Cardiovascular System (S1-6) Flashcards
S1: Intro To CVS + Histology Of The Heart S2: The Heart As A Pump S3: Congenital Heart Defects S4: Cellular And Molecular Events In The CVS / The ANS And The CVS S5: Pressure, Flow And Resistance / The Peripheral Circulation S6: Control Of Cardiac Output / Response Of Whole System (273 cards)
1
Q
Why do we need a cardiovascular system? (S1)
A
We have many cells (to the order of 10^14), many of which are far from the source of O2 and nutrients. Diffusion alone cannot efficiently exchange O2 and nutrients around the body. It is too slow. A cardiovascular system, which comprises of gas exchange and a circulatory system, allows us to have efficient exchange.
2
Q
What does blood transport around the body? (S1)
A
O2, metabolic substrates, CO2 and waste products.
3
Q
Where does diffusion between blood and tissues take place? (S1)
A
At the capillaries
4
Q
What is the composition of capillaries? (S1)
A
They have one layer of endothelial cells - simple squamous epithelium - surrounded by basal lamina
5
Q
At the capillaries, what does O2 and CO2 diffuse through? What do other molecules such as glucose, lactate and amino acids, which are hydrophillic, diffuse through? (S1)
A
O2 and CO2 diffuse through the lipid bilayer.
Larger molecules diffuse through small, aqueous pores between endothelial cells, in the membranes.
6
Q
What factors affect the rate of diffusion? (S1)
A
The area, diffusion ‘resistance’, concentration gradient.
7
Q
How does area affect the rate of diffusion? What is area like with regards to capillaries? (S1)
A
The rate of diffusion depends on the area available for exchange; the more available, the quicker diffusion will be.
Area available for exchange between capillaries and tissues are very large, although it depends on capillary density. A more metabolically active tissue will have more capillaries.
8
Q
What three factors affect diffusion resistance? (S1)
A
It depends on the nature of the molecule (lipophilic/hydrophilic, size), nature of the barrier (eg pore size and number of pores for hydrophillic substances) and the path length. The path length depends on capillary density and the path is shortest in the most active tissues. Diffusion resistance is mostly low.
9
Q
What is the rate of blood flow known as? (S1)
A
The perfusion rate.
10
Q
How much blood flow does the brain, heart and kidneys need? (S1)
A
Brain: 0.5 (constant flow); Heart: 0.9 to 3.6 (increases during exercise); Kidneys: 3.5 (constant flow). All units are ml.min-1.g-1
Something different…
How much roughly do the brain, heart and kidneys weigh if flow l.min-1 is 0.75 (brain), 0.3 to 1.2 (at rest and pumping to its maximum capacity; the heart) and 1.2 (kidneys)?
Brain: 1.5kg (probably an over-estimate); Heart: 0.3kg; Kidneys: 0.3kg
11
Q
When is blood flow to skeletal muscle high? And to the gut?
A
Skeletal muscle: during exercise (can go from 1 l.min-1 to up to 16 l.min-1)
The gut: high after a large meal (1.4 lmin-1 at rest, can increase to 2.4 l.min-1
12
Q
How much blood flows to the body’s tissues in a minute at rest? (S1)
A
5 l.min-1
13
Q
What proportion does the brain, heart and kidneys make up of the total blood flow around the body (at rest)? (S1)
A
0.45
14
Q
How much blood flows to the skin in a minute - does this ever change? (S1)
A
0.2 litres. No.
15
Q
What is the maximum blood flow to the body’s tissues in a minute when might this occur? (S1)
A
24.5 l.min-1 seen during intense exercise.
16
Q
What are the components of the cardiovascular system? (S1)
A
Pump: the heart;
Distribution system: vessels & blood;
Exchange mechanism: capillaries;
Flow control: arterioles and precapillary sphincters.
17
Q
Why is the brain harder to perfuse than the kidneys? (S1)
A
Due to gravity’s effects.
18
Q
What must be added to regulate blood flow? (S1)
A
Resistance reduces the ease with which some regions are perfused in order to direct blood flow to the more difficult regions to perfuse.
19
Q
Which vessels can increase resistance (in doing so regulating blood flow)? (S1)
A
Arterioles. Precapillary spinchters will also play a part in regulating blood flow.
20
Q
How can veins control the total flow in the system? (S1)
A
Veins have thin walls which can easily distend or collapse enabling them to act as a variable reservoir for blood. This capacitance of the veins provides the temporary store… This process requires a temporary store of blood which can be returned to the heart at a different rate.
21
Q
How is blood distributed in the cardiovascular system? (S1)
A
65% in the veins, 20% heart & lungs, 10% arteries & arterioles, 5% capillaries
22
Q
How much blood will a large man contain? (S1)
A
6 litres.
23
Q
How much surface area does the capillaries have for exchange? (S1)
A
About 600m^2.
24
Q
What do arteries do? (S1)
A
They are blood vessels that carry blood away from the heart to the capillary beds.
25
Which three major arterial trunks arise from the arch of the aorta? (S1)
The brachiocephalic artery, common carotid artery and the left subclavian artery.
26
In the abdominal cavity the aorta terminates by bifurcating into the... (S1)
Left and right common iliac arteries in the pelvis.
27
What does left ventricle contraction cause blood pressure in the aorta to rise to? (S1)
Approx. 120 mm Hg. The walls of the aorta will stretch (as well as other elastic arteries).
28
What happens during diastole? (S1)
The aortic semilunar valve closes and the walls of the aorta recoil. This maintains the pressure on the blood and moves it towards the smaller vessels.
29
What does aortic pressure drop to during diastole? (S1)
70-80 mm Hg.
30
What three types (from widest to narrowest) are arteries classified into? (S1)
Elastic conducting arteries (which will have more elastic fibres), muscular distributing arteries (which have more smooth muscle fibres) and arterioles.
31
What is the diameter of arteries and arterioles controlled by? (S1)
The autonomic nervous system.
32
What do the arterioles branch into before reaching the capillaries? (S1)
Metarterioles.
33
What are the three layers of the walls of the arteries and veins called (starting from nearest to the lumen)? (S1)
Tunica intima, tunica media and tunica adventita.
34
Why might elastic arteries appear yellow? (S1)
This may be the case if there is abundant elastin. It will normally be seen in the fresh state.
35
Outline the main features of each layer of the elastic arteries. (S1)
Tunica intima: Endothelial cells; narrow subendothelium of connective tissue with discontinuous internal elastic lamina.
TUNICA MEDIA: 40-70 fenestrated elastic membranes, with smooth muscle cells and collagen between these lamellae.
Tunica adventitia: Layer of fibroelastic connective tissue containing vasa vasorum, lymphatic vessels and nerve fibres.
36
What are vasa vasorum? (S1)
Vasa vasorum are a network of small blood vessels that supply the walls of large blood vessels.
37
Outline the main features of each layer of the muscular arteries. (S1)
Tunica intima: Endothelium, subendothelial layer, thick internal elastic lamina.
TUNICA MEDIA: 40 layers of smooth muscle cells (connected by gap junctions for coordinated contraction). Prominent external elastic lamina.
Tunica adventitia: THIN layer of fibroelastic tissue containing vasa vasorum, lymphatic vessels and nerve fibres.
