Contents

Acute Coronary Syndrome 1

STEMI 1

NSTEMI 5

Angina Pectoris (IHD) 6

Heart Failure 9

Heart Valve Disease 13

Mitral Stenosis 13

Mitral Regurgitation 14

Aortic Stenosis 15

Aortic Regurgitation 15

Heart Catheterisation 16

Acute Pulmonary Oedema 16

Arrhythmias 17

Supraventricular Arrhythmias 17

Ventricular Arrhythmias 18

Ventricular Tachycardia 18

Torsade de Pointes 19

Ventricular Fibrillation 19

Bradycardias 19

Antiarrhythmic Drugs 20

Infective Endocarditis 21

Chest Pain Summary 23

Acute Coronary Syndrome

STEMI

• Most common cause of mortality in Western World. Affects ~0.5% of the population/year

• Majority due to occlusive coronary artery thrombus overlying an ulcerated or fissured stenotic plaque

• Pathogenesis involves a dynamic interaction between severe coronary atherosclerosis, acute plaque rupture, superimposed thrombosis with platelet activation and vasospasm

Microscopic changes following acute MI

Diagnosis

1. Cardiac Enzymes (intracellular enzymes leak out of infarcted myocardium)

   • CK – peaks at 24h. Also produced by skeletal muscle + brain therefore request myocardium-bound fraction (CK-MB) which is specific for myocardial damage. Serum level of the enzyme relates to site of infarct

   • Troponin – most reliable 12h post event. Highly specific (proteins involved in muscle contraction). Remain elevated for weeks therefore use CK to assess infarction in pt whose trop remains high from previous MI

2. ECG

   • Hyperacute changes = tall, pointed T-waves followed by ST elevation. This is followed by T wave inversion. R wave voltage then decreases and Q waves develop

   • Weeks – months = T wave may become upright again, Q waves remain

Site of infarction can be deduced from affected leads:

Inferior MI – involves leads II, III and aVF

Anterior MI – affects precordial leads

Anteroseptal MI – affects leads V1-V3

Lateral MI – affects leads I and aVL and V5-V6

Posterior MI – tall R wave in V1 and V2 with ST depression and upright T waves

Note that there may be reciprocal ST-depression in leads opposite the site of infarction

Development of new LBBB is an indicator of acute MI. However, it is a common abnormality – look at old ECGs

Management

• Emergency Care

  • Aspirin 300mg PO

  • Pain-relief 5-10mg morphine + metoclopramide (anti-emetic)

  • Sublingual GTN (unless hypotensive)

  • Oxygen via non-rebreathe (if sats <94%)

  • Iv access and bloods for FBC, U&E, cardiac enzymes, BM, lipids, ABG

Aim of early care is to initiate reperfusion therapy, limit infarct size and treat life-threatening arrhythmias

• Thrombolysis

  • Should be given if PCI is not available within 90mins of symptom onset

  • Should be given to pts with ST elevation or new LBBB within 12h of onset of pain. Greater benefit if given earlier as efficacy of lysing thrombus decreases with time

  • Largest benefit seen in those at highest risk (elderly, hypotensive, anterior infarct)

  • Can only be given if no contraindications:

• Major bleeding seen in up to 3% of pts

• 2 main thrombolytics are streptokinase + alteplase (recombinant tissue plasminogen activator tPA). Streptokinase induces an antibody response which effectiveness of repeat dose + risk of anaphylactic reaction. Should not be readministered 5days – 2 years following initial treatment

• Primary Coronary Angioplasty (PCA)

  • Primary PCI with stent placement is now the preferred method of revascularisation and is indicated if the pt presents within 90mins of onset of pain

  • Involves immediate transfer to cath lab with intention of opening artery with stent placement (drug-eluting stents are preferred)

  • Many hospitals now have 24h PCI facilities

  • Early revascularisation prevents scar formation, occurrence of heart failure in the future and incidence of ventricular arrhythmias caused by scar formation

• Other therapy in the acute phase

  • Aspirin: 300mg prescribed early 30% in deaths. Use clopidogrel if aspirin sensitivity

  • Β-blockers: iv in acute phase to limit infarct size, risk of arrhythmias and pain. Particularly appropriate when pt has tachycardia (in absence of HF), relative HTN or pain unresponsive to opioids

  • ACEIs: most valuable in pts with Sx of HF or impaired LV function

  • Statins: started immediately as per management of NSTEMI

  • Heparin: forms part of most thrombolytic regimes over 1^st 24h. should then be given until pt mobile

  • Control of BM: Even if pt not a known diabetic as blood glucose often with a variety of physical stressors

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