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cardiovascular system Flashcards

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1
Q

the pumping action of the heart is called bulk flow- what does bulk flow distribute?

A

ions , water and CO2- pH, osmolarity and body water
heat- body temp
hormones, various substrates- metabolism

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2
Q

what is a typical stroke volume at rest?

A

60-80ml

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3
Q

what is the arrangement between the pulmonary and systemic circuits, does their arrangement increase or decrease resistance to flow?

A

systemic and pulmonary are in SERIES flow
series= higher total resistance
ie r=1+1

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4
Q

what is the arrangement of flow in the systemic system, does this arrangement increase or decrease overall resistance to flow?

A

systemic blood can flow through a choice of paths, these paths are arranged in parallel.
parallel = lower total resistance
r=1/2+1/2

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5
Q

what is the relationship between resistance, flow and pressure?

A

blood flow= change in blood pressure/ resistance to flow
*resistance dependent on the radius of the tube

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6
Q

where is most of your blood volume located?

A

about half of your blood at any point is sitting in your venous system

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7
Q

what occurs to pulse pressure as you move further away from the heart?

A

further from the heart=dampening of pulse pressure
elasticity of the arteries helps to dampen this

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8
Q

determinants of blood pressure (equation)

A

MABP= CO x TPR

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9
Q

primary structure and role of the aorta and large arteries

A

high pressure vessels, drives blood through the systemic system
lots of smooth muscle and connective tissue

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10
Q

primary structure and role of smaller arteries and arterioles?

A

resistance vessels
control of these vessels determines the volume of flow through that circulation
wrapped in smooth muscle to accomidate these changes (vasoconstriction/dilation)

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11
Q

primary structure and function of capillaries

A

exchange vessels
single layer of endothelial cells so nutrients can be easily transferred

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12
Q

primary structure and function of veins and venules

A

primary reservoir- abilities to hold the blood. Thin walled and large lumen, elastic layers allowing them to stretch

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13
Q

what makes up cardiac cells (discuss the two types)

A
  1. contractile myocardial cells- form bulk of cells in the atria and ventricles. Attatched via intercalated disks, gap junctions allow electrical signals to spread rapidly. all myocardial cells contract with every heart beat. actin and myosin= striated appearance
  2. nodal tissue (SA and AV node) 1% of cardiac cells, small round cells with no contractile proteins, for generating action potentials, gap junctions are present.
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14
Q

what rate does the SA node generate action potentials?

A

100-110 action potentials per min

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15
Q

what is the action potential conduction speed through atrial muscle compared to ventricular muscle

A

atrial muscle= 0.5ms-1
ventricular myocardium= 0.5ms-1

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16
Q

at what speed does the action potential conduct though the bundle branches (purkinje system) and why is it important its at this rate?

A

5ms-1
want to get the two ventricles to contract at the same time so the signal needs to travel to them quickly

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17
Q

why is the action potential conducted slowly through the av node? what rate is it conducted?

A

slowly at av node because we want to delay the signal so the ventricles will contract after the atria for effective ejection of blood.
AV node conduction= 0.05ms-1

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18
Q

what does the resting membrane potential of nodal and myocardial cells depend upon?

A

high resting permability to potassium
Pk lower in nodal tissue then myocardial cells and RMP is more negative
RM P of SA nodal cells is unstable

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19
Q

what is the pacemaker potential?

A

nodal tissue- pacemaker cells, no true resting membrane potential, they have a pacemaker potential which is a slow steady depolarisation.
lower permeability for potassium and an increasing permeability to sodium= gradual decrease in RMP
at threshold voltage calcium channels open and a ‘slow ap’ occurs

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20
Q

ventricular cells resting membrane potential

A

they have a higher potassium permeability therefore a more negative resting membrane potential (stable RMP)
depolarisation= opening of voltage gated sodium channels (due to a signal).
much faster process that requires a stimulus

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21
Q

how can we increase size of contraction in the cardiac cells?

