acute MI Flashcards

1
Q

ACS

A
acute coronary syndrome:
 acute presentation of coronary artery disease and there are loads of them ! ie 
-unstable angina 
-acute non STEMI 
-STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

AMI

A

acute myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

chronic stable angina

A

fixed stenosis, demand led ischaemia, predictable, safe
ask patients to : sit and breath !
only comes along with increased demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cardiac chest pain

A

often described as:
heavy feeling
weight on chest
pressure, tightness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

nonSTEMI and STEMI

A

have the same pathogenic trigger > take safe atherosclerotic plaque > make it unsafe ie with plaque rupture + thrombosis = dynamic stenosis&raquo_space; supply led ischaemia&raquo_space; leading to symptoms at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

risk factor for stemi/nonstemi

A

spontaneous plaque rupture !! ie platelet cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

factors affecting plaque rupture / fissure

A
  • lipid content of plaque
  • thickness of fibrous cap
  • sudden changes in intraluminal pressure or tone
  • bending and twisting of an artery during
  • each heart contraction
  • plaque shape
  • mechanical injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

chronic stable angina is :

A

predictable, safe
is demand led ischaemia
fixed stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ACS is : (ua / mi)

A

unpredictable and dangerous
is supply led ischaemia
dynamic stenosis (subtotal or complete occlusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PCI

A

percutaneous coronary intervention ! angioplasty damages endothelium, exposing sub endothelial tissue and body will react as an injury … platelet cascade etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treatments (2)

A

aspirin > inhibit cyclooxyrgenase and stops the production of thromboxane A2
clopidogrel, prasugrel, ticagrelor > are ADP receptor antagonist
blocks , and so prevent the binding of ADP to the platelet surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

after an MI - left sided heart failure

A

even if a patient survives an MI, the tissue that suffered from the infarct, scar tissue will form - the muscle is damaged
the volume within the LV cavity increased and so heart function will decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

left sided heart failure

A
causes : dizziness 
orothpnea 
paraxysmal nocturnal dysopnea 
5 year survival rate : 
death due to HF (25%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

diagnosis of STEMI

A

history !
of ..
severe crushing central chest pain
radiating to jaw and arms - left is worse
similar to angina but more severe, prolonged and not relived by GTN (glyceryl trinitrate)
associated with sweating, nausea and often vomitting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

diagnosis of STEMI (3)

A

history !
of ..
severe crushing central chest pain
radiating to jaw and arms - left is worse
similar to angina but more severe, prolonged and not relived by GTN (glyceryl trinitrate)
associated with sweating, nausea and often vomitting
ECG !
ST elevation
-more than or 1mm ST elevation in 2 adjacent limb leads
or
- more than or 2mm ST elevation in at least 2 continuous precordial leads
or
-new onset bundle branch block
T wave inversion
Q waves
cardiac enzymes and proteins markers !
but ..
may be normal at presentation
and do not have time to wait for results
>CK - creatinine kinase
>troponin - Tn (what is preferred)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

anatomical site of MI (ECG)

A

inferior : II III AVF
anterior : v1-v6
anteroseptal v1-v4
anterolateral I avL V1-V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

early treatment of STEMI (1)

A

> clopidogrel etc blocks the action of ADP on platelet surface
aspirin is good at inhibition COX system thus prevention the product of thromboxane A2
> use aspirin in combination with clopidogrel/prasugrel/ticagrelor

18
Q

aspirin

A

300mg

patients asked to chew

19
Q

thrombolysis

A

breaks up clot

|&raquo_space; can get prehospital thrombolysis ie paramedics

20
Q

indications for PCI / thrombolysis

21
Q

risks of thrombolytic therapy

A
  • failure to re-perfuse (mortality risk doubled if artery didn’t open
  • haemorrhage (minor, major, intracranial)
  • hypersensitivity
22
Q

treatment of STEMI with regards to time

A

if : TS elevation ACS they should b treated immediately with PCI
if : PCI cannot be provided within 120m of ECG diagnosis then patients should receive immediate / prehospital thrombolytic therapy

23
Q

early treatment of STEMI (2)

