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Integrated physiology > The cardiovascular system > Flashcards

The cardiovascular system Flashcards

1
Q

the pericardium

A

triple layered (visceral, pericardial, parietal), fused to diaphragm, great vessel

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2
Q

the heart contains

A

chambers- atria and ventricle. vessels ,great, coronary artery

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3
Q

internal structures of the heart

A

right atrium, coronary sinus, SA/AV nodes, fossa ovalis, ventricles, valves, pulmonary trunk, AV valves (prevent backflow up), semi lunar valves (prevent backflow down) chordae tendinea

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4
Q

why is electrical conduction in the heart important

A

it acts as a trigger for contraction of cardiac muscle (excitation-contraction coupling phenomenon), allows trigger to be very rapidly distributed to all cells of myocardium enabling the heart to contract as a single unit- normal heart function requires synchronisation. heart functions as syncytium. cardiac muscle (unlike skeletal) does not require nerve input for activity.

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5
Q

pacemaker cells

A

many cardiac myocytes are capable of depolarising spontaneously and contracting- specialised cells which undergo this spontaneous depolarisation set the rate of heart beat

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6
Q

cardiac muscle;

A

involuntary, striated, branched. intercalated discs formed by interlocking ‘fingers’ of plasma membrane, held tightly together by desmosomes. in this way, the tissue can resist the enormous stresses placed on it during cardiac contraction. gap junctions are also found in this region; these junctions permit ion flow allowing electrical signals to pass rapidly from cell-cell
consists of two different networks- atrial and ventricular

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7
Q

cardiac muscle and concentration gradients

A

current flows across plasma membrane of each of the cardiac muscle cells. the distribution of ions gives rise to concentration gradients (ions not evenly distributed due to membranes being selectively permeable e.g. higher concentration of sodium outside the cell than inside). gives rise to potential difference because ions are charged, inside cell is negative with respects to outside. combination of concentration gradient and potential difference created the electrochemical gradient, this is what determines what happens when membrane permeability is altered.

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8
Q

excitation contraction coupling-myosin

A

cardiac muscle cells contain an arrangement of thin and thick muscle fibres. thick filament has a myosin head which during contraction binds to specific sites on the thin filament. this brings about a conformational change in myosin that causes it to move, pulling the thin filament along in a sliding motion. the head detaches and can then bind to next site, pulling filament in further. requires ATP but also crucially dependant on calcium, in absence of calcium, protein troponin covers up the myosin binding site. however, calcium binding to troponin brings about a conformational change that reveals the binding site for the myosin head therefore in the absence of calcium there is no contraction and muscle remains relaxed. in presence of calcium muscle will contact

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9
Q

contraction related to ECG

A

the myosin/calcium activity is what is being picked up on ECG, AP arises when an increase in electrical activity in nearby cells trigger increase in permeability to sodium, polarity is reversed, triggers outflow of potassium. sodium/potassium pumps activated, returns to resting potential

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10
Q

sarcomere

A

sarcomere-contractile unit of cardiac muscle fibre.

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11
Q

what is preload

A

mechanical stretch placed on muscle fibres prior to contraction, and the bigger the stretch, the harder the contraction will be . in the case of the heart the stretch is caused by the volume of blood in the heart- has important implications for cardiac output and function
preload=end diastolic volume

therefore preload is the resting length proportional to force of subsequent contraction
the length of the sarcomere prior to contraction

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12
Q

electrical activity and contraction;

A

closely related but not the same thing

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13
Q

cardiac action potentials

A

last much longer than in nerves (1000ms compared to 10-30ms)

APs differ in shape and duration for different parts of the heart, depends on the nature of ion channels present

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14
Q

electrical activity in the heart

A

auto-rhythmic activity. depolarization begins in the sino-atrial (SA-pacemaker) node and spreads rapidly through atrial myocardium to the atria ventricular (AV) node. conduction slows at the AV node (allows time to complete contraction before ventricles start)) and enters ventricular conducting system. (the bundle of his and purkinje fibres) which takes the electrical signal to the apex of the ventricles first before spreading upwards. this means contraction follows in a similar way, and blood is ‘milked’ from apex of heart towards opening of great vessels