A

cant recruit more cardiac cells as they all contract with every beat, but we can increase the amount of calcium.
more calcium= stronger contraction

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22
Q

why does tetanus not normally occur in heart muscle?

A

Has a long absolute and relative refractory period- these prevent the re-excitation of the heart muscle during the contraction period

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23
Q

depolarisation moving towards a lead results in a ___ wave

A

positive

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24
Q

depolarisation away from a lead results in a ____ wave

A

negative

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25
repolarisation away from a lead ___ wave
positive
26
what are arrhythmias?
abnormal rhythms of the heart uncoordinated atrial and ventricular contractions
27
atrial fibrilation vs ventricle fibrilation
atrial- can cause clotting and ineffective filling of ventricles ventricular- more life threatening, ventricles pump without filling, if rhythm not rapidly fixed then blood circulation stops and brain death occurs. ECG shows no QRS complex
28
what is occurring in isovolumetric relaxation (diastole 1) re valves, blood flow, volume and pressure differences
all valves are closed, no blood flow or change in blood volume atrial pressure is lower then ventricular pressure- atria fill with blood returning to the heart, when atrial pressure greater then ventricular pressure AV valves open passively and ventricles begin to fill
29
what is occurring during ventricular filling
AV valves have been passively opened 80-90% of blood will move passively down pressure gradient into the ventricles further 20-10% moved when atria contract
30
what is occurring during isovolumetric contraction?
ventricles are filled ventricular depolarisation causing them to contact, pressure rises AV valves close (first heart sound) no blood flow or volume change
31
what is occurring during ventricular ejection?
ventricular pressure exceeding aortic pressure aortic valves open - rapid ejection 2/3 of blood ejected in first 1/3 of ejection time late systole both LVP and AP fall= slow ejection repolarisation of ventricles the pressure in left ventricle falls below the aortic pressure. SL valves close (2nd heart sound)
32
intrinsic vs extrinsic control
intrinsic- controls that originate entirely from within a system extrinsic- controls that involve input from outside
33
what does chronotropic impact?
anything affecting HR
34
what does ionotropic impact?
anything affecting stroke volume
35
what type of control is preload and what does it impact?
intrinsic mechanism when left ventricle end diastolic volume and left ventricle end diastolic pressure increase then preload increases increasing preload increased stroke volume more fill= more empty
36
what accounts for the frank starling mechansims for increased stroke volume?
length tension relationship- muscle being stretched they become better aligned increase in calcium sensitvity which causes greater strength of contraction
37
what type of control is afterload and what does it impact?
intrinsic control (negative regulator) afterload is the resistance the heart has to overcome during systole increased pressure= heart has a harder time ejecting blood
38
what is an extrinsic control of contractility of the heart?
catecholamines (from adrenal medulla and sympathetic nerves) alter ventricular function without changing left ventricle end diastolic volume. They improve contractility, causes contraction and relaxation to occur more quickly
39
what is an ejection fraction and what is it used for?
quantifying contractility- ratio of stroke volume to end-diastolic volume, expressed as a percentage increased contractility= increased ejection fraction.
40
how big are the impacts on heart rate of intrinsic and extrinsic mechanism
intrinsic- limited role extrinsic mechanism (nervous and endocrine) are the major controllers of heart rate.
41
extrinsic mechanisms operate in a ___ manner
tonic always active, they just increase or decrease their amount of activity rather than switching on and off.
42
how does increase in parasympathetic vs sympathetic activity alter heart rate?
parasympathetic- reduced nervous activity to SA node therefore reduced heart rate. sympathetic- increase in frequency of AP generation in the SA node therefore increasing heart rate.
43
how does sympathetic stimulation impact the pacemaker potential?
increases the permeability of Na and Ca which speeds up the rate of depolarisation therefore increased heart rate
44
how does parasympathetic stimulation impact the pacemaker potential?
