19 9-14 Flashcards

1
Q

Blood pressure

A

Force per unit area exerted by the blood against a vessel wall.

Expressed in mmHg.

Pressure is a result when BF is opposed by resistance.

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2
Q

Blood pressure gradient

A

The change in blood pressure from one end of a vessel to the other end; it is the driving force for moving blood.

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3
Q

Blood Flow

A

Volume of blood flowing through a vessel, organ or the entire circulation in a given period.

May be expressed as ml/min.

Pumping action of the heart generates BF.

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4
Q

Resistance

A

A measure of friction between blood and the vessel wall.

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5
Q

4 sources of resistance?

A

Blood viscosity, blood vessel length, blood vessel diameter, obstructions

(Level of resistance can be regulated neurally/hormonally/by local influence. physical dimensions of the vessel and properties of the fluid.

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6
Q

Total peripheral resistance

A

Adding up the combined resistance of all the blood vessels in a particular circuit.

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7
Q

What is the most important factor influencing local blood flow?

A

Peripheral resistance - because vasoconstriction/dilation can alter local blood flow while systemic BP remains unchanged.

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8
Q

Relationship between flow/pressure/resistance?

A

If the difference in BP between two points (the gradient) is large, then BF ↑
Small difference, slow flow
Example: when arterioles serving a particular tissue dilate, their pressure drops increasing the difference in pressure and therefore increasing blood flow.

If peripheral resistance ↑, BF ↓
Most important factor!

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9
Q

Pulse pressure

A

The difference between systolic and diastolic pressure. A measure of elasticity and recoil of arteries.

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10
Q

Calculate MAP

A

MAP = diastolic pressure + 1/3 pulse pressure.

Map is a good indication of how tissues and organs are perfused.

(70-110mmHg = good perfusion; lower than 60 may mean insufficient blood flow.)

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11
Q

When does diastolic pressure occur?

A

When blood is prevented from flowing back into the ventricles by the closed semilunar valve and the aorta recoils

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12
Q

When does systolic pressure occur?

A

When the L ventricle contracts and blood is forced into the aorta producing a peak in pressure.

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13
Q

What does arterial BP reflect?

A

How much the arteries close to the heart can be stretched (compliance/distensibility), and the volume forced into them at a given time.

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14
Q

Explain the mechanisms that help overcome the small pressure gradient in veins to return blood to the heart.

A

Structural: 1. large diameter 2. valves.

Functional: 1. Skeletal muscle pump (skel musc contraction milks blood toward heart)

  1. Respiratory pump (shifting pressure between ab cavity and thoracic cavity)
  2. Sympathetic venoconstriction (veins can be constricted)
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15
Q

What variables affect BP and what are house variables determined by?

A

Variables: blood volume, CO, R

These are determined primarily by venous return, neural and hormonal controls.

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16
Q

Formula to determine bp

A

BP = HRSVR

pumping action of the heart generates BF (=CO which =HR*SV), pressure results when flow is opposed by resistance

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17
Q

How does short term vs long term regulation late BP? (Mechanisms)

A

Short term regulation (NS and hormones) alters blood pressure by changing peripheral resistance and CO.

Long term regualtion alters blood volume via the kidneys.

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18
Q

Short term neural controls alter what?
What is the goal of short term goal?
How is it done

A

Alter both cardiac output and peripheral resistance.

Goals:

  1. Maintain adequate MAP by altering vessel diameter on a moment to moment basis (vessel diameter) and
  2. alter blood distribution to respond to specific demands of various organs (peripheral resistance).

Short term regulation occurs via ANS reflexes involving nuclei in the medulla oblongata.

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19
Q

What are the short term neural controls?

A

baroreceptor relexes,
chemoreceptor reflexes,
higher brain centers.

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20
Q

Role of the cardiovascular center (cardiac and vasomotor centers) in maintaining BP

A

Cardiac center:

  1. Cardioaccelatory center - symp stimulation to SA and AV nodes and ventricles ↑ HR and ↑ force of contraction.
  2. Cardioinhibitory center - parasym to SA and AV ↓ HR.

Vasomotor center
1. Regulation of resistance via degree of vasoconstiction

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21
Q

How is cardiovascular center activity modified?

A

Input from baroreceptors, chemoreceptors, and higher brain centers.

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22
Q

What type of receptors does the vasomotor center receive info from?

