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Physiology and Pharmacology > The Cardiovascular System > Flashcards

The Cardiovascular System Flashcards

1
Q

why do we have a circulatory system?

A
  • evolutionary consequence of increase in size and complexity of multicellular organisms
  • our SA:V ratio is poor
  • steep conc gradient is needed to deliver nutrients/remove waste from centrally located cells
  • blood acts as a convection system
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2
Q

what is the primary function of the circulatory system?

A

distribution of gases and molecules for nutrition, respiration, growth and repair

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3
Q

what are the secondary functions of the circulatory system?

A
  • fast chemical signalling via hormones
  • dissipation of heat around the body and from the body via vasodilation
  • mediates inflammatory response and immune system to invading microbes
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4
Q

what changing demands in the organism require regulation?

A
  • sleep/wake
  • body position and change to interthoracic pressure due to standing/sitting
  • rest/exercise
  • acceleration/deceleration
  • digestion
  • emotional stress
  • thermal stress
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5
Q

what are the 3 functional parts of the human circulatory system?

A
  1. heart - pump
  2. blood - fluid
  3. blood vessels - containers
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6
Q

what percentage of blood does the brain receive and why?

A
  • 15% of blood

- as it is susceptible to oxygen deficit

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7
Q

what are the 2 pumps of the heart?

A
  1. Systemic circulation

2. Pulmonary circulation

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8
Q

what is systemic circulation?

A
  • left side of heart
  • thicker myocardial walls for greater force of contraction
  • parallel circuit from left to right
  • usually flows through single extensive capillary bed
  • can have 2 capillary beds in series e.g. kidneys
  • can have capillary beds in parallel and series e.g. spleen and liver
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9
Q

what is pulmonary circulation?

A
  • right side of heart
  • single pathway from right to left
  • thinner walls
  • requires less contraction force as it goes to lungs which are closer
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10
Q

what are the 3 main groups of blood vessels?

A
  1. arteries: distribution system
    - away from heart
  2. microcirculation: diffusion and filter system
    - capillaries and lymphatic vessels from first-order arterioles to first-order venules
  3. veins: collection system/reservoir
    - to the heart
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11
Q

how do blood vessels vary with branching?

A
  • vessel radius decreases with branching (1.1cm in aorta, 3um in capillary)
  • combined cross-sectional area of daughter vessels is greater than parent vessel
  • sharpest increase occurs in microcirculation
  • total volume of flow is the same, so velocity is low to enable gas exchange
  • important in lungs to maximise O2 collection in blood
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12
Q

how does the function of vessels relate to its structure?

A
  • pressure of veins is lower than arteries, so has valves to prevent backflow
  • pressure of arteries is high to quickly distribute blood to tissues
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13
Q

what are the 4 building blocks of the vascular wall?

A
  1. endothelial cells: single, continuous, inner layer
  2. elastic fibres: provide vessel stretch
    - can be 100% stretch due to attachment to other elements of walls
  3. collagen fibres: maintain integrity of vessels to prevent bursting
  4. smooth-muscle: enable change in diameter
    - vary depending on muscular and elastic arteries
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14
Q

what are the 3 layers of blood vessel walls?

A
  1. Tunica intima: endothelial cells on basement membrane
    - found in all vessel types
  2. Tunica media: smooth-muscle and elastic fibres, with elastic core in microfibrils
  3. Tunica externa/adventitia: collagen fibres, elastic fibres
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15
Q

what blood vessel wall layer do capillaries have?

A
  • only the tunica intima

- one endothelial cell thick to shorten diffusion distance to tissues

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16
Q

how does the composition of vascular walls vary among blood vessels?

A
  • variation contributes to differences in elastic properties between arteries and veins
  • more elastic fibres in aorta than arterioles and veins to propel blood
  • more smooth muscles in arterioles to redirect blood to tissues that need oxygen
  • more collagen fibres in aorta where greatest pressures are so it doesn’t collapse
  • vena cava also has lots of collagen fibres as it is a reservoir of blood
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17
Q

what are the features of elastic arteries?

A
  • largest arteries e.g. aorta
  • highly compliant: walls stretch easily without tearing in response to pressure increase
  • enables vessels to cope with peak ejection pressures
  • recoil of elastic fibres forces blood to move forward, even when ventricles are relaxed
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18
Q

what are the features of muscular arteries?