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15
Q

purkinje fibre/ventricular myocyte

A

AP condensed into 5 phases;
0-immediate depolarisation (sodium)
1- sodium channels deactivate; potential declines to zero.
2; plateau- calcium and potassium flows balances
3- falling membrane potential decreases permeability to calcium and increases permeability to potassium, initiates repolarisation
4- steady state

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16
Q

pacemaker AP

A

slope of pacemaker potential controls the heart rate, ANS transmitters alter ionic currents e.g. sympathetic increases calcium entry
phases;
0- depolarisation occurs as a result of a slow influx of calcium ions
1-3- occur as a single phase, membrane repolarises as a result of potassium efflux
4- not stable, climbs back towards threshold potential which when reached, triggers a complete spontaneous depolarisation. this feature gives it its pacemaker activity.

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17
Q

the electrocardiogram (ECG)

A

measures electrical activity in the heart
P wave- atrial depolarisation
QRS complex- reflects ventricles are larger
T wave- ventricular repolarisation
allows to investigate arrhythmias- heart rhythms which are different to normal
regular- 72 depolarisations/min
too much- tachycardia
too little- bradycardia

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18
Q

ventricular fibrillation

A

disordered electrical activity- heart fails to act as a syncytium- no coordinated pumping activity

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19
Q

what does the cardiovascular system do

A

supply oxygen and nutrients to the rest of the body

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20
Q

stress response

A

provide an increase in oxygen and glucose to tissues such as skeletal muscle to allow body to fight or run away

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21
Q

control system of the heart

A

autonomic control

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22
Q

intercalated disks

A

represent specialised regions of the heart-heart contact. in these areas, the cell membranes of adjacent cells form interlocking digitations and may contain desmosomes and gap junctions

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23
Q

desmosomes

A

allow for very strong cell attachment that prevent the cardiac myocytes from pulling apart during contraction

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24
Q

gap junctions

A

allow rapid conduction of electrical activity through the heart

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25
Q

where is the heart located

A

the middle mediastinum-right in the middle of the chest behind the sternum. contained in a triple layered sac (pericardium)
outer fibrous layer fused to diaphragm and great vessels- anchor. between visceral and parietal layers there is a small amount of fluid that allows the heart to move easily within pericardium as it beats

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26
Q

how does blood return to the heart

A

deoxygenated blood returns t the heart through the veins-get larger as they approach the heart.

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27
Q

what are the 2 veins which enter the heart

A

superior vena cava- draining the head and neck

inferior vena cava-draining lower limbs and trunk

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28
Q

what is the coronary sinus

A

thick vein like structure entering RA, collects blood from veins of cardiac muscle tissue itself

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29
Q

circulation

A

deoxygenated blood from RA transferred to RV, which when contracts, ejects blood to PT-divides into R and L pulmonary arteries that carry deoxygenated blood to lungs. blood returns to LA via L and R pulmonary veins. LA>LV which when contracts, ejects deoxygenated blood into aorta. first part of aorta- ascending aorta AA which curves to form aortic arch AAR, before becoming the descending aorta.

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30
Q

3 arterial branches arising from aortic arch

A

brachiocephalic trunk (BC)
left common carotid (LCC)
left subclavian (LS)
BC later forms right carotid and right subclavian. common carotids supply head and neck while S arteries supply trunk and upper limbs
coronary arteries arise from AA- immediately as it leaves the heart

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31
Q

difference between atria and ventricle walls

A

atria- thin as they don’t have to pump blood very far
ventricle walls are much thicker as they need to pump blood around blood vessel, L thicker than R as pumps blood around body whereas R is only the lungs

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32
Q

right atrium

A

important structures; vena cava, coronary sinus. fossa ovalis FO ‘left over’ from foetal life. (wall between R and L atria)

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33
Q

SA node

A

sino atrial node- pacemaker- sets pace of heartbeat. from SA node, electrical impulse (depolarisation) spreads through the walls of the atria to arrive at the AV node

34
Q

AV node

A

atrioventricular node- ;located between atria and ventricles. from AV node, depolarisation spreads through specialised structures in the intraventricular septum (IVS) before being distributed to ventricle walls. results spreading wave of contraction from apex towards aorta (LV) and pulmonary trunk (RV)

35
Q

functions of valves

A

prevent backflow of blood
4 valves of the heart; between A and V (AV valves) and between V and great vessels. valves between A and V only open when pressure in V falls below A. valves between V and GV only open when P In V is greater than P in GV. the right AV valve has 4 sections (cusps) and is called tricuspid valve, left AV valve is bicuspid.
valve between V and GV is known as tricuspid semi-lunar valves

36
Q

what is the chordinae tendinae

A

string like supporting structures- attach at one end to valve cusp and to other to little muscular papillae in wall of ventricle.

