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Physiology > Chapter 8 (Blood Vessels) > Flashcards

Chapter 8 (Blood Vessels) Flashcards

1
Q

Reconditioning

A

Blood needs to be constantly “reconditioned” so it’s composition remains relatively stable.
Kidneys, digestive, and the skin are reconditioning organs that require the most blood flow to achieve homeostasis.
- They withstand temporary reductions in blood flow (during exercise), whereas the brain cannot.

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2
Q

Pressure Gradient

A

F = ΔP/R
F: flow rate of blood through a vessel
ΔP: pressure gradient
R: resistance of blood vessels

The pressure gradient is the difference in pressure between the beginning and end of a vessel (from high to low). NOT the absolute pressure within the vessel.

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3
Q

Resistance in a Blood Vessel

A 
It's a measure of the opposition to blood flow through a vessel. Usually caused by friction. Resistance causes the flow rate to decrease, as long as ΔP stays constant. 
Factors that influence resistance
1. Blood viscosity (thickness)
2. Vessel length (constant)
3. Vessel radius (biggest influence)

R ∝ 1 / r^4

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4
Q

Poiseuille’s Law

A

Flow rate = ((ΔPπr^4)/8ηL)
η: viscosity of blood
All factors that affect flow rate are integrated into this formula

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5
Q

Vascular Tree

A

Arteries - Arterioles - Capillaries - Venules - Veins

Arteriorles, capillaries and venules are called microcirculation.

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6
Q

Structure of Blood Vessels

A
  • Alternating layers of connective tissues (fibrous and elastic), smooth muscle cells and epithelial cells.
  • Outer layer “tunica adventitia”
  • External elastic lamina
  • Middle layer “tunica media”
  • Inner layer “tunica intima”. Made of a single layer of endothelial cells (endothelium), surrounded by a basement membrane of connective tissues.
  • Sometimes there’s an additional layer of elastic fibers called the internal elastic lamina
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7
Q

Arteries

A

Highly elastic and carries blood away from the heart.
The wall is lined with,
- a single layer of flat endothelial cells
- smooth muscle
-connective tissue (collagen and elastic fibers) to provide tensile and elastic strength to the artery.
There is low resistance because of the large diameter. It also acts as a pressure reservoir to provide a force when the heart is relaxing.

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8
Q

Arterial Pressure and Diastole

A

The arterial walls’ compliance or distensibility (stretchiness) helps determines blood pressure.
During systole, blood enters the arteries (maximum pressure occurs here)
During diastole, no blood enters the arteries, but blood continues to leave them (least pressure here)
120mmHg/80mmHg

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9
Q

Sphygmomanometer and Korotkoff Sounds

A

Sphyg: An inflatable cuff that measures blood pressure.
Korotkoff: Distinct from heart sounds associated with valve closure

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10
Q

Pulse Pressure

A

Pulse pressure = systolic - diastolic

120 - 80 = 40

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11
Q

Mean Arterial Pressure

A

It’s the average pressure driving blood forward to the tissues.
MAP = Diastolic pressure + 1/3 pulse pressure.
120/80 MAP = 80 + (1/3)40 = 93 mmHg (arteries)
- 37 for arterioles
- 20 for capilaries
It is monitored and regulated by blood pressure reflexes.
MAP is usually constant in arteries due to low resistance.
Requirements:
1. Needs to be high enough that organs and tissues have an adequate blood supply
2. Needs to be low enough that it doesn’t put too much strain on the heart.
Short-term Control Adjustments
- occurs within seconds
- adjustments made by alterations in cardiac output and total peripheral resistants
- mediated by ANS influences on heart, veins, and arterioles
Long-term Control Adjustments
- requires minutes to days
-involves adjusting total blood volume by restoring normal sal and water balance through mechanisms that regulate urine output and thirst.

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12
Q

Arterioles

A
  • Major resistance vessels
    Contains:
    1. Less elastic connective tissues, less flexibility
    2. More thick smooth muscles are innervated by sympathetic nerve fibers, and they are sensitive to many local chemicals and a few hormones.
    3. They experience vasoconstriction and vasodilation. This is facilitated by the smooth muscles, rather than connective tissues in arteries.
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13
Q

Arteriole Vasoconstriction

A

Caused by:

  • increased myogenic activity
  • increased oxygen
  • increased endothelin
  • increased sympathetic stimulation
  • decreased carbon dioxide and other metabolites
  • vasopressin; angiotensin II
  • cold
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14
Q

Arteriole Vasodilation

A

Caused by:

