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PathoPhys > Tutorial 6 - Cardiac & case studies > Flashcards

Tutorial 6 - Cardiac & case studies Flashcards

1
Q

State some confirmed risk factors for the development of coronary artery disease (CAD)?

A
  1. Hypercholesterolemia (especially LDL)

2. Hypertension (especially systolic BP)

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2
Q

State some significant, but indirect risk factors for CAD?

A
  1. Lack of exercise
  2. alcohol
  3. stress
  4. diet - high sat fats, low antioxidants
  5. obesity
  6. age - men over 60, women over 65
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3
Q

Explain how the pathophysiology of coronary circulation can be described as a ‘vicious cycle’

A

Basically - Ischemia induced contractile dysfunction precipitates hypotension, and therefor, further myocardial ischemia.

Extended way to say it - The heart’s function is to supply blood to systemic circulation, however it’s ability to do so depends upon its own perfusion with blood (and O2) - which is determined by the blood pumped into systemic circulation. It is a paradoxical problem whereby the cause (impeded delivery of blood to the heart) becomes the effect (impeded systemic circulation and thus impeded delivery of blood to the heart). This is a POSITIVE FEEDBACK CYCLE!

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4
Q

Define the term ‘nadir’

A

the lowest or most unsuccessful point in a situation

(not that related just a cool new word haha)

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5
Q

Control of coronary blood flow - explain what occurs during systole, and why.

(hint: think subendocardial and subepicardial layers)

A
  1. subendocardial, intramural vessels become compressed and so blood flow in these areas halts completely
  2. coronary venous outflow from the subendocardial layers peaks, as small intramural vessels collapse and empty their contents
  3. subepicardial blood flow hindered but much less so then subendocardial
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6
Q

Control of coronary blood flow - explain what occurs during diastole, and why.

(hint: think subendocardial and subepicardial layers)

A
  1. coronary arterial inflow (of subendocardial vessels) increases as transmural gradient favors perfusion, vessels open up
  2. blood flow through subepicardial layers increases also, however not as much as subendocardial
  3. coronary venous outflow falls
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7
Q

How is increased oxygen delivery to the heart achieved and why?

A

Must be met by increased blood flow as heart takes extracts 60-80% of O2 from Hb at rest

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8
Q

What’re the major determinants of myocardial oxygen consumption?

A
  1. HR
  2. SV
  3. Left ventricular contractility
  4. systolic pressure (or ‘myocardial wall stress’)
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9
Q

The major determinants of myocardial oxygen consumption are SV, HR, L.V. contractility and systolic pressure. A two fold increase in any of these determinants requires a __% increase in coronary blood flow.

A

50%

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10
Q

State the basal myocardial oxygen requirements needed to maintain critical membrane function.

A

15% of resting O2 consumption (low)

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11
Q

t/f: cost of electrical activation is trivial when
mechanical contraction ceases during diastolic arrest and diminishes during
ischemia.

A

true

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12
Q

define coronary autoregulation

A

the capacity of the heart to maintain steady myocardial perfusion across a range of perfusion pressures

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13
Q

Coronary autoregulation - what occurs when pressure falls to the lower limit? What is the lower/ upper limit for coronary autoregulation?

A

Coronary resistance arteries maximally dilate and flow becomes pressure dependent - end result is onset of sub-endocardial ischemia

MAP of 70-150 mmHg are tolerance limits

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14
Q

Resting coronary blood flow under normal
hemodynamic conditions averages __ to
__ mL/min

A

0.7-1.0 ml/ min

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15
Q

By how much may coronary blood flow increase due to vasodilation

A

4-5 fold

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16
Q

The ability to increase flow above resting values in

response to pharmacologic vasodilation is termed what?

A

Coronary flow reserve

(It’s not really ‘in response to vasodilation’, vasodilation is how it’s achieved, mauro just worded like that bc he is super clever)

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17
Q

When are maximal perfusion of heart and coronary flow reserve reduced?

