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ACS (CLINICAL FEATURES (NSTEMI
chest pain/discomfort -…
ACS
CLINICAL FEATURES
- NSTEMI
- chest pain/discomfort - tight/heavy/burning - usually retrosternal but can radiate to left arm, neck, both arms, back, epigastrium (mimics heartburn)
- diaphoresis
- physical exertion
- dyspnoea - due to low CO
- ↑JVP
- pulmonary oedema
- cariogenic shock
- weak, syncope (uncommon), nausea, vomit, adnominal pain (might be only symptom) - common in women + old + diabetics
- HTN or hypotension depending on location + extent of infarction
- STEMI
- central heavy chest pain at rest+exertion; radiates to left arm/jaw; 20mins
- dyspnoea - due to pulmonary congestion from diastolic dysfunction
- pallor
- diaphoresis
- nausea, vomiting
- dizzy, weak - due to hypotension/bradycardia
- tachycardia - anterior wall MI
- additional ♥ sounds - S3 or S4 - indicates poor ♥muscle complicate of infarcted muscle
- systolic murmur if mitral regurgitation or ventricular septal defect develops
- ACS - common S+S:
- chest pain
- central/left-sided
- radiate to jaw or left arm
- heavy/constricting/elephant sitting on chest
- diabetics/elderly might not get chest pain
- Px can present with wide variety of types of chest pain, can confuse ischaemic pain for other causes e.g. dyspepsia
- dyspnoea
- diaphoresis
- nausea, vomiting
- pale, clammy
- Px often have few physical signs:
- pulse, BP, temp, O2sats usually normal/mildly altered e.g. tachycardia
- Unstable angina
- chest pain on exertion
- increasing frequency/severity of chest pain
- decreasing levels of activity needed to trigger pain + can occur at rest
- retrosternal pressure/heaviness radiates to jaw, arm, neck
- dyspnoea - can occur alone in atypical
- 4th ♥ sound indicates ↓ ♥ relaxation due to ischaemia
- 2 types:
- typical: chest pain on exertion + relieved by GTN
- atypical: chest pain on exertion - NOT relieved by GTN
- epigastric pain, pleuritic chest pain - common in F/old/diabetic/renal failure Px
- sinus tachycardia
MANAGEMENT
STEMI - acute management:
- Primary percutaneous intervention (PCI) to revascularise
- but thrombolyse if PCI not available
- blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery
- coronary angiography with follow on PCI within 12 hours of symptoms
- For STEMI PCI always offered
- But for NSTEMI need to assess the risk of them getting STEMI and risk of dying - GRACE calculator, tells you how long
- Aspirin - chew
- Ticagrelor** - CI in active bleeding
- Heparin IV - LMWH or unfractionated
- Analgesia morphine IV
- O2
- Anticoagulation after PCI - fondaparinux unless on NOAC already
- Manage hyperglycaemia e.g. with insulin infusion
- ACE inhibitor in all STEMI unless renal failure or systolic BP <90mmHg
- B-blocker
- Statins/lipid-lowering agents
- Nitrates
Post-STEMI management:
- ACE inhibitor (pril) or ARB (sartan; Afro-Caribbean Px; dry cough)
- before starting, measure: renal function, U&E, BP - continued indefinitely
- B-blocker - LOL
- continued >12 months post-MI in PX w/o LV systolic dysfunction or HF; after 12 months review continuation
- if intolerant use CCB:
- verapamil or diltiazem - w/o HF
- amlodipine - if HF
- Statin
- indefinitely continued post-MI
- Anti-platelet therapy
- aspirin indefinitely continued PLUS clopidogrel/other grel
- or clopidogrel alone if aspirin intolerated
- annual flu vaccine
- manage other co-morbidities
- adopt cardioprotective diet; exercise
- cardiac rehabilitation
- psychological support
NSTEMI acute management
- M - morphine
- O - O2
- N - Nitrates - GTN
- A - Aspirin
- C - Clopidogrel (with aspirin but mono therapy if aspirin intolerated)
- B-blocker
- CCB if ischaemic symptoms continue despite GTN + b-blocker
- PCI - for some
- Anticoagulation - heparin - for all Px
Post NSTEMI-management - ballsack
- B-blocker
- Statin
- ACE or ARB
- Asprin
- Clopidogrel
Both unstable/stable angina:
- GTN
- B-blocker or CCB
Statin, anti-hypertensive treatment
Unstable angina
Stable angina - not an ACS
- GTN, B-blocker or CCB
- Anti-platelet therapy - 2ry prevention
- ACE inhibition - 2ry prevention
-
DEFINITION
MI is:
- Necrosis of section of myocardial tissue due to ischaemia (poor supply of blood)
- aka heart attack
- Necrosis due to prolonged mismatch between perfusion + demand due to occlusion in coronary arteries
- STEMI or NSTEMI
- Under ACS umbrella term for acute presentations of ischaemic heart disease:
- STEMI
- ST↑ persistent >20 mins on ECG
- ↑troponin - marker of myocardial cell death/necrosis
- NSTEMI
- Unstable angina
- ST depression
- Note: ST↓ also in stable angina, but ST↑ in Prinzmetal/variant
- no rise in blood troponin in unstable angina
- Stable angina - not an ACS
- occurs predictably with physical exertion or emotional stress
- no more than 10 minutes (usually less)