A

Alpha receptors: vasoconstriction upon stimulation (most vessels).

Beta receptors: Vasodilation in response to epinephrine from adrenal medulla (vessels in skeletal muscle and coronary vessels)

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23
Q

Baroreceptors do what?

Are located/named/transmit via?

A

Detect stretch in blood vessel walls

Aortic arch baroreceptors trasmit via Vagus

Carotid sinus baroreceptors trasmit via glossopharangeal.

24
Q

Steps if baroreceptors detect a rise in BP

A
  1. BP rises above normal
  2. Baroreceptors in carotid sinus and aortic arch are stimulated
  3. Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit vasomotor and cardioaccelatory)
    4a. ↓ Sympathetic impulses to the heart cause ↓HR, ↓ contractility, ↓ CO↓
    4b. Rate of vasomotor impulses allows vasodilation causing ↓ R
  4. ↓ CO and ↓ R return blood pressure to homeostatic range
25
Q

Steps if baroreceptors detect a drop in BP

A
  1. ↓ BP
  2. Baroreceptors in carotid sinuses/aortic arch are inhibited
  3. Impulses from baroreceptors stimulate cardioaccelatory center and vasomotor center (and inhibit cardioinhibitory center)
    4a. ↑ sympathetic impuses to heart cause ↑ HR, ↑ contractility, ↑ CO
    4b. Vasomotor fibers stimulate vasoconstriction causing ↑ R
  4. ↑ CO and ↑ R return BP to homeostatic range
26
Q

Chemoreceptors

A

Detect ↑ in carbon dioxide, low ph and very low o2.

They stimulate the cardioaccelatory and vasomotor centers which ↑ CO and vasoconstriction.

Aortic bodies/Carotid bodies

27
Q

Influence of higher brain centers as a short term neural control

A

Cerebral cortex/hypothalamus can modify arterial pressure by signalling medullary centers

28
Q

What are short term hormonal controls?

A

Influence BP via vascular smooth muscle and vasomotor center.

NE, E, Angiotensin II, ANP, BNP, ADH, Endothelins, NO, Inflammatory chemicals, alcohol

29
Q

Hormonal control E/NE

A

↑ BP by:

↑ CO (both HR and contractility, beta1 receptors of heart)
AND
↑peripheral resistance/vasoconstriction @ alpha receptors in arterioles)

30
Q

Hormonal control Angiotensin II

A

↑ BP by:

↑ peripheral resistance/vasoconstriction of arterioles.

Also promotes release of aldosterone and ADH.

31
Q

Hormonal control ANP/BNP

A

↓ BP by:

↓ peripheral resistance/vasodilation of arterioles,
AND
↓ blood volume (from ↑ h2o and salt loss in kidney tubules).

Also, antagonist to aldosterone. Atrial natriuretic peptide/brain natruiretic peptide

32
Q

Hormonal control ADH/Vasopressin

A

↑ BP by:

↑ peripheral resistance/vasoconstriction of arterioles
AND
↑ water conservation by kidneys increasing blood volume

33
Q

Hormonal control Endothelins

A

↑ BP by:

↑ peripheral resistance/vasoconstriction.

Released in response to low blood flow.

34
Q

Hormonal control NO

A

↓ BP produced in response to high blood flow or other signalling molecules and promotes systemic and localized vasodilation

35
Q

Hormonal control Inflammatory chemicals

A

↓ BP by:

potent vasodilators.

Histamine, prostacyclin, kinins

36
Q

Hormonal control Alcohol

A

↓ BP by:

vasodilator due to inhibiting ADH and the vasomotor center.

37
Q

How do kidneys maintain BP long term?

A

By regulating blood volume

38
Q

Direct renal mechanism?

A

Counteracts an ↑ in BP or blood volume because kidney filtering/reabsorption can’t keep up with fluid from bloodstream which increases the rate urine production.

As a result, BP and BV fall.

39
Q

Indirect renal mechanism?

A

RAAS - renin-angiotensin-aldosterone system. Counteracts a ↓ in arterial BP by causing systemic vasoconstriction.

