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Cardio Exam 2 > Myocardial Infarctions > Flashcards

Myocardial Infarctions Flashcards

1
Q

Classifications on MI:

A
    1. Spontaneous MI related to ischemia caused by a primary event (atherosclerotic plaque erosion or rupture)
    1. MI secondary to ischemia caused by increased oxygen demand or decreased supply (coronary spasm, anemia, embolism)
    1. Sudden, unexpected cardiac death- cardiac arrets, with sympt of ischemia, ST elevation, BBB, or obstruction of a coronary, death before biomarkers obtained
      1. MI associated with PCI (per cutaneous coronary intervention - might clog up vessel just by procedure)
      2. MI associated with stent thro mbosis (stent causes coagulation)
      3. MI associated with CABGS
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2
Q

Sudden cardiac death reasoN?

A

MI with fibrillation

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3
Q

3 Acute coronary syndromes (ACS) are:

A

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

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4
Q

Within first 24 hours of infarction patients have this symptom due to the inflammation…

A

low grade fever!

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5
Q

Anterior/anteroseptal infarction - which artery?

A

left anterior descending (LAD)

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6
Q

Inferior infarction which artery?

A

right coronary (RCA)

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7
Q

Lateral/inferolateral infarction which artery?

A

-circumflex or RCA

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8
Q

ST elevation MI

A
  • full thickness necrosis
  • thrombosis of a single coronary artery
  • commonly forms Q wave on ECG
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9
Q

Non ST elevation MI

A
  • subendocardial layer
  • non Q wave
  • non-transmural
  • often denotes multivessel disease

-WORSE PROGNOSIS = more arrhythmias due to reentry

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10
Q

***What is the most important indicator of prognosis in any heart disease ?

A

LEFT VENTRICULAR FUNCTION

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11
Q

Acute MI pathophys - what are consequences?

A
  • loss of viable myocardium = reduced LV systolic function

- ventricular remodeling-combo of LV dilation and hypertrophy of non-MI myocardium

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12
Q

What happens in ventricular remodeling?

A

-dilation and hypertrophy

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13
Q

Diagnosis of MI based on:

A

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)

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14
Q

What is unstable angina?

A
  • new onset
  • inc frequency or severity
  • onset with less activity
  • angina decubitus
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15
Q

Patient with angina comes in with what complaint?

A
  • 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
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16
Q

Chest pain differential diagnosis:

A
  • costochondritis
  • pericarditis
  • aortic dissection
  • pulmonary embolus
  • GI-GERD
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17
Q

Physical exam finding for AMI:

A

-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

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18
Q

Levines sign

A

clenched fist in from of percordium - not pathomnemonic (doesnt mean that you have it for sure)

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19
Q

S3 is an indicator of what?

A

volume overloaded left ventricle

NOT NECESSARILY LV FAILURE!!!!!

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20
Q

Killip Class 1:

A

No rales
No S3
8% mortality

21
Q

Killip Class 2:

A

Rales over <50% height of posterior chest
OR
S3
30% mortality

22
Q

Killip Class 3:

A

Rales over >50% of posterior chest

44% mortality

23
Q

Killip Class 4

A

Shock - high mortality too much myocardium lost here

24
Q

AMI heart exam findings:

A
  • 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
25
Q

S4 heart sound is a sign of

A

myocardial ischemia! the heart doesnt have the energy to relax so its stiff!!

-goes away with rest if exertional

26
Q

Acute MI labs:

A

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

27
Q

Troponins-types and release/elevation

A
  • troponin I and T both from myocardium
  • rise within 3 hrs of AMI
  • I = elevated 5-10 days
  • T= elevated 10-14 days
28
Q

Creatine Kinase MB (CKMB)

  • rise in levels?
  • peak?
  • specificity
A
  • 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
29
Q

Earliest finding of AMI on ECG?

A

-hyper acute T-waves

30
Q

ECG findings of AMI

A
  • 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
31
Q

Inferior MI in RCA–> Pathologic Q waves in leads?

A

2, 3, F

32
Q

Lateral MI in Circumflex or diagonal LAD–> Pathologic Q waves in leads?

A

1 and L

33
Q

Anterior MI in LAD–> Pathologic Q waves in leads?

A

V1 to V4

34
Q

AMI -imaging:

A
  • Chest X-ray (pulmonary fluid, cardiomegaly..)

- echocardiography (see motion abnormalies, pressures, hemodynamics)

35
Q

What prehospital care to do if someone is having an AMI?

A
  • Reperfusion therapy if possible

- -> FIBRINOLYSIS - GIVE FIBRINOLYTICS

36
Q

Pain control drugs to give?

A

morphine

nalbuphine

37
Q

Stabilize patient process:

A
  • 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
38
Q

MONA for MI:

A

GIVE CLOPTIDOGRIL?

Morphine (DONT GIVE TOO MUCH - respiratory depression - nalbuhpine has no resp depression)
oxygen
nitrates
Aspirin

39
Q

Purpose for Aspirin?

A
  • reduces mortality and non-fatal re-MI

- makes platelets slippery stops clotting

40
Q

Nitroglycerin purpose?

A

-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

41
Q

Purpose for beta blocker

A
  • reduces mortality, pain, and arrhythmias

- reduces myocardial oxygen demand (limit infarction size = MORE LV FUNCTION PRESERVED = IMPROVES MORTALITY!!!!!!!!!!!)

42
Q

Thrombolytic agent of choice?

A

-tPA - INFUSION

43
Q

Prefered therapy for AMI?

A

percutaneous coronary intervention (PCI) SEND THEM TO THE CATH LAB!

44
Q

Which beta blocker to use?

Most benefit where?

A

metoprolol (or atenolol) - most benefit in those with the highest risk of dead after MI

45
Q

Do not use beta blockers if:

A
  • AV blocks
  • lung disease
  • bradycardia
46
Q

risk of thrombolytics:

A

-significantly increases risk of stroke or major bleed vs no fibrinolytic

47
Q

When give t-PA?

A

pretty much whenever you want - within 6hrs and up to 12hrs or more

48
Q

Streptokinase benefit?

A

fewer strokes but more MIs!

t-PA has double the stroke risk

49
Q

Long term therapy for AMI?

A
  • Aspirin + Clopidogrel (reduce platelet adherence)
  • beta blocker
  • statin
  • ACE inh (dec afterload but hard to decide who gets - def not if contraindication)
  • cardiac rehab

Cardio Exam 2 (16 decks)

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