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Section 4B Heart & CV > Cardiac Output & Blood Pressure > Flashcards

Cardiac Output & Blood Pressure Flashcards

1
Q

What is the formula for cardiac output?

A

CO = HR x SV

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2
Q

What is the formula for blood pressure?

A

BP = CO x HR

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3
Q

What are the factors affecting stroke volume?

A

Preload:

  • degree of stretch before contraction
  • Frank Starling law: increased stretch = increased force of contraction
  • increased venous return increases preload

Contractility
- intrinsic strength of contraction

Afterload:
- degree that ventricle must pump against resistance in the pulmonary or systemic circuits (not usually a problem in healthy systems)

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4
Q

What is the formula for stroke volume?

A

SV = EDV - ESV

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5
Q

What is cardiac output?

A

The amount of blood pumped out by one ventricle in 1 minute

average: 5 L minute

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6
Q

What is heart rate?

A

Contractions per minute

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7
Q

What is stroke volume?

A

the amount of blood pumped out by one ventricle in 1 systolic contraction (EDV - ESV)

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8
Q

What is EDV and ESV?

A

End diastolic volume:
- amount of blood in the ventricle at the end of diastole (relatively full)

End systolic volume:
- amount of blood in the ventricle at the end of systole (relatively empty)

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9
Q

What is total peripheral resistance?

A

the amount of friction encountered by the bloodstream as it passes through vessels

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10
Q

What is blood pressure?

A

the pressure exerted by the bloodstream against vessel walls (measured in mm of mercury)

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11
Q

What is MAP?

A

Mean arterial pressure - average pressure in the arteries during one cardiac cycle

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12
Q

What are systolic and diastolic pressure?

A

Systolic - pressure exerted on blood vessel walls during ventricular systole (pump)

Diastolic - pressure exerted on blood vessel walls during ventricular diastole (relaxation)

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13
Q

What increases total peripheral resistance?

A

SNS activation:
- vasoconstriction (activation of alpha 1 adrenergic receptors in tunica media, especially in arterioles)

  • high blood viscosity
  • long blood vessels
  • small blood vessel diameter
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14
Q

What decreases total peripheral resistance?

A

PNS activation:

- vasodilation

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15
Q

What is pulse pressure?

A

the difference between systolic and diastolic pressures

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16
Q

What affects pulse pressure?

A

Sclerotic vessel walls increase pulse pressure (walls cannot absorb systolic pressure effectively)

Elastic vessel walls decrease pulse pressure (walls can absorb systolic pressure effectively)

17
Q

What affects preload?

A

Increases preload:
- increased venous return

Decreased preload:

  • hypoxia
  • decreased thyroid hormones or calcium ions
18
Q

What affects contractility?

A

Increases contractility:

  • SNS stimulation
  • high intracellular calcium ions
  • high thyroid hormones

Decreases contractility:

  • SNS stimulation
  • hypoxia
19
Q

What affects afterload?

A

Increased afterload:

  • high TPR
  • semilunar valve damage

Decreased afterload:
- decreased vascular resistance

20
Q

What is the effect of SNS stimulation on blood pressure?

A

SNS stimulation via cardioaccelaratory centre:

  • vasoconstriction of arterioles increases TPR
  • increased HR
  • increased contractility increases SV and CO
21
Q

What is the effect of PNS stimulation on blood pressure?

A

PNS stimulation via cardioinhibitory centre:

  • decreased HR
  • vasodilation of arterioles decreases TPR
22
Q

What are the short term reflexes for controlling blood pressure?

A

Baroreceptor:

  • stretch receptors in aortic arch, carotid sinuses and walls of elastic arteries
  • can stimulate or inhibit CV centres in order to either raise or lower BP

Chemoreceptor:

  • chemical receptors in aortic bodies and carotid bodies
  • respond to drop in O2/ ph and increase in CO2 levels (decreased BP)
  • stimulates cardioacceleratory and vasomotor centres to increase BP
23
Q

What is the long term regulation of blood pressure?

A

Direct renal mechanism:

  • decreased BP
  • decreases filtration by kidneys and urine filtration
  • raises BV and therefore BP

Indirect renal mechanism (RAAS):

  • decreased pressure
  • renin release from kidneys
  • angiotensinogen to angiotensin 1 to angiotensin II

Actions of RAAS:

  • stimulates adrenal cortex to release aldosterone, which increases sodium reabsorption by kidneys
  • stimulates posterior pituitary to release ADH which increases water reabsorption by kidneys
  • thirst reflex via hypothalamus
  • vasoconstriction and increased TPR
24
Q

What are the 4 actions of the RAAS system?

A
  • stimulates adrenal cortex to release aldosterone, which increases sodium reabsorption by kidneys
  • stimulates posterior pituitary to release ADH, which increases water reabsorption by kidneys
  • stimulates thirst impulse via hypothalmus
  • stimulates vasoconstriction, which increases TPR
25
Q

What is the Frank-Starling Law?

A

Increased stretch = increased force of contraction

26
Q

What is the difference between a baroreceptor and a chemoreceptor?

A

Baroreceptors:
stretch receptors that respond to a change in BP - can stimulate or inhibit CV centres in order to either raise or lower BP

Chemoreceptors
chemical receptors that respond to a drop in O2/pH or an increase in CO2 - stimulate cardioacceleratory & vasomotor centres to increase BP

27
Q

Where are baroreceptors and chemoreceptors located?

A

Baroreceptors:

  • aortic arch
  • carotid sinus & bifurcation of carotid arteries
  • walls of large arteries in neck and thorax

Chemoreceptors:

  • aortic bodies
  • carotid bodies
28
Q

Which visceral afferents carry information from the baroreceptors and chemoreceptors?

A

CNIX (Glossopharyngeal)

  • carotid arteries (baroreceptor and chemoreceptor)
  • carotid sinus (baroreceptor)

CNX (Vagus)

  • aortic arch (baroreceptor)
  • aortic bodies (chemoreceptor)
  • large arteries in neck and thorax (baroreceptor)
29
Q

What are the 4 elements that can be affected by short term regulation of blood pressure?

A
  1. TPR (via vasoconstriction)
  2. HR (via input to SA node)
  3. SV (via SNS input to heart affecting contractility and HR)
  4. CO (via HR and SV)
30
Q

What is the impact of the cardioacceleratory centre on BP?

A

Increases BP

Mechanisms:
- increased contractility of myocardium
- increased heart rate
increases CO

31
Q

What is the impact of the cardioinhibitory centre on BP?

A

Decreases BP

Mechanisms:
- decreased rate of firing in SA node (decreases CO)

32
Q

What is the impact of the vasomotor centre on BP?

A

Increases BP

Mechanisms:
- vasoconstriction (contraction of tunica media) increases TPR and BP

33
Q

What is the direct renal mechanism when blood volume / blood pressure is too low?

A

Kidneys conserve more water and return water to bloodstream (causing blood volume and blood pressure to increase)

34
Q

What is the direct renal mechanism when blood volume / blood pressure is too high?

A

Kidneys can’t reabsorb filtrate quickly enough to keep up with amount of blood being filtered through kidneys

means that more filtrate leaves the body as urine rather than being returned into the bloodstream

means that blood volume and blood pressure drops

35
Q

What is the difference between direct and indirect renal mechanisms?

A

Direct renal mechanisms:
- amount of water filtered by the kidneys from the blood stream manipulated to either raise or lower blood volume and blood pressure

Indirect renal mechanism:
- RAAS system responds to low blood pressure by releasing rening into bloodstream, which converts angiotensinogen to angiotensinogen II

Section 4B Heart & CV (6 decks)

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