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ACP Study > Ischemic Heart Disease and ACS > Flashcards

Ischemic Heart Disease and ACS Flashcards

1
Q

Differentiate between type 1 and type 2 MI and give 3-5 causes of type 2 MI

A
  • type 1: typical MI caused by atherosclerotic plaque rupture (or erosion) and thrombosis
  • type 2: oxygen supply/demand mismatch MI
    • Coronary embolism
    • Severe coronary artery spasm (spontaneous or cocaine-induced)
    • SCAD
    • Vasculitic syndromes
    • Severely increased mVO2 or reduced global DO2
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2
Q

Which of the following is not a functional alteration of myocardium following MI

  1. arrythmogenesis
  2. stunned myocardium
  3. ischemic preconditioning
  4. ventricular remodelling
  5. impaired contractility/compliance
A

a. arrythmogenesis

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3
Q

Compare and contrast PCI vs CABG for ischemic heart diseas

A

PCI

  • Less invasive with shorter convalescence
  • Superior to medical therapy for uncontrolled angina
  • No benefit to survival / MI risk in stable angina

CABG

  • More invasive, with greater risk and longer convalescence.
  • Better revascularization of critical occlusions
  • Confers a survival advantage in pts. with severe CAD
  • Pts. with Hx of multiple CABG are highly suspected for re-occlusion.
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4
Q

Decribe how papillary muscle rupture in MI may be rapidly fatal

A
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5
Q

Patients who sustain an MI in the context of recent angina are likely to experience more/less morbidity and mortality vs. non-anginal patients

A

LESS!

due to ischemic pre-conditioning.

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6
Q

List and briefly describe the three non-infarction ischemic syndromes

A
  • Stable Angina
    • transient angina associated with exertion that relieves with rest
  • Unstable Angina
    • increase in tempo and duration of angina, with reduced exertion or at rest
  • Variant (prinzmetal) angina
    • Caused by transient, intense coronary casospasm. Usually occurs at rest due to endothelial dysfunction
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7
Q

List 3-5 factors which influence the size of myocardial infarction resulting from coronary occlusion

A
  1. the mass of myocardium supplied by the occluded vessel
  2. the magnitude and duration of flow impairment
  3. the oxygen demand of the affected region
  4. the adequacy of collateral circulation
  5. the degree of tissue response to the ischemic process (less in severely atherosclerotic tissue due to endothelial dysfunction)
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8
Q
A
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9
Q

What is the duration of total coronary occlusion required to cause irreversible myoacardial occlusion?

  1. 30-60s
  2. 2-4min
  3. 6-10min
  4. 20-24min
A

d. 20-24 minutes

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10
Q

What are the two major causes of myocardial ischemia in CAD?

A
  1. Fixed vessel narrowing
    * due to atherosclerotic plaques or thrombi
  2. Endothelial cell dysfunction
    • Inappropriate vasoconstriction
    • Loss of normal antithrombotic properties
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11
Q

The three key components to diagnosis of ACS are:

A
  1. Pt Hx
  2. ECG findings
  3. Cardiac biomarkers (troponin I/T and CK-MB)
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12
Q

Which of the following would not normally be part of a conservative (medical) approach for acute UA/NSTEMI?

  1. clopidogrel
  2. tenecteplase
  3. metoprolol
  4. enoxaparin
A

b. tenecteplase
* tenecteplase is a recombinant tPA. Fibrinolysis is not part of routine management of UA/NSTEMI

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13
Q

First- and second-line therapies for STEMI are:

A

First: Primary PCI

Second: Fibrinolysis (tPA)

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14
Q

List 5 differentials for recurrent chest pain (CVS, GI, or MSK)

A
  • Myocardial ischemia (angina)
  • Pericarditis
  • GERD
  • Peptic ulcers
  • Esophageal spasm
  • Biliary colic
  • Costochondritis
  • Cervical radiculitis
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15
Q

One outcome of ischemic myocardial injury is necrosis (i.e. infarction). List and describe two other direct outcomes of myocardial ischemia (not reperfusion injury)

A
  • Stunned myocardium
    • A region of myocardium that suffers acute ischemia but no necrosis, that exhibits a period of systolic dysfunction followed by spontaneous recovery
  • Hibernating myocardium
    • A region of myocardium that suffers chronic ischemia and persistent systolic dysfunction, but may fully recover with restoration of appropriate blood flow
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16
Q

What are two factors that determine coronary vascular resistance?

