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Cardiology M2 > 11 11 2014 Ischemic Heart disease > Flashcards

11 11 2014 Ischemic Heart disease Flashcards

1
Q

List the major determinants of myocardial oxygen supply

A

Oxygen requirements of the myocardium are continuously matched by coronary artery supply.

Coronary Blood flow:

  • 02 content
  • coronary perfusion pressure
  • coronary vascular resistance
  • external compression
  • intrinsic regulaion
  • local metabolites
  • endothelial factors
  • neural innervation
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2
Q

Oxygen content of blood depends on what?

A
  1. amount of hemoglobin
  2. degree of systemic oxygenation
  • anemia, lung disease
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3
Q

Coronary perfusion pressure’s role in oxygen supply

A
  • predominane of coronary perfusion takes place during diastole

Coronary perfusion pressure is approximated by the aortic diastolic pressure.

Q (flow) = P/R

Things that decrease aortic diastolic pressure ( hypotension, aortic valve regurgitation) decrease coronary artery percussion pressure = lessen myocardial oxygen supply.

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4
Q

Coronary vascular resistance is governed by what two things?

A
  1. compression of coronary arteries (external)

2. Factors that alter intrinsic coronary tone.

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5
Q

Why do we need metabolic factors to help with O2 supply?

A

*Because unlike other cells, the heart cannot increase oxygen extraction on demand.

Therefore, any increase in O2 demand must be met by increase in blood flow.

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6
Q

Metabolic factors during hypoxemia

A

hypoxemia because of change in demands of O2.

inhibits oxidative phosphorylation
ADP is now degraded to ADENOSINE

ADENOSINE = vasodilator
* prime metabolic mediator of vascular tone.

Other vasodilators:
Lactate
Acetate
Hydrogen ions
Carbon Dioxide
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7
Q

Adenosine

A

vasodilator
Binds to recptors on vascular smooth muscle and decreases calcium entry into cells
= relaxation, vasodilation,

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8
Q

What are the determinants for myocardial oxygen demand?

A

HR
Wall Tension
Contractility

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9
Q

Name the endothelial derived factors that contribute to regulation of coronary artery tone:

A

Endothelium cells of the atrial wall produce vasoactive substances:

Endothelium- derived NO
Prostacyclin
EDHF
Endothelin 1

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10
Q

Endothelium derived NO

  1. mechanism
  2. main role
  3. increase release by what?
A

Diffuses into and relaxes neighboring arterial smooth muscle via a cGMP mechanism.

Vasodilator

Release is enhanced when exposed to ACh, thrombin, products of aggregated platelets, or even shed stress of blood flow.

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11
Q

Prostacyclin

  1. overall function?
  2. how does it work/ mechanism?
  3. Where does it come from?
  4. When is it released?
A

Vasodilator
Relaxation via cAMP mechanism

Arachidonic acid metabolite

Released from endothelial cells in response to hypoxia, shear stress, ACh, platelet products (serotonin)

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12
Q

EDHF ( Endothelium-derived hyper-polarizing factor)

  1. overall function?
  2. how does it work/ mechanism?
  3. Where does it work best?
A

Vasodilator
Hyperpolarizes vascular smooth muscle
= relaxation – less firing

  • more important in modulating smaller arteries vs. large conduit arteries
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13
Q

Endothelin 1

  1. overall function?
  2. what triggers release?
A

postent vasoconstrictor

Stimulated by thrombin, Angiotensin II, epinephrine, and shear stress of blood flow.

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14
Q

Normal vs. damaged endothelium secretion of metabolites that regulate coronary artery tone?

A

Normally, NO and Prostacyclin dominate over catecholamines! at arteriole vascular smooth muscle.

