Myocardial Infarctions Flashcards
Classifications on MI:
- Spontaneous MI related to ischemia caused by a primary event (atherosclerotic plaque erosion or rupture)
- MI secondary to ischemia caused by increased oxygen demand or decreased supply (coronary spasm, anemia, embolism)
- Sudden, unexpected cardiac death- cardiac arrets, with sympt of ischemia, ST elevation, BBB, or obstruction of a coronary, death before biomarkers obtained
- MI associated with PCI (per cutaneous coronary intervention - might clog up vessel just by procedure)
- MI associated with stent thro mbosis (stent causes coagulation)
- MI associated with CABGS
- Sudden, unexpected cardiac death- cardiac arrets, with sympt of ischemia, ST elevation, BBB, or obstruction of a coronary, death before biomarkers obtained
Sudden cardiac death reasoN?
MI with fibrillation
3 Acute coronary syndromes (ACS) are:
1) ST-elevation MI (STEMI) - complete occlusion of epicardial coronary with tarnsmural MI (q wave infarction)
2) Non-STEMI (NSTEMI) - results from subtotal coronary occlusion (subendocardial MI - ST depression)
3) Unstable angina pectoris
- new onset angina
- less effort
- more severe
Within first 24 hours of infarction patients have this symptom due to the inflammation…
low grade fever!
Anterior/anteroseptal infarction - which artery?
left anterior descending (LAD)
Inferior infarction which artery?
right coronary (RCA)
Lateral/inferolateral infarction which artery?
-circumflex or RCA
ST elevation MI
- full thickness necrosis
- thrombosis of a single coronary artery
- commonly forms Q wave on ECG
Non ST elevation MI
- subendocardial layer
- non Q wave
- non-transmural
- often denotes multivessel disease
-WORSE PROGNOSIS = more arrhythmias due to reentry
***What is the most important indicator of prognosis in any heart disease ?
LEFT VENTRICULAR FUNCTION
Acute MI pathophys - what are consequences?
- loss of viable myocardium = reduced LV systolic function
- ventricular remodeling-combo of LV dilation and hypertrophy of non-MI myocardium
What happens in ventricular remodeling?
-dilation and hypertrophy
Diagnosis of MI based on:
1) Biomarkers + one of the below:
- ischemic symtpoms (chest pain…)
- development of Q waves on ECG
- ischemic ST segments (up or down)
- image evidence of new loss of myocardium or loss of wall motion
2) Pathologic evidence of MI (biopsy or section)
What is unstable angina?
- new onset
- inc frequency or severity
- onset with less activity
- angina decubitus
Patient with angina comes in with what complaint?
- chest just doesnt feel good - tight, heavy, squeezing, crushing
- comonly retrosternal and radiates occasionally to shoulder, jaw, ulnar side of left arm
- up to half-ish people have silent AMI —> you only notice when you do the ECG!
- often gets mistaken for GI symptoms - same innervation as cardia of stomach
- diffuse pain - IF THE POINT TO THE SPOT WHERE IT HURTS THEN ITS NOT MI
Chest pain differential diagnosis:
- costochondritis
- pericarditis
- aortic dissection
- pulmonary embolus
- GI-GERD
Physical exam finding for AMI:
-anxious, distressed, diaphoretic levines sign
-variable HR
BP normal or high [unless Bezold harisch reflex or cardiogenic shock (dec BP)]
-afebrile until inflammation
-occular fundi - atherosclerosis, DM, HTN
-carotid pulses can give clue to LV function
-lung congestion (rales) or may be clear
Levines sign
clenched fist in from of percordium - not pathomnemonic (doesnt mean that you have it for sure)
S3 is an indicator of what?
volume overloaded left ventricle
NOT NECESSARILY LV FAILURE!!!!!
