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Physio Test 2 > Garman CV5 > Flashcards

Garman CV5 Flashcards

Special Circulation

1
Q

3 Mechanisms of local control of blood flow

A

1) Metabolic regulation
2) Autoregulation
3) Shear stress induced vasodilation

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2
Q

What are metabolic regulation of blood flow?

A

Active hyperemia

Reactive hyperemia

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3
Q

What is active hyperemia?

A

Increased blood flow with increased metabolism

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4
Q

What is reactive hyperemia?

A

Increased blood flow after occlusion. Changes in flow reflect effects of metabolic products

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5
Q

How do arterioles know that the tissues need more blood flow?

A
  • Tissue release metabolic products in proportion to level of metabolism. Substance released include CO2, H, K, adenosine, lactate, prostaglandins
  • These metabolites produce vasodilation at precapillary sphincter, causing more blood to flow to area
  • Thus, increased metabolism results in higher local blood flow

-Low o2 also contributes to metabolic vasodilation

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6
Q

What is myogenic regulation?

A

AKA- Autoregulation of blood flow
- If perfusion pressure into vascular bed such as skeletal muscle, is raised artificially, flow initially rises, but returns to orginal level after a short period

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7
Q

How does autoregulation/myogenic regulation happen?

A

Constrictor of vascular smooth muscle in response to higher transmural pressure (Stretch)

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8
Q

Why is autoregulation/myogenic regulation important?

A

It keeps you from stroking out everytime you get excited.

Keeps local flow relatively constant in face of fluctuating pressure through myogenic regulation

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9
Q

Where is autoregulation effective?

A

60-160 MAP

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10
Q

What leads to the muscle contraction in autoregulation/myogenic regulation?

A

Stretch induced depolarization leads to muscle contraction

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11
Q

What is the relationship between pressure, resistance and flow?

A

Q=P/R
Flow= pressure/resistance

Pressure increaes with constant resistance= increase in flow
Increase pressure with proportional increase resistance= no change in flow

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12
Q

What is shear stress-induced endothelium-dependent vasodilation?

A

Increased blood flow in blood vessel causes greater shear stress (force of blood running across endothelium), this causes endothelium to synthesize NO, which dilates smooth muscle

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13
Q

What is required for shear stress-induced vasoldilation require?

A

Healthy endothelium (theory on why athletes have decreased performance overtime)

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14
Q

What causes precapillary sphincters to close on capillary bed after period of increased blood flow?

A

Metabolites are “washed away” from increased blood flow causing more alkalotic environment. Triggers precapillary sphincters to close

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15
Q

What are 3 energy sources for additional ATP during aerobic exercise?

A
  1. Phosphagen system
  2. Glycogen-lactic acid system
  3. Aerobic system
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16
Q

What does ATP change to?

A

ATP—> ADP—>AMP (goes back and forth between each stage)

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17
Q

What is phosphagen system?

A

Phosphocreatine—> Creatine + PO3 (phosphate)

Creatine kinase converts creatine–> creatine phosphate by adding phosphate group (given off from ATP)

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18
Q

What do we rely on to maintain dynamic exercise?

A

Oxidation of glucose, fatty acids, amino acids (aerobic system)

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19
Q

What is glycogen-lactic acid system?

A

Glycogen–> lactic acid

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20
Q

What is aerobic system?

A

Glucose/FA/AA+ O2–> CO2 + H2O + urea

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21
Q

You are in a ________ when going from rest to steady state of work.

A

O2 deficit

You’re working on anaerobic energy

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22
Q

You are ____ _____ when going from steady state to recovery

A

Repayment of O2 debt

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23
Q

Which organ can do gluconeogenesis?

A

Liver and Kidney

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24
Q

How does HR react to level of work?

A

Increase HR with increase work

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25
Q

How is SV affected by level of work?

A

At small increase in work (0-600 kg/m/min), SV increases, but as HR increases more and more, not enough filling time, so SV falls (around 900 kg/m/min)

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26
Q

How does CO respond to aerobic exercise?

A

Direct increase with work until you become anaerobic.

linear relationship

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27
Q

How is arterial pressure affected by aerobic exercise?

A

Systolic pressure has slight increase. Mean and diastolic around the same (very small increase)

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28
Q

How is peripheral resistance affected by exercise?

A

Resistance decreases as work increases. (indirect)

Reason: we’re recruiting more muscle, more tissue, more capillary, increasing surface area and decreasing resistance

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29
Q

How does oxygen consumption change with exercise?

A

oxygen consumption increases with work (direct)

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30
Q

Which blood flow decreases significantly during aerobic exercise?