A

> analgesia - diamorphine IV -reduces workload of heart and reduced infarct size
anti emetic - IV (treats motion sickness)
aspirin - 300mg AND ticegralor 180mg/clopidogrel 600mg to start as a loading dose for anti-platelet work
can considerGTN if bp > 90mmHg
oxygen if hypoxic
primary angioplasty
thrombolysis (if angioplasty not available within 2 hours)

24
Q

complications of AMI

A

death, arrhythmic complications
structural complications
functional complications

25
arrhythmic complications
> ventricular fibrillation
26
structural complications
``` > cardiac rupture >ventricular septal defect >mitral valve regurgitation -LV aneurysm formation -mural thrombus (sometimes with systemic emboli) -inflammation -acute pericarditis -dressler's syndrome ```
27
dressler's syndrome
inflammation of the pericardium
28
functional complications
>mainly just ventricular function ... >acute ventricular failure of LV/RV/both >chronic cardiac failure >cardiogenic shock
29
killip classification
1 - no signs of heart failure 2 - crepitations <50 % of lung fields 3 - crepitations >50% of lung fields 4 - cardiogenic shock
30
acute NSTEMI and UA
the pathogenic trigger is the spontaneous plaque rupture and so antiplatelets are the solution ie clopidogrel and aspirin (standard therapy) >>associated with poorer outcomes , potentially have a higher risk than STEMI
31
diagnosis of NSTEMI
history - heart pain ECG - it may be normal !! biomarker of troponin - can reflect microscopic zone of myocyte necrosis (actin and myosin)
32
treatment of NSTEMI
``` >in the presence of an ischaemic ECG changes or elevation of cardiac troponin patents with ACS should be treated immediately with both aspirin 300mg and ticagrelor 180mg > patients with ACS should be considered for aspirin and clopidogrel where the risks outweigh the benefits of ticagrelor and prasugrel >in the presents of an ishaemic ECG changes or elevation of cardiac markers patients with ACS should be treated immediately with fondaparinux or LMWH > in the absence of bradycardia or hypotension, patients with ACS in killip class 1 should be considered for immediate IV and oral beta blockers ```
33
GP IIb - IIa
open another receptor on platelet starting synthesis of fibrinogen which would them go on to aggregate more platelets > so can get GP IIb - a inhibitors
34
troponin-itis
``` misdiagnosis of an ACS based solely off of troponin levels .. troponin levels are also elevate in a series of other conditions ie CCF hypertensive crisis renal failure PE sepsis stroke/tia pericarditis/myocarditis post arrhythmia ```
35
task force criteria for the diagnosis of MI
detection of a rise/fall of carina biomarker values w at least one value above the 99th percentile upper reference limit and with one of the following : - symptoms of ischaemia - new or presumed new significant ST segment - T wave changes on the left branch block - imaging evidence of new loss of viable myocardium or new regional wall motion abnormality - identification of an intracoronary thrombus by angiography or autopsy
36
diagnosis of type II of myocardial infarction
``` is secondary to an ischaemic imbalance .. increased myocardial demand for oxygen ie sustained tachycardia significant hypertension marker LVH hypertrophic cardiomyopathy valvular disease ... reduced myocardial oxygen / blood supply anaemia hypoxia and resp. failure bradycardia hypotension vasospasm coronary embolism ```
37
type I vs type II MI
``` I = sudden symptoms major ECG changes no obvious other cause higher trop. with rise then fall severe CAD on angiography II = less chest pain minor ECG changes tach/low bp/illness smaller more static troponin mild moderate coronary disease ```
38
non ischaemic myocardial injury with necrosis
not type II cos they don't have a coronary artery disease ... ie pacing , cardiac contusion , received chemotherapy
39
mechanisms of aspirin
it inhibits cyclooxyrgenase, preventing the production of prostaglandins and thromboxane A2 from arachnoid acid, TXA2 promotes the expression of the GP IIb/IIIa binding site on the platelet - allowing fibrinogen to bind
40
mechanism of clopidogrel (thienopyridine)
is a potent inhibitor of ADP-induced platelet aggregation irreversibly inhibiting the binding of ADP to its platelet membrane receptor (ADP binding is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen) Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding to fibrinogen.