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cardiovascular > physiology > Flashcards

physiology Flashcards

1
Q

mean arterial pressure is equal to

A

cardiac output multiplied by the total peripheral resistance

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2
Q

the carotid baroreceptors signals are taken by what nerve?

A

glossopharyngeal

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3
Q

angiotensin 2 causes

A

arteriolar constriction

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4
Q

aldosterone causes

A

sodium reabsorption and therefore increases plasma volume

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5
Q

ADH/Vasopressin cause

A

causes arteriolar constriction, and increase collecting duct permeability

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6
Q

atrial and bran natriuretic peptides cause

A

arteriolar dilation, and sodium excretion

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7
Q

what is the effect of standing

A 
decreased:
venous return
end diastolic volume
preload
stroke volume
cardiac output
mean arterial pressure
baroreceptor AP rate
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8
Q

the reflex response to standing is

A

reduce vagal tone and increase sympathetic tone

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9
Q

the stages of the Valsalva manoeuvre are

A

1) increased thoracic pressure
2) decreased cardiac output and mean arterial pressure
3) reduce baroreceptor AP’s, reflex response increasing total peripheral resistance
3) thoracic pressure decreases
4) venous return is restored and stroke volume is increased as effects of reflex still hasn’t worn off
5) normal

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10
Q

the sympathetic response of the reflex by baroreceptors induce

A

increased:
heart rate
cardiac output
contractility, stroke volume
vasoconstriction increasing venous return, end diastolic volume
arteriolar constriction increasing total peripheral resistance

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11
Q

why does standing reduce venous return?

A

there is increased hydrostatic pressure causing the pooling of blood in veins and venules

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12
Q

sympathetic nervous system works on what receptors for modulating heart rate?

A

beta 1 on the sinoatrial node

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13
Q

sympathetic nerves release what transmitter for increasing heart rate?

A

noradrenaline

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14
Q

why does end diastolic volume alter stroke volume?

A

ensure SV matches LV and RV

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15
Q

an inotropic effect is

A

one that increases contractility

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16
Q

the definition of contractility is?

A

The ability or property of a substance, especially of muscle, of shortening, or becoming reduced in size, or developing increased tension.

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17
Q

stroke volume is effected by

A

preload (EDV) afterload (TPR), neural with the sympathetic supply and pathological effects.

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18
Q

hypercalcemia effect on SV/EDV

A

increases stroke volume but reduces EDV

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19
Q

hypocalcaemia effect on SV/EDV

A

reduces stroke volume but increases EDV

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20
Q

ischaemia effect on SV/EDV

A

reduces stroke volume and increases EDV

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21
Q

barbiturates effect on SV/EDV

A

reduces stroke volume but increases End diastolic volume

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22
Q

ischaemia refers to

A

restriction of blood flow to the tissues

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23
Q

heart pumps are in

A

series

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24
Q

vascular bed are in

A

parallel

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25
Q

flow is equal to

A

pressure divided by resistance

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26
Q

describe the sequence of events from the vascular tree

A

drop to arteries from LV (95-90)
large drops through arterioles (90-40)
capillaries to veins (20-5)

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27
Q

what are the changes of the aortic pressure wave?

A

pressure increases up to systole, the aortic valve closes and then gradually decreases until diastole .

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28
Q

what factors effect the aortic pressure wave

A

stroke volume, velocity of ejection, elasticity and peripheral resistance.

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29
Q

how are the korotkoff sounds produced?

A

use of a sphygmomanometer and a stethoscope

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30
Q

what triggers renin production?

A

activation of sympathetic nerves to the juxtaglomerular cells, distension of afferent arterioles, decreased delivery of sodium/chloride.

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31
Q

how is fibrinogen converted into fibrin?

A

thrombin

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32
Q

how is platelet aggregation inhibited

A

prostacyclin and NO

33
Q

what inactivates thrombin

A

thrombomodulin and heparin

34
Q

what’s the function of plasminogen activator

A

forms plasmin which digests clots

35
Q

everyday how much fluid is lost by capillaries

A

20 L and 17 regained, 3L taken by the lymphatic system

36
Q

what are the causes for an oedema?

A

lymphatic obstruction
raised CVP
hypoproteinemia
increased capillary permeability

37
Q

rough stages of the cardiac cycle?

