Icm Acute Mi

Front 1

whats the relationship btwn the onset of MI sx and treatment

Back 1

the faster you are treated the better the outcome!!!

we want reperfusion in 90 min

Front 2

what is the benefit of tx at the indicated time after MI

60 min
60-120 min
2-12 hours

Back 2

60 min: when treated with antithrombolytics/reperfusion, mortality 1.3 (>70 min mortality 8.7)

1-2 hrs: myocardial salvage, affects survival and L vent fx

2-12 hrs: less vent remodling, rediced vent aneurysm, increase blood to myocardium still in danger, improved electrophysiological stability

Front 3

what is thrombolytic therapy aimed at

Back 3

myocardial salvage

**try to treat 90 min form onset of sx

Front 4

if you start treatment how many hours after sx of MI will you have substantial myocardial salvage, with decreased mortality and increased L vent fx

Back 4

1-2 hours


2-12 hrs: modest benefit bc necrosis has already begun, less adverse remodling, decreased vent aneurysm, increased blood to parts of mycardium still in danger, improved electrophys stability

Front 5

so our pt had an MI 4 hrs b4 being seen, should we still try to tx with thrombolytics

Back 5

sure thing!

benefits 2-12 hrs after onset of sx:
decreased remodling
decreased L vent aneurysm
improved electrophys

Front 6

so we see MAJOR benefit id tx of MI when its 60 min from onset. still good benefit 2 hrs after and little but still some benefit 12 hrs. when do pts usually come in

Back 6

4 hours!!! educate patients about sx and to come in soon!!!

Front 7

what is the largest delay for pts to get therapy for their MI

Back 7

patent delay! they wont come in for like 4 hours. they dont have the education of sx of MI and ways to get fast appropriate care

**TEACH THEM about sx and reasons to be seen

Front 8

what is the role of the pts hx in determining MI

classic features of ischemia

Back 8

HUGE!!! CORNERSTONE

Ischemia: pressure, radiation (L arm, teeth, jaw), sweat, male. can have normal initial EKG, do serial EKG

Front 9

for a sweaty male pt with radiating pressure/pain in the chest what would initial EKG look like

Back 9

could be normal even though he is having an MI, do serial EKG

Front 10

ok so we know that hx is HUGE for MI dx, what should we ask

Back 10

C: character: pressure, squeezing, fullness, heaviness)
O: onset, include evolution of sx
L: location. typically substernal, L border
D: duration, evolution of sx
E: exacerbating factors
R: relief. Nitro, antacid
A: associated sx: sweat, nausea, vomit, SOB, syncope, fatigue, palpitations, edema, cough
S: pain scale. will be HIGH

Front 11

what are the classic associated signs and sx of MI

what is the classic characteristic


what % of ppl wont have this typical presentation

Back 11

A: nausea, vomit, radiation of pain, diaphoresis, SOB, syncope, fatigue, palpatations, edema, cough

C: pressure, squeezing, fullness, heaviness, something sitting on chest

25%: atypicals- dyspnea, syncope, confusion, stroke, fatigue, generalized weakness, nausea, vomit

Front 12

will older or younger pts typically describe MI as pain (can be pressure, squeezing, fullness, heaviness)

Back 12

younger

**older ppl dont intrepret pain pathways as well

Front 13

ok so a pt have severe pain just under breast bone that feels like something is pressing or squeezing, fast onet lasts for hours radiates to back of neck/jaw, SOB, nausea, sweat. menopausal woman who smokes and whos dad had an MI

Back 13

its an MI

typical presentation (seen 75% OF the time)

Front 14

what are some key things to look for for MI PE

Back 14

altered mental status
diaphoresis
rales- fluid in lungs (pneumonia, CHF, pulm edema)
JVD
Edema
S3 S4

RE EXAMINE FREQUENTLY!! take serial EKG's they can be normally initially

Front 15

after you have done a PE on a person with a suspected MI are you done

Back 15

nope, MI is dynamic, reexamine (do serial EGK's the first can be normal)

