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CVS & IBL - Physiology 🫁 > L5: Physiological regulation of arterial blood pressure > Flashcards

L5: Physiological regulation of arterial blood pressure Flashcards

1
Q

What is the definition of the cardiac cycle?

A

The cardiac events that occur from the beginning of one heartbeat to the beginning of the next.

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2
Q

What does the cardiac cycle include?

A

A period of contraction (systole) and a period of relaxation (diastole) occur during the cardiac cycle

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3
Q

What is ABP?

A

It is the lateral force exerted by the blood on the arterial wall.

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4
Q

What are the characteristics of ABP?

A
  • Pulsatile.
  • It is not constant during a cardiac cycle.
  • The systolic BP is caused by the sudden ejection of blood into the aorta during systole.
  • The diastolic BP is caused by the passive elastic recoiling of the arteries (elastic recoil or windkessel effect)
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5
Q

What is systolic pressure?

A

It is the highest arterial pressure during a cardiac cycle, It is measured after the heart contracts (systole) and blood is ejected into the arterial system.

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6
Q

What is diastolic pressure?

A

It is the lowest arterial pressure during a cardiac cycle, It is measured when the heart is relaxed (diastole) and blood is returned to the heart via the veins.

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7
Q

What is pulse pressure?

A

is the difference between the systolic and diastolic pressures.

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8
Q

What is the most important determinant of pulse pressure?

A

SV

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9
Q

What does pulse pressure equal?

A

40mmHg

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10
Q

What is mean arterial pressure?

A

It is the average arterial pressure with respect to time.

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11
Q

How can we calculate mean arterial pressure?

A

Can be calculated approximately as diastolic pressure plus one-third of pulse pressure.

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12
Q

What is the importance of arterial blood pressure?

A

1) It maintains sufficient pressure to keep the blood flowing.
2) It provides enough hydrostatic pressure inside the capillaries essential for the formation of interstitial fluid, urine, etc.

“The pressure in the capillaries causes the ejection of nutrients and vitamins to the cells, it also allows the absorbance of wastes from them”

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13
Q

How does age affect arterial blood pressure?

A
  • The ABP is about 50/30 mmHg.
  • After birth, Increase of age will increase ABP till adulthood where it is 120/80.
  • After the age of 50 years it increases gradually due to normal gradual loss of arterial elasticity.
  • It may become normally 140/90
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14
Q

How does gender affect arterial blood pressure?

A
  • ABP is generally slightly higher in adult males than in females.
  • However, it becomes slightly higher in females after menopause.
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15
Q

How does the bodybuilt affect arterial blood pressure?

A

ABP is higher in obese persons

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16
Q

how does environmental temperature affect arterial blood pressure?

A

Exposure to cold increases both Systolic and systolic pressures due to cutaneous vasoconstriction.

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17
Q

How do emotions affect arterial blood pressure?

A

Increase the ABP considerably

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18
Q

How does exercise affect arterial blood pressure?

A

Systolic ABP increases while the diastolic is often not changed or decreases due to arteriolar vasodilatation.

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19
Q

How do meals affect arterial blood pressure?

A

The ABP increases slightly after meals due to VD of the splanchnic area which increases both VR and COP.

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20
Q

How does posture affect arterial blood pressure?

A

On standing, the force of gravity increases the mean ABP below a reference point in the heart and decreases it above that point by about 0.77 mm/cm height.

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21
Q

What are the factors maintaining normal ABP?

A
  • Cardiac output
  • Peripheral resistance
  • Elasticity of the arterial wall
  • The total blood volume in relation to the capacity of the circulatory system
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22
Q

What do changes in stroke volume affect?

A

Changes in the stroke volume with the HR constant affect the systolic more than the diastolic pressure.

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23
Q

What do changes in heart rate affect?

A

Changes in the HR with constant SV affect the diastolic more than the systolic blood pressure.

24
Q

What are the factors that determine peripheral resistance?

A

PR = VL/r4

a) Viscosity of blood (V): It is the property by which a fluid resists a change in shape, It represents the force with which the fluid particles adhere to each other and resists
their separation

b) Length of the blood vessels (L)
c) The diameters of arterioles (r)

25
Q

What does atherosclerosis cause in terms of ABP?

A

there is a marked increase in systolic “pushing of blood” and a decrease in diastolic blood “decrease in elasticity” pressure resulting in higher pulse pressure.

26
Q

The effect of the factor: (The total blood volume in relation to the capacity of the circulatory system) in ABP?

A

Changes in blood volume:-

  • Mild to moderate
  • Severe

Changes in the capacity of the circulatory system:

  • Increase
  • Decrease
27
Q

What are the most important mechanisms in the regulation of ABP?

A

1- Fast, neurally mediated baroreceptor mechanism

2- Slower, hormonally regulated renin-angiotensin–aldosterone mechanism

28
Q

What are the characteristics of the Baroreceptor reflex?

A

fast, neural mechanisms.

29
Q

What is the definition of baroreceptor reflex?

A
  • It is a negative feedback system that is responsible for the minute-to-minute regulation of arterial blood pressure
  • Baroreceptors are stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.
30
Q

What are the steps in baroreceptor reflex?