38
What are end arteries and where might they be found in the body? (S1)
End arteries are terminal arteries supplying all or most of the blood to a body part without significant collateral circulation. The coronary artery, splenic and renal arteries as well as the central artery to the retina are all end arteries.
39
What is the issue if end arteries are occluded? (S1)
End arteries branch without the development of channels connecting with other arteries. This means if they are occluded there will be insufficient blood supply to the dependent tissue.
40
When is an artery considered an arteriole? (S1)
When it has a diameter less than 0.1mm.
41
Outline the main features of each layer of the arterioles. (S1)
Tunica intima: layer of endothelial cells and very thin layer of subendothelial connective tissue.
TUNICA MEDIA: only one to three layers of smooth muscle, although in small arterioles the tunica media is composed of a single smooth muscle cell that encircles the endothelial cells.
Tunica adventitia: scant
42
Define a metarteriole. (S1)
It is an artery that supplies blood to capillary beds.
43
How do metarterioles differ from arterioles? (S1)
The smooth muscle layer is not continuous in metarterioles. Rather, the individual muscle cells are spaced apart and each encircles the endothelium of a capillary; this is known as the precapillary sphincter. Each muscle cell acts as a spinchter, upon contraction, controlling blood flow into the capillary bed.
44
During strenuous exercise how is blood flow to skeletal muscles increased? How would this differ after eating a hearty meal? (S1)
Dilation of arterioles to skeletal muscle, and constriction of arterioles to the intestine. The reverse is true for a large meal.
45
How wide are the narrowest arterioles? How much wider than an ordinary capillary is this? (S1)
30um. 3-4 times.
46
What are the three types of capillaries and where are they found? (S1)
Continuous: found in nervous, muscle and connective tissues, exocrine glands and the lungs.
Fenestrated: in parts of gut, endocrine glands and renal glomerulus. There are small holes across thin parts of the endothelium, bridged by a thin diaphragm (except in the renal glomerulus).
Discontinuous (sinusoidal): seen in liver, spleen and bone marrow. They have a larger diameter (30-40um) and slower blood flow.
47
What is angiogenesis? (S1)
The development of new blood vessels from pre-existing vessels.
48
What is the diameter of postcapillary venules? Are they more or less permeable than capillaries? (S1)
10-30um, they are more permeable than capillaries.
49
Why does fluid tend to drain into postcapillary venules? What is the exception? (S1)
This is due to the pressure being lower in them than that of capillaries and surrounding tissue. When there is an inflammatory response operating fluid and leukocytes emigrate. These venules are the preferred location for emigration of leukocytes from the blood.
50
What is the diameter of venules? (S1)
50um and they can increase to 1mm.
51
Outline the main features of each layer of the vein. (S1)
Small and medium-sized veins have:
Tunica intima: thin
Tunica media: 2 or 3 layers of smooth muscle
Tunica adventitia: well developed
Large veins have diameters >10mm
Tunica intima: thicker
Tunica media: not prominent but have circularly arranged smooth muscle
Tunica adventitia: well-developed logitudinally orientated smooth muscle
52
Why might the superficial veins of the legs have a well-defined muscular wall? (S1)
Possibly to resist distension caused by gravity.
53
What are venae comitantes? What does the pulsing of the artery promote? (S1)
They are the deep paired veins that, in certain anatomical positions, accompany one of the smaller arteries on each side of the artery. The three vessels are wrapped together in one sheath. The pulsing of the artery promotes venous return within the adjacent, parallel, paired veins.
54
What are some examples of arteries that have venae comitantes? (S1)
The brachial, ulnar and tibial arteries.
55
What are some examples of large veins? (S1)
Vena cavae, pulmonary, portal, renal, internal jugular, iliac, and azygous veins.
56
What is the mitral valve between? (S2)
The left atria and the left ventricle. It is sometimes known as the bicuspid valve.
57
What is the tricuspid valve between? (S2)
The right atria and the right ventricle.
58
What does the action potential cause (in relation to the concentration of ions within the cell)? (S2)
It causes intracellular calcium to rise.
59
How long is an action potential? (S2)
A single contraction lasts 280ms.
60
What are action potentials triggered by? (S2)
The spread of excitation from cell to cell.
61
What is the contraction period referred to as?
| And the relaxation period? (S2)
Systole
| Diastole
62
What do pacemakers do? (S2)
They generate one action potential at a regular interval.
63
How often does the sino-atrial node generate an action potential at rest? (S2)
About once a second.
64
How long does ventricular systole last for? (S2)
280ms
65
How long does ventricular diastole last for? (S2)
At rest, it will last for 700ms before the next systole.
66
When does the mitral valve open? When does it close? (S2)
It opens when atrial pressure exceeds intraventricular pressure i.e. early diastole and closes at a point in ventricular systole, when ventricular pressure exceeds atrial pressure and back flow of blood causes the valves to close shut.
67
When does the aortic valve open? When does it close? (S2)
It opens in systole, after the ventricles contract so that intra-ventricular pressure exceeds aortic pressure. It closes when aortic pressure exceeds ventricular pressure - this is towards the end of systole - and blood flows backwards shutting the valve.
68
How is ventricular muscle organised in order to facilitate the pumping of blood? (S2)
Ventricular muscle is organised into figure of eight bands. These squeeze the ventricular chamber forcefully in the most effective way to allow ejection through the outflow valve.
69
How does the contraction of the ventricle ensure back flow of blood is reduced? (S2)
The apex of the heart contracts first and relaxes last to reduce back flow of blood.
70
What is the main difference between the right and the left heart? (S2)
The left side has a thicker myocardium and so must pump blood around the body and therefore harder, than just around the lungs.
71
What is the origin of the first heart sound? (S2)
As the atrioventricular valves close oscillations are induced in a variety of structures, producing a mixed sound with a crescendo-descendo quality – ‘lup’
72
What is the origin of the second heart sound? (S2)
As the semi-lunar valves close oscillations are induced in other structures, including the column of blood in the arteries. This produces the sound of shorter duration, higher frequency and lower intensity than the first – ‘dup’
73
Why may a 3rd or even 4th sound be heard? (S2)
A 3rd sound may be heard early in diastole and a 4th may be heard during atrial contraction.
74
What is a heart murmur? (S2)
The turbulent flow of blood.
75
What are the two types of murmur? (S2)
Stenosis, incompetence or regurgitation
76
What is stenosis? (S2)
There is a narrowed valve, normally due to calcification - (in the case of aortic stenosis it could be due to acute rheumatic fever).
77
What is incompetance of a valve? (S2)
It is where a valve does not close properly and so there is back flow of blood.
78
When do murmurs occur? (S2)
When blood flow is at its highest, e.g. aortic stenosis produces a murmur in the rapid ejection phase.
79
What is cardiac output? (S2)
Cardiac output is stroke volume times heart rate. The stroke volume is the amount of blood one ventricle of the heart ejects with each beat.
80
Outline the entirety of the cardiac cycle (starting from early diastole)! (S2)
INFLOW VALVES OPEN
In early diastole, the ventricular mass relaxes.
The intraventricular pressure falls below atrial pressure = inflow valves opening.
RAPID FILLING PHASE
The atria, having been distended by continuous venous return from throughout the preceding systole, so initially blood is forced rapidly from the atria into the ventricles – the ‘rapid filling’ phase.