A
  • medium-sized arteries
  • smooth muscle cells are arranged circumferentially to enable contraction of lumen
  • capable of greater vasodilation/constriction to adjust rate of blood flow
  • vascular tone: vessel is never completely relaxed
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19
Q

what is vascular tone?

A
  • state of partial contraction to maintain vessel pressure and efficient flow
  • vessel is never completely relaxed
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20
Q

what are the features of arterioles?

A
  • smooth muscle to enable regulation of blood flow to capillaries
  • regulates microcirculaion
  • metarterioles = terminal regions that have larger diameter and can reform into a venule
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21
Q

what are precapillary sphincters?

A
  • located at end of arteriole
  • monitor blood flow into capillary via mesenteric/cerebral circulation
  • contains high amounts of smooth muscle
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22
Q

what are the features of venules?

A
  • postcapillary venules
  • porous: act as exchange sites for nutrients and waste
  • muscular venules have thin smooth muscle layer (less muscular than arteries)
  • thin walls allow expansion without loosing integrity: reservoirs
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23
Q

what are the features of veins?

A
  • less muscular and elastic
  • distensible enough to adapt to variations in volume and pressure of blood
  • can store a large volume of blood due to high compliance and large lumen
  • contain largest % of blood in the CV system – ‘unstressed volume’ (70% of blood in body)
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24
Q

what are the features of large veins?

A
  • more muscular than venules
  • possess valves to prevent backflow
  • valves are extensions of the inner endothelial layer
  • if valves are defective, backflow of blood can occur, leading to varicose veins
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25
Q

what is capillary exchange?

A
  • function of CVS to maintain suitable environment for tissues
  • capillaries are principle exchange sites for gases, water, nutrients and waste products
  • tissue capillaries allow glomerular filtrate, skin temperature regulation, hormone delivery, platelet delivery
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26
Q

what are the features of capillaries?

A
  • composed of only endothelial cells and basement membrane

- exchange substances between blood and interstitial fluid

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27
Q

what are the 3 groups of capillaries?

A
  1. continuous: have inter-endothelial junctions to prevent leakage
  2. fenestrated: have pores to allow larger molecules to pass through
    - more leaky
  3. sinusoidal: in liver and bone marrow
    - allows whole blood cells to pass through
    - most leaky
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28
Q

what are Starling’s forces?

A
  • fluid transfer across capillary walls driven by sum of hydrostatic and osmotic pressures from fluid inside capillaries and interstitial fluid outside
  • oncotic pressure (colloid osmotic pressure) due to dissolved serum albumin
  • Kf hydraulic conductance (water permeability of capillary wall) varies with tissue
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29
Q

what are the Starling pressures across the capillary wall?

A
  • Pc (capillary hydrostatic pressure) declines along length of capillary via fluid filtration
  • net filtration becomes net absorption
  • arteriole filtration exceeds venular absorption
  • 2-4L fluid/day in interstitium

net filtration = +6mmHg
net absorption = -5mmHg

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30
Q

what is the lymphatic system?

A
  • drains excess interstitial fluid
  • transport of dietary lipids
  • immunology: lymph nodes/organs
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31
Q

how is blood volume maintained?

A
  • lymphatic system maintains circulating volume of blood

- returns lymph to CVS via subclavian veins

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32
Q

what is the pericardium of the heart?

A
  • protective fluid-filled sac
  • lubricates the heart to reduce friction between the heart and surrounding tissue
  • limits infection of the heart
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33
Q

what are the 4 chambers of the heart?

A
  1. Right atrium: receives deoxygenated blood from systemic return (vena cava)
  2. right ventricle: pumps deoxygenated blood to lungs in pulmonary circulation for oxygenation (pulmonary artery)
  3. left atrium: receives oxygenated blood from pulmonary circulation (pulmonary vein)
  4. left ventricle: pumps oxygenated blood under high pressure to head and body (aorta)
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34
Q

what is the difference between atria and ventricles?

A

atria act as reservoirs: passive

ventricles contract: active

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35
Q

what are the atrioventricular valves?

A

Mitral/bicuspid (left) and tricuspid (right):

  • connected to cardiac wall by chordae tendinae and papillary muscles
  • maintain valve integrity
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36
Q

what are the semilunar valves?

A

aortic and pulmonary:

  • have small fibrous nodules which are close together to fill triangular opening
  • fibrous nodules maintain integrity
37
Q

what is the role of the AV valves and SL valves?

A
  • control the unidirectional flow of blood from atria to ventricles to arteries during the cardiac cycle
38
Q

what are the 3 layers of the heart wall?

