[356] Physiology - Coronary Physiology Flashcards

1
Q

LV is perfused during systole or diastole? How does exercise affect this perfusion (Hint: recall exercise effect on diastole)?** In which ventricle do we see a bigger difference in pressure between systole and diastole? Why?**

A

Systolic or Extravascular compression: Phasic Coronary Blood Flow
* LV is perfused during diastole
* During exercise
-Duration of systole decreases
-Duration of diastole decreases (more than systole)
-Can risk less perfusion to heart (because diastole
is shortened)
* RV contracts much less, so the right coronary artery is not compressed as much during systole (blood is not stopped from going in as much) so we dont actually see much of a difference between systolic & diastolic BP in RV

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2
Q

3 organs with autoregulation?

A

(Flow) Autoregulation:
* heart
* brain
* kidney
*

These organs bring flow back to normal if there is a sudden change in bl

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3
Q

If you decrease perfusion pressure, what does autoregulation reflex do to coronary blood flow?

A

Immediate and Steady -State Effects:
* Decreasing perfusion pressure: reflex increase in coronary flow
* Opposite when perfusion pressure increased

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4
Q

Explain what is sensed when metabolic//myogenic control increases blood flow (what triggers flow increase)?

A

Two Mechanisms or Components of Autoregulation:
1. Metabolic control of blood flow
-Dec. arterial pressure in organ → low blood flow to organ → decrease O2, increase waste products in organ → arteriolar dilation in organ → restoration of blood flow to normal
2. Myogenic control of blood flow
-Dec. arterial pressure in organ → low blood flow to organ → decreased wall stretch sensed by organ → arteriolar dilation in organ → restoration of blood flow to normal

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5
Q

What is the Bayliss effect?

A

Myogenic Mechanism of Autoregulation -Sir William Maddock Bayliss:
* Experiment:
-If both columns of water are 50cm tall, pressure in the whole tube is 50 cm H20
-What happens if we raise both water columns to 60 cm H20?
-No flow
-In an arteriole: Arteriolar constriction: Called the Bayliss effect

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6
Q

Is Bayliss effect dependant on state of endothelium? Is the Bayliss effect an example of metabolic or myogenic control of autoregulation?

A

Bayliss Effect (1902):
* The bayliss effect underlies the myogenic component of autoregulation
-If transmural pressure through an arteriole/artery increases, the artery vasoconstricts
* The bayliss effect is endothelium-independent
-Regardless of whether endothelium is present or disrupted, the Bayliss effect occurs

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7
Q

What do we owe the decrease in heart disease to (what changed)? What is the leading cause of death in men//women?

A

Mortality (male, U.S.A.):
* 50% decrease in heart-disease death rate due to decrease in smoking
* Heart disease is still leading cause of death

Mortality (female, U.S.A.)
* Cancers are more deadly than heart disease in women

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8
Q

What is meant by endothelial dysfunction?

A

Endothelial dysfunction:
* A systemic pathological state of the endothelium
* Can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium
* Risk factors :
-Age
-Family history
-Smoking
-Diabetes
-Obesity
-Hypercholesteremia
-Hypertension
* On average male smokers die 13.2 years earlier than male non-smokers and female smokers die 14.5 years earlier than female non-smokers

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9
Q

2 vasoactive substances produced by EnCs? Which vasodilates//vasoconstricts? **4 functions of NO? **

A

The vascular endothelium makes many vasoactive factors
* EnCs produce different substances
-NO causes relaxation of SM
-Endothelin causes constriction of SM
* NO is vasoactive, atheroprotective, antithrombotic & antiproliferative
1.Reduce Ca concentration in cell →Vasodilation
2.Protects from atherosclerosis
3.Prevents clotting
4. Prevents SM cells from multiplying & migrating into the lumen and ending up in the plaque

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10
Q

What happens to Bayliss effect//flow if PerfP on both sides of an arteriole are changed in opposition (+10 on one side, -10 on other)? Bayliss effect engages when pressure changes?

A

Experiment
* If you bring one side up by 10 and one side down by 10 cmH20:
- No Bayliss effect: Perfusion pressure increases but overall pressure across the vessel (transmural pressure) is the same (50+50 → 60+40)

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11
Q

How does increased flow affect diameter of a vessel? Is this positive of negative feedback? What happens to PP//R if flow is increased then?

