloon angioplasty >BMS > DES.

POST-MI COMPLICATIONS

LV Failure

•  Presentation ranges from pulmonary edema to frank cardiogenic shock

•  Tx

Diuresis for pulmonary edema w/o e/o shock

↓ afterload: IV NTG or nitroprusside

Inotrope: If the above Rx’s fail, give dopamine or dobutamine

Other: For cardiogenic shock, consult cardiology. Avoid diuretics, start w/ inotropes, ↓ afterload. May need IABP. Will need revascularization ASAP (NEJM 1999;341:625).

IMI Complications (Circulation 1990;81:401; Annals 1995;123:509)

•  Heart block

2° RCA involvement (supplies AV node), can develop high-degree AV

Block abruptly. Rx: Atropine/place TC pacer pads on pt & prepare for TV pacing, if necessary.

•  Precordial ST ↓

DDx includes (1) anterior ischemia, (2) posterior STEMI, (3) reciprocal Δs. Obtain posterior leads to r/o posterior STEMI.

•  RV infarct

P/w signs of right-sided failure: Hypotension, JVD 2° prox RCA occlusion

Obtain right-sided leads → 1 mm STE in V4R. Avoid nitrates, as these pts are preload dependent. Give dobutamine for persistently low BP (↑ contractility), consult cardiology, urgent reperfusion (NEJM 1998;338:933).

Mechanical Complications

•  Typically several days post-MI

•  Free wall rupture

Tear occurs in the myocardial wall @ junction b/w nl/infarcted muscle, most commonly in elderly person w/ large MI. P/w PEA, ↓ BP, cardiac tamponade. Tx w/ IV fluids (preload dep.), bedside echo (? peric effusion). Consult surgery/cardiology. If +effusion & unstable → bedside pericardiocentesis. If stable → operative repair.

•  Papillary muscle rupture

Occurs in small MI, IMI > AMI, p/w new murmur. Rx:

Diuretics, vasodilators, IABP, surgery consult for operative repair

•  Arrhythmias

AF most common. VT/VF → r/o MI, √ lytes. Monomorphic VT w/i 48 h MI → benign. AIVR: Slow VT (HR <100), often s/p reperfusion, self-limited/benign. New 2°/3° AVB → TC pacing ± TV pacing, esp if a/w BBB. TV for new 3° AVB, new BBB + 2° AVB type II, alternating LBBB/RBBB. Consult cardiology.

•  Other

LV thrombus: Anticoagulate

Ventricular aneurysm: Suspect if persistent STE post-MI. Obtain echo for Dx. Consult surgery, admit.

Pericarditis: Pericardial rub 1–4 d post-MI. ASA, NSAIDs, minimize anticoagulation.

Dressler syndrome: Inflammatory syndrome 2–10 wk post-MI. Fever, pericarditis, pleuritis. ASA, NSAIDs.

PULMONARY EMBOLISM AND DVT

Definition

•  PE: Thrombosis from a vein that embolizes to the pulmonary arterial system

•  DVT: Thrombosis of lower extremity (popliteal, femoral [incl SFV], iliac) or upper extremity (basilic, cephalic) veins

Approach

•  (1) Assess PreTP, (2) perform basic test (labs, CXR, ECG), (3) D-dimer, (4) imaging studies, to obtain (5) post-TP

•  If HD stable perform Dx tests; if unstable, consider empiric tx ± thrombolytics if potential benefit outweighs risk of bleeding (Chest 2004;126(suppl):401S)

History (Chest 1991;100:598; Am J Card 1991;68:1723)

•  RFs: Prior DVT/PE, hypercoagulable state, pregnancy/OCPs, malignancy, prolonged immobilization, recent surgery, FHx DVT/PE

•  PE: Dyspnea (73%), pleuritic CP (66%), cough (37%), syncope, ↓ BP, PEA

•  Assess PreTP: May use PERC (to decide whether any testing is necessary) or Wells criteria (to decide whether D-dimer is sufficient w/u)

•  PERC: If (1) low likely by gestalt + (2) “Yes” to all PERC criteria → 1.8% PE miss rate

Findings

•  PE: Unexplained ↑ HR, ↑ RR, ↓ SpO₂, fever, JVD

•  DVT: Leg edema/pain. Clinical signs DVT ∼50% pts.

Evaluation (PE)

•  Obtain ECG (sinus tachycardia, S1Q3T3 not sens/spec, simultaneous TWI in inferior & anterolateral leads), Hct, PT/PTT, Cr

•  CXR: R/o other causes; “classic” PE CXR findings (Hampton’s hump & Westermark’s sign) not sens/spec

•  D-dimer (sens 95–98%, spec 40–55%, ELISA or Rapid Quant. ELISA; Ann Intern Med 2004;140:589, NPV >99% for low pre-TP; JAMA 2006;295:172). Sens/spec vary by assay/cutoff.

•  False+: Pregnancy, trauma, infection, malignancy, inflammatory conditions, surgery, ↑ age, SCD, AF, ACS, CVA, acute UGIB, DIC

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