IHD Flashcards
definition of IHD
characterised by reduced blood supplu (ischemia) to heart muscle = chest pain
stable angina/ACS
ACS
unstable angina and STEMI (transmural infarction)/NSTEMI -
share underlying pathology: plaque rupture, thrombosis and inflammation.
Can be due to emboli, coronary spasm or vasculitis in normal coronary arteries
MI
myocardial cell death releasing troponin
ischemia
lack of blood supply +- cell death
angina
symptomatic reversible myocardial ischemia
Stable angina: Induced by effort, relieved by rest. Good prognosis.
Unstable angina: (Crescendo angina.) Angina of increasing frequency or severity; occurs on minimal exertion or at rest; associated with very increased risk of MI.
Decubitus angina: Precipitated by lying flat.
Variant (Prinzmetal) angina: Caused by coronary artery spasm (rare; may coexist with fixed stenoses).
RF for IHD
non-modifiable
- age
- male
- FH of IHD - MI in 1st degree relative <55yrs
modifiable
- smoking
- hypertension
- DM control
- hyperlipidaemia
- obesity
- sedentary life style
- cocaine use
controversial
- stress
- type A personality
- LVH
- high fibrinogen
- hyperinsulinaemia
- high homocysteine levels
- ACE genotype
aetiology of MI
sudden occulsion of coronary artery due to rupture of atheromatous plaque and thrombus formation
aetiology of angina
myocardial ox demand exceeds supply - most common cause is atherosclerosis
all 3 features = typical angina, 2 = atypical, 0-1 = non-anginal chest pain:
- constricting/heavy discomfort to the chest, jaw, neck, shoulders or arms
- symptoms brought about by exertion
- symptoms relieved within 5 mins by rest or GTN
atherosclerosis
Endothelial injury is followed by migration of monocytes into subendothelial space and differentiation into macrophages. Macrophages accumulate LDL lipids insudated in the subendothelium and become foam cells. They release growth factors, which stimulate smooth muscle proliferation, production of collagen and proteoglycans. This leads to the formation of an atheromatous plaque.
angina precipitants
cold weather
emotion
heavy meals
causes of angina
atheroma
rarely
- anaemia
- coronary artery spasm eg from cocaine
- AS
- tachyarrhythmias
- HCM
- arteritis/small vessel disease (microvascular angina/cardiac syndrome X)
- emboli
epidemiology of IHD
incidence 5/1000 per annum UK for STEMI
IHD - Common, prevalence is>2%.
More common in males.
Sx of MI
centralised chest pain
sudden onset
crushing
SOB
previous MI
high score out of 10 for intensity
dm - suggests underlying coronary artery disease
sx pf ACS
acute onset chest pain radiates to arms, usually L, neck jaw or epigastrium
occurs at rest
increased severity and frequency of previously stable angina
heavy, gripping pain
may be associated with breathlessness, sweating, nausea and vom
increased severity and frequency of previously unstable angina
may be silent in elderly/dm
sx of stable angina
Brought on by exertion and relieved by rest.
sx of ischemia
acute central chest pain,
lasting >20mins
often associated with nausea, sweatiness, dyspnoea and palpations
silent ACS sx
mostly seen in elderly and dm pts. no chest pain
- syncope
- pul oedema
- epigastric pain
- vomiting
- post op hypotension or oliguria
- acute confusional state
- stroke
- diabetic hyperglycaemic states
angina associated sx
dyspnoea
nausea
sweatiness
faintness
features that make angina less likely
pain that is continuous, pleuritic or worse with swallowing,
pain associated with palpitations,
dizzyness or tingling
signs of acs
distress
anxiety
pallor
sweatiness
high or low pulse and BP
4th heart sound
signs of HF - increased JVP, 3rd heart sound, basal crepitations
pansystolic murmur - papillary muscle dysfunction/rupture, VSD (ventral septal defect)
low grade fever may be present
later a pericardial friction rub or peripheral oedema might develop
check both radial pulses for aortic dissection
signs of arrhythmia
look for signs of complications
low grade pyrexia
disturbance of BP
Signs of complications, i.e. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oliguria).
