Cardiovascular Physiology Flashcards

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1
Q

Whats the function of the CVS?

A

Bulk flow system - Transports:

  • Oxygen/Carbon Dioxide
  • Nutrients
  • Metabolites
  • Hormones
  • Heat
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2
Q

How is blood flow produced?

A

By pressure differences produced primarily by the Left ventricle and the pressure gradient between it and the Right atrium

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3
Q

How is blood flow regulated?

A

Flow = Pressure/Resistance

Pressure = Mean arterial pressure (Diastolic pressure + pulse pressure/3) - Central venous pressure

Resistance = controlled by vessel radius : selectively redirects flow

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4
Q

How does blood pressure change throughout the cardiovascular system?

A

Systemic pressures are highest in the aorta (120mm Hg)

Drops to a minimum of 2mm Hg in the right atrium.

The mean arterial pressure drops gradually as the blood moves from the aorta to the elastic and muscular arteries; when it reaches the arterioles it drops dramatically; by the time it reaches a pre-capillary sphincter, no pressure fluctuations remain - blood pressure = 35mm Hg

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5
Q

Blood Vessel Histology: What are the 3 general features to arteries and veins? (1)

A

(1) Tunica Intima/interna: inner layer of a blood vessel

  • Endothelial lining and a surrounding layer of CT with a variable number of elastic fibres.
  • In arteries, the outer margin of the tunica intima contains a thick layer of elastic fibres called the INTERNAL ELASTIC MEMBRANE
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6
Q

Blood Vessel Histology: What are the 3 general features to arteries and veins? (2)

A

(2) Tunica media: middle layer of blood vessels
- Contains concentric sheets of smooth muscle tissue in a framework of loose CT. The collagen fibres bind the tunica media to the tunica intima and tunica externa.

  • Commonly the thickest part in a small artery
  • Separated from the surrounding tunica externa by a thin band of elastic fibres called the external elastic membrane.
  • Smooth muscle cells of the tunica media encircle the endothelium that lines the lumen of the blood vessel : when they contract the vessel decreases in diameter and when they relax the diameter increases
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7
Q

Blood Vessel Histology: What are the 3 general features to arteries and veins? (3)

A

(3) Tunica externa: outer layer of a blood vessel

  • CT sheath
  • In arteries, it contains collagen fibres with scattered bands of elastic fibres
  • In veins, it is generally thicker than the tunica tunica media and contains networks of elastic fibres and bundles of smooth muscle cells
  • The CT fibres of the tunica externa typically blend into those of the adjacent tissues; stabilising and anchoring the blood vessel
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8
Q

What are the features of of a typical artery?

A

General appearance: Round + relatively thick walls

Tunica Intima:

(1) Usually rippled endothelium
(2) Present interal elastic membrane

Tunica media:
Thick + dominated by smooth muscle cells and elastic fibres
(1) Present external elastic membrane

Tunica externa:
Collagen and elastic fibres

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9
Q

What are the features of of a typical vein?

A

General appearance: Usually flattened or collapsed with relatively thin wall

Tunica Intima:

(1) Smooth endothelium
(2) No internal elastic membrane

Tunica Media:
Thin, dominated by smooth muscle cells an no collagen fibres
(1) No external elastic membrane

Tunica Externa:
(1) Collagen and elastic fibres and smooth muscle cells

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10
Q

Classification of Blood vessels - Arteries: What is an Elastic artery?

A
  • Also known as conducting arteries (carry large volume of blood away from the heart)
  • Large vessels with diameter around 2.5cm
  • E.g. Pulmonary trunk of aorta + major branches (common carotid & subclavian)
  • Walls are extremely resilient - tunica media has a high density of elastic fibres + few smooth muscle cells = cope with high pressure changes
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11
Q

Classification of Blood vessels - Arteries: What is an muscular artery?

A
  • Distribution arteries - distribute blood to the body’s skeletal muscles and internal organs
  • Most common vessel in the arterial system
  • Thick tunica media with more smooth muscle than elastic arteries.
  • Lumen diameter = 0.4 to 0.05 cm
  • Superficial muscular arteries are important pressure points*
  • Low resistance conduit

E.g. external carotid arteries of the neck, brachial arteries of the arm etc

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12
Q

Classification of Blood vessels - Arteries: What is an Arteriole?