SLOWER FILLING OF VENTRICLES
Filling of the ventricles continues through diastole, at a steadily decreasing rate until the intra-ventricular pressure has risen to match atrial pressure. At low heart rates, ventricles are more or less full before the next systole begins.
ATRIAL SYSTOLE
Atrial systole forces a small extra amount of blood into the ventricles. After a delay of about 100-150ms the ventricles begin to contract.
CLOSING OF INFLOW VALVES
As intraventricular pressure rises, blood tends to flow the wrong way through the Mitral valve, producing turbulence that closes the valve forcibly.
OUTFLOW VALVES OPEN
Ventricles then contract isovolumetrically; intraventricular pressure rises rapidly until it exceeds the diastolic pressure of the pressure in the arteries, when the outflow (Aortic/Pulmonary) valves open.
RAPID EJECTION PERIOD
There is then a rapid ejection period, where both intraventricular and arterial pressure rise to a maximum.
OUTFLOW VALVES CLOSE
Towards the end of systole intraventricular pressure falls and once below the arterial pressure the outflow valves close due to the backflow of blood.
When the intraventricular pressure falls below atrial pressure the whole process starts again.
81
Explain how the... AV VALVES OPEN, RAPID FILLING PHASE and the SLOWER FILLING OF VENTRICLES. (S2)
In early diastole, the ventricular mass relaxes.
The intraventricular pressure falls below atrial pressure = Tricuspid/Mitral valves opening.
The atria, having been distended by continuous venous return from throughout the preceding systole, so initially blood is forced rapidly from the atria into the ventricles – the ‘rapid filling’ phase.
Filling of the ventricles continues through diastole, at a steadily decreasing rate until the intra-ventricular pressure has risen to match atrial pressure. At low heart rates, ventricles are more or less full before the next systole begins.
82
What happens after the SLOWER FILLING OF THE VENTRICLES? (S2)
ATRIAL SYSTOLE
Atrial systole forces a small extra amount of blood into the ventricles. After a delay of about 100-150ms the ventricles begin to contract.
83
Why do the AV VALVES CLOSE? (S2)
CLOSING OF AV VALVES
As intraventricular pressure rises, blood tends to flow the wrong way through the Mitral valve, producing turbulence that closes the valve forcibly.
84
What happens after ATRIAL SYSTOLE and the INFLOW VALVES CLOSE? What is the RAPID EJECTION PERIOD? (S2)
OUTFLOW VALVES OPEN
Ventricles then contract isovolumetrically; intraventricular pressure rises rapidly until it exceeds the diastolic pressure of the pressure in the arteries, when the outflow (Aortic/Pulmonary) valves open.
RAPID EJECTION PERIOD
There is then a rapid ejection period, where both intraventricular and arterial pressure rise to a maximum.
85
What happens after the RAPID EJECTION PERIOD? What action leads to the OPENING OF THE INFLOW VALVES? (S2)
OUTFLOW VALVES CLOSE
Towards the end of systole intraventricular pressure falls and once below the arterial pressure the outflow valves close due to the backflow of blood.
When the intraventricular pressure falls below atrial pressure the whole process starts again.
86
How prevalent are congenital heart diseases? (S3)
6-8 in a 1000
87
Which are the most common congenital heart diseases? (S3)
Ventricular septal defect (VSD), followed by atrial septal defect (ASD)
88
What is an ASD? (S3)
An atrial septal defect is where there is an opening between the two atria, which persists following birth.
89
Why would ASD eventually lead to heart failure? (S3)
Left atrial pressure > Right atrial pressure, so oxygenated blood flows from the left atria to the right atria. This can mean the right ventricle is overloaded and will lead to failure. The fact no deoxygenated blood mixes with the systemic circulation explains partly why ASD's are usually asymptomatic until late in adulthood.
90
Which structure closes postnatally in order to prevent the shunting of blood from right to left, as seen in an ASD? (S3)
Foramen ovale
It exists prenatally to permit blood from right --> left and is designed to close shortly after birth.
91
Where are the most common sites for ASDs? (S3)
ASDs can occur anywhere along the atrial septum but are most common in the foramen ovale (Ostium secundum ASD). They can also be found at the inferior part of the septum (Ostium primum ASD).
92
What is a VSD? (S3)
A ventricular septal defect is an opening in the interventricular septum.
93
Where does a VSD most commonly occur? (S3)
In the membranous portion of the septum, but it can occur anywhere.
94
Which way does blood flow when there is a VSD? (S3)
Left --> Right ... Left ventricular pressure > Right ventricular pressure; blood moves from high to low pressure.
95
How would a VSD patient typically present? (S3)
With left heart failure, normally presenting as an infant. If untreated, it can lead to inoperable pulmonary hypertension.
96
Will there be right or left ventricular overload with a VSD and why? (S3)
There would be left ventricular overload.
The blood moves from the left ventricle to the right.
So this means the RV is overloaded initially.
But that 'extra' blood goes to the pulmonary circulation and means more blood is flowing into the left heart. The left heart is therefore more prone to fail. More blood is moving through the pulmonary veins. This explains the fact there is pulmonary venous congestion.
97
What is tetralogy of Fallot? (S3)
```
It is a group of 4 defects that occur together due to a single developmental defect (specifically the interventricular septum is too far in the anterior and cephalid directions).
The 4 defects are:
Pulmonary stenosis
Right ventricle hypertrophy
VSD
Over-riding aorta
```
98
Is tetralogy of Fallot acyanotic or cyanotic? Why? (S3)
It is cyanotic.
This is because the pressure in the right ventricle is higher due to the pulmonary stenosis. This means blood moves from the right to the left ventricle. Therefore deoxygenated blood moves into the systemic circulation - explaining the cyanosis.
99
How would a tetralogy of Fallot patient present? (S3)
There are different severities of tetralogy of Fallot. They, and the magnitude of the shunt, depend on the extent of the pulmonary stenosis. Severe cases present in early childhood with cyanotic spells. More mild cases are compatible with adulthood.
100
What is tricuspid atresia? (S3)
It is the lack of development of the tricuspid valve i,e, the right ventricular inlet.
101
How can the body 'get around' a tricuspid atresia? (S3)
A shunt, so that blood can move from the right to the left can be created. Then blood moves to the lungs via a VSD or a PDA.
102
What is pulmonary atresia? (S3)
It is the lack of development of the pulmonary valve i.e. the right ventricular outlet.
103
How can the body 'get around' a pulmonary atresia? (S3)
There would be a shunt created between the atria so blood can move from the right to the left. Blood will then flow to the lungs by a PDA.
104
Is tricuspid atresia acyanotic or cyanotic? What about pulmonary atresia? (S3)
They are both cyanotic.
105
What is transposition of the great arteries? (S3)
The right ventricle is connected to the aorta and the left ventricle is connected to the pulmonary artery. It is not viable unless the two circuits communicate, i.e. through atrial, ventricular or ductal shunts.
106
How does transposition of the great arteries usually present? (S3)
As a neonatal emergency, due to reduced pulmonary blood flow.
107
What is hypoplastic left heart? (S3)
It is where the left ventricle is underdeveloped. This means the mitral and aortic valves are also underdeveloped. Therefore there is a necessity for an ASD (or PFO) and PDA. The right ventricle supports the systemic circulation as the ascending aorta is very small.
