AIMS: CHEST PAIN. Causes of chest pain. Causes of chest pain: Cardiac causes: Acute coronary syndromes pericarditis thoracic aortic dissection

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1 CHEST PAIN Dr Susan Hertzberg Emergency Department Prince of Wales Hospital AIMS: To identify causes of chest pain in patients presenting to the ED. To identify and risk stratify patients presenting with acute coronary syndromes. To initiate management of patients with acute coronary syndromes in the ED Causes of chest pain: Causes of chest pain Pulmonary causes:usually involve the pleura; pleurisy PE pneumonia pneumothorax tumours Cardiac causes: Acute coronary syndromes pericarditis thoracic aortic dissection

2 Causes of chest pain: Causes of chest pain: GIT causes: gastroesophageal reflux disease (GORD) Peptic ulcer disease esophageal spasm biliary tract disease Chest wall causes: trauma musculoskeletal pain rib fractures thoracic nerve root pain herpes zoster Pathology of ACS Acute coronary syndromes Imbalance between supply and demand for myocardial oxygen Atherosclerotic plaques cause narrowing Plaques thicken Plaques rupture exposing thrombogenic surface, platelets aggregate and thrombi form. Angina-stable/ unstable Non-stemi Stemi Variant angina (Prinzmetal angina)

3 Unstable angina Stable angina New-onset exertional angina Angina at rest Angina of increasing frequency or duration or refractory to nitroglycerin Similar nature and pattern of previous episodes episodic pain lasting 5-15 minutes provoked by exertion relieved by rest or nitroglycerin STEMI NON-STEMI Chest pain with acute ST elevation on ECG. ST elevation of 1mm or more in 2 or more contiguous limb leads ST elevation of 2mm or more in 2 continuous chest leads Ischaemic chest pain ST-T wave changes consistent with ischaemia ( ST depression, T wave inversion) plus biochemical marker elevation

4 Variant angina History: nature of the pain Coronary artery spasm occurs primarily at rest transient ST elevation Pain described as pressure or heaviness Pain may be in neck, jaw or arms Pain may be absent in elderly, diabetic or female Associated with SOB, nausea, vomiting, diaphoresis, dizzy History Risk Factors for ACS Past cardiac history past vascular history risk factor profile 5 primary risk factors diabetes family history cigarette smoking hypercholesterolaemia hypertension

5 Other risk factors Gender Male gender Advanced age Prior cerebrovascular accident 7.5% of pts with ACS) Methamphetamine use Incidence of ACS is higher in males if younger than 70 years At 15 years post-menopause, incidence of angina equal frequency in both sexes Age Incidence of angina increases with age years of age angina more common in men. Over age 70 incidence is the same in both sexes. Likelihood of CAD There are 5 major factors on history (ranked in order of importance) : 1. Typical angina pain 2. Prior MI 3. Male gender 4. Age 5. Number of risk factors

6 Likelihood (cont) Physical examination Other features relating to likelihood: Examination revealing hypotension, cardiac failure, sweating New ECG changes- ST deviation or T wave inversion Elevated troponins Usually normal look for CCF, new murmurs, hypotension ECG ECG (2) Most important diagnostic tool in the ED Moment in time-repeat liberally. Normal ECG does not exclude ischaemic cause of chest pain Abnormalities: transient ST elevation ST depression (0.5 mm significant) dynamic T wave changes: inversion, flattening, hyperacute changes Deep symmetrical T wave inversion (consider CNS events)

7 Bloods Troponins 1 Troponin CKMB FBC Renal function Troponin is a contractile protein not normally found in serum. TnI and TnT are immunologically distinct in both skeletal and cardiac muscle TnI and TnT are both used to detect myocardial damage Troponins 2 Troponins 3 Most bound to myofilaments some cytosolic pool cf CK sensitivity at 12 hours is approx 98% Both are detectable in the serum 3-6 hours after infarction with increased sensitivity up to 12 hours after onset of pain Very sensitive minor elevations identify patients at risk for subsequent cardiac events elevation proportional to mortality remain elevated for 7-10 days (TnI) and days ( TnT) may be elevated in other conditions

8 CKMB CXR Begins to rise within 4 hours of injury peak hours subside over 3-4 days ULN is 3-6% of total CK at 6-9 hours sensitivity increases to approx 90% and by 24 hours near 100% Looking for other causes of chest pain Looking for signs of LVF Goals of ED care Risk stratification Identify patients with acute coronary syndromes Exclude alternative causes of chest pain Risk stratify patients with ACS into low, intermediate or high risk groups, Risk stratification in the ED is aimed at determining the likelihood of symptoms representing ACS and then the short-term risk of death or nonfatal MI in those patients with ACS.

9 High risk Intermediate risk CP at rest >10mins needing IV ST deviation (>0.5mm) T wave inversion (>2mm) in 3 leads, new BBB Elevated serum markers A/w syncope, hypotension, new LVF or new murmur CP at rest >10 mins now resolved Diabetes Age >65 yrs Nocturnal pain History of MI or revascularisation Pathological Q waves or T wave inversion <3 leads Low risk ED CARE New onset angina more than 2 weeks before presentation No high or intermediate risk features. Normal ECG and serum markers. Normal ECG during period of discomfort. Obtain IV access, administer O2 if saturation <95%, apply BP and heart monitoring Obtain ECG within 5 minutes of arrival Complete focused history, including relevant risk factors, physical examination Identify complication of ACS

10 ED CARE Goals of care in ACS patients Serial ECGs may be required Frequent reassessment of vital signs To preserve or improve patency of coronary artery and improve blood flow through stenotic lesions thus reducing myocardial damage. Bloods for biochemical markers Early appropriate consultation Medications Analgesia Analgesics Nitrates Antiplatelet agents Anti-coagulants beta-blockers Reduce pain and decrease sympathetic stress morphine reduces preload morphine 2.5-5mg bolus titrate to effect caution in hypotension

11 Nitrates Anti-platelet agents Oppose coronary artery spasm, causes relaxation of vascular smooth muscle thus reducing preload and after load nitroglycerin-sublingual tablet or spray, topical, of intravenous infusion titrate to MAP and effect Aspirin clopidogrel Glycoprotein llb/llla antagonists ( tirofigan, abciximab, eptifibatide) Aspirin Anticoagulants Inhibits cylcooxygenase which produces thromboxane A2 a potent platelet activator Early administration of aspirin may reduce mortality in patients with AMI by up to 23% mg po To prevent recurrence of clot after spontaneous fibrinolysis does not actively lyse the clot but inhibits further thrombogenesis Fractionated (LMWH) or unfractionated (UFH) heparin

12 Heparins Low molecular weight heparins Augments activity of antithrombin lll and prevents conversion of fibrinogen to fibrin continuous intravenous infusion monitored by APTT testing Enoxaparin reduces cardiac ischaemic events and death by up to 15% in patients with unstable angina Main effect via inactivation of factor Xa, higher anti Xa to anti factor lla ratio 1mg/kg bd sc convenient- no need for APTT monitoring Beta-blockers Have anti-ischaemic, anti-hypertensive and anti-arrhythmic properties Reduce myocardial oxygen demand, reduce wall stress and afterload decrease infarct size in AMI reduce short and long term mortality after MI