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Cardio Week 4 > Lecture 42: Pathophysiology of Myocardial Ischemia and Infarction > Flashcards

Lecture 42: Pathophysiology of Myocardial Ischemia and Infarction Flashcards

1
Q

What are the general principles of myocardial ischemia?

A

Imbalance between oxygen supply and demand due to impaired or inadequate perfusion
Consequences include
i. hypoxia
ii. accumulation of waste products
Not the same as anoxia, which is oxygen deprivation with normal perfusion (so byproducts can be removed for anaerobic metabolism)
Oxygen demands of the myocardium are dynamic

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2
Q

What happens when you decrease metabolic activity?

A

It is possible to have complete interruption of blood flow for extended periods of time without ischemia
That’s why heart is dynamic (because you would get ischemia instantly upon vigorous exercise)

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3
Q

What is anoxia?

A

When there is enough blood being supplied to muscle but there is no oxygen in that blood!
Less detrimental because at least the toxic byproducts are washed out lol

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4
Q

What dictates myocardial oxygen demand?

A
  1. heart rate
  2. systolic wall tension
  3. myocardial contractility
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5
Q

What are anti-pyretics?

A

Drugs that reduce fever such as ibuprofen

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6
Q

What is wall tension determined by?

A

Tension = pressure x radius/wall thickness

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7
Q

How can wall tension be raised?

A

Disease states that elevate LVEDVolumes

And increase afterload like HTN and aortic stenosis

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8
Q

What dictates myocardial oxygen supply?

A
  1. Coronary blood flow
  2. diastolic perfusion pressure
  3. coronary vascular resistance
  4. Oxygen carrying capacity of blood
  5. hemoglobin concentration and oxygen saturation
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9
Q

What is the significance of diastole to coronary blood flow?

A

This is when there is the greatest pressure gradient towards perfusing the coronaries

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10
Q

What can alter coronary blood flow?

A

When there is a change in the diastolic phase of the cardiac cycle
Decreasing diastole through tachycardia or AR = less CBF
Atherosclerosis that leads to stenotic coronary arteries (>80%)
Coronary spasm or platelet aggregation occurs at stenosis

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11
Q

How does an imbalance between demand and supply come about? Significance?

A

Significance = myocardial ischemia

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12
Q

What is the relationship between CBF and myocardial O2 consumption?

A

CBF increases in proportion to myocardial oxygen consumption

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13
Q

What is reactive hyperemia? Significance?

A

An adaptation of the blood vessels to reduce resistance of vascular bed by releasing substances like prostacyclin, adenosine, NO and acetylcholine
This effect is reduced in those with moderate CAD

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14
Q

What is an impairment of coronary flow rate?

A

When the difference between max CBF and rest CBF starts to fall off
Less reactive hyperemia = less ability to maintain luminal area

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15
Q

What are the effects of ischemia on glycolysis?

A

FFAs account for 60-90% of myocardial energy
Toxic TG builds up during anaeraobic metabolism since it has detergent like properties
Lactic acid builds up to inhibit glycolysis
Without enough ATP (<30%), irreversible injury occurs to sarcolemma, results in cell death, sodium accumulation and calcium depletion

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16
Q

What layer is most vulnerable to ischemia?

A

Subendocardium
Intramural compressive forces increase the resistance in subendocardium
-more resistance = less flow
Autoregulation is better in epicardium

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17
Q

What are the electrophysiologic effects of ischemia?

A

Reductions in
i. resting membrane potential (extracellular K)
ii. action 4 upstroke
iii. AP amplitude and duration
iv. conduction velocity
and reduction in production of ATP and creatine phosphate (notes pg 3)
protein synthesis and protein degradation is also suppressed
Arrhythmias because ion channels and transport is fucked up

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18
Q

What is the mechanism for sarcolemma disruption in ischemia?

A

Acidosis
Hypoxia
Ca accumulation lead to worsening of contractility and excitability

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19
Q

What metabolites are not washed out during myocardial ischemia? Significance?

