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Anatomy & Physiology 208 > Physiology of Circulation > Flashcards

Physiology of Circulation Flashcards

1
Q

key players in circulation

A

Heart = pump
Arteries = pressure reservoirs and conduits
Arterioles = resistance vessels
Capillaries = sites of exchange
Veins = conduits and blood reservoirs

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2
Q

Blood Flow:

A
  • The volume of blood flowing through a vessel, organ, or circulation system in a period of time
  • Blood flow remains fairly constant, and it is relatively equivalent to CO
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3
Q

Blood Pressure

A
  • The force per unit area exerted on a vessel wall by the contained blood
  • Typically measured in the largest arteries near the heart
  • The hydrostatic pressure gradient – the difference in blood pressure within the vascular system – provides the driving force to keep blood moving
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4
Q

Resistance:

A
  • Opposition to flow, the amount of friction that blood encounters
  • Most friction is encountered well away from the heart – total peripheral resistance (TPR)
  • Sources of resistance: blood viscosity, vessel length, and vessel diameter
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5
Q

Blood Viscosity

A

internal resistance to flow that exists in all fluids
- Thickness or “stickiness” of the fluid
- Greater viscosity = less movement
- Blood viscosity is fairly constant – exceptions being the anemias and polycythemias

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6
Q

Blood Vessel Length

A

Longer vessel = greater resistance

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7
Q

Blood Vessel Diameter

A

Smaller diameter = greater resistance

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8
Q

mechanics of blood flow

A

flows from high to low pressure against resistance

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9
Q
A
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10
Q

Relationship of Flow, Pressure, and Resistance

A
  • Blood viscosity and vessel length are relatively constant
  • Blood vessel diameter changes frequently and significantly alters TPR
  • Example: River-Bank Flow
  • Resistance varies inversely with the 4th power of the vessel radius
  • If the size of the vessel doubles, resistance drops to 1/16th of its original valve
  • Smaller-diameter arterioles are the major determinants of TPR
  • Turbulence – such as the disrupted flow caused by atherosclerosis – increases resistance
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11
Q

flow, pressure, resistance equation

A

F = delta P / TPR
- TPR is the more important factor influencing blood flow
- TPR is changed by changes in the diameter of the small arterioles

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12
Q

Overview of Blood Pressure

A
  • Blood flows through the vessels on a pressure gradient – always from higher to lower pressure!
  • The pumping action of the heart generates blood flow – resistance to flow generates pressure
  • Systemic pressure is highest in the aorta and steadily declines
  • Steepest drop occurs in the arterioles – where resistance is highest
  • Pressure in the right atrium is 0mmHg
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13
Q

2 factors of arterial blood pressure

A
  1. How much can the elastic arteries close to the heart stretch?
  2. What volume of blood is forced into the arteries?
    - Blood pressure is pulsatile – it rises and falls in a regular fashion
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14
Q

Systolic Pressure

A

blood is expelled into the aorta, the walls are stretched, aortic pressure peaks
Average = 120 mmHg

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15
Q

Diastolic Pressure:

A

aortic walls recoil, aortic valve closes, and pressure drops
Average = 80 mmHg

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16
Q

how is blood driven further forward

A

The volume and energy of the blood stored in the elastic arteries during systole is given back during diastole, and blood is driven further forward

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17
Q

Pulse Pressure

A

the difference in systolic and diastolic pressure
- Increased SV and contractility can temporarily increase PP
- Atherosclerosis chronically increases pulse pressure

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18
Q

MAP - mean arterial pressure

A

the pressure that propels blood into the tissues – useful tool for determining tissue perfusion
- Because diastole lasts longer than systole, MAP is NOT simply the halfway point between SBP and DBP
- diastolic pressure + pulse pressure/3
- Both MAP and PP decrease with increasing distance form the heart

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19
Q

Pulse

A
  • Typically, the radial or carotid pulse
  • Pulse Points = pressure points
  • Used to stop blood flow during hemorrhage
  • Pulses are monitored to assess the effects of activity, postural changes, and emotions
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20
Q

Blood Pressure

A
  • Typically, measured in the left brachial artery
  • Auscultatory Method: practitioner uses a sphygmomanometer and a stethoscope to listen to the Sounds of Korotkoff
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21
Q

