Ischaemic heart disease Flashcards
angina
due to myocardial ischaemia
presents with central chest tightness or heaviness
brought on by exertion and relieved by rest
may radiate to on eor both arms, neck, jaw or teeth
other precipitants: emotion, cold weather, heavy meals
ass. Sx: dyspnoea, nausea, sweatiness, faintness
causes of angina
mostly atheroma
rarely: anaemia
types of angina
stable:
induced by effort and relieved by rest
unstable:
angina of increasing freq or severity. occurs after minimal exertion or at rest. ass. w/ ++ increased risk of MI
decubitus:
precipitated by lying flat
variant (Prinzmetal’s):
caused by coronary artery spasm (rare, may coexist with fixed stenoses). ST elevation that reduces as pain subsides
tests
ECG - usually normal but may show ST depression
flat or inverted T waves
signs of past MI
management
stop smoking, increase exercise, weight loss, control HTN/DM etc
statins if cholesterol >4mmol/L
aspirin
B-blockers eg atenolol (CI in asthma, COPD, LVF, bradycardia, coronary artery spasm)
nitrates for Sx control. GTN spray
long acting calcium antagonists eg amlodipine. particularly useful if B-blockers are contraindicated
K channel activator eg nicorandil if still not controlled
vasoconstriction
increased Ca in smooth muscle leads to contraction
increased K causes vasodilation
acute coronary syndromes
includes unstable angina and evolving MI
pathology:
plaque rupture, thrombosis and inflammation
may also rarely be due to emboli or coronary artery spasm in normal coronary arteries or vasculitis
ACS with ST elevation
or new onset left bundle branch block
what most of us mean by acute MI
LBBB: activation of the left ventricle is delayed, so it contracts after the right ventricle
ACS without ST elevation
ECG may show ST depression (angina), T wave insertion, non-specific changes or be normal
the degree of irreversible myocyte death varies
significant necrosis can occur without ST elevation
risk factors
non-modifiable:
age, gender, FH of IHD (MI in 1st degree relative <55yo)
modifiable:
smoking, HTN, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use
controversial risk factors include:
stress, type A personality (impatient and aggressive), increased fibrinogen, hyperinsulinaemia, increased homocysteine levels, ACE genotype
diagnosis
acute MI is defined by several criteria:
an increase and then decrease in cardiac biomarkers ie troponin and either:
Sx of ischaemia, ECG changes of new ischaemia, development of pathological q waves or loss of myocardium on imaging
Sx of acute coronary syndromes
acute central chest pain lasting >20mins
often ass. w/ nausea, sweatiness, dyspnoea, palpitations
may be silent in the elderly of DM
if silent, presentations may include:
syncope, pulmonary oedema, epigastric pain and vomiting, post-op hypotension or oliguria, acute confusional state, stroke, DKA, HONK
signs of acute coronary syndromes
distress anxiety pallor sweatiness pulse increase or decrease BP increase or decrease 4th heart sound
may be signs of HF (raised JVP, 3rd heart sound, basal creps) or a pansystolic murmur (papillary muscle dysfunction/rupture, VSD)
low grade fever
later, pericardial friction rub, or peripheral oedema
ECG findings ACS
classically hyperacute (tall) T waves
ST elevation or new LBBB occur within hours of transmural infarct
T wave inversion and development of pathological q waves over hours to days
in 20% of MI the ECG may be normal initially
CXR ACS
look for: cardiomegaly pulmonary oedema widened mediastinum (aortic rupture) don't routinely delay Tx whilst waiting for an CXR