A
  • forces that externally compress the arteries (i.e. myocardial contraction during systole)
  • Intrinsic coronary arterial tone
    • Includes metabolic, endothelial, and neural factors
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17
Q

Briefly describe Laplace’s law as it relates to myocardial wall tension and mVO2

A

σ = (P x r) / 2h

  • σ is wall stress, P is intraventricular pressure, r is radius of the ventricle, h is ventricular wall thickness
  • wall stress increases with increasing pressure and ventricular radius (dilated cardiomyopathy) and decreases with increasing wall thickness (myocardial hypertrophy)
  • Increasing wall stress is one of 3 factors in mVO2 (the other two are contractility and HR)
18
Q

Which region of the myocardium is most susceptible to ischemia and why?

A

the subendocardium, because it is more subjected to ventricular systolic pressures (compression of coronary arteries) and blood supply to the subendocardium must pass through several layers of conttracting myocardium.

19
Q

Describe the two common management strategies for UA/NSTEMI

A
  1. Invasive therapy
    • PCI for revascularization, usually attempted when TIMI ≥3
  2. Conservative therapy
    • anti-ischemic treatments (beta-blockers, nitrates, CCBs)
    • antiplatelets (clopidogrel, ticagrelor)
    • anticoagulants (heparins)

fibrinolysis is not standard care for UA/NSTEMI

20
Q

What are the three classes of medication most commonly prescribed for recurrent ischemic episodes (angina)

A
  • Beta-blockers
    • First-line treatment. Reduces myocardial oxygen demand (negative chronotropy and inotropy) and may improve supply (increased diastolic filling time)
  • Organic Nitrates
    • primarily act through reduced preload and wall stress. MAY improve coronary supply (controversial)
  • Calcium Channel blockers
    • Reduced preload and improved supply (coronary dilatation). Third-line treatment if angina not controlled by first two
21
Q

What is the “levine sign”?

A

placing a clenched fist over the chest during periods of ischemic chest pain

22
Q

Which of the following is not part of the spectrum of ACS?

  1. STEMI
  2. NSTEMI
  3. unstable angina
  4. stable angina
A

d. stable angina
* considered a chronic, transient ischemic condition, not an acute coronary syndrome

23
Q

Roughly, what are normal ranges for troponin T and I values

A
  • TnT: <3 is good, 3-14 concerning, >14 diagnostic of MI
  • TnI: <0.8 is good, >0.10 is diagnostic of MI
  • Multiple biomarkers needed to definitely rule out NSTEMI
  • Troponins have best diagnostic value >6 hrs. after onset of symptoms
24
Q

Describe potential outcomes of coronary thrombosis and relate them to the spectrum of ACS

A
  • Partial occlusion with rapid inclusion into plaque or fibrinolysis. No necrosis. Unstable angina
  • Substantial partial occlusion with prolonged or severe downstream ischemia leading to necrosis = NSTEMI
  • Total occlusion with rapid lysis or extensive collateral circulation and necrosis limited to subendocardium = NSTEMI
  • Total occlusion with transmural downstream necrosis = STEMI
25
Q

The most common cause of sudden cardiac death during acute MI is:

  1. Ventricular wall rupture
  2. Acute heart failure
  3. Bradycardic PEA
  4. Ventricular fibrillation
A

d. Ventricular fibrillation

26
Q

What is the purpose of exercise stress testing?

A
  • non-invasive detection of significant coronary artery disease
  • Exercise is performed to a target HR with continuous ECG monitoring. Ischemic ECG changes, paradoxical BP reduction, ventricular arrythmogenesis, or inability to complete the test are indicative of advanced CAD
27
Q

List two factors which influence myocardial oxygen supply and three factors which influence myocardial oxygen demand

A
  • Supply
    • Coronary artery blood oxygen content
    • Coronary blood flow
      • Combination of coronary perfusion pressure and coronary vaascular resistance
  • Demand
    • Wall stress (P x r /2h)
    • Heart rate
    • Contractility
28
Q

Which of the following is not a component of myocardial oxygen demand?