increased permeability to potassium, hyperpolarises and and slows depolarisation therefore decreasing heart rate
45
true or false- increased afterload increases cardiac output
false- increased afterload decreases cardiac output as it makes it harder to pump blood out.
46
when sympathetic activity increases heart rate ____ Conduction velocity ____ duration of diastole ____ contractility __ __ synchronisation of contractions
hr increases conduction velocity increases duration of diastole decreases contractility increases better synchronisation of contractions
47
what is cardiac work determind by? describe the components of law of lapace
determind by the tension development in the cardiac muscle. muscle tension that must be generated to develop a given ventricular pressure depends on the radius and the thickness of the ventricle wall tension= ventricular pressure x radius/ 2 x wall thickness
48
for a constant afterload how is tension requirement determind for a constant radius how is tension requirement determind
the tension that has to be generated by ventricular muscle increases as the radius increases tension generation required increases as afterload increases
49
what does acute heart failure impact?
preload of the heart- left ventricle unable to contract effectively at a normal left ventricle end diastolic volume therefore left ventricle fills more to generate a normal stroke volume. larger radius thinner wall= increased tension continously operating with a larger volume the ventricles have to generate more tension to pump blood out of the heart
50
what does arterial hypertension impact?
afterload ventricle has to generate higher pressure then normal which requires greater tension development. hypertrophy of the ventricle walls brings tension development back down
51
what is poiseuilles relationship
flow= change in pressure/ radius of a tube increased radius increases flow
52
how do the large arteries reduce fluctuations in flow and pressure by ejection of stroke volume?
highly elastic walls of the vessles systole energy is stored, that energy then released in diastole prevents larger swings in blood pressure (reduces pulse pressure)
53
what is ateriosclerosis?
stiffening of the artieries decrease in arterial compliance
54
what are the three most important factors for determining the magnitude of pulse pressure?
1- stroke volume 2- speed of ejection of the stroke volume 3- artierial compliance
55
what is the control hirearchy of vascular regulation
extrinsic factors at the bottom localised endothelial secretions, vasoactive metabolites and autacoids in the middle myogenic regulation has the hirearchy control
56
what are the extrinsic controls of blood vessels?
vasomotor nerves (vasocontrictor, vasodilator) hormones ( adrenaline, vasopresson
57
what do alpha adrenoceptors always cause?
vasoconstriction fibres are tonically active varicosities contain noradrenaline which activates the alpha- adrenoreceptors
58
how does reduced sympathetic activity lead to vasodilation?
increase in blood pressure activates baroreflex inhibits sympathetic activity decreases blood pressure
59
what does impact does angiotensin II have on controlling circulation?
it is a vasoconstrictor important in the response to blood loss
60
what impact does adrenaline have on controlling circulation?
depended on ratio of alpha to beta receptors more alpha receptors we will get vasoconstriction, more beta then we get vasodilation
61
atrial natriuretic peptide is a moderate _____
vasodilator
62
how is intrinsic regulation of vascular tone controlled?
myogenic autoregulation paracrine factors (local release= local response) physical factors (ie temp, pressure)
63
what is occurring in myogenic autoregulation?
myogenic autoregulation- wanting to maintain blood flow. Recognises stretch on the blood vessel and responds directly to an increase in pressure by vasoconstriction or vasodilation ie vessel wall stretched increased blood flow, myogenic autoregulation causes vasoconstriction which decreases blood flow back down this mechanism well developed in the brain, myocardium, kidney
64
what is occuring in metabolic regulation of intrinsic control mechanisms?
blood flow to organs ie brain, heart muscle, and skeletal muscle is adjusted to match its metabolic activity high metabolic activity, high oxygen use produces lots of metabolites, vasodilate to this area to allow it to have a larger blood flow
65
give examples of a endothelium produced vasoconstrictor (2) and a vasdodilator (2)
vasoconstrictor= angiotensin II, endothelian vasodilator= nitric oxide and prostacylcin
66
what impact does vasopressin have in controlling circulation?
vasoconstriction an important response to blood loss
67
