Myocardial infarction/acute coronary syndrome

Question 1

Pathogenesis of MI

Answer 1

1. endothelial cell injury and inflammation
2. plaque formation
3. plaque rupture and thrombogenesis
4. reduce blood supply and increase oxygen demand
5. myocardial ischemia
6. myocardial cell necrosis
7. acute myocardial infarction

Question 2

MI Is result of prolonged ischemia - prolonged ischemia is result of

Answer 2

• most commonly = coronary thrombus
• prolonged vasospasm
• inadequate myocardial blood flow
• excessive metabolic demand
• embolic occlusion (not commonly from distal body)
• vasculitis/coronary artery dissection/trauma
• congenital abnormalities
• hematological disorders
• cocaine

Question 3

What does the arteries supply?
1. right coronary artery
2. left coronary artery
3. posterior circumflex artery
4. anterior interventricualr descending

Answer 3

1. SA/AV node - right side of heart
2. splits into circumstancesflex/LAD
3. lateral and posterior heart
4. left ventricle and septum

Question 4

SA/AV node blood supply

Answer 4

• variations exist in right and left coronary artery distribution
• in MOST people the RCA supplies both SA and AV node
• circumflex can supply SA/AV node in some people

Question 5

Patient presentation with MI

Answer 5

• sudden onset of chest discomfort
• may be described as crushing
• Levines sign: flexed forward slightly at hip and clutching chest
• dramatic surge in sympathetic nervosa system activity
• diaphoresis
• cool, clammy skin
• nausea/vomiting
• fever

Question 6

Diagnostic criteria for MI/ACS

Answer 6

• must have 2/3:
  1. pain
  2. ECG changes
  3. Biochemical markers/presence of enzymes

Question 7

Pain with MI is located where?

Answer 7

• any place above the diaphragm

Question 8

EKG changes with MI

Answer 8

• ST segment
• Q-wave: larger
• T-wave - tall = hyperacute phase or inverted = fully evolved
• elevated ST segment = tissue death
  ST elevation does not have to present for tissue death

Question 9

Cardiac enzymes with MI

Answer 9

• true indicators/appear with tissue death
• take a couple hours to later to look at how the levels are changing
• MI can develop over hours/days
• Troponin T/I = immediately increase
• CKMB = specific to cardiac muscle; increases with myocardial degeneration and clear quickly
• AST, LDH increase later on as troponin decreases
• before mobilizing make sure troponin levels are trending down

Question 10

Acute coronary syndrome stages

Answer 10

• Stage 1: stable angina
• Stage 2: unstable angina
• Stage 3: NSTEMI
• Stage 4: STEMI

Question 11

Stage 1: stable angina

Answer 11

• angina pain develops when there is increase in demand
• setting of a stable atherosclerotic plaque
• vessel is able to dilate enough to allow adequate blood flow to meet myocardial demand
• ECG/Troponins normal

Question 12

Stage 2: unstable angina

Answer 12

• The plaque ruptures and a thrombus forms around the ruptured plaque causing partial occlusion of vessel
• angina pain occurs at rest or progresses rapidly over short period of time
• ECG: inverted T-wave, normal or ST depression
• Troponin = normal

Question 13

Stage 3: NSTEMI

Answer 13

• plaque rupture and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium
• ECG = normal, inverted T-waves, or ST depression
• Troponin = elevated

Question 14

Stage 4: STEMI

Answer 14

• complete occupation of blood vessel
• results in transmural injury and infarction to myocardium
• ECG = hyperacute T-waves or ST elevation
• Troponins = elevated
• tissue death through whole depth of muscle
• lose contractility and conductibility

Question 15

Pathogenesis for MI once the blockage has occured

Answer 15

• a complete interruption of blood supply to an area of myocardium
• cells die and tissue becomes necrotic
• at risk are is within the Zone of perfusion
• the area of tissue death is called zone of necrosis
• if reperfused quickly then surrounding damaged tissue can be spared

Question 16

After MI body heals itself by

Answer 16

• inflammatory process
• scar development
• remodeling process

Question 17

Initial goal is to limit infarction size by

Answer 17

• reperfusion to improve oxygenation
• anticoagulation therapy
• decrease workload of heart (beta blockers, Ca channel blockers)
• improve oxygenation
• manage arrhythmias if needed for hemodynamic stability

Question 18

How can reperfussion occur

Treatments?

