CRD Flashcards
Epidemiology and risk factors for ACS
Most common cause of death in the UK (1/5 men, 1/6 women) More common in men Mortality equal in both sexes Increases with age Increased in South Asians
RF
Modifiable - smoking, diabetes, metabolic syndrome, hypertension, obesity, hyperlipidaemia, physical inactivity
Non-modifiable - male, increased age, FHx of premature CHD, premature menopause, south Asian
Definition of ACS
STEMI, NSTEMI and unstable angina
Symptoms of ACS
Chest pain (central or epigastric) lasting longer than 15 minutes Radiates to arms, shoulders, neck or jaw Sweating Nausea and vomiting Collapse/syncope Dyspnoea Fatigue Palpitations
Atypical presentation is seen in women, older men, diabetics and ethnic minorities.
- abdominal discomfort, jaw pain, altered mental state
Signs of ACS
Tachycardia (sympathetic) Hypotension Pallor Sweating Vomiting, bradycardia (vagal) Pale, cool, clammy Cold peripheries 3rd heart sound Oliguria Narrow pulse pressure Raised JVP Lung crepitations
Diagnostic criteria for MI
Detection of rise and/or fall of troponin and at least one of:
- symptoms of ischaemia
- ECG changes
- Imaging evidence of new loss of myocardium or wall motion abnormality
Causes of MI
Atherosclerosis Infected cardiac valve coronary occlusion secondary to vasculitis coronary artery spasm cocaine use congenital coronary abnormality coronary trauma raised O2 requirement (hyperthyroid) decreased oxygen delivery (severe anaemia)
Investigations for ACS
Observations - stabilise
FBC - anaemia, CRP, ESR
U&Es - potassium and electrolytes
Lipid profile
Troponin
(can use CK-MB or myoglobin)
ECG (ST elevation, Q waves, T wave inversion)
ABG - high lactate and hypoxia
Echo for extent of infarction
Angiography
Myocardial perfusion scintigraphy (SPECT)
Cardiac enzymes
Troponin
- increases within 3-12 hours from pain onset, peak at 48 hours, returns to baseline in 5-14 days
- measure at presentation and 10-12 hours after onset
- T binds to tropomysin, I binds to actin, C bind to calcium
Myocardial muscle creatinine kinase (MB-CK) - increase within 3-12 hours, peak at 24 hours, baseline within 3 days. Not as sensitive or specific
Myoglobin - most sensitive early marker
Causes of raised troponin
ACS Congestive heart failure Sepsis PE CKD Myocarditis
ECG changes in anterior STEMI
Which artery is occluded?
LAD
V3-V4 (septal may be involved V1-V2)
Reciprocal ST depression in III and AVF
ECG changes in inferior STEMI
Which artery is occluded?
80% R coronary, 20% L circumflex
ST elevation, ST depression, T wave inversion, Q waves
II, III, aVF
ECG changes in lateral STEMI
Which artery is occluded?
V5-V6
1st diagonal branch of LAD or obtuse branch of L circumflex
Management for STEMI
Stabilise
Troponin, ECG
Pain relief (GTN, opioids)
300mg aspirin
Supplemental O2 if hypoxic
PCI if able within 12 hours of onset
Fibrinolysis if not - alteplase, reteplase or streptokinase
Secondary prevention - ACEi, aspirin, 2nd anticoagulant (usually NOAC), beta blocker, statin
Management of NSTEMI
Stabilise
Troponin, ECH
Pain relief (GTN, opioids)
300mg aspirin
Supplemental O2 if hypoxic
Fondaparinux or unfractionated heparin within 24 hours
GRACE risk assessment
Lowest risk - aspirin only (no angio)
Low risk - aspirin + clopidogrel + consider angio
High risk - aspirin + clopidogrel + urgent coronary angiography
Secondary prevention - ACEi, aspirin, 2nd anticoagulant (usually ticagrelor), beta blocker, statin
When is a CABG required?
Failed PCI (occlusion not amendable or refractory symptoms)
Cardiogenic shock
Mechanical complications (rupture, mitral regurgitation)
Multivessel disease
What is the secondary prevention post ACS?
Aspirin +/- clopidogrel
Beta blocker
Ace inhibitor - check GFR and BP prior
Statin
Stop smoking, lower cholesterol, lower weight, increase exercise
Prognosis of MI
50% die in 30 days with 1/3 dying in first hour
Earlier perfusion = decreased mortality
What are the risk scores used in ACS?
GRACE - risk stratification in ACS - probability of in-hospital death. Uses Kilip class, SBP, HR, age, creatinine, ST deviation, Cardiac arrest, trop levels
Kilip’s classification - severity of cardiac failure after MI
1-4 from 1 no crackles, no added heart sounds to 4 - cardiogenic shock
TIMI score - risk of death post NSTEMI/UA
Complications post-MI
angina, re-infarct, heart failure cardiogenic shock valve dysfunction cardiac rupture arrhythmia PE Pericarditis Depression
Epidemiology and RF for angina
8% men, 3% women aged 55-64, 14% men, 8% women over 65
Increased in South Asian and Afro-Caribbean
Increasing age
RFs FHx Metabolic syndrome Smoking Diabetes Obesity Decreased exercise Hypertension Hyperlipidaemia Past CHD
Symptoms of angina
Constricting discomfort in the chest
Precipitated by physical exertion
Relieved by GTN or rest in minutes
Precipitating factors: physical exertion, heavy meals, cold exposure, intense emotion
What are the different types of angina?
Stable - precipitated by predictable factors
Unstable - symptoms occur at rest and occur at any time
Refractory - symptoms cannot be controlled by medication
Prinzmetal - occurs at rest and exhibits a circadian pattern - most episodes in the early hours of the morning
Causes of angina
Atherosclerosis Aortic stenosis Hypertrophic obstructive cardiomyopathy Hypertensive heart disease Arrhythmias Anaemia
Investigations for angina
12 lead ECG - LBBB, ST or T wave abnormalities (not NICE recommended)
FBC - rule out anaemia U&E for renal function Fasting blood glucose LFTs Check TFTs Troponin
Echo
Exercise tolerance test
Estimate likelihood of coronary artery disease
- 90%+ treat as angina
- 61-90% - invasive coronary angiography
- 30-60% - non invasive functional testing for myocardial ischaemia
- 10-29% - CT calcium testing