Acute Coronary Syndromes

Acute Coronary Syndromes

16/2/11

PY Mindmaps

FANZCA Notes

OHOA page 42-43

Dr Scott Harding’s (Cardiologist) Talk on Perioperative Cardiovascular Evaluation – 2009

- coronary artery disease accounts for > 30% of death in West

CLASSIFICATION

- unstable angina: ischaemic pain that is more severe, frequent or prolonged than normal

- MI: ischaemic symptoms + raised biomarkers (NSTE-ACS and STE-ACS)

HISTORY

- take pain history

- assess severity

- recent MI’s

- previous thrombolysis, stent or CABG

- CHF symptoms

- functional ability (MET’s)

- medications

Canadian Cardiovascular Angina Scale

I – ordinary physical activity doesn’t cause angina (> 4 METS)

II – slight limitation or ordinary activity (2-4 METS)

III – marked limitation of ordinary activity (1-2 METS)

IV – inability to carry out any physical activity (angina @ rest)

EXAMINTION

- standard CVS examination

- may be nothing to find

- look for CCF symptoms

RISK FACTORS

- DM

- HT

- lipids

- family history

- male

- obesity

- previous MI

- hormone replacement for menopause

- inactivity

INVESTIGATIONS

CARDIAC BIOMARKERS

ADVANTAGESDISADVANTAGES

TNT and TNI- elevates after 8 hours- elevates in non-MI cases

- elevated for 7-10 days- assay variability for ref range

- cardiac specific- reperfusion alters peak

- cut of covers 99th percentile of popn.- need second test if first too early

- new assays very sensitive- some TNT in skeletal muscle

- negative test = low 30 day cardiac risk- incomplete understanding of

- stratifies short and long term risk well in AMIelevation post cardiac and non-

- detects reinfarctioncardiac surgery

- AUC correlates to extent of MI- baseline higher in CRF

CK- widely used and available- non-specific as in brain and sk

muscle

CK-MB- level and ratio improves specificity of CK- less sensitive and specific than TN

Myoglobin- theoretically rapid detection- lacks specificity and doesn’t

elevate earlier than TN

AST- historically used with CK and LDH- non-specific

LDH- late onset and offset- present in many tissues

- LD1 and LD2 in muscle- requires isoenzymes

CRP- marker of inflammation- non-specific

ESR- additive prognostic benefit- non-specific

Novel Biomarkers

Copeptin- if levels low -> rules out MI- not specific

Troponin H-FABP- early marker of ischaemia- disappointing in studies

BNP- prognostication in AMI- difficult to interpret in critical ill.

GP-BB- not superior to TN

Myeloperoxidase- not superior to TN

Pregnancy associated plasma protein A- not superior to TN

ECG

- acute AMI changes: peaked T waves with ST elevation -> gradual loss of R wave -> development of pathological Q wave and TWI

Anteroseptal = LAD

Anterolateral = Cx

Inferior = RCA

Posterior = Cx or PDA (off RCA)

Location of InjuryAffected LeadsArtery

Anterior/SeptalV2, V3, V4Mid or Diagonal LAD

InferiorII, III, aVFRCA or posterolateral Cx

LateralI, aVL, V3, V6Cx

True PosteriorV1 and V2Posterolateral of Cx or PDA of RCA

AnterolateralI, aVL, V2-V6Proximal LAD

InferolateralII, III, aVF, aVL, V5, V6Proximal Cx or Large LV in left

dominant system

Right ventricularV3R, V4RRCA

- criteria for AMI in LBBB:

(1) new LBBB

(2) concordant ST elevation of > 1mm

(3) concordant ST depression of > 1mm in V1, V2 or V3

(4) discordant ST elevation of > 5mm

ETT

- gives an assessment of functional capacity

- looking for; ST depression, hypotension, arrhythmias

CPX Testing

- bike or hand ergometer

- under exercise O2 consumption is a linear function of Q and thus LV function

- aerobic threshold of >11mL/min/kg is able to predict survival after major abdominal surgery accurately

