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Flashcards in lecture 5b Deck (38):
1

UA/NSTEMI definition

- 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

NSTEMI=

UA + myocardial necrosis

3

UA/NSTEMI pathophys

- 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

UA/NSTEMI manifestatins

- 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

UA/NSTEMI cardiac biomarkers

- CKMB& troponin- distinguish pts w/ NSTEMI from UA

6

there is a direct relationship between the degree of troponin elevation and

mortality

7

minor troponin elevations can be caused by

congestive heart failure
myocarditis
PE
or can be false +

8

prinzmetal's variant angina

- 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

STEMI definition

- myocardial cell death due to prolonged & severe ischemia
- ST elevation

10

STEMI pathophys

- 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

coronary plaque prone to disruption are those with

a rich lipid core and thin fibrous cap

12

extent of myocardial damage depends on

- 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

STEMI risk factors

- multiple coronary risk factors
- UA
- hypercoagulability
- collagen vascular disease
- cocaine abuse
- intracardiac thrombi
- coronary emboli

14

STEMI clinical manifestations

- 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

what are considered in differential diagnosis of STEMI?

acute pericarditis, PE, acute aortic dissection, costochondritis & GI disorders

16

STEMI diagnosis

ECG
biomarkers
imaging
non-specific indicators or tissue necrosis & inflammation

17

STEMI physical findings

- 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

STEMI ECG

ST elevation
Q wave

19

STEMI biomarkers

- cardiac specific troponin
& toponin-1
- CK
- CKMB

20

myocardial infaction

death of cardiac muscle due to prolonged severe ischemia

21

MI pathology

- 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

longer occlusion->

larger area of tissue damage

23

STEMI

-transmural infarction
- full thickness
-ST elevation

24

NSTEMI

-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