108
How would hypoplastic left heart present? (S3)
As a neonatal emergency, due to reduced pulmonary blood flow. There must be surgical intervention.
109
How common are Patent Foramen Ovale? (S3)
They may be found in up to 20% of the population.
110
What is a paradoxical embolism? (S3)
A PFO may be the route by which a venous embolism reaches the systemic circulation if pressure on the right side of the heart increases (even transiently). This is called a paradoxical embolism.
111
What is a PDA? (*)
A public display of affection.
112
What else can a PDA be? (*)
A personal digital assistant - i.e. a palmtop computer. Essentially a Blackberry but not shite.
113
Finally, what is a PDA? (S3)
It is a Patent Ductus Arteriosus. The Ductus Arteriosus is a vessel that exists in the foetus to shunt blood from the pulmonary artery to the aorta when the lungs aren't functioning. A Patent Ductus Arteriosus is where the Ductus Arteriosus remains open. Blood flow will reverse and move from the aorta to the pulmonary artery (high pressure --> low pressure).
114
Why does the Ductus Arteriosus close in a healthy indiviudal? (S3)
It closes following the drop in pressure in the pulmonary artery following perfusion of the lungs.
115
What problems can a Patent Ductus Arteriosus lead to? (S3)
It can lead to an increase in pulmonary resistance through vascular remodelling of the pulmonary circulation.
116
What will an increase in pulmonary resistance lead to? (S3)
This will lead to the right heart working harder than the left heart. This will mean the shunt reverses and blood flows from the pulmonary artery to the aorta. This is known as Eisenmenger's Syndrome!
117
What is coarctation of the aorta? (S3)
This is the place where the aorta narrows due to the ductus arteriosus' insertsion.
118
In coarctation of the aorta, why are the head and upper limbs not affected? (S3)
This is because the vessels to the head and upper limbs usually emerge proximal to the coarctation; the blood supply to these regions is not compromised.
119
What are the clinical signs of coarctation of the aorta? (S3)
A delayed and weak femoral pulse.
| Upper body hypertension.
120
Preductal coarctation is known as the neonatal variety of coarctation of the aorta. How would it present? (S3)
As it is associated with a PDA and there is a right to left shunt it would present as a neonatal emergency often due to reduced pulmonary blood flow.
121
Does the Na+/K+ ATPase set the resting membrane potential? (S4)
No. It is set largely due to K+ permeability of the cell membrane at rest.
122
Why does the resting membrane potential not exactly equal Ek (-95mV)? (S4)
This is due to the fact there is a very small permeability to other ion species at rest.
123
What is a cardiac myocyte and what do they do? (S4)
They are cardiac muscle cells and they fire action potentials which trigger increases in cytosolic [Ca2+].
124
What is the resting membrane potential of ventricular cells? (S4)
It is -90mV.
125
Describe the action potential of ventricular cells. (S4)
At diastole, the resting membrane potential is ~-90mV, close to Ek.
The initial depolarisation is caused by the spread of electrical activity of the pacemaker cells.
Once threshold is reached, fast voltage-gated Na+ channels open. This causes depolarisation towards Ena (which is ~+61mV), ~+30mV is reached..
K+ flows out of the cell (through voltage-gated channels); this causes a brief repolarisation returning the membrane potential to ~0.
Then Na+ channels deactivate whilst Ca2+ channels open, keeping the membrane depolarised (they take longer to activate). The influx of Ca2+ causes the release of further Ca2+ from cellular stores, causing contraction.
After ~250ms Ca2+ channels close. K+ efflux causes the membrane potential to return to resting i.e. ~-90mV.
126
What is the maximum -ve voltage of the membrane potential of pacemaker cells? What does it cause? (S4)
-60mV. It results in fast voltage-gated Na+ channels remaining inactivated.
127
What is the 'funny current'; how is a pacemaker cell depolarised? (S4)
The 'funny current' is the 'spontaneous gradual depolarisation' of the pacemaker cells. This is due to the influx of Na+ through slow Na+ channels; these channels open during the repolarisation of the membrane as the potential reaches its most -ve values.
128
What happens after the threshold of a pacemaker cell is reached? (S4)
The Ca2+ channels open giving a relatively slow depolarisation (with respect to the fast Na+ channels being inactivated). Once Ca2+ channels close, the cell repolarises due to K+ efflux.
129
Which channels allow the influx of Na+ ions in pacemaker cells? (S4)
HCN channels... or... Hyperpolarisation-activated, Cyclic Nucleotide-gated channels.
130
Which cells in the heart are fastest to depolarise? (S4)
Those making up the SA node.
131
Histologically what is remarkable about cardiac muscle cells? (S4)
1. Cells are joined together at intercalated disks, allowing action potentials to spread across the myocardium.
2. Gap junctions permit movement of ions and electrically couple cells. The gap junctions are formed by connexon (very large channels) proteins on each side of the cell which join together. Ions can move through these pores so allowing the electrical excitability to spread.
3. Desmosomes rivet (or mechanically join) cells together and cardiac myocytes have a single central nucleus.
132
If skeletal muscles were put in a Ca2+ free solution, would they carry on to contract? (S4)
Yes. This is due to the fact it does not require the movement of Ca2+ to contract.
133
For contraction to take place, cytosolic calcium must increase, how does this occur? (S4)
Depolarisation opens L-type Ca2+ channels in the T-tubule system. Localised Ca2+ entry opens calcium-induced calcium release (CICR) in the SR.
134
How much calcium enters across the sarcolemma, how much across the sarcoplasmic reticulum (SR)? (S4)
25% and 75% respectively.
135
How is cardiac myocyte contraction regulated? (S4)
It is the same as skeletal muscle. Ca2+ binds to troponin C and a conformational change shifts tropomyosin to reveal myosin binding site on actin filament.
136
What must happen for cardiac myocytes to relax? How does this happen? (S4)
There must be a decrease in cytosolic [Ca2+].
SERCA pumps most of it back into the sarcoplasmic reticulum, NCX and the sarcolemmal Ca2+ ATPase also move Ca2+ to the exit across the cell membrane.
137
What is 'tone of blood vessels'? (S4)
Tone refers to how stiff blood vessels are in their baseline state. Tone of blood vessels is controlled by contraction and relaxation of vascular smooth muscle cells. Smooth muscle (non-striated) is used to adjust resistance and distensibility; it does not help to pump the blood.
138
How is excitation contraction coupling in smooth muscle cells controlled? (S4)
Ca2+, once it enters vascular smooth muscle cells, will bind to calmodulin. This binding of Ca2+ to calmodulin controls the excitation contraction coupling in smooth muscle cells. This can be through channels or can happen when G protein coupled receptors (an α-adrenoreceptor) are activated, Gαq produces IP3 and DAG. IP3 causes the release of Ca2+ from sarcoplasmic reticulum. 4 Ca2+ ions bind to one calmodulin. This complex subsequently activates MLCK (myosin light chain kinase). It phosphorylates a (regulatory) light chain on the myosin head. When the light chain is phosphorylated, the myosin head binds to the actin.
139
How does relaxation in smooth muscle cells occur? (S4)
Relaxation occurs as Ca2+ levels decline. MLCP (myosin light chain phosphatase) dephosphorylates the light chain of the myosin head and puts myosin into the resting stage. MLCP is constitutively active (i.e. always active).