A

Lactic acid
Long-chain acyl carnitine
Lysophospholipids
They cause arrhythmogenesis and myocardial depression
Acyl carnitine and lysophospholipids are detergent like and can render sarcolemmal ion channels dysfunciotnal (top of pg 5)

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20
Q

What does myocardial ischemia do to the FFA pool for oxidation/energy?

A

It prevents FFA from being esterified so they can leave the cell
Less FFA pool means that after an ischemic insult, there is prolonged recovery because so much of the energy of the heart is derived from FFA

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21
Q

What are the effects of ischemia on contractile function?

A
  1. Impairs active relaxation in early diastole
  2. causes regional stiffness (decreased compliance) shifting P-V relation up/sleft
  3. very sensitive early measure of ischemia
    Curve is shifted up
    Fucks with both systolic contraction and diastolic relaxation
    Can lead to heart failure and cardiogenic shock if can contract and relax sufficiently
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22
Q

What are the effects of ischemia on systolic function?

A

Contraction decreases proportionately to the decrease in flow
Mechanism involves interference with Ca release, binding to troponin or impaired actin/myosin interaction
Effects = dyskinesis in central zone and hypokinesis/akinesis in adjacent areas
Compensatory mechanisms = hyperkinesis through adrenergic stimulation and Starling mechanism

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23
Q

What is the mechanism by which ischemia causes contractile dysfunction?

A

May involve interference with systolic calcium binding to troponin

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24
Q

What is the mechanism by which ischemia causes diastolic dysfunction?

A

Early part of diastole is isovolumic relaxation, an ACTIVE energy requiring pahse
But if not enough ATP then you are less compliant and you have greater pressure in the ventricle

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25
Q

What is the definition of infarction?

A

Prolonged ischemia that leads to irreversible contractile dysfunction

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26
Q

What is the definition of stunning?

A

When acute ischemia with reperfusion causes prolonged contractile dysfunction
Transient instead of permanent
Caused by:
i. Accumulation of phosphate and hydrogen which depress myocardial contractility (because these are the accumulated toxins)
ii. altered calcium uptake
iii. increased neutrophil-derived free radicals

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27
Q

What is hibernation?

A

Chronic hypoperfusion causing contractile dysfunction
BUT
Still reversible with reperfusion
Chronic state of stunning
Occurs with severe CAD impairing resting CBF

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28
Q

What is angina?

A

Chest discomfort produced by ischemia
Not known why but thought to be due to
-lactate, bradykinin byproducts on cervicothoracic receptors
Chest tightness radiating to left arm, neck and jaw

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29
Q

What is stable angina?

A

Chronic, transient, demand-related
Reproducible at a greater workload/when your body performs vigorous exercise
Resolves after stressor is removed

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30
Q

What is unstable angina?

A 
Defined as
1. new onset angina
2. angina occurring shortly after MI
3. angina increasing in frequency, duration or severity
4. angina occurring at lower workload
5. angina at rest
EMERGENT
Supply related
31
Q

What is variant or Printzmetal’s angina?

A

When vasospasm causes abrupt reduction to myocardial blood flow
Occurs in the morning and at rest (conditions when perfusion should be normal)

32
Q

What is silent angina?

A

Increased in transplant, diabetes

Detected with ECG and stress test

33
Q

How is ischemia diagnosed?

A

When there is angina an consistent changes in ST and T waves for a patient (downward ST segment)

34
Q

What are the symptoms of myocardial ischemia?

A

Angina

Dyspnea

35
Q

What are the signs of myocardial ischemia?

A

Diaphoresis (sweaty)

CHF

36
Q

What are the lab tests for myocardial ischemia?

A
  1. ECG
  2. Echo
  3. Cath
  4. Stress testing
37
Q

What is the significance of the ST segment in diagnosing myocard ischemia?