A
  1. Tachycardia - when the diastolic time available for subendocardial perfusion is decreased
  2. Preload increase - compressive determinants of diastolic perfusion increased
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18
Q

Define coronary flow reserve (real definition, not Mauro’s shitty one)

A

maximum increase in blood flow through coronaries above resting volume; achieved by vasodilation

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19
Q

Other then tachycardia and preload increase, what else may reduce coronary flow reserve?

A

Anything increasing resting flow…

  1. increases in hemodynamic determinants of O2 consumption - systolic pressure, HR, contractility
  2. reductions in arterial O2 supply - anemia, hypoxia
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20
Q

Subendocardial flow occurs primarily in ____ and begins to decrease below a mean coronary pressure of __ mm Hg.

A

diastole; 40mmHg

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21
Q

Sub-epicardial flow occurs ________ and is maintained until coronary pressure falls below __ mm Hg.

A

throughout the cardiac cycle; 25mmHg

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22
Q

t/f: Epicardial conduit arteries contribute significantly to coronary vascular resistance.

A

false

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23
Q

The net effect of many agonists on coronary arteries is critically dependent upon what?

A

whether or not a functional endothelium is present

24
Q

What is the most common endothelium-dependent relaxing factor for the dilation of coronaries?

A

nitric oxide

so drug, ie. ACh –> effects NO in wall –> dilation

25
Q

ACh:

a. ) Vasodilation or constriction?
b. ) Mode of action on coronaries?

A

a. ) dilation
b. )
1. ACh release induces…
2. release of NO
3. NO binds to guanylyl cyclase
4. increased cyclic guanosine monophosphate (cGMP)
5. reduction in intracellular Ca+2 thus SM relax

26
Q

resistance arteries are?

A

arterioles; small diameter BV’s

27
Q

resistance arteries are?

A

arterioles; small diameter BV’s

28
Q

When the endothelium of a coronary artery is removed (due to damage), how does ACh effect this vessel?

A

Instead of dilating it causes vasoconstriction (due to muscarinic receptor)

29
Q

t/f: shear stress and paracrine mediators effect on resistance vessels vary with the size of resistance vessel

A

true

30
Q

t/f: NO is an endothelium derived constricting factor

A

false - dilating

31
Q

NO:

a. ) What cells produce it?
b. ) How is it produced - what enzyme?
c. ) Where does it move once it’s produced?
d. ) Why does it cause SM to relax?

A

a. ) endothelial cells produce it
b. ) type III NO synthase (NOS)
c. ) diffuses abluminally (other side BV wall, away from lumen) into vascular smooth muscle
d. ) increased cGMP thus decreased Ca+2 relaxes SM

32
Q

How is NO mediated vasodilation affected by cyclic or pulsatile changes in coronary shear stress?

A

Changes in coronary shear stress enhance NO mediated vasodilation - chronic upregulation of NOS occurs in response to increased coronary flow, such as during exercise

33
Q

How is NO mediated vasodilation affected by CAD?

A

CAD and risk factors associated impair NO mediated vasodilation of coronary vessels

34
Q

CAD and risk factors associated impair NO mediated vasodilation of coronary vessels - how?

A
  1. CAD/ other things cause oxidative stress
  2. oxidative stress produces superoxide anion
  3. superoxide anion inactivates NO
35
Q

Other then NO mediated vasodilation, state another endothelium-dependent mechanism for dilation of BV’s?

A

Endothelium dependent hyperpolarisation factor

36
Q

What may stimulate EDHF?

A
  1. selected agonists (ie. bradykinin)

2. shear stress-induced

37
Q

EDHF:

a. ) What’s it stand for?
b. ) What does it do?
c. ) Where is it produced?
d. ) How does it bring about it’s action - mechanism?

A

a. ) Endothelium-dependent hyperpolarising factor
b. ) Hyperpolarizes vascular SM causing dilation
c. ) Endothelium
d. ) Opens Ca+2 dependent K+ channels (KCa)

38
Q

State the “hallmark of impaired NO-mediated vasodilation in atherosclerosis, hypertension and diabetes”.

A

superoxide anion (produced due to oxidative stress) inactivates NO, thus impairing ability of BV’s to dilate

39
Q

Exact biochemical species for EDHF - what chemical causes it?

