Myocardial Infarction

Front 1

What is an acute MI?
What causes it/pathogenesis behind it?

Back 1

Irreversible necrosis of myocardial tissue resulting from an acute insufficiency in blood supply

Occurs when there is sudden occlusion of a major coronary artery --> severe and prolonged ischemia leads to PERMANENT death of heart muscle
- usually due to thrombosis within coronary artery from sit of unstable atherosclerotic plaque

Front 2

When do the post-MI electric, mechanical, gross and microscopic dysfunctions become apparent?

Back 2

- Electrical (ECG) and mechanical dysfunction almost immediately apparent
- **ECG is indispensible

- Gross and microscopic pathologic changes not apparent for several hours...
-Scar tissue gradually replaces necrotic tissue for up to 6 wks

Front 3

What percent of people die due to v.fib before reaching hospital?

Back 3

21% sudden death

Front 4

What percent of ppl die during hospitalization for MI? WHY?

Back 4

5-10% die due to electrical and/or mechanical complications

Front 5

What percent of ppl die within first year of MI?

Back 5

5-10%

Front 6

What are the main components of the clinical diagnosis of MI?

Back 6

1. Pt history of acute onset of ischemic symptoms

2. ECG changes

3. Subsequent elevation in serum levels of cardiac enzymes

Front 7

How long must angina-like pain persist to be considered an acute MI (until proven otherwise)?

Back 7

>30 min

Front 8

What are the autonomic symptoms associated with an acute MI?

Back 8

diaphoresis, nausea, sense of impending doom

Front 9

What percent of patients have "silent MIs"?
Who is particularly at risk for "silent MIs"?

Back 9

25% of MIs are "silent MIs"

most common in:
diabetics, elderly, women

Front 10

What characteristics determine the ECG changes of an acute MI?

Back 10

- age of infarct
- location of infarct
- size of infarct

Front 11

What are ECG changes associated with an acute MI?

Back 11

EARLY PHASE:
- ST segment elevation = transmural ischemia, potentially reversible
*** After 30 min of ST elevation, necrosis ensues

HOURS TO DAYS POST-MI:
- Broad, deep Q wave in leads overlying infarcted region (sine qua non for MI) (due to continued depol of normal myocardium opposite to area of infarction - shows a "neg" wave on the infarcted area's lead = Q wave)
- Loss of R wave
- Some remaining ST seg elevation

SERVERAL DAYS TO WEEKS POST-MI:
- Pathologic Q wave persists
- T wave becomes inverted
- ST seg back to isoelectric

CHRONIC PHASE (months to years post-MI):
- ST and T wave changes normalize
- Pathologive Q wave remains forever

Front 12

What artery is occluded in an ANTERIOR MI?
What are the ECG findings?

Back 12

- LAD occlusion
- Leads V1-V6 = pathologic Q waves

Front 13

What artery is occluded in an INFERIOR MI?
What are the ECG findings?

Back 13

- PDA (Post Descending Art) - supplied 80-90% of the time by R Coronary Artery Occlusion (other 10-20% by L Circumflex)
- Leads II, III, aVF = pathologic Q wave

Front 14

What artery is occluded in an POSTERIOR MI?
What are the ECG findings?

Back 14

- Left Circumflex Artery occlusion
- **No leads for post heart, so must use MIRROR IMAGE of ant leads, such as V1 and V2 = ST segment depression; Tall R wave

Front 15

What percent of MIs present with pathologic Q waves?

What percent of MIs present as non-Q wave?
- what are good diagnostic tools for these MIs?

Back 15

Q Wave = 2/3 MIs
Non-Q wave = 1/3 MIs --> must use ST elevation and inverted T waves on ECG; elevated cardiac enzymes in serum

Front 16

What is door-to-balloon time?

Back 16

DTBT = goal to get balloon in occluded coronary artery within 90 minutes from presentation to ER

Front 17

What is the most sensitive and specific diagnostic test of Acute MI?

Back 17

serum cardiac enzyme levels --- specifically, CARDIAC TROPONIN!

Front 18

Creatine Kinase
- when should it be measured?
- when do serum CK levels peak?
- what do the levels mean?
- what are the isoenzymes and their locations?

