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Yr 3 cardio > IHD > Flashcards

IHD Flashcards

1
Q

definition of IHD

A

characterised by reduced blood supplu (ischemia) to heart muscle = chest pain

stable angina/ACS

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2
Q

ACS

A

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

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3
Q

MI

A

myocardial cell death releasing troponin

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4
Q

ischemia

A

lack of blood supply +- cell death

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5
Q

angina

A

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).

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6
Q

RF for IHD

A

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
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7
Q

aetiology of MI

A

sudden occulsion of coronary artery due to rupture of atheromatous plaque and thrombus formation

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8
Q

aetiology of angina

A

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
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9
Q

atherosclerosis

A

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.

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10
Q

angina precipitants

A

cold weather

emotion

heavy meals

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11
Q

causes of angina

A

atheroma

rarely

  • anaemia
  • coronary artery spasm eg from cocaine
  • AS
  • tachyarrhythmias
  • HCM
  • arteritis/small vessel disease (microvascular angina/cardiac syndrome X)
  • emboli
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12
Q

epidemiology of IHD

A

incidence 5/1000 per annum UK for STEMI

IHD - Common, prevalence is>2%.

More common in males.

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13
Q

Sx of MI

A

centralised chest pain

sudden onset

crushing

SOB

previous MI

high score out of 10 for intensity

dm - suggests underlying coronary artery disease

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14
Q

sx pf ACS

A

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

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15
Q

sx of stable angina

A

Brought on by exertion and relieved by rest.

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16
Q

sx of ischemia

A

acute central chest pain,

lasting >20mins

often associated with nausea, sweatiness, dyspnoea and palpations

17
Q

silent ACS sx

A

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
18
Q

angina associated sx

A

dyspnoea

nausea

sweatiness

faintness

19
Q

features that make angina less likely

A

pain that is continuous, pleuritic or worse with swallowing,

pain associated with palpitations,

dizzyness or tingling

20
Q

signs of acs

A

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).

21
Q

Ix for IHD

A

ECG

CXR

blood

echo

22
Q

ECG for STEMI

A
  • 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
23
Q

ECG for NSTEMI/unstable angina

A

ST depression

T wave inversion

non specific changes

or normal

Q waves may indicate a previous MI

24
Q

cxr for acs

A

cardiomegaly

pul oedema

widened mediastinum

signs of HF

ddx eg aortic dissection

25
Q

bloods for ACS

A

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

26
Q

echo for acs

A

regional wall abnormalities

measure LVEF - early measurements misleading because of myocardial stunning

exercise or dobutamine stress echo may detect inducible wall motion abnormalities

27
Q

ix results for angina

A

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

28
Q

exercise ECG testing

A

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

29
Q

radionucleotide myocardial perfusion imaging (rMPI)

A

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

30
Q

pharmacologic stress testing

A

if pts cant exercise or if exercise test is inconclusive

pharm induce tachy - dipyridamile, adenosine or dobutamine

imaging detect ischemic myocardium

31
Q

cardiac catheterisation/angiography

A

in ACS with positive troponin or TIMI score 5-7, or if high risk on stress testing

32
Q

coronary ca scoring

A

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)

33
Q

summary of ix results for IHD

A

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

34
Q

Ix approach for angina

A
  • 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.

35
Q

Mx of stemi and nstemi

A

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

36
Q

sx control for ACS

A

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

37
Q

RF mx for ACS

A

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

38
Q

cardioprotection for ACS

A

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%)

39
Q

revascularisation for acs

A

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

Yr 3 cardio (38 decks)

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