A

Flow induced (vaso)dilation, Flow mediated (vaso)dilation, positive feedback!
* Increase flow causes dilation of the vessel (positive feedback effect)
- R decreases
- Perfusion pressure increases

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12
Q

**Explain both mechanisms of NO-induced vasodilation? **What enzyme catalyses NO formation? **What amino acid is NO produced from? **

A

Two mechanisms controlling NO release
1. Flow induced dilation
- Increased flow activates eNOS
- eNOS, and other enzymes → catalyse L-arginine turning to NO
* NO then diffuses across the space and affects SM
* NO is produced and released by EnCs

  1. Receptor mediated dilation (below)
    - ACh receptor (“M”) stimulation on EnCs activates eNOS
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13
Q

What happens if increasing concentrations of ACh is applied to endothelium of a vessel when endothelium is intact//not intact?

A

Receptor mediated vasodilation
* ACh binds to a receptor on endothelial cells, causing synthesis and release of NO (as do many other vasodilators: e.g., bradykinin and histamine)
- Receptor mediated dilation is endothelium dependant

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14
Q

Flow equation (Flow = *)? Vasodilation causes increase or decrease in velocity of blood flow?

A

ACh infusion: diagnostic test to assess NO system
* Injecting increasing amounts of ACh into coronary arteries → More NO synthesized & released → more vasodilation → increasing flow
* Flow equations
-flow=vA (v = velocity)
-flow=𝚫P/8vL/𝛑A2
-(v = viscosity; v = velocity)
-v∝A → dilation will result in increase in flow velocity

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15
Q

Endothelial dysfunction is a precursor for what disease?

A

The vascular endothelium makes makes many vasoactive factors
* Endothelial dysfunction is a precursor for atherosclerosis

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16
Q

ACh effect on vascular smooth muscle? What would happen therefore if EnC was scraped away and ACh was applied to the vessel? Why?

A

Furchgott’s Discovery of EDRF
* ACh has a direct vasoconstrictor effect on vascular smooth muscle
-So you get constriction on SM cells
-If you scrape away Endothelium, infusing ACh would cause vasoconstriction because the EnCs are not there to receive ACh and produce NO, instead the SM ACh-Rs constrict.

17
Q

O2 content of arterial blood (ml O2/L blood)? **Heart muscle O2 consumption//blood flow//arteriovenous O2 difference compared to other organs? **What is the only other organ that receives comparable blood flow to heart?

A

Fick Principle
* O2 content of arterial blood = 200 mL O2/L blood
* Heart muscle O2 consumption: 9.7 ml/(100g tissue * minute)
-Most of any organ
* Heart muscle blood flow: 84 ml/(100g tissue * minute)
-Kidney is only organ that receives this much flow
-Because of the filtering of blood done by the kidney that it receives this much flow
* Arteriovenous O2 difference: 114 ml O2/L blood
-Heart extracts most O2 out of passing blood in comparison to other organs.

18
Q

Coronary O2 consumption equation? Can heart extract much more O2 from blood than it already does? If you want to increase myocardial work, what must be changed then?

A

Myocardial oxygen consumption and coronary blood flow
* Equation: Myocardial O2 consumption = coronary blood flow x arterio-venous O2 difference
* If you want to increase work of heart, only way to do this is to supply more blood to heart
-Cannot extract any more O2 from blood (see graph on left, as heart consumes more oxygen the venous O2 concentration does not change much; this demonstrates that heart is extracting as much O2 as it can no matter what)

19
Q

What is coronary flow reserve (CRF)? What is CRF in humans (number)?

A

Coronary flow reserve (CFR)
* CFR= maximum coronary blood flow/resting coronary blood flow ≅ 5

20
Q

4 determinants of O2 need of the heart?

A

Work of the Heart
* E.g. hypertension → heart failure
* Determinants of O2 need of heart:
1. HR increase
2. Afterload increase
3. Preload (EDV) increase
4. Contractility increase
-Increase O2 need of heart

21
Q

Rate pulse pressure formula? RPP use?

A

Rate-Pressure product [RPP]
* Rate-pressure product = heart rate x systolic BP
-RPP is used as an index/idea for myocardial work (taking into account 2 easily measurable determinants of myocardial O2 consumption)