1
Q
UA/NSTEMI definition
A
- angina with at least 1/3:
- occurs at rest, usually last >10 minutes
- it is severe and new onset (w/in the last 4-6 weeks)
- occurs with a crescendo pattern
2
Q
NSTEMI=
A
UA + myocardial necrosis
3
Q
UA/NSTEMI pathophys
A
- atherosclerotic plaque rupture or erosion with a superimposed nonocclusive thrombus
- dynamic obstruction
- progressive mechanical obstruction
- secondary to increased myocardial oxygen demand &/or decreased supply
4
Q
UA/NSTEMI manifestatins
A
- chest pain
- usually severe enough to be described as frank pain
- dyspnea & epigastric discomfort may also occur
- large ischemia or NSTEMI: diaphoresis; pale, cool skin; sinus tachycardia; a 3rd &/or 4th heart sound; basilar rales and sometimes hypotension, resembling STEMI
5
Q
UA/NSTEMI cardiac biomarkers
A
- CKMB& troponin- distinguish pts w/ NSTEMI from UA
6
Q
there is a direct relationship between the degree of troponin elevation and
A
mortality
7
Q
minor troponin elevations can be caused by
A
congestive heart failure
myocarditis
PE
or can be false +
8
Q
prinzmetal’s variant angina
A
- syndrome of severe ischemia paint that occurs at reast but NOT usually with exertion and is associated with transient ST elevation
- due to focal spasm of an epicardial coronary artery
9
Q
STEMI definition
A
- myocardial cell death due to prolonged & severe ischemia
- ST elevation
10
Q
STEMI pathophys
A
- thrombotic occlusion of a coronary artery prevsiously affected by atherosclerosis
- thrombus develops rapidly at site of vascular injury
- surface of plaque becomes disrupted ->thrombogensis
- in rare cases can also be caused by coronary emboli, congenital abnormalities, coronary spasm, inflammation, etc
11
Q
coronary plaque prone to disruption are those with
A
a rich lipid core and thin fibrous cap
12
Q
extent of myocardial damage depends on
A
- territory supplied by the affected vessel
- extent of occlusions
- duration
- quantity of collateral vessels
- demand for oxygen
- endogenous factors that can produce early spontaneous lysis of the occlusive thrombus
- adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery
13
Q
STEMI risk factors
A
- multiple coronary risk factors
- UA
- hypercoagulability
- collagen vascular disease
- cocaine abuse
- intracardiac thrombi
- coronary emboli
14
Q
STEMI clinical manifestations
A
- pain is deep and visceral; heavy, squeezing & crushing & sometimes stabbing or burning
- similar to angina pectoris but occurs at REST, more severe and lasts longer
- weakness, sweating, N/V, anxiety
15
Q
what are considered in differential diagnosis of STEMI?
A
acute pericarditis, PE, acute aortic dissection, costochondritis & GI disorders
16
Q
STEMI diagnosis
A
ECG
biomarkers
imaging
non-specific indicators or tissue necrosis & inflammation
17
Q
STEMI physical findings
A
- angina >30 min & diaphoresis strongly suggests STEMI
- tachycardia &/or hypertension (anterior MI)
- bradycardia &/or hypotension (inferior MI)
- a pericardial friction rub is heard in many pts w/ transmural STEMI
- temp elevation up to 38*C
- arterial pressure is variable; systolic BP declines 10-15mmHg from preinfarction rate
18
Q
STEMI ECG
A
ST elevation
Q wave
19
Q
STEMI biomarkers
A
- cardiac specific troponin
& toponin-1 - CK
- CKMB
20
Q
myocardial infaction
A
death of cardiac muscle due to prolonged severe ischemia
21
Q
MI pathology
A
- in most cases of acute MI, PERMANENT DAMAGE to the heart occurs when the perfusion of the myocardium is severely reduced (usually at least 2-4 hours)
22
Q
longer occlusion->
A
larger area of tissue damage
23
Q
STEMI
A
- transmural infarction
- full thickness
- ST elevation
24
Q
NSTEMI
A
- subendocardial infarction
- partial thickness
- ST depression
25
histology prior to 24 hours post MI
- very minimal
26
histology after 24 hours post MI
- first changes involve the mycoytes
- wavy appearance
- still have nuclei
27
histology 3-4 days post MI
- neutrophils are recruited
- lack of nuclei
- can only see the remnants of nuclei
28
histology 7-10 days post MI
- macrophages come
- process of healing starts
- elongated cells=fibroblasts
- tiny capillaries formed
- granulation of tissue
29
histology of day 10-14 post MI
- collagen
| - repair process leads to formation of scar
30
histology weeks post MI
- complete healing
| - damaged tissue replaced by collagen
31
reperfusion
- RESCUE!
| - restore circulation
32
complications
- acute LVF, PE, shock
- arrhythmias
- myocardial rupture, hemopericardium, cardiac tamponade
- pericarditis (Dressler syndrome)
- RV infarction
- infarct extention (new necrosis)
infarct expansion (stretching, thinning, & dilation)
- mural thrombus
- ventricular aneurysm
- papillary muscle dysfunction->mitral regurgitation
- progressive late HF
33
cerebrovascular disease- stroke
thrombosis
emolism
hemorrhage
34
cerebrovascular disease
1. hypoxia, ischemia & infarction due to impairment of blood supply & oxygen to CNS tissue
2. hemorrhage resulting from rupture of CNS vessels
35
acute ischemic injury
global cerebral ischemia
| focal cerebral ischemia
36
global cerebral ischemia
- (ischemic/hypoxic encephalopathy)
- cardiac arrest
- shock
- severe hypotension
- affects entire brain
- mild cases: transient post-iscehmic confusional stat followed by complete recovery
- severe case- brain death or a persistent vegitative state
37
focal cerebral ischemia
- (reduction/cessation of blood flow to localized area of the brain)
- embolic occlusion
- thrombotic occlusion
- vasculitis: infections
- atherosclerosis
- only a portion of the brain is affected
- if sustained, leads to infarction
38
brain infarction
- hemorrhagic: multiple, sometimes confluent petichial hemorrhages, typically associated with emboli
- nonhemorrhagic: thrmbosis
Cardio Exam 2
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