140
How can protein kinase A interfere with MLCK? (S4)
It can phosphorylate it, making it inactive.
141
The sympathetic and parasympathetic nervous systems have two neurones arranged in series. How are the two neurones divided into the central and peripheral nervous system? (S4)
A pre-ganglionic neurone cell body falls under the central nervous system (CNS). The synapse and post-ganglionic nervous system fall under the peripheral nervous system (PNS). Together these two neurones act on the target cell.
142
What is the peripheral nervous system divided into?
The PNS is divided into the somatic nervous system and the autonomic nervous system (ANS).
143
What is the ANS divided into? (S4)
The sympathetic nervous system and the parasympathetic nervous system ('rest and digest'). The division is based on anatomical grounds. There is also an enteric nervous system which is a network of neurones surrounding the GI tract. It is normally controlled via sympathetic and parasympathetic fibres.
144
Where do the roots of the sympathetic nervous system come from? (S4)
The thoraco-lumbar region.
145
Where do the roots of the parasympathetic nervous system come from? (S4)
The cranio-sacral region.
146
What is the autonomic nervous system (ANS) important for? (S4)
For regulating heart rate, blood pressure, temperature etc. (homeostasis) and co-ordinating the body’s response to exercise and stress.
147
Is the ANS controlled voluntarily? What does it control? (S4)
It is largely outside voluntary control. The ANS exerts control over smooth muscle (both vascular and visceral), exocrine secretion and the rate and force of contraction in the heart.
148
In the sympathetic division, which segments do preganglionic neurones arise from? (S4)
T1 to L2 (or L3).
149
In the parasympathetic division, where do preganglionic neurones arise from? (S4)
It has preganglionic fibres which travel in cranial nerves (III, VII, IX & X) or sacral outflow from S2-S4.
150
What do preganglionic neurones of the sympathetic division synapse with? (S4)
Most synapse with postganglionic neurones in the paravertebral chain of ganglia although some do in a number of prevertebral ganglia (coeliac, superior mesenteric, inferior mesenteric ganglia).
151
What do preganglionic neurones of the parasympathetic division synapse with? (S4)
They synapse with neurones in ganglia close to the target tissue and thus have short postganglionic neurones.
152
What do preganglionic neurones of the sympathetic division release? (S4)
Acetylcholine.
153
What do preganglionic neurones of the parasympathetic division release? (S4)
Acetylcholine.
154
What does acetylcholine act on in the postganglionic cell? (S4)
Nicotinic ACh receptors (have an ion channel).
155
Are postganglionic neurones of the sympathetic division usually cholinergic? (S4)
They are usually noradrenergic (noradrenaline is the transmitter). The exception is sympathetic innervation of the sweat glands – postganglionic neurones release ACh which acts on muscarinic ACh receptors.
156
Are postganglionic neurones of the parasympathetic division usually cholinergic? (S4)
Postganglionic parasympathetic neurones are usually cholinergic (have ACh as a transmitter).
157
In the parasympathetic divison, what does ACh released from postganglionic neurones act on? (S4)
It acts at muscarinic ACh receptors on the effector cells – these are G protein-coupled receptors, M1, M2 & M3 and have no integral ion channel).
158
What do chromaffin cells of the adrenal medulla do? (S4)
They are like specialised postganglionic sympathetic neurones. They release adrenaline which circulates in the blood stream.
159
What do noradrenaline and adrenaline act on? (S4)
They act on adrenoreceptors. These are G protein-coupled receptors (they have no integral ion channel). There are α1 and α2 adrenoreceptors as well as β1 and β2.
160
What is the advantage of having different subtypes of adrenoreceptors? (S4)
Different tissues can have different subtypes which allows for diversity of action and selectivity of drug action.
161
What receptor is found in the heart for sympathetic and parasympathetic effect? (S4)
β1 for sympathetic effect: i.e. increase rate (chronotropic effect) and force of contraction (ionotropic effect). M2 in order to decrease (chronotropic effect) rate.
162
What receptor is found in the lungs for sympathetic and parasympathetic effect? (S4)
β2 for sympathetic effect: i.e. relaxation of airways. M3 in order for contraction.
163
What receptors is found for sympathetic action of sweat glands? (S4)
α1 for localised secretion (e.g. palms) and M3 for generalised secretion.
164
What receptors are found for parasympathetic action of sweat glands? (S4)
There are none :)
165
What receptors is found in the pupil of the eye for a sympathetic and a parasympathetic effect? (S4)
α1 for sympathetic effect: dilation (radial muscle contracts)
M3 for parasympathetic effect: contraction (sphincter muscle contracts).
166
Is sympathetic drive to different tissues independently regulated? (S4)
Yes. This means sympathetic activity to the heart can be increased without increasing activity to the GI tract.
167
In the CVS, what does the ANS control? (S4)
Heart rate (chronotropic effect), force of contraction (ionotropic effect) of the heart and the body's total peripheral resistance.
168
What is the parasympathetic input to the heart derived from? (S4)
The cranial (X) or vagus nerve.
169
What do the preganglionic fibres of the vagus nerve synapse with and where? (S4)
They snapse with postganglionic cells on the epicardial surface or within the walls of the heart (located at the SA and AV node).
170
In the parasympathetic input to the heart, what do the postganglionic cells release? (S4)
Acetylcholine.
171
In the postganglionic parasympathetic input to the heart, what receptors does ACh act on? What do these receptors do when activated? (S4)
M2 receptors. They decrease heart rate (negative chronotropic effect) through decreasing AV node conduction velocity.
172
For the sympathetic input to the heart, where are the postganglionic fibres from? What parts of the heart do the innervate? (S4)
The sympathetic trunk. These fibres innervate the SA node, the AV node and the myocardium.
173
In the sympathetic input to the heart, what do the postganglionic cells release? (S4)
Noradrenaline.
174
In the sympathetic input to the heart, what does noradrenaline act on and what do the receptors do when activated? (S4)
It acts on β1-adrenoreceptors. This increases heart rate (positive chronotropic effect) and force of contraction (positive ionotropic effect).
175
What are some features of HCN channels? (S4)
The hyperpolarising cyclic nucleotide (HCN) channels are are opened by hyperpolarisation and are activated by cyclic nucleotides (e.g. cAMP).
176
What does sympathetic activity do to the pacemaker potential? How does it do this? (S4)
Sympathetic activity increases the slope of the pacemaker potential thereby reaching threshold quicker. It is mediated by β1 receptors (noradrenaline bind to them) which are G-protein coupled receptors associated with adenylate cyclase. The Gαs subunit stimulates adenylate cyclase, increasing the production of cAMP, thereby increasing the pacemaker potential.
177
What does parasympathetic activity do to the pacemaker potential? How does it do this? (S4)
The Parasympathetic activity decreases the slope of the pacemaker potential. It is mediated by M2 receptors. They are known as Gαi (G-protein coupled receptors) and are therefore inhibitory. They inhibit adenylate cyclase, decreasing the production of cAMP, this means the HCN channels are activated less.
178
How else do M2 receptors effect the pace of the heart? (S4)
The β-gamma subunit increases K+ conductance.
179
During the action potential of pacemaker cells, what contrasting effects would increasing K+ conductance have (during the downstroke)? (S4)
This hyperpolarises the membrane potential. This has two effects, it means the membrane potential is further away from threshold, but it is more likely to activate the HCN channels.
