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phty251 > CVS > Flashcards

CVS Flashcards

1
Q

role of the circulatory system?

A

bulk flow and distribution of blood and all that it contains

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2
Q

how is blood flow arranged in systemic circuit?

A

through branches and blood flows through in parallel

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3
Q

what is the equation that describes blood flow?

A

blood flow = change in pressure/resistnace to flow

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4
Q

(poiseuilles law) what 3 factors govern resistance?

A

length of tube, viscosity of liquid, radius of tube.

R = 8nL/pi r^4

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5
Q

increasing the blood vessel of a radius by 2, does what to resistance?

A

doubling radius, reduces resistance by 16

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6
Q

what is the name and sequence of flow of vessels in systemic and pulmonary circuit?

A

aorta - arteries - arterioles - capillaries - venules - veins - vena cava.

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7
Q

how does flow change between and within circuits?

A

blood flows in series between each type of circuit, and in parallel within each circuit

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8
Q

where is the most blood volume located?

A

in veins - 40% of blood is in veins at any given time

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9
Q

how does the CSA and velocity of blood flow change at each level of circuit flow?

A

moving away from heart, blood flow velocity decreases by half going from arterial to venous system. velocity is slowest at capillaries, and CSA of blood vessels peak at capillaries

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10
Q

what determines the blood pressure gradient through each circuit?

A

pulsatile bloodflow decreases moving away from heart due to pulsatility causing damage at small vessels

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11
Q

primary function of aorta and large arteries?

A

high pressure resevoir, drives blood through systemic circuit

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12
Q

primary function of smaller arteries and arterioles?

A

resistance vessels, determines volume flow through circulation

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13
Q

primary function of capillaries?

A

exchange vessels

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14
Q

primary function of venules and veins?

A

return conduits, primary resevoir or capacitance of the vasculature

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15
Q

heart wall layers from inside - outside

A

endocardium - myocardium - epicardium-pericardial fliud/space - pericardium

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16
Q

path of blood through heart, after circulating body:

A

RA - R AV valve - RV - PV - P trunk - P arteries - lung capillaries - Pveins - LA - L AV valve - L- Aortic valve - aorta - body

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17
Q

how are contractile myocardial cells arranged and associated with each other?

A

arranged in layers and are associated with each other through intercalated disks at each end (like bricks)

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18
Q

where and why are gap junctions associated with contractile heart cells?

A

gap junctions have low electricla resistance, and are present in the intercalated disk

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19
Q

how are filaments of cardiac muscle cells arranged?

A

actin and myosin arranged in a striated appearance

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20
Q

what is nodal tissue and where in the heart is it located?

A

nodal tissue are small round cells with minimal contractiel protein. they are specialized for generation and conduction of AP in the atria (SA node)

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21
Q

to get to the ventricles, wheat does the AP have to pass through?

A

the atrioventricular ring (via AV node)

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22
Q

why does the AP slow down once it reaches the AV node?

A

slowing down AP at AV node allows atria to fully depolarise and contract

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23
Q

what are the modified myocardial cells in the conducting system?

A

purkinje fibres

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24
Q

what is the difference in K+ permeablity between nodal tissue and myocardial cells and what does this cause?

A

permeablity to K+ is lower in nodal tissue than myocardial tissues and the RMP is less negative

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25
Q

explain the pacemaker potential

A

the slow depolarisation where K+ permeablity reduces as Na+ & Ca+ permeability increase, causing a gradual decrease in RMP

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26
Q

why does tetanus not occur in heart muscle?

A

summation of heart muscle contractions is not possible

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27
Q

What prevents re-excitation of heart muscle during most of the contraction period?

A

long absolute and relative refractive periods (due to Ca+ entering/ ‘plateau’ phase) so heart cell cant be activated again

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28
Q

at what end of the electrode would the camera be located for an ECG?

A

camera in an ECG would be located at the positive end of the electrode

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29
Q

what would depolarisation moving toward a lead cause in an ECG trace?

A

positive wave

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30
Q

what would depolarisation moving away from lead cause in an ECG trace?

A

negative wave

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31
Q

what would repolarisation moving away from lead cause in an ECG trace?

A

positive wave

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32
Q

what is the clinical implication of a missing QRS complex on an ECG trace?

A

missing QRS complex = block in signal at AV node, disturbance in communication between atria and ventricles

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33
Q

what is an arrhythmia?

