Session 4 - MI

Question 1

In the assessment of chest pain, what indicators would make you think of cardiac ischemia?

Answer 1

Site- most often central

Onset- gradually over a few MINUTES! if Angina, will come on exertion.

Character- crushing, tightness, heavy, compressing. Not likely sharp, shouldn’t be reproducible on palpation.

Radiation- often radiates to (left) arm or neck and jaw in MI

Associated symptoms- sweating, N/V, going grey, SOB, syncope

Timing- if it lasts around 15-20 mins or more, likely Ischemic. so not chronic or quickly coming and going.

Exacebators/Eleviators- angina, exacerbated by exertion, elevate by rest or GTN spray

Severity- high for MI

Question 2

In the assessment of chest pain, what indicators would make you think of cardiac ischemia?

Answer 2

Site- most often central

Onset- gradually over a few MINUTES! if Angina, will come on exertion.

Character- crushing, tightness, heavy, compressing. Not likely sharp, shouldn’t be reproducible on palpation.

Radiation- often radiates to (left) arm or neck and jaw in MI

Associated symptoms- sweating, N/V, going grey, SOB, syncope

Timing- if it lasts around 15-20 mins or more, likely Ischemic. so not chronic or quickly coming and going.

Exacebators/Eleviators- angina, exacerbated by exertion, elevate by rest or GTN spray

Severity- high for MI

Question 3

When taking a history of chest pain, you should concentrate on?

Answer 3

history of the pain (SOCRATES)
cardiovascular risk profile (QRISK2)
previous personal or family history of IHD

Question 4

what does the QRISK2 score measure?

Answer 4

probability of having a cardiovascular event (MI or stroke) in the next 10 years based on someones risk factors

Question 5

differential diagnosis of chest pain includes?

Answer 5

ACS/MI
stable angina 
pericarditis 
aortic dissection
PE

pleuritis
pneumonia
pneumothorax

oesophageal spasm
GORD

Question 6

risk factors for IHD include:

Answer 6

non-modifiable: age, male, family history of IHD, personal history of IHD

Clinical: hypertension, hyperlipedemia, diabetes

modifiable: sedentary lifestyle, poor diet, smoking, high alcohol intake, obesity,

‘Type A personality’?- aggressive/ambitious

Question 7

what are you looking for in the ECG of someone having a STEMI?

Answer 7

Tall T waves
T wave inversion
ST elevation!!!! (hence STEMI)
pathological Q waves

Question 8

what are you looking for in the blood results of someone with suspected NSTEMI?

Answer 8

raised troponin I/T
troponin is a contractile protein which is not normally found in the serum, it is only released during myocardial necrosis. Should see a rise and fall within serial tests.

Question 9

what are you looking for in the blood results of someone with STEMI?

Answer 9

raised troponin I/T

raised creatinine kinase

Question 10

When taking a history of chest pain, you should concentrate on?

Answer 10

history of the pain (SOCRATES)
cardiovascular risk profile (QRISK2)
previous personal or family history of IHD

Question 11

what does the QRISK2 score measure?

Answer 11

probability of having a cardiovascular event (MI or stroke) in the next 10 years based on someones risk factors

Question 12

differential diagnosis of chest pain includes?

Answer 12

ACS/MI
stable angina 
pericarditis 
aortic dissection
PE

pleuritis
pneumonia
pneumothorax

oesophageal spasm
GORD

Question 13

risk factors for IHD include:

Answer 13

non-modifiable: age, male, family history of IHD, personal history of IHD

Clinical: hypertension, hyperlipedemia, diabetes

modifiable: sedentary lifestyle, poor diet, smoking, high alcohol intake, obesity,

‘Type A personality’?- aggressive/ambitious

Question 14

Management of acute MI?

Answer 14

brief history and physical, ECG and bloods

M- morphine (+antiemetics)
O- oxygen
N- nitrates
A- aspirin

try to get to PCI (percutaneous coronary intervention - i.e. sending within 2 hours)
if can’t, fibrinolysis with streptokinase/tissue plasminogen activator

Question 15

what are you looking for in the ECG of someone having an acute MI?

Answer 15

Tall T waves
T wave inversion
ST elevation!!!! (hence STEMI)
pathological Q waves

Question 16

what are you looking for in the blood results of someone with STEMI?

Answer 16

raised troponin I/T

raised creatinine kinase

Question 17

How is an NSTEMI treated differently to a STEMI?

Answer 17

as there is no ECG indication of MI, rely more on troponin in blood tests to diagnose.

still get MONA, but rather than referring them to a PCI centre, use anticoag: LMW heparin.

then they are discharged with preventative drugs: ACE-i, beta blockers, statins

Question 18

what secondary prevention lifestyle advice would you give to someone post-MI?

Answer 18

lifestyle changes: quit smoking, more exercise, less alcohol, better diet (less fat, more veg) lose weight if they are overweight (put them in cardiac rehabilitation programme)

Question 19

what drugs should be given to someone to take home, post MI?

Answer 19

should all be discharged with the following:

ACE-I or Calcium Channel Blocker - treat hypertension

Beta Blockers - negative into and chronotropes, reduce workload on heart

Statins - to lower LDL, reduce plaque formation

Aspirin - anti platelet, prevent clotting

(GTN spray if they get angina)

Question 20

How do you decide whether to give someone an ACE-I or a calcium channel blocker to treat their hypertension? give example of each

Answer 20

age/ethnicity

if they are under 55 and not afrocaribean, give ACE-I such as ramipril/enalapril

if they are over 55 or afrocarribean give calcium channel blocker such as amlodipine/nifedipine

Question 21

What is the pathophysiology of an MI?

Answer 21

Normally by mechanism of atherosclerosis

High LDL levels, deposited in the walls of coronary artery, oxidises, which causes expression of adhesion molecules, allowing macrophages come in

Macrophages take up the LDL, but they form foam cells and also get stuck. in the lipid core.

Other cytokines are released by the endothelial cells and cause smooth muscle proliferation, which then synthesises collagen and forms a fibrous cap, which overlies the lipid core.

The lipid core continues to grow if there is a high serum level of LDL, so inflammation continues and the T lymphocytes activate the macrophages to release matrixmetalloproteinases, which weaken the fibrous cap.

This leads to plaque rupturing, causes thrombosis, leads to partial/total occlusion of the coronary artery, ischemia of the myocardium, myocardial necrosis occurs