A
  • Internal diameter ~20-30 µm
  • Poorly defined tunica externa : in larger arterioles, the tunica media consists of 1 or 2 layers of smooth muscle cells
  • Smallest arterioles, tunica media contains scattered smooth muscle cells that do not form a complete layer
  • Diameter changes in response to local conditions or to sympathetic or endocrine stimulation. E.g. Arterioles in most tissue vasodilate when oxygen levels are low
  • Changes in diameter affect amount of force required to push blood around the CVS. More pressure is needed to push blood through constricted vessels than through a dilated one
  • Force opposing blood flow is called RESISTANCE (R) = arterioles are RESISTANCE VESSELS
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13
Q

Classification of Blood vessels - Capillaries: What is a capillary?

A
  • Permeate most tissue : weave throughout active tissues, forming intricate networks that surround muscle fibres
  • Radiate through CT & branch beneath the basement membrane of epithelia
  • Only blood vessel whose walls permit exchange between blood and surrounding interstitial fluids : thin capillary walls
  • Slow blood flow through capillaries, allowing sufficient time for diffusion or active transport of materials
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14
Q

Classification of Blood vessels - Arteries: What are the typical features?

A
  • Endothelium tube inside a thin basement membrane
  • No Tunica media nor externa
  • Diameter = ~7-10 µm : similar to that of a single RBC
  • x2 main types: Continuous & Fenestrated
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15
Q

Classification of Blood vessels: What is a continuous capillary?

A
  • Supply blood to most areas of the body
  • Endothelium is a complete lining. In large continuous capillary, a cross section may show numerous epithelial cells : in a small one it might be a single cell encircling the lumen
  • Located in all tissue except Epithelia and Cartilage
  • Permit water/small solutes/lipid soluble materials to diffuse into the interstitial fluid
  • Prevent loss of blood cells and plasma proteins
  • In specialised continuous capillaries (most of CNS + thymus); endothelial cells are bound together by tight junctions = very restricted permeability
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16
Q

Classification of Blood vessels: What is a Fenestrated capillary?

A
  • Contain “windows” or pores, that penetrate the endothelial lining
  • Pores allow rapid exchange of water and solutes between blood and interstitial fluid
  • E.g. Chorid plexus of the brain
  • Found along absorptive areas of the intestinal tract and at filtration sites in the kidneys
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17
Q

Classification of Blood vessels: What is a Sinusoidal capillary?

A
  • Resemble fenestrated capillaries that are flattened and irregularly shaped
  • Have gaps between adjacent endothelial cells, and the basement membrane is either thinner or absent
  • Permit the free exchange of water and solutes as large as plasma proteins between blood and interstitial fluid
  • Blood move relatively slowly, maximising the time available for exchange across the sinusoidal walls.

Found in: Liver, bone marrow, spleen, endocrine glands

E.g. Liver sinusoids: plasma proteins secreted by liver cells enter the bloodstream

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18
Q

Classification of Blood vessels: What is a Capillary bed?

A
  • Capillaries function as part of an interconnected network = capillary bed/plexus
  • A single arteriole generally gives rise to dozens of capillaries - they empty into several venules (smallest vessels of the venous system
  • Contains several direct connections between arterioles and venules
  • Wall of the first part of the passage contains smooth muscle tan can change its diameter = METARTERIOLE/precapillary arteriole
  • The rest of the passagewat resembles a typical capillary in structure = THOROUGHFARE CHANNEL
  • More than 1 artery can supply a capillary bed; multiple arteries = COLLATERALS - they fuse before giving rise to arterioles
  • Fusion of x2 collaterals = arterial anastomosis
  • Arteriovenous anastomoses = direct connections between arterioles and venules
19
Q

Classification of Blood Vessels: Whats the function of Atriovenous anastomses?

A
  • When they dilate, blood bypasses the capillary bed and flows directly into the venous circulation.

Flow is regulated primarily by sympathetic innervation under control of the cardiovascular centre of the medulla oblongata

20
Q

Classification of Blood Vessels: What is a precapillary sphincter?

A

Guards the entrance to each capillary

Contraction of the smooth muscle cells of this sphincter narrows the capillary entrance = reducing or stopping the flow of blood

When one closes it diverts blood flow to another branch

21
Q

Classification of Blood Vessels: What is a Venule?