Answer 18

• thrombolytics: tissue plasminogen activator (tPA) to reduce clot
• PTCA - percutaneous transluminal coronary angioplasty (through skin)

Question 19

Medications for MI treatment aims to

Answer 19

• reduce the clot
• prevent further clots
• reduce myocardial O2 demand
• increasing O2 supply (coronary vasodilators
• improving/maintaining myocardial function (digitalis/digoxin)

Question 20

Surgical treatment for MI

Answer 20

• percutaneous transluminal coronary angioplasty (PCTA) via cauterization
• PCTA with stent placement via catheterization
• Coronary ArteryBypass Grafting (CABG) - open procedure with harvest of vein and artery graft

Question 21

PCTA/PCTA with stent

Answer 21

• fed into coronary artery with balloon that compresses plaque against a wall
• or the ballon can have a Stent around it that will hold the artery open
• often medicated with anticoagulants
• can reocclude if lifestyle is not changed

Question 22

CABG

Answer 22

• Coronary artery bypass graft
• single = one graft (bypass one clot)
• double: two grafts
• triple = three grafts
• quadruple = 4 grafts
• reperfused lower than the blockage to hit the zone of perfusion

Question 23

CABG graft sites

Answer 23

• greater saphenous (leg)
• left internal mammary artery (only needs to be attached at one end)
• radial artery

Question 24

CABG procedures on pump verse off pump

Answer 24

• on pump = bypass machine to stop the heart from beating and keep it in place
• off pump: newer, takes less trauma and incisions, with a device that stabilize the area of the heart they are working on

Question 25

PT interventions of MI patients in acute care

Answer 25

- when patient is stable and cleared by physician - early attention to surgical sites - low level activity, functional activity (HR 20-30 above resting) - out of bed to chair, walking - goal: get to next level of care

Question 26

PT interventions for MI patients after remodeling period and cleared for increased activity

Answer 26

- cardiac rehab phase (progressing into low end of age predicted HRmax) - appropriate exercise prescription based on a submaximal exercise test, careful monitoring and progression - attention to post surgical deficits as well as aerobic conditioning - include strengthening - goals previous level of function o better

Question 27

Don't start exercise if vitals: - pulse rate - RR - SPB - DBP - Fever - SPO2 - Ejection fraction - Arryhmias - RPE

Answer 27

- pulse rate: >120-130 or <40 - RR: >30 bpm - SPB: >200 - DBP: >110 - Fever: >100 - SPO2: <88% - Ejection fraction: <50% - Arryhmias: >6/min - RPE: n/a

Question 28

Terminate exercise if - pulse rate - RR - SPB - DBP - Fever - SPO2 - Ejection fraction - Arryhmias - RPE

Answer 28

- pulse rate: Post MI/CABG_ 20-30 above resting; post med surge >130 - RR: unable to talk - SPB: >220 - DBP: 110 - Fever: N/A - SPO2: <88% - Ejection fraction n/A - Arryhmias: >6/min - RPE13

Question 29

phase 1 of cardiac rehab | For MI

Answer 29

- uncomplicated MI, hospitalization for 3-5 days - complicated MI hospitalization for 7-10 days

Question 30

Phase 2 cardiac rehab | For MI

Answer 30

- outpatient hospital based cardiac rehab for 8-12 weeks - extension of inpatient cardiac rehab for 2 weeks

Question 31

Phase 3 of cardiac rehab

Answer 31

- self exercise/community cardiac rehab