A

ST segment reflects period of relative inactivity between systole and repolarization
Ischemic cells have decreased resting membrane potential with current flowing from normal myocardium into ischemic zone
Results in ST segment DEPRESSION in leads opposite the area of ischemia
ST elevation is seen in myocardial infarction rather htan ischemia

38
Q

What are the principles to treating myocardial ischemia?

A
  1. Reduce demand

2. Improve supply

39
Q

How do you reduce myocardial demand?

A
  1. nitrates (reduce LVEDP so decrease wall tension, vasodilate coronaries)
  2. Beta blockers (reduce HR, contractility and BP, prolongation of diastole) … firstline treatment for ischemia
  3. Ca channel blockers (reduce preload, afterload, HR, BP, contractility)
    Reducing preload = less contractility because of FrankStarling relationship
40
Q

What is the first-line treatment for ischemia?

A

Beta-blockers
Lowering contractility = less demand
Lowering HR = more diastolic filling = more CBF

41
Q

How do you reduce demand in the heart?

A

Calcium channel blockers (verapamil, diltiazem)
Beta-blockers
Nitrates
All three reduce contractility
Nitrates reduce contractility because it reduces LVEDP or preload

42
Q

How do you improve supply in heart (opening up the lumen)?

A
  1. anti-platelet agents like aspirin or clopidogrel
  2. anti-coagulants like heparin
  3. Percutaneous coronary intervention (PCI)
  4. Stent implantation (bare-metal or drug0eluting)
  5. coronary artery bypass graft surgery (CABG)
43
Q

What are the consequences of plaque rupture?

A
  1. unstable angina
  2. MI
  3. ischemic stroke
44
Q

What is the MoA of heparin?

A 
Binds to antithrombin III (AT)
AT then inactivates thrombin 
And factor Xa
Also binds thrombin into a
Complex that inactivates the mofo
Effect is SIZE dependent
45
Q

What is the pathophysiology of MI?

A

Often proceeded by unstable angina (aka acute coronary syndrome)
Plaque rupture due to macrophage derived metalloproteinases degrading the fibrous cap

46
Q

What is the role of metalloproteinases to plaque rupture?

A

Degrades the fibrous cap

Released by foam cells (according to notes pg 10)

47
Q

Can MI occur in absence of atherosclerosis?

A

Yes 10% of time

Can be due to coronary embolism, severe vasospasm trauma or extreme increases in myocardial O2 demand

48
Q

How many patients progress to MI with unstable angina?

A

10%

49
Q

What is acute coronary syndrome?

A

An umbrella term that refers to situations where blood supplied to the heart is suddenly blocked
Examples: unstable angina and MI

50
Q

What is MI?

A

Irreversible heart muscle necrosis resulting from prolonged ischemia

51
Q

What are the factors that affect the extent of MI damage?

A

Location of plaque
Size of vasc bed
Collaterals, local tissue factors
Time occlusion/reperfusion

52
Q

How do you diagnose MI?

A
  1. Angina
  2. diaphoresis
  3. dyspnea
    ECG abnormalities (ST elevation, loss of R wave and new Q wave)
    Elevation in myocardial proteins such as:
    i. creatine kinase
    ii. CK-M
    iii. myoglobin
    iv. troponin T and I
53
Q

What are enzymes that indicate MI?

A
  1. CK
  2. CK-M
  3. myoglobin
  4. Troponin T and I
54
Q

What is the significance of creatine kinase in blood?

A

Shows patient just had MI

55
Q

What is the difference between myocardia ischemia and myocardial infarction presentation?

A

Ischemia = ST depression
Infarction = ST elevation
-current is flowing out of the infarct

56
Q

What are the ECG changes of MI?

A

ST elevation

57
Q

What are the arrhythmic complications of MI?

A
  1. sinus tachycardia (due to pain, anxiety or shock)
  2. sinus bradycardia (when there is RCA involvement)
    • brady due to vagal efferents near RCA
  3. atrial flutter and fibrillation
  4. isolated ventricular premature beats
  5. conduction block (all the types of bundle branch block lol)
58
Q

What are the LV dysfunction complications of MI?