Back 18

- measured every 8 hours for 24 hours post-MI
- levels peak 16-24 hours post-MI
- larger the infarct, the higher the CK peak
- 3 isoenzymes:
- CK-BB = in brain, kidney
- CK-MM = in skeletal, cardiac muscle
- CK-MB = in cardiac muscle ONLY

Front 19

What should type of CK elevation be for an MI?

Back 19

Elevation of the CK-MB isoenzyme is sensitive and specific for MI

Front 20

What does it mean when there is an elevated serum CK but not an elevated CK-MB?

Back 20

Non-cardiac source of CK

Front 21

What is cardiac troponin?
What are the cardiac isoenzymes?
When is Tn most diagnostic?

Back 21

= Protein complex (3 distinct proteins) that regulate Ca-dependent interaction of actin and myosin

- Tn I and T are expressed only in cardiac muscle

- Tn elevated within 4-6 hrs post-MI; remain elevated for several days

Front 22

What is cardiac troponin?
What are the cardiac isoenzymes?
When is Tn most diagnostic?

Back 22

= Protein complex (3 distinct proteins) that regulate Ca-dependent interaction of actin and myosin

- Tn I and T are expressed only in cardiac muscle

- Tn elevated within 4-6 hrs post-MI; remain elevated for several days

Front 23

When a pt presents with an acute MI, what general measures should be taken within the hospital?

Back 23

1. ECG monitoring should be started immediately; continue for 48-72 hrs

2. Narcotic analgesia to relieve chest pain --> reduces anxiety and sympathetic drive (catecholamine release), which increases myocardial work load and O2 demand
= Morphine Sulfate

3. Nasal O2

4. Bedrest

5. Diet- clear liquids only for first day (digestion increases cardiac demand) (minimizes potential for aspiration)

Front 24

What are the "ABCs" of routine MI tx?

Back 24

Aspirin --> prevents clotting
Beta-Blockers --> reduces infarction
Cholesterol-lowering Drugs (statins)

Front 25

How effective are B-Blockers in reducing future sudden death and reinfarction?

Back 25

Reduce by ~25%

Front 26

In absence of complications following MI, how long before a patient is typically discharged?

Back 26

3-5 days

Front 27

When are ACE Inhibitors indicated for MI patients?

Back 27

When it is a large, anterior MI;
Congestive Heart Failure

Front 28

What are the main complications of an acute MI?

Back 28

- post-infarction angina
- pericarditis
- electrical complications: cardiac arrhythmias
- mechanical complications: L ventricular failure, R ventricular infarction, myocardial rupture (free wall, IV septum, papillary muscle)

Front 29

Post-infarction angina
- what does it mean?
- prognosis?
- tx?

Back 29

= residual areas of viable myocardiam remain in jeopardy of reinfarction
- poor prognosis :-(
- cardiac catherterization to check it out.... assess the need for balloon angioplasty or bypass surgery

Front 30

Pericarditis
- clinical features?
- early v late?
- tx?

Back 30

Clinical Features:
- pleuritic pain (sharp, localized, worse on inspiration)
- pericardial friction rub on auscultation
- ST segment elevation in almost all ECG leads

Early Pericarditis (first few days) - large transmural infarcts involving pericardium
Late Pericarditis (weeks after infarct) - Dressler's Syndrome = autoimmune reaction

Early cases often self-limited;
Dressler's Syndrome might require anti-inflammatory tx

Front 31

What are the electrical complications that might follow an acute MI?

Back 31

ARRHYTHMIAS

Ventricular Arrhythmias
- Premature Ventricular Contraction (PVC) - worst when multifocal
- Ventricular tachycardia
- Ventricular fibrillation

Supraventricular Arrhythmias
- Atrial Fibrillation or Atrial Flutter (secondary to L ventric failure)
- Atrial Infarction
- Pericarditis

Bradyarrhythmias

Conduction Disturbances
- 1st degree AV Block - within AV node itself - more favorable prognosis
- 2nd degree/3rd degree AV Block - poorer prognosis; might require pacing

Front 32

What is the cause of most instances of sudden death early on in an acute MI?

Back 32

Ventricular tachycardia and ventricular fibrillation

Front 33

When is bradyarrhythmia most commonly found in MI?

Tx?