40
Q

Effect of Direct renal mechanism

A

Initial stimulus:
↓ arterial pressure

Physiological response:
↓ filtration by kidneys
↓ urine formation
↑ blood volume

Result: ↑ MAP

41
Q

Effect of Indirect renal mechanism

A

Initial stimulus:
↓ arterial pressure

Physiological response:
Inhibits baroreceptors
↑ symp NS activity
↑ renin release from kidneys → angiotensinogen →ang I → ang II

(4 different actions)

1.  Adrenal cortex 
aldosterone 
↑ sodium reabsorption by kidneys 
↑ water resorption by kidneys 
↑ blood volume  
  1. ↑ ADH release by posterior pituitary
    ↑ water reabsorption by kidneys
    ↑blood volume
  2. ↑ thirst via hypothalamus
    ↑ water intake
    ↑ blood volume
  3. Vasoconstriction/↑ peripheral resistance

Result: ↑ MAP

42
Q

MAP factor/initial stimulus - ↑ activity of muscular pump and respiratory pump

A

Physiological response:
↑ venous return
↑ stroke volume

Result: ↑ CO ↑ MAP

43
Q

MAP factor/initial stimulus - ↓ release of ANP

A
Physiological response: 
↑ conservation of Na+ and water by kidneys 
↑ blood volume 
↑ venous return 
↑ SV  

Result: ↑CO ↑MAP

44
Q

MAP factor/initial stimulus - Fluid loss from hemorrhage, excessive sweating

A

Physiological response:
↓ blood volume and BP

(2 actions)

  1. ↑ conservation of Na+ and water by kidneys
    ↑ blood volume
    ↑ venous return
    ↑ SV

Result: ↑CO ↑MAP

  1. Baroreceptors
    Activation of vasomotor and cardioacceleratory centers in brain stem (which leads to 3 effects)
    (a.) ↑ SV and (b.) ↑ HR resulting in ↑ CO ↑ MAP

(c). ↓ diameter of blood vessels results in ↑ peripheral resistance ↑ MAP

45
Q

MAP factor/initial stimulus - Crisis stressors: exercise, trauma, ↑ body temp

A

Physiological response:
↓ blood ph/↑CO2/↓O2
chemoreceptors
activation of vasomotor and cardio-acceleratory centers
↑Stroke volume/↑HR and ↓ diameter of blood vessels

Result: ↑CO and ↑Peripheral resistance
↑ MAP

46
Q

MAP factor/initial stimulus - bloodborne chemicals (E/NE/ADH/Angiotensin II and ↓ ANP)

A

Physiological response:
↓ diameter of blood vessels

Result: ↑ peripheral resistance
↑ MAP

47
Q

Effect of exercise on CO

A
Physiological response:  
↑ activity of respiratory pump 
↑ activity of muscular pump 
↑sympathetic venoconstriction  
↑venous return 
↑ EDV 
↑SV  

Result ↑CO

48
Q

Effect of ↓ BP (activating cardiac centers)

A
Physiological response:  
↑ symp activity 
↑ contractility directly (or ↑ epi in blood then ↑ contractility) 
↓ ESV 
↑ SV  

AND
↑ symp activity
↑ HR

AND
↓para
↑HR

All result in:
↑ CO

49
Q

MAP factor/initial stimulus - Dehydration, high hemacrit

A

Physiological response:
↑ blood viscosity

Result:
↑ peripheral resistance
↑ MAP

50
Q

MAP factor/initial stimulus - ↑ Body size

A

Physiological response:
↑ Blood vessel length

Result:
↑ peripheral resistance
↑ MAP

51
Q

Pressures in: arteries, capillaries, veins

A

Arteries: 80-120

Capillary 20-40

Veins 0-20

52
Q

Regulation of BP - lines of defense

A

Short term

1st line

  1. Neural, ANS - medulla oblongata, baroreceptors
  2. Neural - chemoreceptors
  3. Higher brain centers

2nd line
4. Chemicals

Long term

3rd line of defense
1. Kidney/blood volume

53
Q

Regulating BP - systemic vs. local

A

Systemic/intrinsic - goal is to maintain MAP

  1. ANS
  2. Chemicals
  3. Other/kidney

Local/autoregulation/intrinsic- goal is to meet local metabolic needs

  1. Myogenic - inherent in all smooth muscle, if stretched it will recoil
  2. Metabolic controls - watching chemical levels (co2, O2, ph)
54
Q

Hormonal vasoconstrictors

A

NE/E
Angiotensin II
ADH/vasopressin
Endothelins

55
Q

Hormonal vasodilators?

A
ANP/BNP
NO
Inflammatory chemicals
Alcohol (because it inhibits ADH)
Adenosine