In endothelium injury – dysfunctional endothelium secretes reduced amounts of vasodilators
- balance switches to vasoconstriction

  1. inappropriate vsoconstriction
  2. loss of normal antithrombotic properties (due to impaired NO and prostacyclin )
    - allows platelets to aggregate and secrete pro-coagulants and vasoconstrictors
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15
Q

Fixed vessel narrowing and hemodynamic significance of coronary artery narrowing:

  1. two main points
  2. plaque >70%
  3. plaque >90%
A

Atherosclerotic plaque in coronary artery
* length and degree of vessel narrowing

  1. amount of stenosis ( atherosclerotic plaque)
  2. amount of compensatory vasodilation the distal resistance vessels are able to achieve.

If plaque is >70% occlude – full dilation of resistance vessels (distal) is not enough to cover oxygen demand upon exertion = ischemia
* resting blood flow is normal.

if plaque is >90% ischemic can occur while at rest

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16
Q

Stunned myocardium

A

prolonged systolic dysfunction even after return of normal myocardial blood flow.

Reversible and contractile function gradually recovers

17
Q

Hibernating myocardium

A

Chronic ventricular dysfunction due to persistently reduced blood supply (usually because of CAD)

Ventricular function can promptly improve if appropriate blood flow is restored

18
Q

Stable angina

A

Chest discomfort during exertion or emotional stress

Fixed obstructive atheromatous plaque in one or more coronary arteries.

Atherosclerotic plaque causes endothelial dysfunction which can cause vasoconstriction instead of vasodilation

19
Q

Unstable Angina

A

Symptoms can be experienced at lesser degrees of exertion and even at rest

Precursor to an acute MI

-disruption of plaque triggers platelet aggregation = thrombus formation

20
Q

Variant Angina

A

Intense vasospasms in the absence of atherosclerotic lesions.

Often occurs at rest because ischemia in this case results from transient reduction of coronary oxygen supply vs. increase in myocardial oxygen demand.

21
Q

Silent Ischemia

A

Episodes of cardiac ischemia that occur in absence of perceptible discomfort or pain

Can happen in people who have experienced Angina before or it can be the only manifestation of CAD.

detected via laboratory techniques or electrocardiography

22
Q

Syndrome X

A

symptoms of angina pectoris who have no evidence of significant atherosclerotic coronary stenoses on coronary angiograms.

May show definite laboratory signs of ischemia during exercise testing.

Inadequate vasodilator reserve – resistance vessels (which don’t appear on coronary angiography) may not dilate appropriately during periods of increased myocardial oxygen demand

23
Q

Symptoms of MI

  1. location/ radiation
  2. longevity of symptoms
  3. what brings symptoms one and what relieves them?
  4. ECG
A

retrosternal tightness or pressure; typically radiates to neck, jaw, or left shoulder and arm.

Lasts a few minutes ( usually < 10 minutes)

Brought on by exertions, relived by rest or nitroglycerin

Transient ST depressions or elevations, flattened or inverted T-waves

24
Q

Electrocardiogram

A

Most useful tool!! obtain during an anginal episode

ST segment elevations = transmural myocardial ischemia
- can be seen during intense vasospasm as well.

T-wave flattened or inversions

ST and T wave deviations are seen

25
Q

Stress test

  1. what are the two types
  2. brief description
A
  1. Exercise
    heart rate and ECG are continuously monitored as patient is doing test (exercise)

(+) if patient get typical chest discomfort OR if ECG abnormalities are consistent with ischemia ( ST segment depressions)

  1. Pharmacological
    inotrope : dobutamine or
    vasodilator: dipyridamole or adenosine.

Drug induced vsodilation increases blood flow to myocardium and steals blood aaa form diseased segments (because those segments were already dilated)
- Coupled with nuclear imaging, echocardiography

26
Q

The effect of ISCHEMIA to:

  1. Systolic function
  2. Distolic compliance
  3. Papillary muscle
  4. Sympathetic tone
A
    1. (decreased) = pulmonary congestion
      = Kyskinetic apical impulse and rales
  2. decrease in diastoli compliance = S4 sound
  3. papillary muscle dysfunction = mitral valve regurgitation
  4. Increase in sympathetic tone = Diaphoresis, increase HR, and High blood pressure

Cardiology M2 (25 decks)

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