Capillary Blood Pressure

A
  • Blood pressure entering a capillary bed is ~35 mmHg
  • Blood pressure exiting a capillary bed is ~17 mmHg
  • Secondary to the fragility of the capillary bed, low pressures are essential
  • Capillaries are so permeable that even low pressure can adequately force filtrate out of the blood stream
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22
Q

Venous Blood Pressure

A
  • Venous pressure is far less pulsatile – pressure gradients are less steep
  • Low venous pressure results from TPR – energy has been dissipated out
  • Despite valves, venous pressure is too low for adequate venous return
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23
Q

Three Functional Adaptations of venous blood pressure

A
  1. muscular pump
  2. respiratory pump
  3. sympathetic vasoconstriction
24
Q

muscular pump

A

activity of the skeletal muscles surrounding the deep veins squeezes the veins and propels blood towards the heart

25
Q

respiratory pump

A

during breathing, pressure changes in the ventral body cavity propel blood towards the heart

26
Q

Sympathetic Vasoconstriction

A

during SNS firing, veins constrict, venous volume is reduced, and blood is pushed towards the heart

27
Q

venous blood pressure flow

A

increased venous return > increased stroke volume > increased cardiac output

28
Q

3 key variables in regulation of blood pressure

A
  1. Cardiac Output
  2. Total Peripheral Resistance
  3. Blood Volume
29
Q

regulation of blood pressure

A
  • Blood Pressure (BP) varies directly with CO and TPR
  • Anything that increases CO or TPR will increase BP
  • Anything that increases HR or SV will increase BP
  • Any change that threatens BP homeostasis will be compensated for
30
Q

Short Term Regulation: Neural Controls

A

Neural controls can alter both CO and TPR
Two Main Goals:
1. Maintain adequate MAP by altering blood vessel diameter – small changes in vessel diameter can cause substantial changes in TPR - and therefore BP
*Example: perfusion of the heart and brain during low blood volume
2. Alter blood distribution to respond to specific demands
*Example: during exercise, blood is shunted to the skeletal muscles

31
Q

baroreceptors

A
  • pressure-sensitive mechanoreceptors that respond to changes in arterial pressure and stretch
  • most neural controls operate via reflex arcs involving these
  • Inputs from baroreceptors are integrated into the Cardiovascular Center of the medulla oblongata
  • Outputs travel via autonomic fibers to the heart and the vascular smooth muscle
32
Q

Neural Controls: 
Role of the Cardiovascular Center

A

The cardiovascular center contains cardioacceleratory, cardioinhibitory, and vasomotor centers

33
Q

vasomotor center

A

transmits impulses along sympathetic efferent fibers called vasomotor fibers

34
Q

vasomotor fibers

A

exit the spinal cord (T1-L2) and innervate the smooth muscle of the blood vessels - mainly arterioles

35
Q

vasomotor tone

A

a result of the arterioles almost always moderately constricting

36
Q

sympathetic activity and vasoconstriction

A

Increased sympathetic activity will increase vasoconstriction and raise BP; decreased sympathetic activity will decrease vasoconstriction and lower BP

37
Q

Neural Controls: Baroreceptor Reflexes

A

Rising arterial BP activates baroreceptors in the carotid sinuses (dilations within the internal carotid arteries), the aortic arch, and the walls of nearly every large artery of the head/neck
- Baroreceptors send impulses to the cardiovascular center –cardioinhibitory center is stimulated; vasomotor and cardioacceleratory centers are inhibited

38
Q

Net Result

A

decreased blood pressure
* Via vasodilation and decreased cardiac output
- Rapid-responding baroreceptors protect against short-term changes in BP
* Ex: Orthostatic Hypotension – a failure of the baroreceptor reflex

39
Q

Chemoreceptors

A

receptors that respond to changes in levels of CO2, H+, and O2 in the blood
- stimulate the cardioacceleratory center to increase CO and the vasomotor center to increase vasoconstriction when:
* CO2 level rises
* pH level falls
* O2 level falls
- Located close to the baroreceptors, the most prominent chemoreceptors are the carotid bodies and the aortic bodies
- play a larger role in regulating respiratory rate