37
Q

2 synchronised pumps of the heart

A

lung loop> pulmonary circulation

other loop> systemic circulation

38
Q

route of blood flow

A

arteries> arterioles>capillaries>(where gas exchange occurs)> deoxygenated blood leaves via venules> join up to form veins

39
Q

pressure of blood

A

highest in arteries- drops around body-lowest in veins

40
Q

anatomy of a blood vessel

A

the internal (luminal) surface of blood vessels is lined with endothelium, a single cell layer with lots of specialised functions. endothelium supported on a connective tissue basement membrane. under this layer there is tunica intima (internal coat)-site of development for the atherosclerotic plaque. separated from muscular tunica by an elastic layer- the internal elastic lamina. tunica media is made up of lots of smooth muscle cells which can contract or relax and alter the diameter of the blood vessel. after tunica media, there is the external elastic lamina and a layer of loose connective tissue called the tunica adventitia

41
Q

parasympathetic

A

the parasympathetic supply comes from the vagus nerve- the tenth cranial nerve- and supplies only a very small area of the heart: the SA and AV nodes (fibres pass to cardiac plexus then SA node etc.) major effect on HR

42
Q

sympathetic

A

branches of the sympathetic nervous system supply nodes and muscle tissue of heart. referred to as accelerator nerves- activation increases HR by acting on specialised myocytes a=in the nodes. because the nerves supply the rest of the tissue, increases force of contraction.

43
Q

functions of endothelium

A

prevents blood clotting, allows adhesion of circulating WBC to enter tissue and carry out immune surveillance and produces nitric oxide which acts on smooth muscle cells to make them relax

44
Q

differences between arteries and veins

A

lumen diameter, wall thickness, relative development of the different layers, specialised such as tight junctions

45
Q

cholinergic synapse

A

found between post-ganglionic fibres of parasympathetic nervous system and tissue ( also in synapse between pre and post ganglionic fibres in both systems bit receptors are different) Acetylcholine Ach is synthesised when nerve is stimulated and released as a neurotransmitter into synaptic cleft. ACh binds to receptors on tissue. duration of Ach controlled by enzyme acetylcholine esterase which breaks down ACh which is then taken up into nerve terminal to be recycled

46
Q

adrenergic synapse

A

found between post-ganglionic fibres of sympathetic system-noradrenaline is synthesised and then when nerve is stimulated and released as a neurotransmitter into synaptic cleft. NA binds to receptors on tissue and on nerve terminal itself. when NA binds to these receptors it inhibits release of NA by nerve terminal; and attenuates (lessens strength) of stimulation of tissue by sympathetic nerve.

47
Q

cholinergic receptors in CVS

A

smooth muscle possess muscarinic (M3) receptors. if these were activated by an agonist leads to contraction. however in blood vessel, smooth muscle ae covered in a layer of endothelial cells (also have M3 receptors). activation of endothelial M3 receptors increase NO production which causes relaxation. net effect=vasodilation M2 receptors also found in heart- activation causes reduction in HR

48
Q

adrenergic receptors in CVS

A

adrenergic receptors also activated by circulating adrenaline released from adrenal medulla as a response to stress
in terms of adrenergic receptors, Beta 1 and beta 2 are found in the heat (predominant subtype beta 1) activation leads to increase In HR and force of contraction

49
Q

alpha 1 receptors

A

most smooth muscle and blood vessel cells will have alpha 1 receptors present in their cell membranes. activation>contraction>vasoconstriction.

50
Q

alpha 2 receptors

A

most smooth muscle and blood vessel cells will also possess alpha 2 receptors which also cause contraction. alpha 2 receptors sometimes found in sympathetic nerve terminals, this often tends to have negative feedback effects on the release of NA from the nerve. this means that the vasoconstriction effect caused by activation of post-synaptic receptors is reduced. this acts to prevent a dangerous and overwhelming response to release of NA.