Dobutamine Stress Echo

- those that can’t exercise

- up to 40mcg/kg/min

- looks @ regional wall motion as an indicator of impaired perfusion

- > 4 wall motion abnormalities = high risk

Nuclear Medicine Scan – Dipyridamole thallium scintography, SESTAMIBI, SPECT MPI, PET

- coronary vasodilator (dipyridamole) and radio isotope (thallium) which is up taken into perfused myocardium

- impaired perfusion shows up as reversible perfusion defects caused by dipyridamole causing a steel phenonmena

- non-perfused areas show up as permanent perfusion defects

- key findings one is looking for = reversible perfusion defects, permanent perfusion defects and cavity dilation

- negative test is very reassuring

CT Coronary Angiogram

- quantification of the amount of Ca2+ in the coronary arteries

- massive dose of radiation

- useful when wanting to completely rule out CAD burden

Dobutamine stress MRI

- elegant up and coming form of stress testing

- identifies wall motion abnormalities

- highly accurate

- safe

TechniqueSensitivitySpecificity

ETT70%80%

Exercise Stress ECHO8085

Dobutamine Stress ECHO8080

Sestamibi MPI8075

SPECT MPI9075

PET scan9080

Coronary arteriography

- delinates who needs PCI, CABG or medical management

- anatomical nature of lesions

- can stent but has issues relevant to surgery (see AHA 2007 Guidelines)

MANAGEMENT

STEACS

Reperfusion therapy

- options: thrombolysis, PCI or CABG

- ideally PCI within 90 minutes (if not thrombolyse)

- thrombolysis contraindications: absolute – active bleeding, closed HI/facial trauma in 3 months, suspected aortic dissection, risk of ICH, relative – anticoagulation, non-compressible vascular puncture, recent major surgery, > 10 minutes of CPR, internal bleeding within 4 weeks, active peptic ulcer, poorly controlled HT, ischaemic CVA within 3 months, pregnancy

Anti-platelet therapy

- aspirin 300mg (reduces risk of death or MI by 50% in USAP or NSTEMI)

- clopidogrel 600mg (all those that require a stent, withhold if needs a CABG)

- glycoprotein IIb/IIIa inhibitors (post NSTEMI and PCI)

Antithrombin therapy

- PCI: UFH

- thrombolysis: UFH or LMWH

Nitrates

- symptomatic relief

- use in CCF

- no mortality advantage however

Beta-blockers

- IV or PO

- reduce mortality

ACE-I

- use in patients with low EF, AMI and those who are vasculopaths.

Statins

- decreases risk of ischaemic events

NSTEACS

Risk stratification

- high: repetitive or prolonged pain, elevated TNT, persistent or dynamic ECG changes, transient ST elevation, cardiogenic shock, VT, syncope, EF < 40%, prior CABG, PCI within 6 months, DM, CRF

- intermediate: rest or prolonged pain, age > 65, known IHD, 2 or more IHD risk factors, CRF, prior aspirin use

- low: none of the above

Management

- high: aggressive medical management and coronary angiography (including LMWH)

- intermediate: inpatient monitoring and provocation testing

- low: discharged and followed up

PERIOPERATIVE MANAGEMENT

- early consultation with cardiology

- keep cardiac medications going

- avoid tachycardia, hypotension, hypoxia, hypercarbia

- good analgesia

- keep Hb > 90g/L

- high index of suspicion for perioperative MI

- 12 lead ECG post op day 1, 2 and 3

- TNT if high risk day 2 and 3

- keep anti-platelets going

- if develops ST elevation -> urgent angiogram

- treat angina and CHF aggressively

COMPLICATIONS

- cardiac failure

- post-infarction ischaemia

- ventricular free wall rupture: pericardiocentesis and repair

- ventricular septal rupture: IABP, inotropes, surgery

- acute MR: afterload reduction, IABP, inotropes, surgery ASAP

- right ventricular infarction: IV fluids, inotropes, AV synchrony, IABP, reperfusion

- arrhythmias: correct hypoxia, acidosis, hypovolaemia, K+, Mg2+ (controversial)

- cardiogenic shock: must get revascularisation (PCI or CABG) within 24 hours

- thromboembolism: mural thrombus -> anticoagulate

- post-MI syndrome (Dressler’s) and pericarditis

Jeremy Fernando (2011)