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Cardiology: Acute Coronary Syndromes (ACS)

Acute Coronary Syndromes (ACS)
Acute Coronary Syndromes (ACS)

Definition
  • Includes unstable angina and evolving MI
  • Most commonly due to atheroma but may also be due to emboli, coronary artery spasm or vasculitis
  • Usually divided into;
    • ACS with ST segment elevation or new onset LBBB (often referred to as an acute MI)
    • ACS without ST elevation, ECG may show ST depression, T wave inversion, non-specific changes o be normal (subendocardial MI)
  • Necrosis can occur without ST elevation

Risk factors
  • Non-modifiable – age, male, FHx
  • Modifiable – smoking, hypertension, hyperlipidaemia, DM, obesity, sedentary lifestyle
  • Controversial – stress, Type A personality, LVH, Increased Apoprotein A, increased fibrinogen, hyperinsulinaemia, increased homocysteine levels, ACE genotype, and cocaine use

Incidence
  • 5/1000 per annum in UK for ST segment elevation

Diagnosis
  • WHO criteria – 2/3 from typical history, ECG changes and cardiac enzyme rise

Symptoms
  • Central chest pain lasting >20mins associated with nausea, sweatiness, dyspnoea, palpitations
  • Silent MI’s without pain may occur in diabetics and the elderly. Presentations include syncope, pulmonary oedema, epigastric pain and vomiting, acute confusion, stoke, diabetic hyperglycaemia states

Signs
  • Distress, anxiety, pallor, sweatiness. Pulse and BP may be up or down. There may be a 4th heart sound
  • There may be signs of heart failure (raised JVP, 3rd heart sound, basal crepitations)
  • Pansystolic mumur (papillary muscle dysfunction/rupture, VSD)
  • A low grade pyrexia may be present
  • Later there may be a pericardial rub or peripheral oedema

Tests
  • ECG
    • Classically tall T waves, ST elevation or new LBBB occur within hours of a transmural infarction
    • T wave inversion and pathological Q waves follow over hours to days
    • In 20% the ECG may be normal
  • CXR
    • Look for cardiomegaly, pulmonary oedema, widened mediastinum (aortic dissection)
  • Bloods
    • FBC, U&Es, glucose, lipids cardiac enzymes
    • Normal CK-MB/CK ratio is <5%
    • Troponin T peaks at 12-24hr and is elevated for 1wk. If normal >6hr after the onset of pain and ECG is normal, the risk of an MI is very slim

Differential
  • Angina, pericarditis, myocarditis, aortic dissection, PE, oesophageal reflux/spasm

Mortality
  • 50% of deaths occur within 2hr after onset of symptoms

Management of ACS

Pre-hospital
  • 300mg aspirin chewed, sublingual GTN
  • IV morphine 5-10mg and IV metachlopromide 10mg

In hospital
  • Oxygen, IVI, morphine, aspirin
  • With ST segment elevation
    • Thrombolysis or primary angioplasty
    • ?-blocker e.g. atenolol 5mg IV unless contraindicated
    • ACE-I in normotensive patients within 24hr after acute MI, especially if there is evidence of heart failure or LV dysfunction
  • Without ST segment elevation
    • ?-Blocker e.g. atenolol 5mg IV
    • Low MW heparin e.g. enoxapain 1mg/kg/12hr for 2-8 days
    • Nitrates – usually given IV
    • High risk patients (those with persistent or recurrent ischaemia, ST-depression, diabetes, raised troponin) require and infusion of GPIIb/IIIa antagonist (e.g. tirofibran) and  ideally urgent angiography. Consider clopidogrel as well as aspirin for the first 12 months

Subsequent management
  • Bed rest for 48hr, continuous ECG monitoring
  • Daily examination of heart, lungs and legs for complications
  • Daily 12 lead ECG, U&Es and cardiac enzymes for 2-3 days
  • Prophylaxis against thromboembolism e.g. heparin 5000U/12hr SC. Of there is a large anterior MI consider warfarin to reduce risk of systemic embolism from an LV mural thrombus. Continue low dose aspirin indefinitely (reduces vascular events by 29%)
  • Start oral ?-blocker (e.g. metoprolol 50mg/6hr) or calcium channel antagonist if CI
  • Consider an ACE-I in all patients. ACE-I in those with heart failure reduces 2 yr mortality by 25-30%
  • Start a statin
  • Address modifiable risk factors
  • Exercise ECG – may be useful in risk stratification 3-4 weeks post MI or in patients without ST elevation or troponin rise