A

uncoordinated atrial and ventricular contractions caused by a defect in conduction system

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34
Q

what is the clinical implication of atrial fibrillation?

A

atrial fibrillation can cause clotting and inefficient filling of the ventricles (atria not emptying properly)

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35
Q

what is the clinical implacation of ventricular fibrillation?

A

more life threatening, the ventricle pump without filling and if rhythm is not corrected circulation stops and brain death occurs

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36
Q

what is systole?

A

contraction phase of cardiac cycle

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37
Q

what is diastole ?

A

relaxation phase if cardiac cycle

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38
Q

when does systole begin and end?

A

systole begins with ventricular contraction, ends when ejection of blood ceases

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39
Q

when does diastole begin and end?

A

begins when ejection ceases as ventricles relax, ventricular filling begins after sufficient relaxation occurs

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40
Q

when does the majority of ventricular filling occur?

A

80-90% of ventricular filling occurs before atria contract, blood flows passively with pressure gradient

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41
Q

what is the first heart sound caused by?

A

AV valves closing

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42
Q

what is the second heart sound caused by?

A

SL valves closing

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43
Q

when is ventricular volume at a maximum?

A

at the end of diastole (EDV)

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44
Q

when is ventricular pressure at a maximum?

A

during ejection phase, P falls during late systole

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45
Q

when is arterila pressure at a minimum and maximum ?

A

minimum at end of diastole (diastolic BP), maximum during systole (systolic BP)

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46
Q

what is the “frank-starling mechanism”?

A

if LVEDV increases, the LV responds by doing more work, thus increasing SV (more fill = more empty)

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47
Q

what does preolad determine?

A

preload determines the initial (pre-contraction) muscle fibre length

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48
Q

what accounts for the Frank-Starling mechanism?

A

length tension relationship: a stretched muscle increases in calcium sensitivity, therefore increasing CB strength and resulting SV

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49
Q

what is afterload?

A

afterload is the tension the fibres must generate before they can shorten. AKA the pressure the ventricles must overcome to force open the aortic and pulmonary valves

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50
Q

what is extrinsic control of contractility of heart?

A

catecholamines released from the adrenal medulla, and from sympathetic nerves in the heart can alter ventricular function without a change in LVEDV. causes contraction and relaxation to occur more quickly

51
Q

what is the ejection fraction normally?

A

EF = SV/EDV between 50-75% under normal resting conditions

52
Q

what plays more of a role in HR?

A

extrinsic mechanism of heart primarily control HR

53
Q

what is the ionotropic effect?

A

increased EDVV, increased activity of sympathetic nerves to heart, increased plasma adrenaline = act on cardiac muscle to increase stroke volume

54
Q

what does an increase in parasympathetic nervous activity (vagus nerve) to SA node, do to HR?

A

reduces HR from 110 - 70 approx

55
Q

what does an increase in sympathetic nervous activity do to HR and how?

A

increases the frequency of AP firing and increases HR

56
Q

what is the law of Laplace? (cardiac work)

A

the muscle tension that must be generated to develop a given ventricular P depends on the radius of the ventricle and the thickness of the ventricle wall.
T = (P x r)/2 x u

57
Q

what is pulse pressure?

A

the difference between systolic and diastolic pressure

58
Q

how to calculate mean BP at brachial artery?

A

mean BP at brachial artery = diastolic pressure + 1/3 (pulse pressure)

59
Q

what is the change in BP as blood flows through the systemic and pulmonary circuits?

A

Blood pressure decreases (including pulsatility) as blood moves further from the heart

60
Q

how does the CSA of blood vessels change as we move through the circulatory system?

A

CSA peaks at capillaries. represented graphically through the system = bell curve

61
Q

how does the mean velocity of blood flow change as we move through the circuit?

A

mean velocity of blood flow fastest at aorta - arteries, begins to slow gradually at arterioles, before becoming slowest at capillaries (for adequate exchange) and then gradually increases to approx 1/2 the original speed in the venous system

62
Q

what is the function of the aorta and large arteries?

A

the aorta and large arteries reduce the fluctuations in flow and pressure generated by the intermittent ejection of the stroke volume, accomplished by their highly elastic walls.

63
Q

how is energy stored in blood vessel walls in the cardiac cycle?

A

during systole, energy is stored in the elastic wall as the elastic elements are stretched. this energy is then released during systole. recoil of vessels maintains blood pressure further down the flow.

64
Q

what is arteriosclerosis and its implications on pulse pressure?