  • decreased myogenic activity
  • decreased oxygen
  • decreased sympathetic stimulation
  • increased CO2 and other metabolites
  • increased nitric oxide
  • histamine release
  • heat
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15
Q

Cardiac Output

A

Depends on:

  1. Local metabolic changes: current demand for blood. When cells are more active they require more blood.
  2. The number and radius of arterioles supplying the area.
  3. The extent of vascularization
  4. Arteriolar resistance in the various vascular beds.
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16
Q

Intrinsic and Extrinsic Control

A
  1. Local (intrinsic) control determines the distribution of cardiac output (blood flow)

a. Local Chemical Influences
i. active hyperemia
ii. local metabolic changes
iii. local vasoactive mediators
iv. effect of Histamine on arterioles

b. Local Physical Influences
i. local heat/cold application
ii. chemical response to shear stress
iii. myogenic response to stretch
iv. reactive hyperemia

  1. Extrinsic control regulates blood pressure by controlling fluid balance
    a. sympathetic activity
    b. epinephrine and norepinephrine
    c. angiotensin II
    d. vasopressin / ADH
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17
Q

Local Vasoactive mediators

A

Chemical and physical changes affect the endothelial cells which release locally acting chemical messengers.
eg. Endothelial-derived relaxing factors act as vasoactive agents (endothelin and nitric oxide). This induces relaxation of arteriolar smooth muscles by inhibiting contraction-induced Ca2+ into smooth muscle cells.

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18
Q

Endothelin / Endothelial Cells

NOT ON EXAM

A
  • lines b.v and heart chambers, physical barrier between blood and remainder of the vessel wall.
  • secretes substances that stimulate new vessel growth
  • participates in capillary exchange
  • influences formation of clots and clot dissolution
  • aids in the determination of capillary permeability
19
Q

Effect of Histamine on Arteriolar Caliber

A

Connective tissue and blood cells release histamine in response to tissue injury or allergy. Histamine induces vasodilation which allows for more leukocytes to the injured area.

20
Q

Myogenic Responses to Stretch

A

Vasoconstriction increases muscle tone (thicker)
Vasodilation decreases muscle tone (thinner)
Endothelial-derived vasoactive substances induces myogenic tone

21
Q

Reactive Hyperemia

A

The spike in blood flower after a period of ischemia (no blood flow)
Dilation occurs when:
1. myogenic relaxation occurs
2. there are changes in local chemical composition

22
Q

Autoregulation

A

It’s a local arteriolar mechanism that keeps tissue blood flow pretty constant despite wide variation in mean arterial pressure
eg, brain and kidneys have better autoregulation than skeletal muscles.

23
Q

Extrinsic Control of Arteriolar Radius

A
  • Includes both neural and hormonal influence that regulate arteriolar radius
  • Sympathetic nerve fibers innervate arteriolar smooth muscles in the systemic circulation, except for the brain
24
Q

Effect of Norepinephrine on arteriolar smooth muscle

A
  • Sympathetic nerve endings release NE, which binds a1- adrenergic receptors. Ths causes smooth muscles of arterioles to contract (vasoconstriction).
  • Cerebral arterioles do not have a1-adrenergic receptors.
  • These cerebral vessels are controlled by local mechanisms that maintain constant blood flow.
25
Q

Epinephrine and Norepinephrine influence

A

Epinephrine
- B2 and a1 stimulate vasodilation (arterioles heart, skeletal muscles)
Norepinephrine
- a1-adrenergic receptors stimulate vasoconstriction (arterioles digestive system and kidneys)

26
Q

Influence of Angiotensin II

A
  1. It’s a part of a hormonal pathway that regulates the body’s salt balance through aldosterone.
  2. Promotes salt and water conservation during urine formation
  3. Maintains plasma volume through fluid balance to regulate long-term blood pressure
  4. Potent vasoconstrictor.
27
Q

Capillaries

A
  • 10-40 billion capillaries
  • Capillary walls are made of a single layer of flat endothelial cells.
  • Radius cannot be adjusted.
  • Maximized surface area and minimized diffusion distance
  • Velocity of blood flow is slow (increased exchange time)
  • 2 passive exchanges
    a. diffusion
    b. bulk flow (no questions)
  • Capillaries are surrounded precapillary sphincters.
  • Can branch from a thoroughfare channel known as a metarteriole (between arteriole and venule)
28
Q

Capillary Pores

A
  • Located at the junctions between cell and capillary.

- They permit passage of small water-soluble substances.