what are the four main pressures that determine the filtration rate between capillaries and interstitual fluid?
biggest= capillary hydrostatic pressure (favours filtration) osmotic force due to plasma protein concentration ( favours absorption) interstitual fluid hydrostatic pressure ( favours absorption) osmotic force due to interstitual fluid protein concentration ( favours filtration) capillary hydrostatic pressure high = net filtration capillary hydrostatic pressure drops= net absorption
68
what do imbalaced absorption/ filtration levels caus when a) absorption is too much b) when filtration is too much
absorption= deep vein thrombosis, too much fluid in capillaries filtration= oedema, too much fluid in the tissues
69
what are the 4 determinants of venous pressure?
sympathetic innervation- small amount of smooth muscle to vasoconstric/dilate skeletal muscle pump -muscles contracting pushing venous return back up blood volume - greater blood volume= likely to pool more at your feet respiratory pump (negative pressure causes vena cava stretches out and draws blood return into it)
70
how does the short term control of MABP through the arterial baroreceptor reflex work?
sensors are aortic and carotid sinus baroreceptors afferent fibres travel in vagus & glossopharyngeal nevres they have tonic activity ie pressure rise increases barorecptor firing parasympathetic activity to hear increases and sympathetic decreases (want to decrease HR) HR, contractility and TPR falls= vasodilation
71
during exercise what organs recieve increased, decreased and the same cardiac output?
increased= brain, heart, skeletal muscle, skin decreased= kindeys, GI tract, other non exercising muscles
72
what is the immeditate response to blood loss?
baroreceptor reflex decreased arterial pressure= decreased firing increased sympathetic decreased parasympathetic ( hr increase), vasocontriction (increased TPR) these mechanisms in place to restore MABP
73
what is the intermediate response for blood loss?
loss of blood volume can be rapidly restored from interstitual fluid (doesnt matter whats in the blood just want the right volume to be pumped around the body) net reabsorption of water from interstitual fluid into the capillaries (typically from gut and skin ie skin going pale)
74
what is the long term response for blood loss?
fluid replacement over hours to days replacement occurs decreased renal perfusion triggers angiotensin II (vasoconstrictor), causes less urine, stimulates thirst and decreases Na loss. replacement of red blood cells through bone marrow, takes around 6 weeks.
75
what role does the ductus arteriosus serve?
structure in fetal circulation that allows the lings to be bypassed as fetus gets all its nutrients and oxygen from the placenta
76
by what structure are the liver/kidneys bipassed in fetal circulation?
ductus venosus
77
what structure does the foramen ovale connect?
right to the left atrium
78
what causes the foramen ovale to close?
right atrial pressure reduces, increased left atrial pressure results in the closing of the foramen ovale
79
what is the pulmonary blood flow like in fetal blood circulation?
high pressure with extreme vasconstriction high resistance to blood flow
80
what are the 3 main features of a pulmonary circulation?
pulmonary circulation recieves 100% of cardiac output- all blood needs to go back to the lungs to become reoxygenated low resistance circulation- high number parallel vessels, larger diametre vessels high compliance- easily distendable low arterial pressure
81
how is gravity a regulator of pulmonary blood flow?
low pressure system- high compliance therefore gravity influences regional blood flow. effect of standing increases blood flow to lower regions of the lungs, blood flow to upper regions decreases (apart from during exercise when the upper regions are increased. decreased resistance to lower increases resistance to upper
82
how is hypoxia a regulator of pulmonary blood flow?
pulmonary vasculature constricts in response to hypoxia (low oxygen) this mechanism optimises the ventilation-perfusion matching for optimal gas exchange (decreases blood flow and directs blood away from poorly ventilated alveoli
83
how is endothelial control a regulator of pulmonary blood flow?
endothelium of pulmonary vasculature releases various vasoactive peptide that regulate vascular tone ie nitric oxide- vasodilator endothelin 1- potent vasoconstrictor
84
how is the sympathetic nervous system a regulator of pulmonary blood flow
SNS has minor role in regulating pulmonary blood flow a-adrenoreceptors= vasoconstriction b-adrenorecepetors= vasodilation they tend to counter eachother out

physiology (10 decks)

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