A

arteriosclerosis is a decrease in arterial compliance, due to stiffening from calcification/plaque formation. thus vessel walls cant stretch as much during systole, therefore can’t store E therefore pulse pressure increases

65
Q

why have extrinsic control of blood vessels?

A
  • to regulate overall TPR

- to allow the brain to alter blood flow selectively to individual organs

66
Q

what are the extrinsic controls?

A
  • vasomotor nerves (vasoconstrictor, vasodilator)

- hormones (adrenaline, vasopressin, angiotensin II)

67
Q

what is the most important and widespread extrinsic control of blood vessels (normally)

A

sympathetic vasoconstrictor fibres (noradrenergic) are the most widespread and important extrinsic control (release adrenaline)

68
Q

what controls sympathetic vasoconstrictor nerves and where fo they innervate?

A

sympathetic vasoconstrictor nerves are controlled by the brainstem (vasomotor centre), and innervate most arterioles and nerves of the body

69
Q

where do sympathetic vasoconstrictor nerves terminate and what do they release?

A

sympathetic vasoconstrictor nerves terminate at edge of tunica media, in strings of synaptic varicosities. varicosities release dense-cored vesicles, containing noradrenaline (NAd) and ATP

70
Q

where/what does NAd do once released from synaptic variscosities?

A

NAd acts on alpha-adrenoreceptors on vascular myocyte and cause vasoconstriction.

71
Q

what activity at a-adrenoreceptors causes vasodilation?

A

a-adrenorecpetors are tonically active, therefore only a decrease in activity (or alpha blockers) causes vasodilation

72
Q

how does reduced sympathetic activity lead to vasodilation?

A

increase in BP - activates baroreceptor reflex - inhibits sympathetic activity - reduced BP (a decreased firing rate causes a decrease in impulse frequency)

73
Q

how does increased sympathetic activity lead to vasoconstriction?

A

tissue blood flow reduced - contraction of local resistance vessels - TPR increased - increased BP - capillary P reduced - contraction of local resistance vessels - allows ISF to be absorbed into the plasma

74
Q

adrenaline - site of secretion and how it affects circulation?

A

adrenaline is a catecholamine released from adrenal medulla and acts as both a vasoconstrictor and dilator

75
Q

action of angiotensin II in circulatory system?

A

antiogensin II is a vasoconstrictor important in the response to hypovolaemia and cardiac failure. tends to increase BP

76
Q

action of vasopressin in circulatory system?

A

vasopressin (anti-diuretic hormone), ADH is a vasoconstricitor and its vascular response is important in response to hypovolaemia

77
Q

atrial natriuretic peptide action in circulatory system?

A

atrial natriuretic peptide is a moderate vasodilator

78
Q

what is autoregualtion?

A

autoregulation is when arterial pressure is altered but blood flow in vascular beds remains constant.

79
Q

what is myogenic autoregulation?

A

myogenic autoregulation is when resistance vessels respond directly to an increase in pressure by vasoconstriction or vasodilation

80
Q

where is myogenic autoregulation well developed?

A

myogenic autoregualtion is well developed in areas that always need consistent blood flow; brain, myocardium, kidney.

81
Q

what is metabolic regulation (active hyperemia)?

A

metabolic regulation is an intrinsic mechanism by which blood flow to organs such as the brain, heart muscle, and skeletal muscle is adjusted to match metabolic activity

82
Q

3 x intrinsic mechanisms of controlling vascular tone

A
  • myogenic response
  • paracrine factors
  • physical factors
83
Q

3 x extrinsic mechanisms of controlling vascular tone

A
  • vasodilator nerves
  • sympathetic vasoconstrictor nerves
  • endocrine factors
84
Q

2 x vasoconstrictors produced by endothelium?

A

vasoconstrictors

  • endothelin
  • angiotensin II
85
Q

3 x vasodilators produced by endothelium?

A

vasodilators

  • nitric oxide (NO)
  • Prostacyclin (PGI2)
  • endothelial-derived hyperpolarizing factor (EDHF)
86
Q

Structure of capillaries

A

thin-walled tube of endothelial cells without smooth muscle cells, covered by basement membrane

87
Q

type of junction in continuous capillaries

A

continuous capillaries have tight functions

88
Q

primary function of capillaries?

A

capillary primary function is fluid and solute exchange

89
Q

what kind of substances easily diffuse across the capillary wall?