A
  • Smallest vessel in the venous system
  • Collect blood from capillary beds
  • Vary widely in size and structure; average internal diameter is roughly ~30 µm
  • Venules smaller than 50µm lack a tunica media, and the smallest venules resemble epanded capillaries
22
Q

Classification of Blood Vessels: What is a Vein (M)?

A

Medium-sized: comparable in size to muscular arteries

  • Thin tunica media and contains relatively few smooth muscle cells
  • Thickest layer of a medium sized vein is the tunica externa, contains longitudinal bundles of elastic and collagen fibres
23
Q

Classification of Blood Vessels: What is a Vein (L)?

A

Large Vein: Include superior and inferior vena cavae and their branches within the abdominopelvic and thoracic cavities

  • Have all 3 layers of Tunica
  • Slender tunica media is surrounded by a thick tunica externa composed of a micture of elastic and collagen fibres
24
Q

How does the Parasympathetic nervous system regulate heart rate?

A
  • Vagus nerve
  • Vagus releases ACh, acts on muscarinic ACh receptors in SA node
  • Slows pacemaker cells
  • Decreases heart rate = Bradycardia
  • Heart is under vagal restrain = constant release of ACh to maintain the low rate
25
Q

How does the Sympathetic nervous system regulate heart rate?

A
  • Sympathetic nerves release Norepinephrine
  • In conjunction with epiinephrine from adrenal medulla
  • Acts on ß1-receptors on SA node
  • Increases slope of pacemaker potential = threshold is reached quicker = increased heart rate= Tachycardia
26
Q

What is Preload?

A

Volume of blood in ventricles at the end of diastole (end of diastolic pressure)

  • Increased in: Hypervolemia, regurgitation of cardiac valves
27
Q

What is Afterload?

A

Resistance left ventricle must overcome to circulate blood

Increased in: Hypertension and Vasoconstriction

Increase in Afterload = Increase in workload

28
Q

What influences Cardiac Output?

A

Heart rate (HR) & Stroke Volume (SV)

29
Q

What factors influence Stroke volume (1)?

A

End-diastolic volume (EDV): The amount of blood in a ventricle at the end of diastole, just before contraction begins

Influenced by: FILLING TIME & VENOUS RETURN

Filling time: Duration of ventricular diastole. Depends entirely on the heart rate –> the faster the heart rate the shorter the time available for filling

Venous return: Variable over this period. Varies in response to changes in cardiac output/blood volume/patterns of peripheral circulation/skeletal muscle activity

Preload: Degree of stretching in ventricular muscle cells during ventricular diastole - preload is directly proportional to the EDV = the greater the EDV the larger the preload

Preload affects the ability of muscle cells to produce tension

30
Q

What factors influence Stroke volume (2)?

A

End-systolic volume (ESV): The ventricle has contracted and ejected the stroke volume, the amount of blood that remains in the ventricle at the end of ventricular systole is ESV

Effected by 3 factors:

(1) Contractility: amount of force produced during contraction, at a given preload.
- factors increasing contractility = have positive inotropic action

E.g. stimulating increased Ca2+ entry into cardiac msucle cells = force and duration of ventricular contraction

  • factors decreasing contractility = have negative inotropic action

E.g. stimulating decreased Ca2+ entry into cardiac msucle cells = force and duration of ventricular contraction

(2) Preload:
(3) Afterload: Amount of tension that the contracting ventricle must produce to force open the semi-lunar valve and egect blood

Increases with increased resistance to blood flow out of the ventricle

  • If afterload increases, so does Stroke Volume
  • Any factor that restricts blood flow through the arterial system increases afterload
31
Q

How can Autonomic activity effect contractility (1)?

A

Sympathetic:

  • Positive iontropic effect
  • Causes Norepinephrine (NE) release by Postganglionic fibres of the cardiac nerves & secretion of of Epineephrine (E) and NE by the adrenal medullae
  • Stimulate alpha and beta receptors on cardiac muscle plasma membrane = increased cardiac muscle metabolism + force/degree of contraction = Lower ESV
32
Q

How can Autonomic activity effect contractility (2)?

A

Parasympathetic:

  • stimulation by the vagus nerves = negative iontropic effect
  • Primary effect of ACh is at membrane surface = produces hyperpolarisation and inhibition = reduced cardiac contraction force
  • Atria shows greatest changes in contractile strength - highly innervated with parasympathetic nerve terminals (ventricles don’t)
  • Increased ESV
33
Q

What factors influence Heart Rate (1)?

