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Cardiovascular > STEMI/NSTEMI > Flashcards

STEMI/NSTEMI Flashcards

1
Q

pathophysiology of stable angina

A

fixed stenosis
demand led ischaemia
atherosclerotic plaque

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2
Q

what is meant by acute coronary syndrome (ACS)

A

any acute presentation of coronary artery disease
provisional diagnosis that covers a spectrum of conditions
e.g. unstable angina, MI

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3
Q

pathophysiology of ACS

A

fibrous plaque
plaque ruptures/fissure and thrombosis
dynamic stenosis (subtotal or complete occlusion)
supply led ischaemia

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4
Q

platelet cascade - initiation

A 
vascular damage (spontaneous plaque rupture)
exposing subendothelial collagen and von Willebrand factor
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5
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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6
Q

platelet cascade - adhesion

A

platelet recruitment and adhesion at site of injury forming a monolayer
adhesion leads to activation

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7
Q

platelet cascade - release of activators

A

ADP and other activators are released through degranulation
thromboxane A2 is generated via cycloxygenase
ADP binds to ADP receptors on circulating platelets and platelet activation accelerates - resulting in platelet aggregation (process that must be managed)

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8
Q

platelet cascade - activation of platelet

A

activated platelets trigger inflammatory cascade

activated platelets express adhesion receptors for leukocytes

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9
Q

symptoms for MI

A

severe crushing central chest pain, may come on at rest
radiates to jaw and arms, especially the left
similar to angina but more severe, prolonged (30 mins or longer) and not relived by GTN
associated with sweating nausea and often vomiting

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10
Q

ECG changes in MI

A

ST elevation (STEMI) - first few hours
T wave inversion - first day
Q waves - first day

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11
Q

ECG changes in STEMI

A

> 1mm ST elevation in 2 adjacent limb leads
2 mm ST elevation in at least 2 contiguous precordial leads
new onset bundle branch block

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12
Q

ECG leads corresponding to inferior MI

A

II
III
aVF

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13
Q

ECG leads corresponding to anterior MI

A

V1-V6

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14
Q

ECG leads to corresponding to anteroseptal MI

A

V1-V4

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15
Q

ECG leads to corresponding to anterolateral MI

A

I
aVL
V1-V6

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16
Q

cardiac enzymes and protein markers for diagnosis

A

indicate cardiac injury (necrosis)
enzyme - CK (creatinine kinase)
protein marker - Tn (troponin)

17
Q

treatment for MI

A 
Morphine - diamorphine (+anti-emetic)
Oxygen - if hypoxic 
Nitrate - GTN
Aspirin 
Clopidegrel

PCI (90 minutes)
thrombolysis (120 minutes)

18
Q

risks of thrombolysis

A

failure to re-perfuse
haemorrhage - minor, major, intracranial haemorrhage
hypersensitivity

19
Q

complications of MI

A

death
arrhythmic complications
structural complications
functional complications

20
Q

arrhythmic complications of MI

A

ventricular fibrillation

21
Q

structural complications of MI

A 
cardiac rupture
ventricular septal defect
mitral valve regurgitation 
left ventricular aneurysm formation
mural thrombus +/- systemic emboli
inflammation
acute pericarditis 
dressler's syndrome
22
Q

functional complications of MI

A

acute ventricular dysfunction (left, right or both - biventricular failure)
chronic cardiac failure
cardiogenic shock

23
Q

killip classification in-hospital mortality

A

I - no sings of HF
II - crepitations <50% of lung fields
III - crepitations >50% of lung fields
IV - cardiogenic shock

24
Q

ECG findings in NSTEMI

A

may be normal!

25
Q

differential diagnosis of elevated troponin levels

A 
MI
CCF
hypertensive crisis
renal failure
PE
sepsis
stroke/TIA
pericarditis/myocarditis 
post arrhythmia
26
Q

type I MI

A

spontaneous MI related to isachaemia due to primary coronary event such as plaque erosion and/or rupture, fissuring or dissection

27
Q

type II MI

A 
MI secondary to ischaemia due to imbalance of oxygen supply and demand;
increase - 
sustained tachycardia
hypertension
left ventricular hypertrophy
hypertrophic cardiomyopathy
valvular disease
decrease;
anaemia
hypoxia
bradycardia
hypotension
vasospasm
coronary embolism

poor prognosis

28
Q

class III MI

A

sudden unexpected cariac death, including cardiac arrest, often with symptoms suggesting ischaemia with new ST-segment elevation, new left bundle branch block, or pathologic or angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings

29
Q

features of type I MI

A 
sudden symptoms 
major ECG changes 
no other obvious cause 
high troponin rise then fall
severe CAD on angiography
30
Q

features of type II MI

A 
less chest pain
minor ECG changes
tach/low BP/illness
smaller more static troponin levels
mild moderate coronary disease
31
Q

describe non ischaemic myocardial injury with necrosis

A

occurs in complex, seriously unwell patients with significant medical or surgical issues
patients have no evidence of significant coronary artery disease absence of ischemic symptoms or ECG chnages
hard to diagnose either type I or II MI

32
Q

conditions associated with non ischaemic myocardial injury with necrosis

A

cardiac injury not related to myocardial ischaemia;
cardiac contusion, ablation, pacing, AICD shocks
myocarditis, cardiotoxic, chemotherapy

multi-factorial or indeterminate myocardial injury;
Severe sepsis or respiratory failure
PE
Pulmonary Hypertension, Cor Pulmonale
Chronic severe heart failure, Chronic Renal failure
Severe acute neurological diseases (stroke, subarachnoid)
Exercise, Burns
Stress (Takotsubo) cardiomyopathy

33
Q

treatment post MI

A

anti-platelet - aspirin/clopidogrel
beta-blocker - atenolol/bisorpolol
ACE - ramipril/perindopril
statins - simvastatin/atorvastatin

Cardiovascular (39 decks)

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