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cardiology > acute MI > Flashcards

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
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2
Q

AMI

A

acute myocardial infarction

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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

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4
Q

cardiac chest pain

A

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

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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

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6
Q

risk factor for stemi/nonstemi

A

spontaneous plaque rupture !! ie platelet cascade

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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
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8
Q

chronic stable angina is :

A

predictable, safe
is demand led ischaemia
fixed stenosis

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9
Q

ACS is : (ua / mi)

A

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

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10
Q

PCI

A

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

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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

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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

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13
Q

left sided heart failure

A 
causes : dizziness 
orothpnea 
paraxysmal nocturnal dysopnea 
5 year survival rate : 
death due to HF (25%)
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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

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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)

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16
Q

anatomical site of MI (ECG)

A

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

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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

A

-

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
Q

arrhythmic complications

A

> ventricular fibrillation

26
Q

structural complications

A 
> cardiac rupture 
>ventricular septal defect 
>mitral valve regurgitation 
-LV aneurysm formation 
-mural thrombus (sometimes with systemic emboli)
-inflammation 
-acute pericarditis 
-dressler's syndrome
27
Q

dressler’s syndrome

A

inflammation of the pericardium

28
Q

functional complications

A

> mainly just ventricular function …
acute ventricular failure of LV/RV/both
chronic cardiac failure
cardiogenic shock

29
Q

killip classification

A

1 - no signs of heart failure
2 - crepitations <50 % of lung fields
3 - crepitations >50% of lung fields
4 - cardiogenic shock

30
Q

acute NSTEMI and UA

A

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
Q

diagnosis of NSTEMI

A

history - heart pain
ECG - it may be normal !!
biomarker of troponin - can reflect microscopic zone of myocyte necrosis (actin and myosin)

32
Q

treatment of NSTEMI

A 
>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
Q

GP IIb - IIa

A

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
Q

troponin-itis

A 
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
Q

task force criteria for the diagnosis of MI

A

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
Q

diagnosis of type II of myocardial infarction

A 
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
Q

type I vs type II MI

A 
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
Q

non ischaemic myocardial injury with necrosis

A

not type II cos they don’t have a coronary artery disease … ie pacing , cardiac contusion , received chemotherapy

39
Q

mechanisms of aspirin

A

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
Q

mechanism of clopidogrel (thienopyridine)

A

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.

cardiology (22 decks)

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