Ix for IHD
ECG
CXR
blood
echo
ECG for STEMI
- hyperacute (tall) T waves
- ST elevation
- new LBBB within hours
- T wave inversion and pathological Q waves follow over hours to days
- Inferior wall II, III, aVF
- Anterior wall Septum (V1–V2), apex (V3–V4), anterolateral wall (V5–V6)
- Lateral wall I, aVL
- Posterior infarct Tall R wave and ST depression in V1–V3
ECG for NSTEMI/unstable angina
ST depression
T wave inversion
non specific changes
or normal
Q waves may indicate a previous MI
cxr for acs
cardiomegaly
pul oedema
widened mediastinum
signs of HF
ddx eg aortic dissection
bloods for ACS
FBC
U&E
CRP
glucose
lipids
cardiac enzymes - CK-MB and cardiac troponin levels (T and I), increase after 12 hours
amylase - pancreatitis might mimic MI
TFTs
AST and LDH increase after 24 and 48hrs respectively - occaisionally used only to make a retrospective diagnosis
echo for acs
regional wall abnormalities
measure LVEF - early measurements misleading because of myocardial stunning
exercise or dobutamine stress echo may detect inducible wall motion abnormalities
ix results for angina
ECG usually normal - may show ST depression, flat or inverted T waves, signs of past MI
blood tests - FBC, U&E, TFTs, lipids, HbA1c
consider echo and CXR
exercise ECG testing
to determine prognosis and management
indicated in trop-negative ACS or stable angina with an immediate or high pre-test probability of CHD
positive test - >= 1mm horizontal or downsloping ST segment depression measured at 80ms after end of QRS
failed test - failure to reach at least 85% of predicted max HR (220-age) and otherwise -ve
radionucleotide myocardial perfusion imaging (rMPI)
Uses Tc-99m sestamibi or tetrofosmin
can be performed under stress or at rest
stress testing would show low uptake in ischemic myocardium
rest test can be used in pts with ACS, no previous MI but non-diagnostic troponin and ECGs
pharmacologic stress testing
if pts cant exercise or if exercise test is inconclusive
pharm induce tachy - dipyridamile, adenosine or dobutamine
imaging detect ischemic myocardium
cardiac catheterisation/angiography
in ACS with positive troponin or TIMI score 5-7, or if high risk on stress testing
coronary ca scoring
using specialised CT - role in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischemia (absence of CAC excludes obstructive coronary artery disease)
summary of ix results for IHD
MI have troponin rises, unstable angina doesnt!
MI may be STEMI - ST elevation (perhaps only in leads V7-9) or new onset LBBB
or NSTEMI - troponin positive ACS w/o ST elevation, may be ST depression, T wave inversion, non-specific changes to ECG, or no changes
increase in cardiac biomarkers eg troponin
ECG changes of new ischemia
development of pathological Q waves
new loss of myocardium
regional wall motion abnormalities on imaging
Ix approach for angina
- exercise ECG - look for ischemic ECG changes
- angiography - either cardiac CT with contrast pr angiography
- functional imaging - myocardial perfusion scinitigraphy, stress echo (echo while undergoing exercise or receiving dobutamine), cardiac MRI
Typical angina in a patient with previously proven IHD: Treat as stable angina; if further confirmation is required, use non-invasive testing, eg exercise ECG.
Typical and atypical angina: CT angiography. If inconclusive, use functional imaging as 2nd line and transcatheter angiography as 3rd line.
Mx of stemi and nstemi
Both will require the same initial management, but a STEMI will require urgent percutaneous coronary intervention (PCI: angiogram +/- stenting).
Manage in ABCDE approach
o Oxygen and cardiac monitoring - myocardial muscle needs Ox - 15L via non-rebreathe mask first and continual cardiac monitoring
o Anti-ischemic therapy – nitrates - GTN spray, administered under tongue and will dilate the coronary arteries
o Antiplatelet agents – aspirin and clopidogrel (300mg of both)
o Call cardiologist - because eventually the coronary vessels need to be opened by angioplasty
o Anti-coagulation – heparin, LMWH, fondaparinux
o Blood: Trop-T, FBC, U&E, VBG - gives instant HB because anaemia worsens ischemia, XMatch
o Call surgical senior
o=ACE inhibitor and statin
sx control for ACS
manage chest pain with PRN GTN and opiates
if this is insufficient give GTN infusion - monitor BP - omit if recent sildenafil use
if pain deteriorating seek senior help
RF mx for ACS
pts should be advised and helped to stop smoking
identify and treat dm, hypertension and hyperlipidaemia
advise a diet high in oily fish, fruit, veg and fibre and low in saturated fats
daily exercise
refer to cardiac rehab programme
flag depression/anxiety to GP - independently associated with poor CV outcomes
cardioprotection for ACS
antiplatelets: aspirin (75mg OD) and 2nd antiplatelet eg clopidogrel for at least 12 months to reduce vascular events eg MI or stroke. Consider adding PPI for gastric protection
anticoagulant until discharge he fondaparinux
B blockage reduces myocardial ox demand - start low and increase slowly, monitoring pulse and BP, if contraindicated consider verapamil or diltiazem
ACE-i in patients with LV dysfunction, hypertension or dm unless not tolerated - titrate slowly monitoring renal function
high dose statin - atorvastatin 80mg
echo to assess LV function - eplerenone improves outcomes in MI patients with HF (ejection fraction <40%)
revascularisation for acs
STEMI and very high-risk NSTEMI (eg haemodynamically unstable) - immediate angiography +- PCI
NSTEMI patients who are high risk (eg GRACE score >140) should have angiography within 24h;
intermediate risk (eg GRACE109–140) within 3d;
low-risk patients may be considered for non-invasive testing.
multivessel disease may be considered for CABG instead of PCI
