Ischaemic Heart Disease Flashcards
What factors affect myocardial demand and supply?
DEMAND: - heart rate e.g. tachycardia - contractility - wall tension (preload & afterload) e.g. aortic stenosis \+ thyrotoxicosis
SUPPLY:
- O2 carrying capacity of blood e.g. anaemia
- coronary blood flow (diastolic BP - perfusion & coronary artery disease) e.g. hypertension, narrowing arteries
What are the differentials for chest pain? Give some examples for each organ type.
HEART & GREAT VESSELS: e.g. IHD, pericarditis, aortic dissection
- central chest pain
- ischaemic myocardium - tight/crushing/”pressue”
- pain on exertion relieved by rest - angina
LUNGS & PLEURA: e.g. pneumonia, pneumothorax, pulmonary embolism
- lateral, sharp chest pain, increases on inspiration + respiratory symptoms
GI: reflux, gallbladder disease, peptic ulcers
- chest & epigastric pain + GI symptoms
CHEST WALL: muscle pain, bony metastases, trauma
- localised pain, movement/pressure increases pain, history of trauma/overuse
What is the area of the heart most vulnerable to ischaemia? Why? What other factors make the heart vulnerable to ischaemia?
Sub-endocardium (coronary bloodflow goes epicardial -> endocardial)
No major collateral circulation (unless there is chronic ischaemia over time)
Coronary arteries fill during diastole, therefore reduces during exercise
Give the modifiable and non-modifiable factors for IHD?
Modifiable:
- smoking
- hyperlipidaemia
- hypertension
- diabetes mellitus
- lack of exercise
- obesity
- stress
Non-modifiable:
- family history
- +++age
- male (until after menopause)
What is the difference between a stable and an unstable atheromatous plaque?
STABLE:
Small necrotic core and thick fibrous cap
UNSTABLE:
Large necrotic core and thin fibrous cap
What are the different ways in which an artery can be occluded by atheromas?
- fibrous cap ruptures -> platelet aggregation -> thrombus formation
- fibrous cap ruptures -> platelet aggregation -> heals over with thicker fibrous cap
- fibrous cap grows
What is stable angina pectoris? How is it diagnosed?
- moderate reduction in bloodflow (>70%) (bloodflow through LAD during diastole)
- transient ischaemia during exertion (particularly after meals and in cold weather); pain relieved by rest in ~5mins and is very predictable
- no myocyte injury or necrosis
- crushing chest pain may radiate up to the neck and jaw, down both arms, back, and epigastrium
No ECG changes at rest; exercise ECG shows ST depression and possibly changes in BP/arrhythmias (OR chest pain occurs)
What is the treatment for stable angina pectoris?
Reduce O2 demand:
- Nitrates: vasodilatation (only veins at therapeutic doses) - reduces preload
- Calcium channel blockers: peripheral vasodilatation - reduces afterload
- Beta-blockers: reduce HR & contractility
Increase O2 supply:
- Aspirin: reduce platelet aggregation to prevent further thrombus formation
- Statins: reduce LDLs (reduce progress of atherosclerosis) & increase plaque stability
- Revascularisation: stent occluded artery
Outline revascularisation of the coronary arteries.
Angiography: catheter inserted into femoral artery and up into the aorta
Percutaneous Coronary Intervention (PCI): inflate a balloon with a stent
Coronary Artery Bypass Grafting:
- internal mammary artery
- radial artery
- saphenous vein (reversed so the valves are the right way around)
What conditions come under acute coronary syndrome ?
Unstable angina pectoris
STEMI
NSTEMI
What is unstable angina pectoris? How is it diagnosed?
- Angina increasing in frequency, severity, & duration (crescendo)
- Angina at rest
- Recent onset of new, effort-limiting angina
No ST elevation (no injury) & no biomakers (no necrosis)
90%+ occlusion
What are the differences between nSTEMI & STEMI?
STEMI = ST elevation myocardial infarction (subepicardial injury)
- ST elevation in 2< leads (1mm limb leads, 2mm chest leads) + new left bundle branch block
- pathological Q waves (necrosis) + T wave inversion (ischaemia)
- full thickness necrosis (90% have total occlusion of an artery)
- biomarkers of necrosis present (CK-MB & troponin)
- PCI (if available in 90min) & thrombolysis
nSTEMI = non-ST elevation myocardial infarction (subendocardial injury)
- possible T wave inversion
- some necrosis (partial occlusion/collateral circulation present)
- biomarkers of necrosis present (CK-MB & troponin)
- does not respond to thrombolysis
- early vascularisation
What are the features of an MI history?
- central crushing chest pain radiating up into the neck & jaw, down the shoulders and back, into the epigastrium
- severe persistent pain and distress/feeling of “impending doom”
- pain at rest with no precipitant (50%) (shearing forces tear fibrous thrombus)
- pain not relieved by rest or nitrates
- sympathetic stimulation: sweating, pallor
- vomiting centre activated (poss. by severe pain) -> nausea/vomiting
- breathlessness (LV dysfunction)
- faint
What are the features of an MI examination? What initial investigations should you do?
Cold/clammy skin
Sweating/pallor
Distressed
May/may not have tachycardia/arrhythmia
May/may not have low BP
Signs of heart failure: S3/S4 heart sounds, crackles in lung bases (due to LV failure)
ECG & cardiac enzymes
What are the characteristics of the cardiac enzymes?
Cardiac troponin T (cTnT) & cardiac troponin I (cTnI)
- released by myocyte death
- onset (3-4hrs), peak (18-36hrs), fall (10-14days)
Creatine kinase CK-MB
- onset (3-8hrs), peak (24hrs), fall (48-72hrs)