A

Autonomic innervation:

  • Nerve plexus’ (cardiac plexus) innervation via the sympathetic and parasympathetic division
  • Postganglionic sympathetic neurons are located in the cervical and upper thoracic ganglia
  • Vagus nerves carry parasympathetic preganglionic fibres to small ganglia in the cardiac plexus
  • Both Para + Symp innervate the SA & AC nodes and atrial muscle
  • Both innervate ventricular muscle cells BUT sympathetic fibres far outnumber para fibres
  • Cardioacceleratory centre = control site in medulla oblongata of sympathetic neurons (increase heart rate)
  • Cardioinhibititory centre = control site in medulla oblongata of parasympathetic neurons (decrease heart rate)
  • Regulated by the reflex pathways
34
Q

What effect does Parasympathetic innervation have on heart rate?

A
  • Dominates in healthy individuals at rest.
  • Changes the ionic permeability of cells in the conducting system

SA Node:
- stimulates the release of ACh, which extends re-polarisation and decreases the rate of spontaneous depolarisation = heart slows

35
Q

What effect does Sympathetic innervation have on heart rate?

A

SA Node:
- Stimulates the release of Norepinephrine (NE) and binds to Beta-1 receptors, leading to the opening of sodium ion channels and calcium ion channels

Shortens re-polarisation and accelerates the rate of spontaneous depolarisation = heart rate increases

36
Q

What factors influence Heart Rate (2)?

A

Hormones:

E/NE/thyroid hormone increase heart rate by their effect on the SA node

37
Q

Haemodynamics: What are the 2 levels of control over the smooth muscle surrounding arterioles? (1)

A

Extrinsic Mechanisms:

Ensure total peripheral resistance of whole body stays in the right range (Global)

Parasympathetic nerves: Little effect - limited to digestive tract, eternal genitalia and salivary glands

Release of Norepinephrine - binds to alpha receptors = arteriolar constriction

Decreases flow through that tissue & increases total peripheral pressure

Decrease in Norepinephrine = blood vessel dilation

In some tissues (cardiac muscle), Epinephine activates Beta2 receptors = arteriole dilation - increases flow through that tissue = decreases TPR

38
Q

Haemodynamics: What are the 2 levels of control over the smooth muscle surrounding arterioles? (2)

A

Local (intrinsic) controls - meets selfish needs of individual tissue

Active (metabolic) hyperaemia: Increased metabolism (localised chemical conditions promote vasodilation) - controlled by concentration of metabolites in the capillaries (CO2/K/H) - Endothelium sense the conc. of metabolites - detects increase - chemical factors released and causes dilation of arterioles - washes out metabolites from local area

Pressure (flow) autoregulation:

Decrease in MEAN ARTERIAL PRESSURE causes a decrease in flow - metabolites accumulate and causes arteriole dilation - flow is restored to normal

39
Q

Central (reflex) control of circulation: How is Mean Arterial Pressure (MAP) calculated?

A

MAP = Cardiac Output (CO) X Total Peripheral Resistance (TPR)

Driving force behind circulation

40
Q

What happens if you have a low MAP?

A

Faint

41
Q

What happens if you have a high MAP?

A

Hypertension (high blood pressure)

42
Q

Whats the short-term management of MAP?

A

Arterial Baroreceptors (baroreflex):

Found in the walls of:
(1) Aortic sinuses (pockets in the walls of the ascending aorta adjacent to the heart)

(2) Carotid sinuses (expanded chambers near the bases of the internal carotid arteries of the neck)
(3) Wall of the right atrium

Monitor the degree of stretch in the walls of expandable organs

43
Q

How do baroceptors respond to increased blood pressure?

A
  1. Homeostasis disturbed
  2. Baroreceptors stimulated
    3a. Cardioinhibitory centre stimulated
    3b. Decreased cardiac output
    4a. Cardioacceleratory centre & Vasomotor centre inhibited
    4b. Vasodilation
  3. Blood pressure decreases
  4. Homeostasis restored
44
Q

How do baroceptors respond to decreased blood pressure?

A
  1. Decrease in bood pressure
  2. Baroreceptors inhibited
    3a. Vasomotor centre stimulated
    3b. Vasoconstriction
    4a. Cardioacceleratory centre stimulated & Cardioinhibitory centre inhibited
    4b. Increased cardiac output
  3. Blood pressure increases
  4. Homeostasis restored