A

late diastole to atrial systole to isovolumic ventricular contraction to ventricular ejection to isovolumic ventricular relaxation

38
Q

what factors influence blood flow in veins

A

gravity, skeletal muscle pumps, respiratory pumps, venomotor tone and systemic filling pressure

39
Q

what is a the general injury response

A

fibrin is formed by fibrinogen through thrombin which binds to the platelet plug formed by adhering to collagen in the basement membrane

40
Q

pressure is equal to

A

flow multiplied by resistance

41
Q

arteriolar constriction is stimulate by sympathetic nerves through

A

norepinephrine being binding to alpha 1 receptors

42
Q

the hormone epinephrine binds to what receptors on blood vessel triggering

A

released by the adrenal medulla bind to alpha 1 receptors causing constriction

however it does also bind to beta 2 receptors on skeletal and cardiac muscles

43
Q

active hyperaemia depends on the release of

A

EDRF

44
Q

Darcy’s and poiseuille’s laws are important because

A

varying radius controls resistance, by controlling the total peripheral resistance also effects change in pressure or the mean arterial pressure because the change in pressure is equal to flow multiplied by resistance

45
Q

SLL I node is connected to

A

left arm with right arm

46
Q

SLL II is connected to

A

left leg and right arm

47
Q

SLL III is connected to

A

left leg with left arm

48
Q

P wave is caused by

A

atrial depolarisation

49
Q

QRS complex is caused by

A

ventricular depolarisation

50
Q

T wave is caused by

A

ventricular repolarisation

51
Q

the PR are interval normally lasts from about

A

0.12 - 0.2 secs

52
Q

QRS lasts for normally

A

0.08 secs

53
Q

QT interval normally lasts for

A

0.42 seconds

54
Q

how long is a cardiac action potential?

A

250 m secs

55
Q

how can the a cardiac cell regulate contraction?

A

Ca2+

56
Q

why cannot cardiac muscle exhibit tetanic contraction?

A

due to its long refractory period

57
Q

Explain the generation of heart sounds (phonocardiogram).

A

the phonocardiogram is a recording of the sounds and murmurs made by the heart using a phonocardiograph. It works by plotting vibrations made by the closure of the atrioventricular valves and the closure of the semilunar valves. It’s more accurate than a stethoscope for tracking heart functions

58
Q

Illustrate the sequence of changes in pressure and volume in the chambers of the heart throughout the cardiac cycle.

A

initially we have the late diastole, in which both sets of chambers are relaxed and fill passively. The next phase is the atrial systole in which the atria contracts and forces a small amount of blood into the already filled ventricle valve through the Atrioventricular valves, but there isn’t sufficient pressure for opening the semilunar valves. The ventricles then contracts, forcing open the semilunar valves and the blood is ejected in ventricular systole, and atria at this point is in diastole. There is the then the isovolumic ventricular relaxation as the ventricles relax, and the pressure falls closing the semilunar valves. Then we go back to the late diastole phase.
closure of the tricuspid and bicuspid valve is S1 which makes the first heart sound, the closure of the semilunar valves is S2 making the two heart sounds.

59
Q

Explain the significance of Starling forces and the lymphatic system in relation to oedema

A

starlings forces varies in capillary bed, due to the osmotic pressure forcing fluid into the capillaries, as fluid if forced out of the capillaries through hydrostatic pressure. Overall 20 litres is lost through this and 17 litres is regained this way, the remaining 3 litres is absorbed by the lymphatic system. An oedema is formed through the accumulation of excess fluid, this may be due to lymphatic obstruction through surgery or filariasis, raised central venous pressure from ventricular failure, hypoproteinaemia from nephrosis, liver failure and nutrition or increased capillary permeability from inflammation or rheumatism.

60
Q

Identify the processes involved in transport between capillaries and tissues.

A

the gross structure of the capillaries is designed for exchange, with lots of thin walled capillaries with such a small diameter resulted in a large surface area to volume ratio. They had either leaky endothelial junctions, or fenestrated pores to allow for exchange or discontinuous with massive channels. The process itself is either through the self-regulating diffusion, or by carrier mediated transport such as the glucose transporter.

61
Q

Describe the mechanism that prevents blood clotting in vessels.

A

clotting involves the formation of a platelet clot and fibrin clot. The fibrin is formed from fibrinogen being activated by thrombin to fibrin which then binds around the platelet plug adhering to the basement membrane. The anti-clotting mechanisms involve stopping blood contacting collagen, the production of prostacyclin and NO which inhibits platelet aggregation, the production of tissue factor pathway inhibitor which prevents thrombin production, the expression of thrombomodulin or heparin which binds to thrombin and inactivates it and the secretion of plasminogen activator which helps form plasmin which breaks down clots.

62
Q

Describe the dominant factors controlling blood flow in cardiac, cerebral, pulmonary and renal vascular beds.