180
How does noradrenaline have a positive ionotropic effect? (S4)
It acts on β1 receptors in the myocardium. This increases cAMP, which activates protein kinase A, which phosphorylates the L-type Ca2+ channels thereby increasing Ca2+ entry during the action potential.
There may also be increased uptake of Ca2+ in the sarcoplasmic reticulum. Contractile machinery will also have an increased sensitivity to Ca2+.
181
Are blood vessels sympathetic or parasympathetically innervated? (S4)
Most blood vessels receive sympathetic innervation. An exception is erectile tissue which has parasympathetic.
182
What receptors do most arteries and veins have? (S4)
α1-adrenoreceptors, coronary and skeletal muscle vasculature also have β2-receptors.
183
Why is vasomotor tone necessary? (S4)
There must be a certain amount of ‘tone’ (stiffness) of smooth muscle vessels. If they are fully dilated at rest, then they cannot both contract and dilate. If you decrease the sympathetic output you get vasodilation, if you increase sympathetic output you get vasoconstriction. This means there is some sympathetic output at rest (to maintain tone).
184
Do α1-adrenoreceptors cause vasoconstriction or vasodilation of smooth muscle vasculature? (S4)
Vasoconstriction.
185
How are α1-adrenoreceptors activated in smooth muscle vasculature? (S4)
Noradrenaline acts on the α1-adrenoreceptors to cause vasoconstriction. These, Gαq-receptors, release inositol triphosphate causing an increase in intracellular [Ca2+] from stores. Via influx of extracellular Ca2+ there is contraction of smooth muscle. There is also depolarisation due to the release of diacylglycerol (DAG).
186
Do β2-adrenoreceptors cause vasoconstriction or vasodilation of smooth muscle vasculature? (S4)
Vasodilation.
187
How are β2-receptors activated in smooth muscle vasculature? (S4)
The β2-receptors are sensitive to circulating adrenaline. They will increase (through the stimulation of adenylate cyclase, Gαs) cAMP when activated. This opens a K+ channel and leads to relaxation of smooth muscle. (Note: β1-receptors would activate Ca2+ channels causing contraction!).
188
Does circulating adrenaline act on α1-receptors as well as β2-receptors? (S4)
It does however it has a higher affinity for β2-receptors than α1-receptors, (it will activate α1-receptors when adrenaline is above a certain concentration).
189
When β2-receptors are activated in smooth muscle vasculature, there is an increase in cAMP leading to vasodilation. Does it effect anything else? (S4)
The increased cAMP activates protein kinase A which will phosphorylate myosin light chain kinase (allowing the cross-chain interaction to take place in smooth muscle). This action will be less effective due to the phosphorylation of MLCK.
190
What is the main mechanism for vasodilation? (S4)
If exercising there is an increase in adrenaline therefore there is an increase in bloodflow to the heart through vasodilation. However local metabolites play a greater role: active tissues produce adenosine, K+, H+ and increase [CO2], these have a strong vasodilator effect.
191
Where are baroreceptors found? (S4)
The aortic arch and the carotid sinus.
192
What do baroreceptors do? (S4)
They are stretch receptors, if blood pressure increases, they stretch more. This increases the firing of the baroreceptors to the medulla. Sympathetic output to the heart is increased: there is bradycardia and vasodilation which counteract mean arterial pressure.
193
What bifurcates at the common carotid artery? (S4)
There is bifurcation of the common carotid artery into the internal and external carotid artery.
194
What are the three main groups of drugs that act on the ANS? (S4)
Sympathomimetics, andrenoceptor antagonists and cholinergics.
195
What do sympathomimimetics do and what are there clinical uses? (S4)
Sympathomimetics are agonists of α and β adrenoceptors therefore mimicking the sympathetic output. These have cardiovascular uses such as the administration of adrenaline to restore cardiac function in a cardiac arrest. It can also be used for anaphylactic shock. β1 agonist, dobutamine, may be given in cardiogenic shock (pump failure). Salbutamol, a β2 agonist, is a more general example .
196
What are the clinical uses of adrenoceptor antagonists? (S4)
Prazosin, an α1 antagonist, is an anti-hypertensive agent – it inhibits noradrenaline action on smooth muscle vasculature (leading to vasodilation). Propanolol is another example; it is a non-selective β1/2 antagonist. It will slow the heart rate, reduce force of contraction but also lead to bronchoconstriction. Atenolol is a selective β1 antagonist and there is therefore less risk of bronchoconstriction.
197
What do cholinergics do and what are there clinical uses? (S4)
Cholinergics act on muscarinic receptors as agonists and antagonists. Pilocarpine, a muscarinic agonist, is used in the treatment of glaucoma (it activates constrictor pupilae muscle). An example of a muscarinic antagonist is atropine or troicamide. These increase heart rate and leads to bronchial dilation (it is also used to dilate pupils; for examination of the eye).
198
What is flow of blood through blood vessels driven by? Is this a proportional relationship? (S5)
Gradient of pressure. Yes, flow is proportional to the pressure difference between the ends of a vessel (the higher the pressure difference the greater the flow).
199
If there is a given pressure gradient, what is flow determined by? (S5)
Resistance of the vessel.
200
What is resistance of the blood vessel determined by? (S5)
The nature of the fluid and the vessel.
201
Define flow. (S5)
The volume of fluid passing a given point per unit time.
202
Define velocity. (S5)
The rate of movement of fluid particles along the tube.
203
If cross sectional area of the blood vessel changes:
| Will flow? Will velocity? (S5)
No. Flow remains constant.
| Yes. Velocity is inversely proportional to cross sectional area (at a given flow rate).
204
Would the aorta have high or low velocity? Why? (S5)
It has a low cross sectional area so it would have a high velocity.
205
What is laminar flow? (S5)
It is flow where there is a gradient of velocity from the middle to the edge of the vessel. Velocity is highest in the centre and stationary at the edge.
206
What is viscosity? (S5)
Fluid moves in concentric layers (the middle layers move faster than the edge layers so fluid layers must slide over one another). The extent to which fluid layers resist sliding over one another is known as viscosity.
207
What is turbulent flow? (S5)
As the mean velocity increases, flow eventually becomes turbulent. Here the velocity gradient breaks down, fluid tumbles over and flow resistance is greatly increased.
208
What are heart murmurs? (S5)
Heart murmurs are unusual, audible (usually with a stethoscope) sounds from the heart. They are examples of turbulent flow, usually across valves. Turbulent flow generates sound.
209
In a vessel with constant pressure driving flow, flow is determined by the mean velocity. What does the mean velocity depend on? (S5)
Viscosity of the fluid: mean velocity is inversely proportional to viscosity. The higher the viscosity the slower the central layers will flow and thus the lower the average velocity.
The radius of the tube. Viscosity determines the slope of the gradient of velocity. If the gradient (or viscosity) is constant, the wider the tube the faster the middle layers move so mean velocity is proportional to the cross sectional area of the tube.
210
What is flow the product of? (S5)
Flow = mean velocity * cross-sectional area
[Where mean velocity is directly proportional to the radius of the tube and indirectly proportional to the viscosity of the fluid.]