A

Acute diastolic dysfunction which leads to pulmonary edema
Systolic dysfunction (systemic hypoperfusion)
-extensive myonecrosis can cause shock, positive feedback loop with lower BP and then Lower CBF which then leads to more myonecrosis, etc.
Pericarditis due to transmural infarct or immulogic response (Dressler’s syndrome)
Ventricular free wall rupture
Ventricular septum rupture (VSD)
Rupture of papillary muscle

59
Q

What is oliguria?

A

Low output of urine

Aka hypouresis

60
Q

What is the relationship of pericarditis and MI?

A

Can occur in 25% of patients following MI
Commonly follow anterior infarcts and majority are reabsorbed spontaneous
Friction rubs are heard 48 hours since infarction

61
Q

What is Dressler’s syndrome?

A

An immunologic cause of post-infarction pericarditis
Manifest as a localized fibrinous pericarditis
Occurs 2-10 weeks psot MI
Distinct from early pericarditis without immunologic cause
Treated with corticosteroids and aspirin

62
Q

What are the mechanical complications of MI?

A
  1. VSD (due to anterior MI)
  2. free wall rupture (anterior/inferior MI)
    -highest mortality >95%
  3. papillary muscle rupture (inferior MI)
    -you see a V wave
    May be predisposed by use of NSAIDs and corticosteroids
63
Q

What are the characteristics of free wall rupture?

A

Occurs in elderly female or hypertensive patients
Transmural infarction in LAD is risk factor
Site is usually border between normal and infarcted myocardium
Causes hemopericardium and tamponade
May form a pseudoaneurysm if rupture is subacute

64
Q

What are the characteristics of VSD?

A

Less catastrophic than free wall rupture
Can result in a serpiginous tract
Murmur is heard

65
Q

What is a serpiginous tract?

A

A descriptive term for a twisted, vermiform radiolumency surrounded by a sclerotic rim, seen in bones or infarction
Accompanied by intramedullary calcification

66
Q

What are the characteristics of papillary muscle rupture?

A

Results in acute MR
Occurs in relatively small infarcts (compared to the other mechanical failures from bigger infarcts)
Murmur is heard

67
Q

How do aneurysms form in heart after MI?

A

These are areas that are dyskinetic (because already infarcted)
Started to bulge out due to pressure increase
But cannot prevent bulge because there is not contractile function!
Other areas of muscle are hyperkinetic, which push more pressure to that area of dyskinesis

68
Q

What are the key characteristics of LV remodeling?

A

Structural alterations during healing
-consists of expansion in infarcted region due to loss of myocytes and aneurysm
-expansion of infarcted region can lead to aneurysm
-compensatory dilation/hypertrophy elsewhere
LV hypertrophy is inadequate which leads to progressive dilation, wall stress elevation, CHF and ultimately sudden death lol
ACE inhibitors favorably alter the remodeling process

69
Q

What is the treatment of MI?

A

PCI or stent
Fibrinolysis
aspirin
Beta blockers to reduce infarct size (reducing demand)
Oxygen and morphine
Same shit, reduce demand and increase supply (as before)
Streptokinase

70
Q

What does streptokinase do?

A

Lyses clots by converting plasminogen to plasmin, something that lyses thrombin in clots

71
Q

What is used to treat POST MI patient?

A
  1. aspirin, clopidogrel and warfarin
  2. beta-blockers (decrease demand)
  3. ACE inhibitors and implantable cardioverter defibrillator
  4. statins
  5. smoking cessation
  6. nutrition counseling
  7. exercise
  8. control of HTN and diabetes
72
Q

What are the 4 thrombolytic agents approved for MI use?

A
  1. anisoylated plasminogen streptokinase activator complex (APSAC)
  2. recombinant tissue-type plasminogen activater (tPA and rPA)
  3. streptrokinase
  4. aspirin
73
Q

What is PTCA?

A

Percutaneous transluminal coronary angioplasty

Cardio Week 4 (12 decks)

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