51
Q

beta 2 receptors

A

some smooth muscle will have beta 2 receptors> activation causes relaxation>vasodilation

52
Q

activation of beta receptor

A

activation of each subtype leads to activation of AC which leads to an increase in cAMP, cAMP activates PKA which increases calcium released for sarcoplasmic reticulum.

53
Q

smooth muscle contraction

A

calcium is still involved but actual contraction brought about by activation of MLCK. this protein kinase is inhibited by cAMP, so activation of beta receptor in this context will cause relaxation>vasodilation

54
Q

adrenergic receptors in smooth muscle

A

alpha 1 receptor cause vasoconstriction, beta 2 receptor causes vasodilation. the receptors have a different distribution throughout the vasculature, and it allows the body to redistribute the blood flow in response to stress.
In response to stress; increased activation of sympathetic nerve fibres and release of adrenaline from adrenal medulla. activate alpha 1 and beta 2 receptors, causing vasodilation in blood vessels where predominant receptor is beta 2 and constriction where alpha 1 receptors predominate. increased blood flow to some tissues and reduce to others.

55
Q

control of blood flow

A

radius controls blood flow and therefore pressure. important as blood pressure is the driving force for delivery of oxygen and nutrients to tissues, but if too high can cause damage. pressure is also important in driving production of tissue fluid, which bathes cells and therefore is a way in which nutrients are delivered to cells.
blood flow is inversely proportional to resistance which is inversely proportional to radius^4

56
Q

autonomic control of heart beat

A

SA node intrinsically auto rhythmic, fires at 110bpm, regulated by ANS. resting HR more like 60bpm. vagal influence dominant at rest
p-symp nerves are largely restricted to the nodes, activation therefore has a negative chronotropic effect . no direct effect on contractility, however, activation of p-symp nerves inhibit sympathetic activity. therefore the indirect effect is a reduction of cardiac contractility

57
Q

factors which control production of tissue fluid

A 
hydrostatic pressure (blood pressure), therefore the greater the blood pressure, the greater the drive to produce tissue fluid. 
net result- tissue fluid returns to blood but at a lower rate than formed. excess handled by lymphatic circulation
58
Q

what is blood flow driven by

A

pressure gradient- 120mmHG in aorta; 0 in RA
aorta and arteries; distribution system- small amount of blood at high pressure. arterioles; variable resistance system where most of the arterial pressure is dissipated. capillaries; large SA for exchange
venules, veins, vena cave; 70% of blood at low pressure

59
Q

pathological excess

A

oedema

60
Q

control mechanisms

A

ANS- major control mechanism for CVS. ensures adequate cardiac output is maintained at all times so that oxygen and nutrient supply is available at all times

intrinsic- those that arise within the CVS
extrinsic- those that arise out with the CVS

61
Q

the baroreceptor reflex (intrinsic control)

A

monitor and modify BP on acute level. consists of sensory (stretch) receptors (mechanoreceptors) located in the wall of the carotid sinus and the aortic arch. stretch wall of vessel proportional to pressure in vessel. CNS linkage in medulla oblongata -cardiac control centre and vasomotor centre. motor pathways through ANS to heart and blood vessels.
increases symp activity and decreases p-symp activity. net effect is increase in BP and HR. symp nerves to muscular arterioles cause vasoconstriction

activation of baroreceptors sends nerve impulses to the control centre that inhibit symp outflow> decrease HR and BP.
note- there is always some degree of symp activity on CVS.

62
Q

the renin-angiotensin-aldosterone system (R-A-A-S, intrinsic control)

A

circulating renin is an enzyme that cleaves the pro-peptide angiotensinogen converting it to angiotensin 1- further modified by action of angiotensin converting enzyme (ACE) to produce angiotensin 2-potent vasoconstrictor which increases BP and stimulates release of aldosterone from adrenal glands. mineralocorticoid acts on kidney to enhance sodium retention and water retention which increases blood volume and therefore increases pressure. detected by juxtaglomerular apparatus of kidney and therefore decrease in renin ad inhibit pathway.