A

Unclear, maybe..

  1. endothelium derived hydrogen peroxide
  2. epoxyeicosatrienoic acid
40
Q

Prostacyclin effect on coronaries?

A

vasodilator

41
Q

Prostaglandins effect on coronaries?

A

vasodilator

42
Q

By how much must a coronary vessel undergo stenosis until symptoms are felt?

A 
50-60% = may be 
80-90% = definitely
43
Q

Describe coronary perfusion following total coronary artery occlusion.

A

Residual perfusion still occurs due to native coronary collateral channels - these open due to development of an inter-coronary pressure gradient (between source and recipient vessel)

44
Q

in most animal species, native collateral flow through coronaries:

a. ) Is what % of resting flow?
b. ) Is able to maintain tissue for what max time?

A

a. ) 10%

b. ) 20 mins max, probs less

45
Q

t/f: Little variation is seen in the function of coronary collaterals amongst patients with chronic stenosis

A

false - it is trememdous how much coronary collateral function varies!
In some, coronary pressure falls below 10mmHg. In others (with hella good coronary collaterals), normal resting perfusion is maintained and stress-induced ischemia is prevented

46
Q

Irreversible myocardial injury begins after ___ minutes of coronary occlusion in the absence of significant collaterals

A

15-20

47
Q

Coronary occlusion causes irreversible injury to myocardium, after 15-20 minutes.

a. ) Where does this begin? Where does it progress toward?
b. ) Why does it occur this way?
c. ) How long does it take for this transmural progression?
d. ) What may accelerate this?

A

a. ) begins sub-endocardial progress to sub-epicardial
b. ) this is reflection of…
1. higher O2 consumption in sub-endocardium
2. redistribution of blood to sub-epicardial layers (due to compressive determinants - it’s harder to get blood into sub-endocardium)
c. ) 4-6 hours
d. ) Increased myocardial O2 consumption (tachycardia), decreased O2 delivery (anemia, hypotension)

48
Q

Coronary occlusion causes irreversible injury to myocardium - what may occur before this stage, to reduce this irreversible injury?

(hint: counter-intuitive one here)

A

Repetitive, reversible ischemia resulting in angina before the full occlusion can actually reduce the permanent damage - as it causes preconditioning of the heart!

(get used to not having O2 bitch!!)

49
Q

What is Echocardiography?

A

a test that uses sound waves to produce live images of your heart - kind of like an ultrasound for your heart!

50
Q

What is left-ventricular remodelling?

A

Surgery to restore natural shape of the heart in those who’ve had a heart attack

51
Q

Studies suggest that failing human cardiac myocytes undergo a number of changes that might lead toa progressive loss of contractile function, including what? (6, get at least 4)

A
  1. decreased alpha-myosin heavy chain gene expression
  2. increase in beta-myosin heavy chain expression,
  3. progressive loss of myofilaments in cardiomyocytes
  4. alterations in cytoskeletal proteins
  5. alterations in excitation-contraction coupling
  6. desensitization of beta-adrenergic signaling
52
Q

a. ) What occurs to the left ventricle (LV) during cardiac remodeling?
b. ) Why does this occur?
c. ) What does this contribute to?

A

a/b/c.) LV dilates due to changed biology of cardiomyocytes, contributing to heart failure

53
Q

With regard to LV heart remodeling - how does it change the morphology of the heart? is this a good or bad thing?

A

LV becomes larger and more spherical, bad thing as contributes to heart failure

54
Q

State some mechanical disadvantages due to LV remodelling?

A
  1. increased ‘meridional’ wall stress (afterload)
  2. increased O2 use - energetic burden
  3. worsening of hemodynamic overloading
    etc.

(basically fucks up the matching of heart structure to function, contributing to heart failure)

55
Q

The LV becomes more large and spherical due to LV remodeling.

a. ) What was it’s original shape?
b. ) What is the consequence of this change?

A

a. ) prolate ellipse

b. ) energetic burden for failing heart - exasperates underlying problems it was there to fix

PathoPhys (25 decks)

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