Cardiac Output & Blood Pressure

Question 1

What is the formula for cardiac output?

Answer 1

CO = HR x SV

Question 2

What is the formula for blood pressure?

Answer 2

BP = CO x HR

Question 3

What are the factors affecting stroke volume?

Answer 3

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)

Question 4

What is the formula for stroke volume?

Answer 4

SV = EDV - ESV

Question 5

What is cardiac output?

Answer 5

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

average: 5 L minute

Question 6

What is heart rate?

Answer 6

Contractions per minute

Question 7

What is stroke volume?

Answer 7

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

Question 8

What is EDV and ESV?

Answer 8

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)

Question 9

What is total peripheral resistance?

Answer 9

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

Question 10

What is blood pressure?

Answer 10

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

Question 11

What is MAP?

Answer 11

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

Question 12

What are systolic and diastolic pressure?

Answer 12

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

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

Question 13

What increases total peripheral resistance?

Answer 13

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

Question 14

What decreases total peripheral resistance?

Answer 14

PNS activation:

- vasodilation

Question 15

What is pulse pressure?

Answer 15

the difference between systolic and diastolic pressures

Question 16

What affects pulse pressure?

Answer 16

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

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

Question 17

What affects preload?

Answer 17

Increases preload:
- increased venous return

Decreased preload:

• hypoxia
• decreased thyroid hormones or calcium ions

Question 18

What affects contractility?

Answer 18

Increases contractility:

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

Decreases contractility:

• SNS stimulation
• hypoxia

Question 19

What affects afterload?

Answer 19

Increased afterload:

• high TPR
• semilunar valve damage

Decreased afterload:
- decreased vascular resistance

Question 20

What is the effect of SNS stimulation on blood pressure?

Answer 20

SNS stimulation via cardioaccelaratory centre:

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

Question 21

What is the effect of PNS stimulation on blood pressure?

Answer 21

PNS stimulation via cardioinhibitory centre:

• decreased HR
• vasodilation of arterioles decreases TPR

Question 22

What are the short term reflexes for controlling blood pressure?

Answer 22

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

Question 23

What is the long term regulation of blood pressure?

Answer 23

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

Question 24

What are the 4 actions of the RAAS system?

Answer 24

• 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

Question 25

What is the Frank-Starling Law?

Answer 25

Increased stretch = increased force of contraction

Question 26

What is the difference between a baroreceptor and a chemoreceptor?

Answer 26

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

Question 27

Where are baroreceptors and chemoreceptors located?

Answer 27

Baroreceptors: - aortic arch - carotid sinus & bifurcation of carotid arteries - walls of large arteries in neck and thorax Chemoreceptors: - aortic bodies - carotid bodies

Question 28

Which visceral afferents carry information from the baroreceptors and chemoreceptors?

Answer 28

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)

Question 29

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

Answer 29

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)

Question 30

What is the impact of the cardioacceleratory centre on BP?

Answer 30

Increases BP | Mechanisms: - increased contractility of myocardium - increased heart rate increases CO

Question 31

What is the impact of the cardioinhibitory centre on BP?

Answer 31

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

Question 32

What is the impact of the vasomotor centre on BP?

Answer 32

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

Question 33

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

Answer 33

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

Question 34

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

Answer 34

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

Question 35

What is the difference between direct and indirect renal mechanisms?

Answer 35

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