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Cardiopulmonary PT > Myocardial infarction/acute coronary syndrome > Flashcards

Myocardial infarction/acute coronary syndrome Flashcards

1
Q

Pathogenesis of MI

A
  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
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2
Q

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

A
  • 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
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3
Q

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

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

SA/AV node blood supply

A
  • 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
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5
Q

Patient presentation with MI

A
  • 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
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6
Q

Diagnostic criteria for MI/ACS

A
  • must have 2/3:
    1. pain
    2. ECG changes
    3. Biochemical markers/presence of enzymes
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7
Q

Pain with MI is located where?

A
  • any place above the diaphragm
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8
Q

EKG changes with MI

A
  • 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
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9
Q

Cardiac enzymes with MI

A
  • 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
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10
Q

Acute coronary syndrome stages

A
  • Stage 1: stable angina
  • Stage 2: unstable angina
  • Stage 3: NSTEMI
  • Stage 4: STEMI
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11
Q

Stage 1: stable angina

A
  • 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
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12
Q

Stage 2: unstable angina

A
  • 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
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13
Q

Stage 3: NSTEMI

A
  • 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
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14
Q

Stage 4: STEMI

A
  • 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
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15
Q

Pathogenesis for MI once the blockage has occured

A
  • 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
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16
Q

After MI body heals itself by

A
  • inflammatory process
  • scar development
  • remodeling process
17
Q

Initial goal is to limit infarction size by

A
  • reperfusion to improve oxygenation
  • anticoagulation therapy
  • decrease workload of heart (beta blockers, Ca channel blockers)
  • improve oxygenation
  • manage arrhythmias if needed for hemodynamic stability
18
Q

How can reperfussion occur

Treatments?

A
  • thrombolytics: tissue plasminogen activator (tPA) to reduce clot
  • PTCA - percutaneous transluminal coronary angioplasty (through skin)
19
Q

Medications for MI treatment aims to

A
  • reduce the clot
  • prevent further clots
  • reduce myocardial O2 demand
  • increasing O2 supply (coronary vasodilators
  • improving/maintaining myocardial function (digitalis/digoxin)
20
Q

Surgical treatment for MI

A
  • 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
21
Q

PCTA/PCTA with stent

A
  • 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
22
Q

CABG

A
  • 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
23
Q

CABG graft sites

A
  • greater saphenous (leg)
  • left internal mammary artery (only needs to be attached at one end)
  • radial artery
24
Q

CABG procedures on pump verse off pump

A
  • 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
25
Q

PT interventions of MI patients in acute care

A
  • 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
26
Q

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

A
  • 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
27
Q

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

A
  • 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
28
Q

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

A
  • 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
29
Q

phase 1 of cardiac rehab

For MI

A
  • uncomplicated MI, hospitalization for 3-5 days
  • complicated MI hospitalization for 7-10 days
30
Q

Phase 2 cardiac rehab

For MI

A
  • outpatient hospital based cardiac rehab for 8-12 weeks
  • extension of inpatient cardiac rehab for 2 weeks
31
Q

Phase 3 of cardiac rehab

A
  • self exercise/community cardiac rehab

Cardiopulmonary PT (25 decks)

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