A
  1. epicardium
  2. myocardium
  3. endocardium
39
Q

what is the epicardium?

A
  • outermost layer
  • comprised of loose connective tissue, elastic fibres and adipose tissue for integrity
  • protects heart
  • produces pericardial fluid for lubrication
40
Q

what is the myocardium?

A
  • composed of involuntary striated muscle cells
  • muscle cells are encased in collagen fibres
  • largest layer
41
Q

what is the endocardium?

A
  • inner layer
  • continuous with valvles
  • contains smooth muscle and elastic fibres
42
Q

what 2 types of cells does the heart consist of?

A
  1. contractile cells: majority of atrial and ventricular tissues
    - APs lead to contraction and generation of force/pressure
  2. conducting cells: found in SAN, atrial internodal tracts, AVM, bundle of His and Purkinje system
    - rapidly spread APs
43
Q

what is the electrophysiology of cardiac cells?

A
  • excitation of myocytes triggers excitation-contraction coupling
  • AP propagation is timed to synchronise ventricular contraction and optimise blood ejection
  • thick myocardium contains branched fibre cells which care connected via intercalated discs
  • this allows APs to propagate from cell-to-cell rapidly
44
Q

how are myocardial cells structured?

A
  • they are electrically coupled via gap junctions for coordinated contraction as a syncytium
  • intercalated disc gap junctions form channels between myocytes allowing depolarisation current to spread
  • intercalated discs are part of sarcolemma via Z-lines which are excitable
  • desmosomes anchor fibres together to maintain integrity
45
Q

what are T-tubules?

A
  • deep invaginations of the sarcolemma
  • enable current to be relayed to cell to release Ca2+
  • larger instantaneous force is produced by SR Ca2+ release near all sarcomeres simultaneously
46
Q

what are sarcomeres?

A
  • repeating, functional units between intercalated discs
  • cardiac muscle is striated
  • sarcomeres have myosin ad actin filaments
  • myosin head binds to actin
  • contains tropomyosin and troponin
  • troponin C-subunit binds to Ca2+ and moves tropomyosin from the actin-myosin binding site
47
Q

how is the sarcomere a sliding filament?

A
  • following depolarisation, cross-bridges form and break between actin and myosin
  • this allows the filaments to slide over each other
  • cross-bridge is formed via ATP and allows tension in the muscle fibre
  • distance between Z-lines shorten
  • overall effect is an organ-level contraction
48
Q

what is titin?

A
  • a scaffold to hold the actin and myosin to the intercalated discs
49
Q

what is the depolarisation sequence of the heart?

A
  1. cells of SAN spontaneously depolarise to fire APs 60-100/min
    - can be affected by ANS
  2. cardiac cells electrically coupled via gap junctions conduct AP from cell to cell through left and right atria - atrial systole
  3. 0.1s later, signal arrives at AVN
    - atrioventricular ring prevents instant impulse spread
  4. conduction spreads to His-Purkinje fibre system in ventricles, leading to ventricular systole for blood ejection
50
Q

what is the overall process of the cardiac cycle?

A
  1. atrial systole
  2. isovolumetric ventricular contraction = ventricular systole
  3. rapid ventricular ejection
  4. reduced ventricular ejection
  5. isovolumetric ventricular relaxation = diastole
  6. rapid ventricular filling
  7. reduced ventricular filling
51
Q

what happens during atrial systole?

A
  1. depolarisation of atria following sitmulation of SAN
  2. contraction of atrium causes increase in atrial pressure
  3. as ventricles are relaxed and AV valves are open, blood flows from atria to ventricles
    - passive filling
52
Q

what is isovolumetric ventricular contraction (ventricular systole)?

A
  1. following electrical activation via Purkinje fibres, ventricles contact and ventricular pressure rises
  2. when ventricular pressure exceeds atrial pressure, AV valves close, producing heart sound S1
  3. pressure increases but volume remains the same
53
Q

what happens during rapid ventricular ejection of blood?

A
  1. pressure rises until it exceeds aortic pressure
  2. SL valves open, and blood is ejected due to pressure gradient from ventricle to artery
  3. most of stroke volume is ejected
  4. ventricular volume falls and arterial pressure rises
  5. atrial filling begins and pressure slowly increases
54
Q

what is reduced ventricular ejection?

A
  1. ventricles repolarise and pressure falls due to no contraction
  2. SL valves still open, so blood is still ejected but at a reduced rate
  3. arterial volume falls as blood moves to arterial tree
  4. arterial pressure increases as blood returns to heart
55
Q

what is isovolumetric ventricular relaxation (diastole)?