A

Splanchnic (GI)
Renal
Endocrine

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31
Q

Which blood flow increases significantly during aerobic exercise?

A 
Coronary
Skeletal Muscle (biggest increase)
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32
Q

Which blood flow stays about the same?

A

Brain, skin (slight increase in skin r/t temperature regulation)

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33
Q

What is biggest factor that affects CO in athlete?

A

Stroke volume is bigger (105mL athlete at rest compared to 75mL for nonathlete)

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34
Q

What gives athlete larger CO than nonathletes?

A

“Physiological hypertrophy” of LV; leads to higher contractility.

Lower resting HR

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35
Q

When is the LV cardiac tissue perfused?

A

During LV diastole.

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36
Q

Why is the RV able to be perfused during systole? (compared to LV?)

A

RV does not generate as much pressure as the LV (25 in RV vs 120+ in LV). This allows perfusion of RV cardiomyocytes to occur during systole and diastole.

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37
Q

What metabolite is important causes vasodilation in cardiomyocytes?

A

Adenosine. The metabolite adenosine builds up in cardiomyocyte during left ventriular systole. The build up of this metabolite causes increased left coronary circulation flow during diastole.

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38
Q

What are thebesian veins?

A

Veins that drain directly into lumen of heart from coronary veins (i.e. LV) and contribute to normal physiologicla shunt (deoxygenated blood return to LV). Deoxygenated blood also returns form bronchial veins and goes into LA.

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39
Q

Which tissue is hardest to perfuse in the heart?

A

Subendocardium

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40
Q

Where is intramyocardial pressure the highest?

A

Subendocardium (inner third myocardium)

41
Q

Extravascular pressure in myocardium ( intramyocardial pressure) _____ LVP during systole.

A

Exceeds

42
Q

Is there a myogenic reflux in the heart?

A

Yes, but not as important as metabolic regulation or effects on extravscular pressure.

43
Q

What results from SNS activation in a normal heart?

A

Metabolic vasodilation of coronary arteries

44
Q

Where do we measure oxygen demand in the heart?

A

During systole

45
Q

Where do we measure oxygen supply in heart?

A

During diastole

46
Q

How does widened PP affect supply/demand on heart

A

Increased systole= increased demand

Decreased diastole= decreased supply

47
Q

What does increased systole pressure do to demand?

A

Increase

48
Q

What does lower diastolic do to supply?

A

Decrease supply

49
Q

How does increased HR affect supply/demand?

A

Decreased supply, increased demand

50
Q

How much blood does brain receive? (% CO)

A

15% CO at rest

51
Q

Why does the brain need so much blood?

A

Brain is least tolerant to organ ischemia. It relies heavily on glucose for metabolism., Death to cells comes within minutes of ischemia

52
Q

Where does brain recieve blood?

A

4 source arteries

  • 2 internal carotids
  • 2 vertebral arteries (branch off of SCL)
53
Q

Cerebral vasculature and CSF compartments housed in _____ cranium with _____ volume

A

Rigid; Fixed

54
Q

Where does the left common carotid come from?

A

Branch of aorta

55
Q

Where does R common carotid artery come from?

A

Branch off of brachiocephalic artery

56
Q

What forms the circle of willis?

A 
Anterior communicating arteries
Anterior cerebral artery
Internal carotid artery
posterior communicating artery
Posterior cerebral artery
57
Q

Is circle of willis present in everyone?

A

No, degeneration starts by 20s

58
Q

What does the circle of willis provide?

A

Collateralization of flow

59
Q

What do the vetebral arteries form?

A

Basiliar artery

60
Q

What gives rise to middle cerebral artery?

A

Left and right common carotid

61
Q

What does basilar artery “give rise” to?

A

L and R posterior cerebral artery

62
Q

What does anterior cerebral artery feed?

A

Medial part of brain

63
Q

What is autoregulatory range for brain?

A

50-150 mmHg

64
Q

What does autoregulation in brain do?

A

Prevent increase in blood flow (and ICP) when blood pressure increases. Maintains adequate blood flow when blood pressure decreases

65
Q

What 2 mechanisms stimulate vasoconstriction or vasodilation?

A

Myogenic and metabolic

66
Q

Does sympathetic nervous system influence cerebral blood flow?

A

No. (although debated)

67
Q

When does cerebral circulation dilate?

A

In response to PaCO2

Very big increase in cerebral blood flow for elevated CO2 (even minor)

68
Q

What does hyperventilation do to cerebral circulation?

A

Decrease CO2, causes vasoconstriction

69
Q

What is response of cerebral circulation to low O2?