A

the dominant factors in controlling blood flow are the basic haemodynamics such as Darcy’s law that flow is equal to the change in pressure over resistance, extrinsic effects of neural and hormonal influences, local intrinsic effect.
special areas include coronary circulation as aortic pressure increases, blood flow decreases s it is interrupted by systole, it demonstrate excellent active hyperaemia and many beta 2 receptors. Cerebral circulation is also must be kept stable at all times, shows excellent autoregulation

63
Q

Justify the importance of Poiseuille’s Law in relation to the control of resistance and blood flow.

A

with darcy’s law and Poiseuille’s law which stated that varying radius controls resistance, therefore the varying radius of arterioles, or the total peripheral resistance and also effects change in pressure or the mean arterial pressure because the change in pressure is equal to flow multiplied by resistance.

therefore, reducing resistance of the vascular bed increases the flow through the bed, where as reducing the total peripheral resistance also reduces the mean arterial pressure. So in order to maintain the blood flow to the vascular bed resistance must be altered and this is achieved through stimuli.

64
Q

Define active hyperaemia, pressure autoregulation and reactive hyperaemia.

A

active hyperaemia in which increasing metabolic activity increased concentration of metabolites such as carbon dioxide, hydrogen and potassium, which triggers the release of EDRF causing arteriolar dilation, the subsequent increase in blood flow is t wash out the metabolites to match blood flow to metabolic needs.
pressure autoregulation occurs when mean arteriolar pressure drops, decreasing flow so metabolites accumulate triggering the release of EDRF which causes dilation and flow is restored to maintain supply despite MAP changes.
Reactive hyperaemia is when the blockage of the blood supply causes a increase in blood flow, this response is essentially and extreme version of pressure autoregulation.

65
Q

identify the various neural, hormonal and local factors affecting arteriolar tone.

A

neural control of the smooth muscle of arterioles include sympathetic nerves which release norepinephrine binding to alpha1 receptors causing constriction reducing flow and increasing total peripheral resistance.

hormonal factors such as epinephrine are released by the adrenal medulla which bind to alpha 1 receptors causing arteriolar constriction, having the same effect as norepinephrine but in some tissue is activates beta 2 receptors such in skeletal muscles increasing flow reducing the total peripheral resistance(TPR). Angiotensin 2 also has a similar effect as epinephrine in response to low blood volume increasing TPR, vasopressin an antidiuretic hormone which like angiotensin is released in response to low blood volume and as a result has a similar effect Atrial natriuretic peptide and brain natriuretic peptide are released in response to high blood volume, having an opposite effect causing dilation and reducing TPR.

66
Q

Indicate the factors affecting pressure and flow in veins.

A

pressure is low and the vessels are distensible and collapsible so they are effected by external factors. Such as gravity which causes venous distension in the legs, decreasing the end diastolic volume, reducing cardiac output and mean arteriolar pressure and causes venous collapse in the neck.
skeletal muscle pump also effects the blood flow, as movement forces blood through the veins. As well as respiratory pump, in that breathing generates a negative upper body pressure and a positive body pressure below it essentially forces the blood up to the heart.
there is venomotor tone, the contraction of smooth muscle around venules and veins, and systemic filling pressure created by ventricles and transmitted through the vascular tree to the veins.

67
Q

Define systolic pressure, diastolic pressure and pulse pressure

A

systolic pressure is the peak pressure of the arteries, the pulse pressure is the difference between the between the systolic and diastolic pressure, and the diastolic pressure is the lowest artery pressure.

68
Q

Explain the origin of the Korotkoff sounds and their use.

A

Korotkoff sounds originate from the use of a sphygmomanometer and a stethoscope of the brachial artery, as blood is pumped passed through from the high decreasing pressure of the sphygmomanometer noise is generated. If the pressure of the sphygmomanometer is above or below systolic pressure there is silence, as it is just under systolic, there is a tapping sound and as it decrease is progresses to a thumping, then muffled

69
Q

Illustrate the changes in the aortic pressure wave as it passes through the vascular tree.

A

the aortic pressure increases up to systole, the aortic valve closes and then gradually decreases to diastole and repeats. The elastic arteries act as a pressure reservoir dampening decreasing variations. The pressure wave can be altered by stroke volume, velocity of ejection, elasticity and peripheral resistance.

as the pressure flows from the left ventricle to the right atrium the pressure gradually decreases.

70
Q

Illustrate the changes in blood velocity and total cross-sectional area of the vessels through the vascuar tree.