A
  1. begins when ventricles fully repolarised
  2. ventricles relax and pressure decreases
  3. when below arterial pressure, SL valves close, causing heart sound S2
  4. all valves are closed and ventricular volume is constant
56
Q

what is rapid ventricular filling?

A
  1. ventricular pressure falls below atrial pressure

2. AV valves open and volume increases rapidly, but pressure stays low (S3)

57
Q

what is indicated if S3 is heard in adults?

A
  • sign of illness
58
Q

what is reduced ventricular filling?

A
  1. longest phase of cardiac cycle
  2. final portion of ventricle filling
  3. atrial systole marks end of diastole
59
Q

what is the electrocardiogram (ECG)?

A
  • measured by magnetic fields
  • depolarisation and repolarisation events of the cardiac cycle detected by electrodes on skin
  • displays electrical activity to identify pathology with aberrant rate
  • records the summed electrical activity of the heart
  • direction of electrical activity can cause positive or negative deflections
60
Q

what is the P wave of an ECG?

A
  • depolarisation of atria
  • duration of P wave= atrial conduction time
  • repolarisation of atria is masked by QRS wave
61
Q

what is the PR interval of an ECG?

A
  • AV node conduction

- reflects the initial depolarisation of atria to that of the ventricles

62
Q

what is the QRS complex of an ECG?

A
  • depolarisation of ventricles

- ejection of blood from heart

63
Q

what is the T wave of an ECG?

A
  • repolarisation of ventricles
64
Q

what are the haemodynamics of arteries?

A
  • under high pressure - stressed volume

- receive blood directly from heart

65
Q

what are the haemodynamics of arterioles?

A
  • site of highest resistance to blood flow
  • walls are always contracted: tonically active smooth muscle to propel blood
  • resistance changed in response to sympathetic nerves, catecholamines and vasoactive substances
66
Q

what are arterioles innervated by? what receptors do they use?

A
  • sympathetic adrenergic fibres
  • alpha1-adrenergic receptors are activated by NA, leading to contraction of smooth muscle to increased resistance and vasoconstriction
  • beta2-adrenergic receptors in skeletal muscle arterioles cause dilation and relaxation
67
Q

how are capillaries innervated?

A
  • controlled by dilation/constriction of precapillary sphincters
  • regulated by sympathetic innervation of vascular smooth muscle and vasoactive metabolites produced in tissue
  • e.g. angiotensin, bradykinin, histamine, nitric oxide, Vasoactive Intestinal Peptide (VIP)
68
Q

what are venules and veins innervated by? what receptors do they use?

A
  • smooth muscle walls innervated by sympathetic nerve fibres - can contract
  • increased activity via alpha1-adrenergic receptors causes contraction, leading to reduced capacitance
  • this causes a decrease in unstressed volume, and an increase in stressed volume
69
Q

what is the velocity of blood flow?

A
  • rate and displacement of blood per unit of time
  • depends on diameter and cross-sectional area of the blood vessel
  • inverse relationship between velocity and cross-sectional area

velocity (cm/s) = flow (mL/s) / cross-sectional area (cm2)

70
Q

what determines blood flow?

A
  • pressure difference between vessel inlet and outlet
  • resistance of vessel to blood flow

flow (mL/s) = change in pressure (mmHg) / resistance (mmHg/mL/min)

71
Q

what factors determine resistance to blood flow?

A
  • blood vessel diameter
  • vessel length
  • series/parallel arrangement
  • blood viscosity

resistance is directly proportional to vessel length and blood viscosity, but inversely proportional to 4th power of radius of lumen

R = (8 x viscosity x vessel length) / radius of blood vessel ^4

72
Q

what is a series blood vessel arrangement?

A
  • series resistance = summed resistance of all blood vessels in an organ
  • pressure decreases through each sequential component
  • largest decrease in pressure in arterioles:

change in pressure = resistance x flow

73
Q

what is a parallel blood vessel arrangment?

A
  • e.g. major arteries branching from aorta
  • parallel resistance is less than any of the individual resistances
  • there is no loss of pressure in blood flow
74
Q

what are the different pressures in the different blood vessels of the CVS?

A
  1. aorta: high pressure, high cardiac output, high-low compliance
  2. arteries: high pressure due to elastic recoil
  3. arterioles: dramatic fall in pressure due to high resistance to flow
    - no longer pulsatile
  4. capillaries: frictional resistance to flow and filtration
  5. venules and veins: low pressure, high compliance
75
Q

why is there a decrease in pressure as blood flows through the vessels?