A

1) A decrease in arterial pressure decreases stretch on the walls of the carotid sinus and aortic arch.
2) Decreased stretch decreases the firing rate of the baroreceptors (which send information to the vasomotor center in the brain stem).
3) The vasomotor center responds to the decrease in mean arterial blood pressure by decreasing parasympathetic outflow to the heart and increasing sympathetic outflow to the heart and blood vessels to increase mean arterial pressure to 100mmHg

31
Q

What are the effects caused by baroreceptor reflex?

A

↑ heart rate
↑ contractility and stroke volume
↑ vasoconstriction of arterioles
↑ vasoconstriction of veins (venoconstriction)

32
Q

What causes ↑ heart rate?

A

resulting from the decreased parasympathetic tone and increased sympathetic tone to the SA node of the heart.

33
Q

What causes ↑ contractility and stroke volume?

A

resulting from increased sympathetic tone to the heart.

34
Q

What are the results of increased heart rate and increased contractility, Stroke volume?

A

They produce an increase in cardiac output that increases arterial pressure.

35
Q

What causes ↑ vasoconstriction of arterioles?

A

resulting from the increased sympathetic outflow.

36
Q

What is the result of ↑ vasoconstriction of arterioles?

A

TPR and arterial pressure will increase.

37
Q

What causes ↑ vasoconstriction of veins (venoconstriction)?

A

resulting from the increased sympathetic outflow.

38
Q

What are the results of ↑ vasoconstriction of veins?

A

causes a decrease in unstressed volume and an increase in venous return to the heart.

39
Q

What are the characteristics of the renin-angiotensin-aldosterone system?

A
  • slow, hormonal mechanism.

- used in long-term blood pressure regulation by adjustment of blood volume.

40
Q

What are the chemicals in the renin-angiotensin-aldosterone system?

A
  • Renin is an enzyme.
  • Angiotensin I is inactive.
  • Angiotensin II is physiologically active.
  • Angiotensin II is degraded by angiotensinase.
  • One of the peptide fragments, angiotensin III, has some of the biologic activity of angiotensin II.
41
Q

What are the steps in renin–angiotensin–aldosterone system?

A

1) A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin.
2) Renin is an enzyme that catalyzes the conversion of angiotensinogen to angiotensin I in plasma.
3) Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs.
4) angiotensin II has many effects

42
Q

What are the effects of angiotensin II?

A

a) It stimulates the synthesis and secretion of aldosterone by the adrenal cortex.
b) It increases Na+–H+ exchange in the proximal convoluted tubule.
c) It increases thirst and therefore water intake.
d) It causes vasoconstriction of the arterioles, thereby increasing TPR and arterial pressure.

43
Q

What is the importance of stimulation and secretion of aldosterone in the RAAS?

A
  • Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure.
44
Q

Why is the action of aldosterone slow?

A

because it requires new protein synthesis.

45
Q

What is the importance of the increase of NA - H exchange in the proximal convoluted tubules in the RAAS?

A
  • This action of angiotensin II directly increases Na+ reabsorption, complementing the indirect stimulation of Na+ reabsorption via aldosterone.
  • This action of angiotensin II leads to contraction alkalosis.
46
Q

What are other regulation systems of ABP?

A

1) Cerebral ischemia
2) Chemoreceptors in the carotid and aortic bodies
3) Vasopressin [antidiuretic hormone (ADH)]
4) Atrial natriuretic peptide (ANP)

47
Q

What are the steps of regulation of ABP in the case of cerebral ischemia?

A
  • When the brain is ischemic, the partial pressure of carbon dioxide (PCO2) in brain tissue increases.
  • Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels.
  • Constriction of arterioles causes intense peripheral vasoconstriction and increased TPR.
  • Blood flow to other organs (e.g., kidneys) is significantly reduced in an attempt to preserve blood flow to the brain.
48
Q

What is an example of the response to cerebral ischemia?

A
  • The Cushing reaction is an example of the response to cerebral ischemia. Increases in intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral PCO2.
  • The vasomotor center directs an increase in sympathetic outflow to the heart and blood vessels, which causes a profound increase in arterial pressure.
49
Q

Where are chemoreceptors located?

A

located near the bifurcation of the common carotid arteries and along the aortic arch.

50
Q

What are chemoreceptors in carotid and aortic bodies sensitive to?

A

have very high rates of O2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2).

51
Q

What does a decrease in pressure of oxygen do to the chemoreceptors in the carotid and aortic bodies?

A

Decreases in PO2 activate vasomotor centers that produce vasoconstriction, an increase in TPR, and an increase in arterial pressure.

52
Q

What is vasopressin hormone involved in?

A

It is involved in the regulation of blood pressure in response to hemorrhage, but not in minute-to-minute regulation of normal blood pressure.

53
Q

How do atrial receptors respond to a decrease in blood volume or blood pressure?

A

Atrial receptors respond to a decrease in blood volume (or blood pressure) and cause the release of vasopressin from the posterior pituitary.

54
Q

What are the effects of vasopressin?

A

Vasopressin has two effects that tend to increase blood pressure toward normal:

  • It is a potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles.
  • It increases water reabsorption by the renal distal tubule and collecting ducts by activating V2 receptors.
55
Q

From where is ANP released?

A

from the atria in response to an increase in blood volume and atrial pressure.

56
Q

What are the effects of ANP?

A
  • ANP causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR.
  • causes increased excretion of Na+ and water by the kidney, which reduces blood volume and attempts to bring arterial pressure down to normal.
  • inhibits renin secretion.

CVS & IBL - Physiology 🫁 (12 decks)

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