A

small drop through the arteries in pressure from 95-90mmHg which is a low resistance conduit, then a large drop through arterioles from 90-40 mmHg as it is the resistance vessels. Pressure is already low when the blood gets to the capillaries for exchange, it then leaves a small pressure difference from 20 – 5 mm Hg for the veins as systemic filling pressure. Pulmonary pressure is then a fifth of that of systemic. As a rule as the cross sectional area decreases, the velocity of the blood flow increases.

71
Q

Describe the components and function of the aterial baroreceptor reflex.

A

the arterial baroreceptor reflex originates from baroreceptors in the aortic arch and the carotid artery sinus’s. if they detect an increase In pressure, they send signals through the vagus nerve and the glossopharyngeal nerves respectively to the cardiovascular centres in the medulla. In response a response parasympathetic in nature is sent through the vagus nerve, it reduces the heart rate and the total peripheral resistance. As a result the cardiac output and blood pressure decrease. If it drops too low, a sympathetic response is sent, stimulating the adrenal gland and the sinoatrial and atrioventricular node to increase the heart rate, the stroke volume, causing increased vasoconstriction increasing the total peripheral resistance and increasing the cardiac output thus the blood pressure.

72
Q

Describe the effect of changes in posture on the cardiovascular system in relations to baroreceptors.

A

as someone stands up, the blood begins to pool in capacitance veins in the legs. As a result the mean arterial pressure will decreases, reducing the signals being fired by the baroreceptors inducing a sympathetic response by the medulla increasing the heart rate, stroke volume and total peripheral resistance increasing blood pressure. Also as a reflex the vagal tone will decrease, contributing to the increase in heart rate and cardiac output.

73
Q

what is the relationship between mean arterial pressure, cardiac output and total peripheral resistance?

A

mean arterial pressure is equal to cardiac output multiplied by the total peripheral resistance.

74
Q

Identify the reflex pathways involving renin-angiotensin-aldosterone, antidiuretic hormome, atrial natriuretic peptide and brain natriuretic peptide in the control of plamsa volume.

A

the release of renin by the juxtaglomerular cells of the kidney occurs in response to a reduced concentration of Chloride and sodium ions, sympathetic nerves or constriction of afferent arterioles in response to the drop-in mean arterial pressure. The renin will convert angiotensin into angiotensin 1 which is then converted into angiotensin 2 which acts as a vasoconstrictor, stimulating the hypothalamus to produce ADH and stimulates the adrenal cortex to produce aldosterone which increases the permeability of the collecting duct to increase the blood volume and reduces diuresis.

the hypothalamus when stimulated by its osmoreceptors detecting changes in the interstitial fluid, angiotensin 2 or by decreased blood volume detected by baroreceptors in the aortic arch and carotid sinus stimulates the pituitary gland to release ADH which increases permeability of the collecting duct and causing vasoconstriction.

atrial natriuretic peptide is released by myocardial cells in the due to the increased pressure in the atrium. In response to increased mean arterial pressure it inhibits renin, decreases the permeability of the collecting duct resulting increased secretion of sodium and stimulates the medulla centres to reduce mean arterial pressure.

75
Q

Recognise the role of the kidneys in regulating plasma volume and therefore blood pressure.

A

Osmoreceptors in the hypothalamus for the interstitial fluid
baroreceptors in the aortic arch and the carotid sinus’s
juxtaglomerular cells in the kidney
myocardial cells in the atrium

76
Q

Explain the effects of the sympathetic and parasympathetic systems on heart rate.

A

sympathetic system releases noradrenaline from nerves and the release of adrenaline from the adrenal medulla, increasing heart rate by acting on beta one receptors on the sinoatrial node. This is called tachycardia.
parasympathetic system the vagus nerve release acetylcholine acting on muscarinic receptors on the sinoatrial node to hyperpolarise cells and reduce heart rate which is called bradycardia.

77
Q

Explain the effects of the sympathetic and parasympathetic systems on stroke volume

A

the sympathetic system nerves release noradrenaline and stimulate the adrenal cortex to secrete adrenaline both operating on beta one receptors increasing contractility making it an inotrope, or a agent which alters contraction by giving a stronger but shorter contraction.

the parasympathetic system has very little effect since the vagus doesn’t innervate the ventricular muscle.

78
Q

Explain the effects of preload and afterload on stroke volume.

A

an important component of preload is that the energy of contraction is as a result of the initial length of muscle. Preload thus is affected by the end diastolic volume, increasing it increases stroke volume and vice versa. Therefore, it is restricted to the influence of the capacitance vessels such as veins.

afterload is the load against what the muscle has to contract, this is determined by the cardiac output and the total peripheral resistance. Therefore, afterload is restricted to the arterioles. Increasing total peripheral resistance decreases stroke volume.

cardiovascular (6 decks)

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