Killip Class 1:
No rales
No S3
8% mortality
Killip Class 2:
Rales over <50% height of posterior chest
OR
S3
30% mortality
Killip Class 3:
Rales over >50% of posterior chest
44% mortality
Killip Class 4
Shock - high mortality too much myocardium lost here
AMI heart exam findings:
- muffled S1 and S2 (the blood isnt moving so well anymore)
- S4 at apex (heart CANT relax bc no energy - active process!! - stiffer myocardium)
- S3 variably present
- pericardial friction rub sometimes
- systolic murmur at apex (mitral regurg - papillary muscles not working well)
- dec perfusion of extremities visible-ish
S4 heart sound is a sign of
myocardial ischemia! the heart doesnt have the energy to relax so its stiff!!
-goes away with rest if exertional
Acute MI labs:
1) serum markers
**-cardiac specific troponin (cTnI or cTnT)
**-creatine kinase MB isoform (CK-MB)
==> measure every 8-12 hours
2) other lab changes/pathologies:
-anemia,
-DM
-dyslipidemia
Troponins-types and release/elevation
- troponin I and T both from myocardium
- rise within 3 hrs of AMI
- I = elevated 5-10 days
- T= elevated 10-14 days
Creatine Kinase MB (CKMB)
- rise in levels?
- peak?
- specificity
- rises 4-8hrs and returns to norm in 2-3 days
- peaks at 24 hrs or earlier if reperfused (if reperfuse in time then you wash out the CKMB that the dying cells released = quicker peak levels)
- also found in skeletal muscle
Earliest finding of AMI on ECG?
-hyper acute T-waves
ECG findings of AMI
- Hyperacute T_waves
- ST elevation elevation (usually drops to isoelectric by end of actual MI occurrence)
- T wave inversion (not reliable)
- Pathologic Q-waves (take hours to develop - wave of depolarization going AWAY from area of infarction bc the infarcted area doesnt electrically cancel out the side
Inferior MI in RCA–> Pathologic Q waves in leads?
2, 3, F
Lateral MI in Circumflex or diagonal LAD–> Pathologic Q waves in leads?
1 and L
Anterior MI in LAD–> Pathologic Q waves in leads?
V1 to V4
AMI -imaging:
- Chest X-ray (pulmonary fluid, cardiomegaly..)
- echocardiography (see motion abnormalies, pressures, hemodynamics)
What prehospital care to do if someone is having an AMI?
- Reperfusion therapy if possible
- -> FIBRINOLYSIS - GIVE FIBRINOLYTICS
Pain control drugs to give?
morphine
nalbuphine
Stabilize patient process:
- REASSURANCE (reduced sympathetics - CALM THEM DOWN)
- support circulation (IV fluids, pressors if needed)
- maintain rhythm (monitor, antiarrhythmics via IV)
- pain control - DO NOT ABOLISH THE PAIN (morphine nalbuphine)
- O2 if needed
MONA for MI:
GIVE CLOPTIDOGRIL?
Morphine (DONT GIVE TOO MUCH - respiratory depression - nalbuhpine has no resp depression)
oxygen
nitrates
Aspirin
Purpose for Aspirin?
- reduces mortality and non-fatal re-MI
- makes platelets slippery stops clotting
Nitroglycerin purpose?
-may reduce/abort angina if given soon enough
if theyve been having chest pain for 4 hrs then it might be a little too late
Purpose for beta blocker
- reduces mortality, pain, and arrhythmias
- reduces myocardial oxygen demand (limit infarction size = MORE LV FUNCTION PRESERVED = IMPROVES MORTALITY!!!!!!!!!!!)
Thrombolytic agent of choice?
-tPA - INFUSION
Prefered therapy for AMI?
percutaneous coronary intervention (PCI) SEND THEM TO THE CATH LAB!
Which beta blocker to use?
Most benefit where?
metoprolol (or atenolol) - most benefit in those with the highest risk of dead after MI
Do not use beta blockers if:
- AV blocks
- lung disease
- bradycardia
risk of thrombolytics:
-significantly increases risk of stroke or major bleed vs no fibrinolytic
When give t-PA?
pretty much whenever you want - within 6hrs and up to 12hrs or more
Streptokinase benefit?
fewer strokes but more MIs!
t-PA has double the stroke risk
Long term therapy for AMI?
- Aspirin + Clopidogrel (reduce platelet adherence)
- beta blocker
- statin
- ACE inh (dec afterload but hard to decide who gets - def not if contraindication)
- cardiac rehab