Complications of MI
  • Cardiac arrest
  • Cardiogenic shock
  • Bradycardia or heart block
    • Sinus bradycardia treat with atropine 0.6-1.2mg IV, consider pacing if no response or not tolerant
    • 1st block – observe closely as 40% progress into higher degrees of block
    • Wenckebach doenst need pacing but Mobitz Type II does at it carries a higher risk of developing complete heart block
    • Complete heart block – consider pacing
    • BBB – MI complicated by trifascicular block or non-adjacent bifascicular disease should be paced
  • Tachyarrhythmias
    • Check for low K+. acidosis, and hypoxia as they can predispose
    • Regular broad complex tachycardia after MI is almost always VT
    • If haemodynamically stable treat with antidysrhythmic
    • Early VT give lidocaine infusion or amiodarone
    • Late VT amiodarone
    • If compromised give DC shock
    • If AF or atrial flutter, if compromised give DC shock, if not digoxin and ?-blocker
  • LV failure
  • RV failure
    • Presents with low CO and raised JVP. If BP remains low consider ionotropes
  • Pericarditis
    • ECG, saddle shaped T wave. Treatment NSAIDs and ECHO for effusion
  • DVT/PE
  • Systemic embolism
    • After large anterior MI consider warfarin for 3mth
  • Cardiac tamponade
    • Presents with low CO, pulsus paradoxis, raised JVP and muffled heart sounds. Diagnosis via ECHO and treatment via aspiration or surgery
  • Mitral regurgitation
    • May be mild following papillary dysfunction or severe following papillary muscle rupture. Presents with pulmonary oedema
  • VSD
    • Presents with pansystolic murmur and raised JVP and cardiac failure. Treat with surgery. Mortality 50% in first week
  • Late malignant ventricular arrhythmias
    • Occur 1-3 weeks post MI. Avoid hypokalaemia as this is the most avoidable cause
  • Dressler’s syndrome
    • Recurrent pericarditis, pleural effusions, fever, anaemia and raised ESR 1-3 weeks post MI. Treat with NSAIDs and steroids if severe
  • Left ventricular aneurysm
    • Occurs late (4-6wk post MI) and presents with LVF, angina, recurrent VT or systemic embolisation. On ECG there is persistent ST segment elevation. Treat by anticoagulation and consider excision


Emergency management

Acute MI
  • Attach ECG monitor and record a 12-lead ECG
  • High flow O2 by face mask (caution if COPD)
  • Get IV access, take blood for FBC, U&Es, glucose, lipids, cardiac enzymes
  • Brief assessment;
    • Any Hx of CVD? Risk factors for IHD
    • Contraindications for thrombolysis
    • Examination – pulse, BP, JVP, cardiac murmurs, signs of heart failure, peripheral pulses, scars from previous cardiac surgery
  • Drugs;
    • Aspirin
    • Morphine 5-10mg IV plus antiemetic metachlopromide 10mg IV
    • GTN sublingually 2 puffs or 1 tablet as required
    • Thrombolysis
    • ?-Blocker (atenolol 5mg IV unless asthma or LVF
  • CXR
  • Consider glucose, insulin and potassium infusion for patients with DM
  • Consider DVT prophylaxis
  • Consider medication unless calcium channel antagonist (unless specific indication)