  1. Endothelial cell dysfunction
  2. Radius of the ventricle
  3. Heart rate
  4. Contractility
A

a. Endothelial cell dysfunction

  • This is a cotributor to decreased myocardial oxygen supply, not demand
  • Contributors to mVO2 are:
    • HR
    • Contractility
    • Wall stress, determined by:
      • Intraventricular pressure
      • Ventricular radius
      • Wall thickness
29
Q

What is the most sensitive and specific biomarker for MI?

A

cardiac troponin (cTnI and cTnT)

  • troponins are also found in skeletal muscle, but the cardiac isozymes are unique
  • CK-MB is a creatine kinase specific to cardiac muscle cells and also used in infarction detection.
    • CK-MB testing is neither as sensitive nor as specfic for MI
30
Q

Compare and contrast unstable angina and NSTEMI in terms of thrombus involvment

A
  • both usually involve a partially-occlusive thrombus
  • NSTEMI involves myocyte necrosis (infarction = necrosis) while unstable angina has none.
31
Q

List 4 modifiable risk factors for atherosclerosis

A
  1. dyslipidemia
  2. smoking
  3. hypertension
  4. diabetes
32
Q

Describe the clinical relevance of a TIMI score ≥ 3

A
  • TIMI is a thrombolysis in MI risk stratification score
  • TIMI ≥ 3 is associated with high risk of morbidity/mortality and is the threshold for early invasive revascularization
33
Q

Which is the most common cause of thrombus formation in ACS, plaque rupture or endothelial erosion?

A

plaque rupture

endothelial erosion without plaque rupture is seen as an increasingly important, but not dominant cause of ACS

34
Q

What are the 2 ways in which atherosclerosis contributes to coronary thrombus formation?

A
  1. plaque rupture
    • exposes blood to thrombogenic substances
  2. endothelial dysfunction
    • impairment of normal antithrombotic and vasodilatory mechanisms
35
Q

The major diagnostic distinction between UA and NSTEMI is:

A

absence/presence of cardiac serum biomarkers (troponin and CK-MB)

36
Q

Which of the following is not a standard treatment for recurrent ischemic chest pain (angina)?

  1. Nitroglycerin
  2. Captopril
  3. Metoprolol
  4. Diltiazem
A

b. captopril

captopril is an ACE-inhibitor. Standard medical care for chronic angina consists of:

  1. Beta-blockers (metoprolol)
  2. Nitrates (nitroglycerin)
  3. Calcium-channel blockers (diltiazem)
37
Q

List two cause of myocardial ischemia not related to CAD

A
  1. Decreased perfusion (as in shock)
  2. Decreased blood oxygen content (anemia or respiratory failure)
38
Q

Differentiate between ECG changes seen in stable/unstable angina vs. variant angina vs. infarction

A

Stable/unstable angina

  • ST-depression and T-wave flattening or inversion. Rapid reversal with resolution of symptoms

Variant angina

  • ST-elevation may be present! Rapid reversal with resolution of symptoms

Infarction

  • Dynamic ST-T changes leading to STE and Q-waves which may not resolve for days/weeks or may be permanent
39
Q

Differentiate between myocardial ischemia, injury, infarction, and angina

A
  • Ischemia = insufficient oxygen supply to meet tissue demand (i.e. local hypoxia)
  • Injury = reversible tissue damage and dysfunction secondary to prolonged ischemia
  • Infarction = a region of non-reversible ischemic damage. i.e. necrosis
  • Angina = the uncomfortable sensation felt in the chest of myocardial ischemia
40
Q

Describe the role of nitric oxide in coronary vacular resistance and identify its source in normal cardiac physiology

A
  • NO is released by endothelial cells in response to a number of aggravating factors
  • NO causes cGMP-mediated vasodilation
41
Q

List three endogenous mechanisms of antithrombosis, and relate them to medical treatments for thrombotic disease

A
  • Inactivation of clotting factors
    • analogous to abticoagulant therapy (blood thinners)
    • includes warfarin, heparin, apixaban, dabigatran, etc.
  • Fibrinolysis
    • tPA used both endogenously and therapeutically for fibrinolysis
  • Platelet inhibition / vasodilation
    • Prostacyclin/NO endogenously
    • ASA and clopidogrel therapeutically
42
Q

Describe the role of adenosine in regulation of coronary vascular resistance

A
  • during hypoxia, excess free adenosine is produced from breakdown of ATP
  • Free adenosine binds to receptors on vascular smooth muscle, inhibiting calcium influx
  • Net effect is hypoxia-induced vasodilation

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