29
Q

Lymphatic System

A

An extensive network of one-way vessels provides an accessory route by which fluid can be returned from te interstitial fluid to the blood.
“storm sewer”

30
Q

Lymphatic System (Def and Functions)

A

An extensive network of one-way vessels provides an accessory route by which fluid can be returned from the interstitial fluid to the blood.
“storm sewer”
1. Return of excess filtered fluid
2. Defence against disease
a. Lymph nodes have phagocytes which destroy bacteria filtered from interstitial fluid.
3. Transport of absorbed fat
4. Return of filtered protein

31
Q

Lymph

A

Lymph: interstitial fluid that enters a lymphatic vessel.
Lymph vessels: lymphatics converge to form larger lymph vessels. They eventually empty into venous system. Has one way valves and surrounded by smooth muscles.

32
Q

Initial Lymphatics

A

Initial lymphatics: small blind-ended terminal lymph vessels permeate almost every tissue of the body.
Pathway: blood capillaries - plasma - interstitial fluid - lymph - lymphatic vessels - venous return - right atrium.

33
Q

Oedema

A

Swelling of tissues because of excess interstitial fluid.
Causes:
1. A reduced concentration of plasma proteins.
a. kidney disease
b. liver disease
c. loss of pl. protein from burned surfaces
2. Increased permeability of capillary wall (allergic reaction)
3. Increased venous pressure (swelling during pregnancy)
4. Blockage of lymph vessels (filariasis and elephantiasis)

34
Q

Venules

A

Venules have little tone and resistance. Capillaries drain into venules, which turn into veins.

35
Q

Veins

A
  • Have a large radius, so the offer little resistance to flow.
  • Serves as blood reservoir
  • “Capacitance vessels”
    Factors that enhance Venous Return
  • Driving pressure from cardiac contraction
  • Sympathetically induced venous vasoconstricion
  • Skeletal muscle activity
  • Effect of venous valves
  • Respiratory activity
  • Effect of cardiac suction.
  • 64% of blood is stored in the veins
36
Q

Blood Pressure

A

Additional reflexes that influence blood pressure.
1. Left atrial receptors and hypothalamic osmoreceptros affect long-term regulation of blood pressure by controlling plasma volume
2. Chemoreceptors in carotid and aortic arteries are sensitive to low O2 or high acid levels in the blood - reflexely increase respiratory activity
3. Associated with certain behaviours and emotions mediated through cerebral-hypothalamic pathway
4. Exercise modifies cardiac responses
5. Hypothalamus controls skin arterioles for temperature regulation.
6. Vasoactive substances released from endothelial cells play a role.
Primary Determinants
- cardiac output
- total peripheral resistance

37
Q

Hypotension

A
  • blood pressure below 100/60 mmHg
    Occurs when
  • there is too little blood to fill the vessels
  • heart is too weak to drive the blood
    Orthostatic (postural) hypotension
  • results from insufficient compensatory responses to gravitational shifts in blood (horizontal to vertical position)
38
Q

Primary Hypertension

A 
- blood pressure is above 140/90 mmHg
Primary
- category for blood pressure elevated by a variety of unknown causes, rather than single disease
Potential Causes
- excessive salt intake
- defects in salt management by the kidneys
- diets low in K+ and Ca2+
- endogenous digitalis-like substances
- excess vasopressin / ADH
Complications:
- congestive heart failure
- stroke
- heart attack
- spontaneous hemorrhage
- renal failure
- retinal damage
39
Q

Secondary Hypertension

A

Secondary

  • 10% of hypertension cases
    1. Renal hypertension (eg, atherosclerotic plaque in renal artery)
    2. Endocrine hypertension (eg, pheochromocytoma- adrenal medullary tumor causes excessive release of E and NE)
    3. Neurogenic hypertension: results from defect in cardiovascular control centre (Medulla Oblongata)
40
Q

Circulatory Shock

A

When the blood pressure falls so low that adequate blood flow to the tissue can no longer be maintained.

41
Q

Hypovolemic Shock

A

Also known as as hemorrhagic shock, results when you lose more than 20 percent (one-fifth) of your body’s blood or fluid supply (severe haemorrhage, excessive vomiting, diarrhoea, urinary losses etc.)

42
Q

Cardiogenic Shock

A

Due to a lessened cardiac output and weakened heart.

43
Q

Vasogenic Shock

A

Shock caused by widening (vasodilation) of the blood vessels, usually from medication. Symptoms include dizziness and loss of consciousness.

44
Q

Neurogenic Shock

A

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury.

Physiology (13 decks)

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