211
What is pressure the product of? (S5)
Pressure = flow * resistance
| [Where flow = mean velocity * cross-sectional area]
212
How are resistance and radius related? (S5)
It decreases with the 4th power of the radius, i.e. very much more difficult to push blood through small vessels than big ones.
213
How do resistances relate to if there are more than one blood vessel? (S5)
If blood vessels are connected in series the resistances add, for vessels connected in parallel the resistance is lower.
214
If flow is constant and we increase resistance, what will happen to the pressure change from one end of the vessel to the other? (S5)
It will increase.
215
Over the whole circulation, flow is the same at all points. How does resistance change in each type of vessels? (S5)
Arteries are low resistance – therefore pressure drop over arteries is small.
Arterioles are high resistance – therefore pressure drop over arterioles is large.
Individual capillaries are high resistance, but there are many connected in parallel so the overall resistance is low.
Venules and veins are low resistance.
216
Why is the pressure within arteries high? (S5)
Due to the high resistance of the arterioles. The greater the resistance of the arterioles, the higher the arterial pressure will be.
217
When there is turbulent flow (say in the aorta), what happens to resistance of the vessels? (S5)
It will increase. Aortic pressure resultantly increases to overcome this.
218
Why would the aorta have turbulent flow? (S5)
It has a small cross-sectional area therefore high velocity. The flow is more likely to become turbulent. Alternatively If a vessel is narrowed, say from atherosclerosis, flow can become turbulent.
219
How does distensibility of blood vessels affect resistance? (S5)
Blood vessels have distensible walls – the pressure within the vessel generates a transmural pressure between inside and outside which tends to stretch the tube. As the vessel stretches resistance falls. Therefore the higher the pressure in a vessel, the easier it is for blood to flow through it.
220
How do distensible vessels achieve capacitance? (S5)
As the pressure within a distensible vessel falls the walls eventually collapse; blood flow ceases before the driving pressure falls to zero. As vessels widen with increasing pressure, more blood transiently flows in than out. Therefore distensible vessels ‘store’ blood, or have capacitance. Veins are the most distensible, and so have the greatest capacitance.
221
Why is viscosity 'increased' due to the location of blood cells in the plasma? (S5)
Blood cells congregate in the middle of the flow, so apparent viscosity is increased as cells go round faster than the plasma.
222
What is cardiac output? (S5)
The product of stroke volume and heart rate.
223
Why must arterial pressure be relatively high? (S5)
Arterial pressure must rise high enough to drive the cardiac output through the high resistance of the arterioles. This is the total peripheral resistance (TPR).
224
Does the CVS show pulsatile flow? (S5)
Yes, the heart ejects blood intermittently. Blood flows into the arteries during systole and in diastole it does not.
225
If arteries had rigid walls then what would happen to pressure in the arteries? (S5)
If the arteries had rigid walls then pressure would rise enough in systole to force the whole stroke volume through the TPR and fall to zero in diastole.
226
Arteries have distensible walls, how does this affect pressure? (S5)
Since arteries have distensible walls, in systole the arteries stretch and more blood flows in than out (this means pressure does not rise so much). As arteries recoil in diastole, flow continues through the arteries.
227
What is normal blood pressure? Pulse pressure? Average pressure? (S5)
Normal blood pressure is 120 / 80 mmHg.
Pulse pressure is the difference between systolic and diastolic pressure.
Average pressure is calculated as diastolic plus one third pulse pressure.
228
When does arterial pressure reach its maximum/minimum? (S5)
Arterial pressure rises to a maximum somewhere in the middle of systole. Arterial pressure falls to a minimum at the end of diastole.
229
What is systolic pressure affected by? (S5)
Systolic pressure is affected by how hard the heart pumps, the TPR and the stretchiness (or compliance) of the arteries.
230
What is diastolic pressure affected by? (S5)
It is affected by systolic pressure and TPR.
231
What is the main reason arterioles and pre-capillary sphincters are resistance vessels? (S5)
Mainly because the lumen is narrow. The lumen is narrowed by tonic contraction of smooth muscle in walls or vasomotor tone. Vasoconstriction will increase resistance to flow.
232
What balance dictates vasodilating factors' (H+, K+, adenosine, etc.) effects? (S5)
Their effect depends on the balance between the rate at which they are produced and that which the blood flow washes them away.
If metabolism increases then more vasodilator metabolites are produced; therefore there is more vasodilatation. This means an increase in flow, vasodilator metabolites are washed away… If there is more metabolism, there is greater blood flow.
233
What is reactive hyperaemia? (S5)
Reactive hyperaemia is seen when the circulation to an arm or the like is cut off for a minute or so. When blood flow is restored there is an enormous increase for a short while because vasodilator metabolites accumulate in the blood (arterioles dilate maximally). When flow is returned, resistance is very low so flow is very high. High flow washes away the vasodilator metabolites so smooth muscle constricts again.
234
What is autoregulation in relation to blood flow when pressure changes? (S5)
If supply pressure changes, blood flow to a tissue will change. This will change metabolite concentration and alter the resistance of arterioles so blood flow returns to an appropriate level for metabolism. Provided that supply pressure remains within certain limits, tissues will automatically take what blood they need.
235
How is total peripheral resistance related to the body's need for blood flow? (S5)
If all tissues in the body alter the resistance of their arterioles to match metabolism then TPR will be inversely proportional to the body’s need for blood flow.
236
What is the pressure of veins determined by? (S5)
Veins are very stretchy, the pressure in the veins is determined by the volume of blood they contain. This depends on the balance between flows in from the body and out via the heart.
237
What is central venous pressure and what is it dependent on? (S5)
CVP (or central venous pressure) is the pressure in the great veins (these are the veins that fill the heart in diastole). CVP depends on return of blood from the body, pumping of the heart and gravity & 'muscle pumping' (in the veins).
238
What happens to total peripheral resistance if tissues need more blood? (S5)
Arterial pressure must be high enough to ensure tissues get the blood they need; TPR will fall as more blood is needed.
239
What is arterial pressure dependent on? (S6)
The heart pumps its cardiac output into the arteries where pressure rises to a level determined by cardiac output and total peripheral resistance.
240
What is venous pressure dependent on? (S6)
Blood drains to the veins where pressure is determined by balance between the rate at which blood enters the veins and the rate at which the heart pumps it out.
241
If we eat a meal the gut needs more blood. Local vasodilators dilate arterioles so TPR falls. If cardiac output stays the same, what will happen to arterial and venous pressure? (S6)
Arterial pressure will fall and venous pressure will rise.
242
If cardiac output increases and TPR stays constant, what will happen to arterial and venous pressure? (S6)
Arterial pressure will rise and venous pressure will fall.
243
Explain how the cardiovascular system will be stable if the cardiac output is increased by rises in venous pressure and falls in arterial pressure and vice versa
The system is demand-led and stable, the TPR changes in response to metabolic demand, altering arterial and venous pressure and the CO changes in response to this.
244
How does the heart respond to falls in arterial pressure and rises in venous pressure? (S6)
By pumping more blood. This action returns arterial and venous pressure back to normal.
245
What causes the stretching of the ventricular myocardium? (S6)
During diastole the ventricles fill; they are isolated from the arteries and connected to the veins. The ventricle fills until the walls stretch enough to produce an intra-ventricular pressure equal to venous pressure.