Front 16

why do an EKG on a pt with possible MI

Back 16

1. dx MI in atypical pts
2. dx non ischemic cardiac problems: PE, pericarditis
3. stratify risk of bad outcomes & determine if pt is admitted
4. establish criteria for theraputic intervention

Front 17

ok so we can use an EKG to determine both ischemic and non ischemic (PE, pericarditis) events. how can we use this to determine therapy

Back 17

1. ST elevation >1 mm in 2 anatomically contigious leads may meet criteria for thrombolytic therapy

Front 18

inferior MI, what leads are affected on EKG

Back 18

ST elevation in II III aVF

reciprocal changes in V1-4

**seeing these things together there is a 90% PPV that its an inferior MI

**inferior MI are larger infarcts with higher mortality

Front 19

what a serial EKG

Back 19

taken at several intervales super important if your thinking MI,

50% of ppl with MI are normal, 20% progress to MI

DO SERIAL EKG ON POSSIBLE MI

Front 20

whats the tx for MI

Back 20

so easy a fireman can do it ;)

A- airway. protection/ability
B- breathing, give O2
C- circulation. check pulses and BP

**start an IV so its there in case the veins collapse

Front 21

ok so you have done your EKG and ABC on a pt with MI, whats next

Back 21

based on progression of disease
1. endo damage by plaque disruption
2. platelet aggregation
3. thrombus formation --> blocked lumen
4. Coronary vasospasm

TREATMENT
1. Increase O2 to myocardium --> give O2 and thrombolytics

2. B block, Ca channel blockers to decrease contractility and decrease O2 demand

3. nitro + thrombolytics to increase metabolis stbstrate availability

4. anti inflammatory

5. prevent reocclusion. inhibit platelet aggregation/thrombus formation with asprin or antithrombins

Front 22

tell me about nitro in pts with MI

Back 22

Decreases preload, some decrease in afterload

2. Direct dilation of coronaries, be sure diastolix is >90

3. Give 3 oral doses, and then IV if more is needed

4. if you give too much and get Hypotension give IV saline

**careful in pts with bradycardia, hypotension, inferior wall MI, R vent infarct

Front 23

will notro affect preload or afterload or both in pts with MI

Back 23

preload more but some afterload

**direct dilation of coronaries, diastolic needs to be more than 90

**caution in pts with bradycardia and hypotension

Front 24

so with MI we get:
1. Endo damage through plaque disruption. shearing injury

2. platelet aggregation

3. thrombus formation, partial block

4. coronary vasospasm

what are the therapies to tx

Back 24

1. increase O2 to myocardium with thrombolytics

2. b block, Ca block to decrease force of contraction and decrease O2 consumption

3. increase metabolic substrate availability to myocardium via nitro and thrombolytics

4. protect injured myocardial cells from fx with antiinflammatories

5. prevent reocclusion with antiplatelets (asprin) and antithrombin

Front 25

what is antiplatelet therapy

Back 25

asprin will decrease mortality 60-325 mg

synergistic with antithrombolytics

CI: if you have a major bleed or are allergic

Front 26

what can be given to destroy the clot

Back 26

asprin

dont use if you have a bleed or an allergy

Front 27

what are some CI for thrombolytic therapy

Back 27

recent surgery
cerebrovascular disease
GI/GU bleed
trauma
HTN (180/110)
allergy

Front 28

what does morphine sulfat do for MI

Back 28

1. pain releif
2. decrease anxiety
3. decrease O2 consumption of heart
4. dialte

**side effect is hypotension, tx with saline bolus

Front 29

why use a b blocker in pt with MI

why not

Back 29

decrease controactility to decrease O2 demand. also decrease Catecholamie mediated tachycardia

**DONT USE:
-bradycardia
-CHF
-COPD
-Hypotension
- reactive airway disease
1 AV block

Front 30

who gets prophylactic lidocain for AMI

Back 30

only pts "at risk"

*premature ventricular beats that are:
- multifocal
-frequent