A

lipid-soluble substances including O2 and CO2 easily diffuse through endothelial cells in capillary wall

90
Q

how do ions and polar molecules pass through the capillary wall?

A

ions and polar molecules are poorly soluble and pass through water-filled channels in endothelial lining/intercellular cleft

91
Q

can proteins diffuse through capillary?

A

no, proteins usually can’t diffuse through the water-filled channels (except liver)

92
Q

what is the transpulmonary diffusion gradient in capillaries due to?

A

diffusion gradient (what diffuses in and out) is based on cellular utilization or production

93
Q

what is the starling principle of fluid exchange for capillaries?

A

capillary blood flow is affected by plasma osmotic pressure (AKA colloid osmotic pressure, COP) as well as hydrostatic pressure.

94
Q

true or false; normally, the filtration is greater than reabsorption at capillaries

A

true - about 4 litres a day of modified ISF/lymph is returned in lymph vessels

95
Q

water is driven across the capillary wall by the sum of what pressures?

A

water is driven across the capillary wall by the sum of hydrostatic and colloid osmotic pressures of the blood and ISF

96
Q

how is the colloid osmotic pressure of the blood generated?

A

colloid osmotic pressure of the blood is generated by the plasma proteins dissolved in the plasma

97
Q

what do hydrostatic and osmotic forces tend to move water in/out of capillary?

A
  • hydrostatic forces tend to move water out of the capillary (filtration)
  • osmotic forces tend to draw water in to the capillary (reabsorption)
98
Q

what is the result when filtration greatly outweighs absorption in the lymph/capillary system?

A

lymph acts as buffer so when there is too much filtration, OEDEMA/swelling occurs as a result

99
Q

4 determinants of venous pressure

A
  • sympathetic innervation
  • skeletal muscle pump
  • blood volume
  • respiratory pump
100
Q

resting arterial blood pressure (MABP) is?

A

approx. resting MABP is 90mmHg

101
Q

explain the arterial baroreceptor reflex (short term control of MABP)

A

(arterial baroreceptor reflex)
- sensors = aortic and carotid sinus baroreceptors
- aortic afferent fibres travel in vagus, carotid sinus afferent fibres travel in glossopharyngeal nerves to CVS centres in brainstem (NTS in medulla)
- there is tonic activity in both afferent nerves from the baroreceptors, and in efferent parasympathetic and sympathetic nerves
- this means system can respond rapidly to incr./decr. in arterial pressure
eg; an incr. in P will incr. activity in baroreceptor afferent fibres- parasympathetic activity to heart incr. - sympathetic activity to heart and BV decr. - HR, cardiac contractility and TPR decr. and vasodialtion occurs - thuus decr. venous return - thus decr. prelaod/CO. - combined drop in CO and TPR due to vasodilation decr. arterial pressure

102
Q

explain orthostatic hypotension - sequence:

A

orthostatic hypotension (if not corrected)

  • decr. CVP (less blood returning to heart)
  • decr. R SV
  • decr. L V filling pressure
  • decr. L SV
  • decr. arterial P
  • decr. cerebral blood flow (O2 lack)
  • thus symptoms of dizziness/visual fade
103
Q

explain reflex response to preserve cerebral perfusion

A

cerebral perfusion preservation reflex:

  • (standing up ) - decr. arterial BP
  • decr. input from low P receptors
  • decr. input from high P receptors
  • results in incr. sympathetic drive to: SA node ( and decr. vagal), myocardium, resistance vessels, capacitance vessels
104
Q

how is TPR maintained in exercise as CO increases?

A

TPR is maintained during exercise by vasoconstriction in abdominal organs, kidneys and other non-exercising muscles (as PAO = CO x TPR)

105
Q

explain the immediate response to haemorrhage

A

baroreceptor reflex; drop in BP sensed by decreased firing of baroreceptors

  • decr. parasympathetic discharge to heart
  • incr. sympathetic discharge to heart, veins and arterioles
  • thus constriction of resistance vessels
  • thus incr. TPR, CO, SV toward normal results in incr. arterial P toward normal
106
Q

explain the intermediate response to haemorrhage

A

intermediate response = absorption of water from the interstitial space:

  • following blood loss, P in capillaries decr.
  • additionally, refelx constriction of small arteries/arterioles decr. capillary P further
  • with this fall in capillary P, large amounts of water cna be withdrawn rapidly into circulation from ISF of the gut and skin (where massive vasoconstriction may occur = skin goes pale)
  • in this way, blood volume and BP caan be restored to normal
107
Q

explain the long term response to haemorrhage

A

long term response = fluid replacement
- even if BP is maintained, still have to replace lost volume.
- decreased renal perfusion triggers renin/angiotensin II
- Angiotensin II is a vasoconstrictor that reduces renal perfusion (less urine (+ADH), reduces renal Na loss, stimulates aldosterone which stimulates thirst
- over next few hours/days total body lost water and slat are replaced (incr. intake/decr. losses)
to restore blood content = replacement of RBC by bone marrow, a nd albumin by liver (takes around 6 weeks)

108
Q

what is generic circulation?

A

generic circulation is when each organ and tissue receives a blod supply that flows through a circuit

109
Q

in fetal circulation, how is blood oxygenated?

A

fetal blood is oxygenated at the site of the placenta vis the maternla bllod supply (relatively hypoxic = 80% saturated)

110
Q

in fetal circulation, what does placenta serve as?

A

in fetal circulation, placenta acts as:

  • intestine (nutrient uptake)
  • kidney (waste removal)
  • lungs (uptake of CO2)
  • receives a large fraction of cardiac output
111
Q

why and how are lungs bypassed in fetal circulation?

A

the lungs are bypassed by the DUCTUS ARTERIOSUS, in fetal circulation due to:

  • extreme pulmonary vasoconstriction
  • high resistance to blood flow
  • airways are collapsed
  • blood moves from L to R side of heart through shunting via foramen ovale (between atria)
  • why? - because fetal blood is oxygented at the site of placenta via maternal blood supply.
112
Q

how and why are liver and kidneys bypassed in fetal circulation?

A 
how = liver and kidney are bypassed via ductus venosus
why = because otherwise fetus will loose nutrients and the fetus is already in water
113
Q

explain how does venous mixing occur in fetal circulation?

A
  • high O2 areterial blood from placenta bypasses liver and connects to inferior vena cava (up toward RA).
  • folds in vena cava guide blood through RA - Foramen ovale - LA (flow is laminar)
  • this blood then crosses with venous blood from superior vena cava and goes to RV
114
Q

at birth, how do lungs start working?

A

lungs sart working at birth as placenta is removed and CO2 acts as a stimulus for breathing.

115
Q

what are the inspiratpry motions at birth?

A

inspiratory motions at birth:

  • generate -ve thorax pressure
  • draws blood out of placenta
  • inflates lungs
  • blood flows into lungs
116
Q

a reduction of what causes the ducus arteriosus to close at birth?

A

a reduction in prostoglandins causes ductus arteriosus to close

117
Q

what causes the foramne ovale to close?

A

a decr. in RA P + incr. LA P causes folds of foramen ovale to close(mostly fuses with time)

118
Q

whis is higher, fetal pulmonary blood pressure or adult pulmonary blood pressure?

A

fetal heart BP is highe as vessels are squished

119
Q

how much of the cardiac output does pulmonary circulation receive?

A

pulmonary circulation receives 100% of cardiac output

120
Q

pulmonary circulation is a vascular bed characterised by?

A

pulmaonry circulation is a vascular bed characterised by:

  • a low resistance circulation
  • a high compliance
  • a low arterial pressure
121
Q

how does gravity regulate pulmonary blood flow?

A

gravity affects pulmonary blood flow as lower rehions of the lung jave increased blood flow compared to upper rehions of the lung (when standing)

122
Q

how does hypoxia regulate pulmonary blood flow?

A

hypoxia = low O2, pulmonary vasculature restricts in response to hypoxia. hypoxic pulmonary vasoconstriction optimizes the ventilation - perfusion matching for optimal gas exchange

123
Q

how does does endothelial control regulate pulmonary blood flow?

A

the endothelium of pulmonary vasculature releases vasoactove peptides that regualte pulmonary vascular tone including:

  • nitric oxide (vasodilator)
  • endothelin 1 (vasoconstrictor)
124
Q

how does the sympathetic nervous system regualte pulmonary blood flow?

A

pulmonary vasculatire is innervated by alpha and beta adrenoreceptors.
alpha adrenoreceptors, located mostly in large vessels = vasoconstriction on stimulation
beta adrenoreptors, located mostly in smaller resistance vessels= vasodilation on stimulation
HOWEVER tend to negate each other, thus SNS plays minor role in regulation

phty251 (6 decks)

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