- relieved on rest + sublingual nitrates
Unstable angina is:
- new onset angina or abrupt deterioration in previously stable angina, often occurring at rest
- angina at rest/exertion due to poor O2 supply reaching ♥muscle
- blood troponin levels DON'T rise i.e. no biochemical evidence of ♥damage
PATHOPHYSIOLOGY
ACS develops in Px with known/undetected IHD:
- IHD same as coronary artery disease/coronary heart disease
- initial endothelial dysfunction triggered by risk factors egg, smoking, HTN, hyperglycaemia → eventually leads to gradual build up of fatty plaques in coronary arteries aka atherosclerosis → narrowing → ↓ less blood and O2 reaching myocardium during increased demand → angina (poor O2 reaching ♥ during exertion)
- sudden plaque rupture in coronary endothelium → sudden artery occlusion → ↓ or no blood/O2 reaching that ♥ area
Complications of coronary atherosclerosis:
- occlusion = ↓blood/O2 →angina
- rupture/erosion = thrombus → COMPLETE occlusion→STEMI
- transmural infarct (zone of necrosis is whole wall thickness)
- rupture/erosion = thrombus → PARTIAL/intermittent occlusion→NSTEMI
MI pathogenesis:
- 3 commonly blocked coronary arteries:
- LAD - left anterior descending - most cases
- supplies anterior wall + septum of LV
- RCA - right coronary artery
- supplies posterior wall, septum, papillary muscles of LV
- LCx - left circumflex
- supplies lateral wall of LV
- coronary artery blocked → within mins muscle becomes ischaemic = cell contractility↓
- initial stage sensitive as ischaemic damage in perfusion zone potentially reversible
- after 20-40 mins → irreversible damage = zone of necrosis
- inner third myocardium affected first
- as furthest from arteries in epicardium so last area to receive blood + subject to higher pressure from inside ♥
- sub-endocardial infarct - partial infarct of wall - NSTEMI
- occurs if block suddenly lyses/breaks down + blood flow returns
- in this case damage can be limited to inner third
- ♥cell death confined to endocardial layers + not full thickness of muscle layers
- due to relatively small branch, good collateral flow around occluded vessel, or bc intervention for ST↑ early+effective
- transmural infarct - zone of necrosis is whole wall thickness - STEMI
- after 3-6 hours zone of necrosis extends through entire wall
- can lead to arrhythmia, death, severe HF
- dead muscle = permanent Q waves on ECG
Major complications of MI:
- 0-24 hours
- arrhythmias as damage disrupts electrical signal conduction
- cardiogenic shock - as ♥ cant pump enough blood to body
- depends on how much contractile muscle affected
- might need inotropic support
- 1-3 days
- pericarditis - inflammation of tissue around infarct + neutrophil invasion
- pericardial effusion; pericardial rub; pain worse on lying flat
- 3-14 days
- myocardial rupture of new connective tissue
- MO invade tissue + healing process begins with formation of new connective tissue (yellow+soft) - risk of rupture at this stage
- 2 weeks-months
- HF - as scar tissue doesn't contract to pump blood
- overtime heart muscle can grow/remodel to compensate for these lost cells + pump harder but ultimately continue to fail = HF
- chronic HF due to V dysfunction
- loop diuretics e.g. furesomide + ACE + B-blockers - to improve prognosis of chronic HF
INVESTIGATIONS
STEMI:
- ECG - first
- ST↑ in 2 or more adjacent leads; >20 mins
- Cardiac troponin blood levels ↑ - first
- Coronary angiogram - use early
- confirms acute MI = shows thrombus with occlusion of artery
- facilitates early re-perfusion to save ♥
- CXR;
- should be normal,
- used to exclude DDx for chest pain + assess♥ functioning
- widened mediastinum = aortic dissection
- pulmonary oedema = impaired ♥ function
- look for cardiomegaly - suggest HF
- U&Es
- Creatinine
- Glucose, lipids, cholesterol
- Echocardiogram - after repercussion therapy
- NSTEMI:
- ECG - first
- downsloping ST depression and/or symmetrically inverted T waves
- usually persistent T wave inversion
- do serial ECGs if chest pain to detect development of STEMI or to guide re-perfusion strategy
- trial sublingual GTN
- cardiac troponin
- confirms diagnosis
- creatine kinase if troponin not available
- FBC
- used to find 2ry cause of NSTEMI (e.g. acute blood loss, anaemia)
- normal; anaemia; thrombocytopoenia
- U&E - normal or deranged
- LFTs - if considering drugs that undergo hepatic metabolism
- normal
- CXR
- normal or may show pulmonary oedema
- look for cardiomegaly
- Unstable angina
- ECG - first
- normal or transient ST↓ or T wave inversion
- Cardiac biomarkers - not elevated
- FBC - low or normal
- ↓Hb can be precipitating factor for angina
- Coronary angiography
- stenosis of coronary artery
- CXR
- excludes DDX for chest pain
- in Px with HF will have pulmonary oedema
- U&E - normal
- Coagulation profile - normal