63
Q

2 wats of controlling BP

A

blood volume and blood vessel volume.
baroreceptor> volume
RAAS>both
blood volume can also be controlled by atrial natriuretic peptide

64
Q

extrinsic control mechanisms

A

local metabolites; hypoxia, lactate, CO2, H etc
endothelial activity; NO, prostacyclin, thromboxane’s etc
temperature
pressure
can override intrinsic control mechanisms

65
Q

cardiac output

A

HR x stroke volume
HR- bpm
stroke volume- amount of blood ejected from ventricle per beat

66
Q

what do heart beats consist of

A

ventricular contraction (systole) and relaxation (diastole) these events of muscular contraction and relaxation determine blood flow through the heart

67
Q

what is flow through the heart determined by

A

valve status which is determined by pressure differentials

68
Q

cardiac cycle 7 stages

A

atrial contraction, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, reduced filling

69
Q

atrial contraction

A

atrial contraction is immediately proceeded by atrial depolarisation- the P wave of the ECG.
the atria contract, this is accompanied by a small increase in left arterial pressure. blood flows from LA to LV through the AV valve. results in only a small increase in LV volume. (because atrial contraction contributes only small amount to ventricular filling (10%). most of the filling happens because ventricle relaxes, this causes pressure in ventricles to drop lower than atrium.
if A pressure is higher than V pressure, Av valve will open and most of the blood will fall into ventricle.
during this phase the aortic and pulmonary semilunar valves are closed because pressure in ventricles is lower than GV.
if HR increases, contribution to V filling becomes more significant but duration of contraction does not change significantly. therefore less time for heart to relax and so less passive filling of V. under conditions of stress, atrial contraction accounts for 40% of ventricular filling.

70
Q

relationship between preload and stroke volume

A

increase in preload= increase in stroke volume

BUT an increase In preload does not mean an increase in HR

71
Q

when will cardiac output increase

A

if stroke volume doesn’t increase

72
Q

factors effecting ventricular preload

A

atrial contractility, heart rate, ventricular compliance, venous pressure, inflow resistance

73
Q

isovolumetric contraction

A

‘same volume’ therefore although heart is contracting, all valves are closed so no blood enters or leaves the ventricles. initiated by ventricular depolarisation - QRS complex. under the influence of symp NS, this excitation-contraction coupling is enhanced. increased EDV, increased ventricular contractility therefore even bigger stroke volume. pressure builds rapidly until pressure in ventricle equal to that in aorta i.e. ejection is opposed by arterial pressure

74
Q

afterload

A

the force (load) against which the heart (ventricle) must eject blood. related to aortic pressure- the higher the aortic pressure the higher the afterload and the harder the heart will have to work to eject blood
so, SV is actually determined by the balance between preload and afterload.
afterload^- decrease blood ejected- decrease stroke volume
however
decrease blood ejected- ^blood left behind-^EDV-^contraction-^ejection of blood

75
Q

aortic pressure during stress

A

arteries also contain smooth muscle cells, response to NA/A by contracting, get arterial and venoconstriction, stress increases both preload and afterload, but preload more

76
Q

rapid ejection

A

ventricles continue to contract, pressure continues to rise. pressure in ventricle will be greater then in the GV and the aortic semilunar valve will open. blood ejected from ventricle, rapid decrease in ventricular volume. this flow of blood from the ventricle to the vessel will cause the ventricular pressure to drop, while the pressure in the ventricle increases.

77
Q

reduced ejection

A

ventricular repolarisation (T-wave)outflow drops, ventricular wall tension, which further reduces the rate of ejection. as the pressure in the ventricle and the great vessel start to equalise, the semilunar valve begin to move to a closed position.

78
Q

isovolumetric relaxation

A

outflow drops, semilunar valves shut abruptly. gives rise to 2nd heart sound. big drop in ventricular pressure/ amount of blood left in ventricle when semilunar valves close- EDV. around 50ml
difference between EDV and ESV is stroke volume=70ml typically. arterial pressure continues to rise due to constant venous return

79
Q

rapid filling

A

pressure in ventricle continues to drop while pressure in atrium continues to rise. eventually the pressure differential becomes sufficient to open the AV valves and blood flows rapidly into ventricle

80
Q

reduced filling

A

as the ventricle fills with blood, the wall becomes more and more distended, with the result that it becomes less compliant. this means that, for relatively small changes in volume, there is a big increase in pressure>slow flow in ventricle

Integrated physiology (8 decks)

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