40
Q

Neural Controls: Higher Brain Centers

A
  • Reflexes regulating blood pressure are integrated into the medulla oblongata of the brain stem – the cerebral cortex and hypothalamus are not involved in routine regulation of BP
  • Higher brain centers can modify arterial pressure via relays to the brain stem
  • Examples: fight or flight response, redistribution of blood flow by the hypothalamus
41
Q

Adrenal Medulla Hormones: Epinephrine and Norepinephrine

A
  • Released in response to stress
  • Enhance sympathetic response by increasing CO and promoting vasoconstriction
42
Q

Angiotensin II

A
  • Renin is released by the kidneys when blood pressure or volume are low
  • Renin generates Angiotensin II
  • Promotes intense vasoconstriction to rapidly increase blood pressure
  • Stimulates release of ADH and Aldosterone – both participate in longer term BP regulation
43
Q

Atrial Natriuretic Peptide (ANP)

A
  • Produced by the atria of the heart to reduce blood volume and pressure
  • Antagonizes aldosterone, promotes vasodilation, stimulates excretion of sodium and water
44
Q

Antidiuretic Hormone (ADH)

A
  • Also called vasopressin, produced by the hypothalamus
  • Stimulates the kidneys to conserve water and widespread vasoconstriction
45
Q

Long Term Regulation: Renal Mechanisms

A

Longer term blood pressure controls regulate blood volume
- Increased BV = Increased BP and vice versa
- The kidneys are a key player in long term regulation

46
Q

Direct Renal Mechanism

A
  • When BV or BP rise, fluid is filtered from the bloodstream to the kidneys more rapidly -> increased urine -> decreased BV and BP
  • The opposite also occurs
47
Q

Indirect Renal Mechanism

A
  • When BP declines, the kidneys release the enzyme renin into the blood
  • Renin splits the plasma protein angiotensinogen to make angiotensin I
  • Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)
  • ACE is found in the capillary endothelium of various body tissues – especially the lungs
48
Q

The Four Actions of Angiotensin II

A
  1. Stimulates the adrenal cortex to secrete aldosterone
  2. Stimulates the posterior pituitary gland to secrete ADH
  3. Triggers the sensation of thirst
  4. Vasoconstriction to increase TPR
49
Q

Homeostatic Imbalances

A

Hypertension (HTN): chronically elevated blood pressure
SBP > 130 mmHg; DBP > 80 mmHg
30% of adults over 50 are hypertensive
HTN strains the heart and damages the blood vessels
Prolonged HTN is a major cause of heart failure, vascular disease, renal failure, and CVA

50
Q

Primary (or Essential) HTN

A

Hypertension without a specific, underlying cause
- Environmental, contributing factors:
* Heredity, Diet, Obesity, Age, Diabetes Mellitus, Stress, Smoking
- Primary HTN can be controlled with improved diet, increased exercise, stopping smoking, managing stress, and taking anti-HTN medications
- Commonly used anti-HTN medications: diuretics, beta-blockers, calcium-channel blockers, ACE inhibitors, and angiotensin II receptor blockers

51
Q

Secondary HTN

A

10% of HTN cases
Secondary HTN as an identifiable cause:
- Obstructed renal arteries
- Kidney disease
- Endocrine disorders – hyperthyroidism or Cushing’s Disease

52
Q

Hypotension

A

Blood Pressure < 90/60 mmHg
- Often hypotension is harmless – or even healthy!
- Chronic hypotension can be a sign of a serious underlying condition
* Addison’s Disease: inadequate function of the adrenal cortex
* Hypothyroidism
* Severe malnutrition
- Hypotension is problematic when it results in inadequate tissue perfusion

53
Q

Circulatory Shock

A

blood vessels are inadequately filled; blood cannot circulate normally – body tissues are not adequately perfused

54
Q

Hypovolemic Shock

A

blood volume is too low
- Results from large scale blood or fluid loss
- HR will increase in response to a dramatic drop in blood volume
- Intense vasoconstriction will shift blood out of reservoirs
- Treatment: replace fluid volume ASAP

55
Q

Vascular Shock:

A

blood volume is normal; poor circulation because of extreme vasodilation and lost TPR
- Anaphylactic: lost vasomotor tone in response to an allergic reaction
- Neurogenic: failure of the autonomic nervous system
- Septic: severe systemic bacterial infection

Anatomy & Physiology 208 (39 decks)

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