Back 33

Inferior Wall MI
- due to excitation of vagal receptors (parasympathetic), which are abundant in inferior L ventricle wall

Tx: usually not necessary bc slower HR is beneficial to re-oxygenate the heart; BUT if HR <40 or hypotension, give atropine or temporary pacing

Front 34

What are the mechanical complications of acute MI?

Back 34

L ventricular failure
- single-most important prognostic factor in hemodynamic compromise
- assessed by Classification of Killip

Right Ventricular Failure
- Might present with hypotension or shock (decreased CO)
- Elevation of Jugular Venous Pressure
- almost always an ACUTE INFERIOR MI
- Must administer adequate fluid to augment L vent filling and, thus, cardiac output

Myocardial Rupture - free wall, IV septum, Papillary Muscle

Front 35

Classification of Killip

Back 35

Assesses level of L ventricular function (thus, hemodynamic)

Class I: No evidence of CHF
Class II: Mild CHF (rales in lower lungs; vascular congestion on CXR)
Class III: Pulmonary Edema (rales throughout lungs; S3 gallop)
Class IV: Cardiogenic Shock (signs of hypotension and low CO - cool clammy skin, mental obtundation, low urine output)

Front 36

What is the single-most important prognostic factor in an acute MI?

Back 36

Hemodynamic Compromise!
- depends on L ventricular function

Front 37

Where is the infarction almost always associated with a R Ventricular MI?

Back 37

Inferior MI

Front 38

Myocardial Rupture
- when does peak incidence occur after MI?
- what areas and what sx?

Back 38

*Peak incidence of rupture 3-5 days post-MI

Free Wall Rupture
- usually sudden death due to massive cardiac tamponade

Ventricular Septum Rupture
- results in CHF or cardiogenic shock
- new holosystolic murmur on auscultation
- palpable thrill across L sternal border
- potentially correctable by surgery

Papillary Muscle Rupture
- extent of rupture determines extent of mitral regurg
- rupture of entire papillary muscle = rapidly fatal
- rupture of one or a few heads = CHF, low CO
- new holosystolic murmur
- potentially correctable by surgery

Front 39

What are the main methods of myocardial repurfusion?

Back 39

1. Thrombolytic Therapy
2. Coronary Angioplasty
3. Emergency Bypass Surgery

Front 40

What are the main methods of myocardial repurfusion?

Back 40

1. Thrombolytic Therapy
2. Coronary Angioplasty
3. Emergency Bypass Surgery

Front 41

Who are the main candidates of urgernt reperfusion therapy?

Back 41

- symptom onset within 12 hours
- ST segment elevation in > or = 2 contiguous ECG leads
- New LBBB

**No contraindication to these drugs

Front 42

Who are the main candidates of urgernt reperfusion therapy?

Back 42

- symptom onset within 12 hours
- ST segment elevation in > or = 2 contiguous ECG leads
- New LBBB

**No contraindication to these drugs

Front 43

What are commonly used IV thrombolytics?

Back 43

- Streptokinase (nonfibrin specific)

- Fibrin specific:
- Tissue Plasminogen Activator (tPA)
- Reteplase
- Tenecteplase (TNK-tPA)

Front 44

What are commonly used IV thrombolytics?

Back 44

- Streptokinase (nonfibrin specific)

- Fibrin specific:
- Tissue Plasminogen Activator (tPA)
- Reteplase
- Tenecteplase (TNK-tPA)

Front 45

What can be done after Thrombolytic drugs to decide upon further procedures? What are these procedures?

Back 45

cardiac catheterization and stress tests help decide....

- Coronary angioplasty
- Coronary bypass surgery

Front 46

What can be done after Thrombolytic drugs to decide upon further procedures? What are these procedures?

Back 46

cardiac catheterization and stress tests help decide....

- Coronary angioplasty
- Coronary bypass surgery

Front 47

What is the most superior therapy post-MI?
Why?

Back 47

CORONARY ANGIOPLASTY
- bc treats underlying stenosis

Front 48

What are the limitations to thrombolytic tx?

Back 48

- time delay to reperfusion (45-60 min)
- acute patency in only 60-80% cases
- **risk of recurrent ischemia/infarction -- dissolves clot, but doesn't get rid of plaque itself
- hemorrhagic risk!!!