A

No significant response to CBF until very low O2 (around 50)

70
Q

What is CNS ischemic reflex?

A

If vasomotor center in medulla becomes ischemic, strong sympathetic outflow on heart afters to increase arterial BP ABOVE autoregulatory range for CBF, thus increasing blood flow in “last ditch” effort to save brain

This reflex is not significantly innervated by sympathetic nerves

71
Q

What is cushing reflex?

A

Increase in intracranial pressure (seen in TBI) may impede CBF. This causes sympathetic outflow which will raise arterial pressure in an attempt to overcome the high ICP that is impeding flow. Also a last ditch effor to preserve cerebral perfusion. High arterial pressure is accompanied by bradycardia because of activation of baroreceptors.

72
Q

What are quickest blood pressure regulators?

A

Baroreceptors

73
Q

What is relative feedback gain for the CNS ischemic response to sudden change in BP?

A

Takes longer than baroreceptors, but is a HUGE response

This is why patients with stroke have a VERY high BP

74
Q

What is stress relaxation response to change in blood pressure?

A

Opposite of myogenic reflux.

Smooth muscles in vessels will slowly start to relax overtime.

75
Q

What is capillary fluid shift’s role in response to change in blood pressure?

A

With decrease in BP– Fluid shift interstitial-> intervascular

With increase in BP– Fluid shift intervascular—> interstitial

76
Q

What percent of CO does pulmonary circulation receive?

A

100% CO from RV

77
Q

What percent blood volume is in lungs?

A

10%

78
Q

What is normal physiologic splitting?

A

Aortic valve closes slightly faster than pulmonic valve

79
Q

Why does normal physiologic splitting happen?

A

Since the pressure is higher in aortic system, it closes first
The pressure in pulmonic circulation is slightly lower, so there’s a lag in closer of pulmonic vein

80
Q

When do you hear physiologic splitting? Why?

A

During inspiration.
Since pulmonic pressure is even LOWER during inhalation (d/t negative pressure breathing) the valve will close even slower during inhalation.

81
Q

Why do you not hear splitting as pronounced during exhalation?

A

Pulmonic pressure is increased, reducing delay in pulmonic closure

82
Q

How are capillaries arranged around alveoli?

A

“Sheet” blood flow around alveoli through alveolar vessels.
This provides efficient gas exchange
-Extra-alveolar vessels are also thin-walled (as are alveoli)

83
Q

What happens to capillaries when alveolar size increases in lungs?

A

Capillaries get squished, decrease blood flow

84
Q

What is effect of pulmonary artery pressure on pulmonary vascular resistance?

A

As PA pressure goes up (more blood in capillaries), PVR decreases. (There’s nothing around the pulmonary capillaries except air, unlike other areas of body. Increase amount of flow, size of capillary will increase)

85
Q

What happens to capillaries/alveoli under normal physiologic, negative pressure breathing

A

Alveoli expand, pulling apart capillaries

86
Q

What happens to PVR while intubated?

A

Increases. Positive pressure increases vascular resistance

87
Q

______ and _______ of vessels accounts for reduction in PVR with elevation of PA pressure.

A

Recruitment; Distention

88
Q

What does the body do when lung tissue is not getting oxygen?

A

Body does not send blood to any part of the lung that is not being ventilated.

89
Q

What is the long term compensation for low O2 atmosphere?

A

Polycythemia

90
Q

What causes mountain sickness?

A

Shunting of blood away from lungs d/t low O2

-high altitude pulmonary edema is pathological response to low po2 atmosphere

91
Q

What is pathway of fetal circulation?

A
  • Blood away from baby on umbilical artery, back to mom
  • Blood comes in from mom on umbilical vein
  • Umbilical vein goes to liver via ductus venosus (shunt between umbilical vein and IVC)
92
Q

What is the foramen ovale?

A

“Right to left” shunt that allows blood from IVC to flow into LA, bypassing RV and pulmonary circulation

93
Q

What is the ductus arteriosus?

A

Right to left shunt b/w pulmonary artery and aorta

94
Q

Why is blood sent to lungs in fetal circulation?

A

To allow growth of lung tissue.

95
Q

What happens to fetal circulation at birth?

A

At birth pressure in R system decreases, L pressure increases. This causes foramen ovale “flap” to close.
-For the ductus arteriosus, it becomes ligamentum arteriosum

96
Q

Which closes permanently, quickest after birth?

A

Ductus venosus (almost 100% closure by 3 months)

97
Q

What % foramen ovale permanently closed by 15 years?

A

60%

98
Q

What % ductus arteriosus close at 3 months?

A

80%

Physio Test 2 (10 decks)

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