A
  • as energy consumed overcomes frictional distance
76
Q

how does arterial pressure vary in systemic circulation?

A
  • oscillations in arterial pressure reflect pulsatile activity of heart
  • diastolic pressure = lowest arterial pressure during ventricular relaxation
  • systolic pressure = highest arterial pressure after blood ejected from ventricles
77
Q

what is the dicrotic notch (incisura)?

A
  • the blip produced when the aortic valve closes

- brief period of backwards flow

78
Q

what is pulse pressure?

A

pulse pressure = systolic pressure - diastolic pressure

  • reflects the volume ejected from the left ventricle (stroke volume)
79
Q

what is mean arterial pressure?

A

mean arterial pressure = diastolic pressure + 1/3 systolic pressure

  • average pressure of arteries in a complete cardiac cycle
80
Q

how does blood pressure change throughout the day?

A
  • higher pressure during the day
  • lower pressure during sleep
  • pressure is regulated to meet the needs of the body and activity levels
81
Q

how is blood pressure rapidly regulated?

A
  • baroreceptors: carotid and aortic sinuses in arteries
  • Nucleus tractus solitarius receives info and directs changes in output of ANS via CVS centres
  • brainstem CVS centres in reticular formation of medulla and pons: cardiac accelerators/decelerators
82
Q

what is the sympathetic control of blood pressure (BP)?

A

elevates BP in 4 ways:

  1. stimulates SAN to increase HR
  2. increases cardiac muscle contractility and stoke volume via b1-adrenoreceptors
  3. stimulate arterioles to vasoconstrict and increase total peripheral resistance (TPR)
  4. stimulate veins to vasoconstrict to decrease unstressed volume and increase stressed volume on arterial side
83
Q

what is the parasympathetic control of blood pressure?

A
  • vagus nerve inhibits SAN to decrease HR and reduce BP
84
Q

how is arterial pressure (Pa) controlled in the long term?

A

renin-angiotensin II-aldosterone system:

  1. decreased Pa causes decrease in renal perfusion pressure
  2. this is detected by mechanoreceptors in afferent kidney arterioles
  3. prorenin is converted to renin
  4. angiotensin is converted to angiotensin I
  5. ACE converts angiotensin I to angiotensin II
85
Q

what are the downstream effects of angiotensin II?

A
  • causes adrenal cortex to secrete aldosterone
  • increases Na+ reabsorption to increase ECF
  • stimulates Na+/H+ exchange in kidney
  • stimulates reabsorption of Na+ and bicarbonate
  • acts on hypothalamus to increase thirst and secretion of vasopressin to increase water reabsorption
  • vasoconstriction of arterioles to increase TPR
86
Q

what are other regulatory hormones in BP homeostasis?

A
  • chemoreceptors for O2 in carotid and aortic sinus bodies stimulate arteriole vasoconstriction
  • chemoreceptors for CO2 in brain stimulate arteriole vasoconstriction
  • ADH (AVP): acts on V1 receptors and causes vasoconstriction in vascular smooth muscle cells/ acts on V2 receptors and causes water retention
  • atrial natriuretic peptide (ANP): vasodilator to increase diuresis and decrease ECF
87
Q

what is chronic hypertension?

A
  • long term elevated blood pressure
  • info from carotid sinus baroreceptors joins CN IX to brainstem
  • aortic arch info via CN X
  • baroreceptors in chronic hypertension do not perceive elevated BP as abnormal
  • therefore hypertension is maintained and not corrected
88
Q

what is the risk hypertension?

A
  • persistent high BP can cause risk of heart disease/attacks via damage to endothelium causing constriction, so loss of O2 to heart tissue
  • can cause stroke if blocked brain artery
  • strain on blood vessels and other organs
89
Q

what are hypertension treatments?

A
  • ACE inhibitors
  • angiotensin II receptor blockers
  • diuretics = thiazide
  • beta-blockers: block effects of epinephrine to lower force of heart contraction
  • Ca2+ channel blocks: limits rate of Ca2+ into heart so contractions weaken and blood vessels relax
  • alpha-blockers: inhibit alpha-adrenoreceptors to stop vasoconstriction
  • alpha-agonists: reduce sympathetic output so reduce BP
  • renin inhibitors: stop angiotensin II release

Physiology and Pharmacology (13 decks)

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