The higher the venous pressure the more the heart fills in diastole.
246
What is the ventricular compliance curve? (S6)
It is the relationship between venous pressure and ventricular volume.
247
What is Starlings Law of the heart? (S6)
If muscle is stretched, contraction is harder.
248
So greater venous pressure has what effect on contraction? (S6)
Therefore the greater the venous pressure, the more the heart fills, the more it stretches, the harder it contracts, the greater the stroke volume. There is a limit however, where if venous pressure is increased the heart becomes over-filled and the myocardium becomes overstretched.
249
What does end systolic volume depend on? (S6)
How much the ventricle empties depends on how hard it contracts and how hard it is to eject blood.
250
What is force of contraction dependent on? (S6)
Force of contraction is determined by end diastolic volume (Starlings Law) and contractility, which is increased by sympathetic activity (i.e. it has a positive chronotropic effect).
251
What does difficulty in ejecting blood depend on? (S6)
Difficulty of ejecting blood, ‘aortic impedance’, depends mainly on TPR. The harder it is to eject blood the higher the pressure rises in the arteries. The easier it is to eject blood the more that will come out in systole.
252
What happens to stroke volume if arterial pressure falls? And if venous pressure falls? (S6)
So if arterial pressure falls, end systolic volume will fall and stroke volume rises. If venous pressure falls, stroke volume will fall.
253
What is autonomic outflow to the heart controlled by? (S6)
Signals from baroreceptors. The carotid sinus senses arterial pressure. It sends signals to the medulla oblongata which controls the heart.
254
If a baroreceptor, such as the carotid sinus, detects a fall in arterial pressure what will be the body's response? (S6)
Increase heart rate: (through increasing sympathetic and reducing parasympathetic activity)
Increase contractility (through increasing sympathetic activity)
Therefore falls in arterial pressure increase cardiac output.
255
What is the 'Bainbridge Reflex'? (S6)
Rises in (central) venous pressure are sensed in the right atrium and lead to reduced parasympathetic activity – also increasing heart rate. This is known as the ‘Bainbridge reflex’.
256
What goes on in the body when eating a meal? (S6)
Increased activity of the gut leads to local vasodilatation. Therefore total peripheral resistance falls. So arterial pressure falls and venous pressure rises.
The rise in venous pressure causes a rise in cardiac output and the fall in arterial pressure triggers an increase in the heart rate (and therefore cardiac output).
Venous pressure is subsequently reduced by extra pumping of the heart. Arterial pressure also increases. This means demand is met and the system is stable.
257
Theoretically, what happens if heart rate increases but everything else remains constant? (S6)
If heart rate increases but everything else remains constant, initally cardiac output will rise. This rise in cardiac output reduces venous pressure, thus reducing stroke volume. This means cardiac output returns to its initial value.
258
What do local vasodilators do to skeletal muscle during exercise and what effect does this have on resistance? (S6)
Skeletal muscle produces local vasodilators during exercise. These dilate the resistance vessels, the pre-capillary sphincters (as opposed to the arterioles).
The pre-capillary sphincters will open during exercise increasing blood to the capillaries massively. This results in a huge fall in resistance; there is a sudden drop in TPR.
259
What is 'muscle pumping'? (S6)
Exercise involves using skeletal muscle, most of which have veins running close to them or through them. These veins are compressed as the muscle begins to contract. Due to valves in the veins, ‘muscle pumping’ drives blood back to the heart (and not to the rest of the body).
260
What are the three issues facing the two ventricles of the heart and matching blood pumped around the body? (S6)
1. The Starlings curve are slightly different in the right and left ventricles.
2. Both sides of the heart must beat at the same rate.
3. They must match stroke volumes.
261
What will happen if the left and right ventricle do not pump the same volume of blood? (S6)
If the outputs are not matched then blood will accumulate in the lungs leading to pulmonary oedema. If 'on top of the Starling curve', the right heart pumps more blood into the lungs than the left can take out of the lungs. This forces fluid into the interstitial spaces of the lungs resulting in pulmonary oedema.
262
How does the body prevent pulmonary oedema developing from mismatching of stroke volumes? (S6)
The body’s mechanism to deal with this challenge is to increase heart rate. This is driven by the brain. Within a second or two of the heart rate increasing, huge amounts of blood go into the veins and because they reach a heart already beating fast, they can beat fast and keep the stroke volume down.
263
What happens to blood pressure when standing up? (S6)
When standing blood ‘pools’ in the superficial veins of the legs due to gravity. Thus central venous pressure falls. By Starlings Law, cardiac output will fall (stroke volume decreases due to a fall in (central) venous pressure) and arterial pressure will ALSO fall.
264
How does the body respond to a fall in arterial pressure? (S6)
Baroreceptors detect the fall in arterial pressure. TPR increases, particularly in the gut or at the skin, increasing arterial pressure.
265
What is 'postural hypotension?' (S6)
As we get older (or become unwell) ‘postural hypotension’ can occur. This is a drop in blood pressure when standing and can result in fainting.
266
What happens to blood volume when there is a haemorrhage? (S6)
There can be significant losses of blood.
267
Why does cardiac output fall when there is a haemorrhage? (S6)
Cardiac output falls because there is blood loss, so the heart is pumping less blood (i.e. stroke volume decreases). TPR will initially stay the same and arterial pressure will also fall.
268
During a haemorrhage how does the body respond to the fall in arterial pressure? Are these actions helpful? (S6)
Baroreceptors detect the fall in arterial pressure and heart rate and TPR rise. The rise in heart rate (and force of contraction due to sympathetic activity) pumps more blood out of the veins, lowering venous pressure further. The rise in TPR helps arterial pressure but lowers venous pressure as blood from the arterial side will not reach the venous side. This makes the problem worse.
You can lose a litre of blood and still be able to cope (without a transfusion).
269
How may a patient with a haemorrhage present? (S6)
A patient may present with a fast heart rate but a weak pulse as the stroke volume is not enough to supply the circulation. They will also be very white due to cutting down blood flow to skin. They may also start sweating due to increased sympathetic action.
270
What does the body do to minimise damage during a haemorrhage? (S6)
Veno-constriction: the muscles in the walls of the veins contract down, squeezing what little of the blood you have left into the heart. This increases venous pressure.
‘Auto-transfusions’: blood gets replaced through fluid moving between the circulation and the extracellular space (through the capillary membrane). The amount that moves is determined by hydrostatic and colloid osmotic pressure. If venous pressure goes down, hydrostatic pressure decreases and fluid moves into the circulation from the extracellular space.
Blood flow to organs where it is not currently essential, such as the gut and the skin will be minimised.
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What controls long-term change in blood volume? (S6)
The kidney. The greater the Na+ in the body, the greater the blood volume.
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If Na+ is too much what will happen? (S6)
There will be too much blood, venous pressure will increase. Stroke volume will increase and therefore cardiac output as well. Arterial pressure will rise and not decrease.
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So how is hypertension a result of having a haemorrhage? (S6)
More blood is forced through the tissues due to increased cardiac output. This removes the chemicals that cause the arterioles to dilate, this will increase the TPR. Arterial pressure will increase further and stay up. The arterioles will eventually become stronger as their action is inducible. Therefore the TPR will stay elevated and hypertension is a result. The higher the blood volume the higher the blood pressure.