Thrombolysis
  • Greatest benefit if given before 12hr, British Heart Foundation recommends within 90mins
  • Indications – chest pain with;
    • ST elevation >2mm in 2 or more chest leads
    • ST elevation >2mm in 2 or more limb lead
    • Posterior infarct – dominant R waves and ST depression in V1-V3
    • New onset LBBB
  • Thrombolysis CI;
    • Internal bleeding
    • Prolonged or traumatic CPR
    • Heavy vaginal bleeding
    • Acute pancreatitis
    • Active lung disease with cavitation
    • Recent trauma or surgery (<2wk)
    • Cerebral neoplasm
    • Severe hypertension (>200/120mmHg)
    • Suspected aortic dissection
    • Previous allergic reaction
    • Pregnancy or <18wk postnatal
    • Severe liver disease
    • Oesophageal varices
    • Recent head trauma
    • Recent haemorrhagic stroke
  • Relative CI;
    • History of severe hypertension
    • Peptic ulcer
    • History of CVA
    • Bleeding diathesis
    • Anticoagulants
  • Types of thrombolysis;
    • Streptokinase – dose 1.5 million units in 100ml given in 0.9% NaCl over 1hr
      • SE – nausea, vomiting, haemorrhage, stroke, dysrhythmias
      • Watch for allergic reactions.
      • Do not repeat unless it is within 4 days of initial dose
    • Alteplase
      • Followed by heparin if patient has had previous streptokinase or responded badly to it
      • Has additional benefit if given within 6hrs to younger patients
    • Reteplase is given as 2 IV boluses 2hr apart
    • Tenecteplase can be given as a bolus injection
  • Complications
    • Recurrent ischaemia or failure to reperfuse (usually detected as persistent pain and ST elevation after thrombolysis
    • Stroke
    • Pericarditis
    • Cardiogenic shock
    • Heart failure

Right ventricular infarction
  • Confirm by either ECHO or by showing ST elevation in RV3/4 (RV4 is when V4 is placed in the right 5th IC spaced midclavicular line)
  • Treat hypotension and oligouria with fluids
  • Avoid nitrates and diuretics
  • Intensive monitoring and ionotropes may be useful in some patients

Acute management of ACS without ST segment elevation
  • Admit to CCU and monitor closely
  • High flow O2 by face mask
  • Analgesia – morphine 5-10mg IV plus metoclopromide 10mg IV
  • Nitrates – GTN spray or subligual tablets as required
  • Aspirin – 300mg PO
  • Oral ?-blocker e.g. metoprolol 50-100mg/8hr or atenolol 50-100mg/24hr (If ?-blocker is contraindicated give a rate limiting calcium channel antagonist instead e.g. verapamil 80-120mg/8hr PO or diltiazem 60-120mg/8hr PO)
  • Low MW heparin e.g. enoxaparin 1mg/kg/12hr
  • IV nitrate if pain continues – GTN 50mg in 50ml 0.9% NaCl at 2-10ml/hr titrates to pain and maintain systolic BP >100mmHg
  • Record ECG whilst in pain
  • High risk patients (persistent or recurrent ischaemia, ST-depression, diabetes, raised troponin)
    • Infusion of tirofibran (GPIIb/IIIa antagonist) and urgent angiography
    • Addition of clopidogrel
    • Optimize drugs
    • ?-blocker, Ca+ channel antagonist, ACE-I and nitrate
    • Intensive statin regime starting at top dosages
    • If symptoms fail to improve then refer to cardiologist for urgent angiography +/- angioplasty or CABG
  • Low risk patients (no further pain, flat or inverted T waves or normal ECG and negative troponin)
    • May be discharged if a repeat troponin is negative
    • Treat medically and arrange further investigation e.g. stress test angiogram

  • The aim of drug therapy is;
    • Anti-ischaemic - ?-blocker, nitrate, calcium channel antagonist
    • Antithrombotic – aspirin, heparin

  • Further measures;
    • Wean off IVI GTN when stabilized on oral drugs
    • Give 3-5 days of heparin
    • Serial ECGs and cardiac enzymes
    • Address modifiable risk factors – smoking, hypertension, hyperlipidaemia, diabetes
    • Gentle mobilization

Prognosis
  • Overall risk of death is 1-2% but 15% for refractory angina despite medical therapy
  • The following are at increased risk;
    • Haemodynamic instability – hypotension, pulmonary oedema
    • T wave inversion or St segment depression on resting ECG
    • Previous MI
    • Prolonged rest pain
    • Older age
    • BM

Indications for consideration of invasive intervention
  • Poor prognosis e.g. pulmonary oedema
  • Refractory symptoms
  • Positive exercise tolerance test at low workloads
  • Non-Q wave MI

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