CVS Flashcards
(104 cards)
0
Q
What branches come from the LCA?
A
Anterior interventricular branch
Circumflex branch
Left marginal branch
Lateral branch
1
Q
What branches come from the RCA?
A
Posterior interventricular branch
Sino-atrial nodal branch
AV nodal branch
Right marginal branch
2
Q
What does the SAnodal branch supply?
A
Pulmonary trunk, SAN
3
Q
What does the right marginal branch supply?
A
RV, apex
4
Q
What does the AV nodal branch supply?
A
AVN
5
Q
What does the posterior interventricular branch supply?
A
The posterior 1/3 of the IVS, LV and RV
6
Q
What does the anterior interventricular branch supply?
A
LV, RV and anterior 2/3 of interventricular septum
7
Q
What does the left marginal branch supply?
A
LV
8
Q
What does the circumflex branch supply?
A
LA, LV
9
Q
Which coronary arteries anastomose?
A
The posterior and anterior interventricular branches
The circumflex and the RCA
Both marginal branches with the IV branches
10
Q
What and when is isovolumetric relaxation in the cardiac cycle?
A
It is when the ventricles are relaxing after systole and both the atrioventricular and outflow valves are closed (as arterial pressure > ventricular pressure > atrial pressure) so the volume of blood in the ventricles stays the same.
11
Q
What and when is isovolumetric contraction?
A
This is when the ventricles are starting to contract in systole, so pressure is rising. All valves are closed because ventricular pressure is > atrial but < arterial so volume of blood in the ventricles remains constant.
12
Q
Explain the heart sounds.
A
1st heart sound = LUB
–> occurs due to closing of atrioventricular valves as ventricular pressure > atrial = systole is beginning.
2nd heart sound = DUB
–> occurs due to closing of outflow valves as arterial pressure > ventricular
13
Q
What can a “whoosh” between the two normal heart sounds represent?
A
Aortic or pulmonary stenosis/incompetence causing turbulent blood flow
14
Q
Describe the inside of the left atrium.
A
- large smooth wall which 4 pulmonary veins enter
- smaller muscular wall formed from pectinate muscles
15
Q
Describe the inside of the right atrium.
A
Posterior smooth wall where coronary sinus and vena cava enter.
Anterior wall formed from pectinate muscles.
Fossa ovalis (remnant of the foramen ovalis)
16
Q
What is the function of the right auricle?
A
It allows the atria to increase its capacity
17
Q
Describe the right ventricle.
A
Tricuspid valve with 3 cusps.
Smooth wall around area of outflow valve
Other wall is muscular (known as trabeculae carnae)
18
Q
What valve is present in the LV and how many cusps does it have?
A
The mitral valve with 2 cusps
19
Q
How are the cusps held in the hearts ventricles and how do they work?
A
Attached to papillary muscles via chordae tendinae. The papillary muscles contract prior to systole to close the cusps and prevent backflow.
20
Q
What are the 4 shunts in foetal circulation and their remnants in an adult?
A
Ductus arteriosus - between PT and aorta, becomes ligamentum arteriosum
Ductus venosus - bypass of the liver, becomes ligamentum venosum
Foramen ovale - from RA to LA, becomes fossa ovalis
Umbilical vein - from mothers circulation to foetal, becomes ligamentum teres.
21
Q
How does birth rid of foetal shunts?
A
Placental support removed
High pO2 causes contraction of ductus arteriosus
Ductus venosus simply closes
LA pressure increases as blood starts to flow to lungs upon breathing = LA pressure > RA = septum primum pushed against secundum, causing closure of foramen ovale.
22
Q
How does atrial septation occur?
A
Septum primum grows down to endocardial cushions with osmium primum inside.
Ostium secundum opens and primum closes
Septum secundum grows, which the foramen ovale in it
= channel for passage formed
23
Q
How does ventricular septation occur?
A
Muscular portion grows up towards the endocardial cushions, leaving a small space known as the primary interventricular foramen.
CT derived from the endocardial cushions then grows down to the muscular portion to form the membranous portion.
24
How does conotruncal septation occur?
Endocardial cushions form in the truncus arteriosus, and grow towards each other to form a spiral septum.
25
What do the parts of the heart tube become in the adult?
Bulbis cordis --> trabeculated wall of RV, outflow tracts, great vessels.
Ventricle --> LV
Atrium --> auricles of atria
Sinus venosus --> smooth wall of RA
26
Describe the order of the branches of the aorta.
Brachiocephalic trunk (gives subclavian and common carotid)
Left common carotid (gives external and internal, external gives maxillary and facial arteries)
Left subclavian
Thoracic/descending aorta
Celiac trunk
Supra renal artery
Superior mesenteric artery
Renal arteries
Testicular/ovarian arteries
Inferior mesenteric artery
Common iliac artery (gives internal and external)
27
Describe the order of the veins, R to L in the body.
Superior vena cava
R. Brachiocephalic (gives branch to arm, external then internal jugular)
L. Brachiocephalic
Hepatic veins
Renal veins
Testicular/ovarian veins (the L stems from hepatic vein)
Common iliac vein (gives nterval and external)
28
What are the nuclei like n cardiac muscle?
Single and central
29
What is the function of intercalated discs?
Hold cells together via desmosomes and contain gap junctions which form non selective ion channels = spread of electrical activity.
30
Describe and explain a ventricular action potentials shape.
1) . Upstroke = depolarisation causes v-gated Na+ channels to open and Na+ to influx
2) . This is followed by a sharp drop, as Na+ channels inactivate so no more influxes, and K+ channels open = efflux of K+
3) . Plateau phase occurs where Ca2+ L type (v-gated) channels open, meaning inflow of Ca2+ is balancing out efflux of K+.
4) . Ca2+ channels close and K+ continues to efflux = repolarisation.
From -90mV to 30mV
Upstroke to repolarisation takes ~280ms
31
Describe and explain the shape of an action potential in the SAN.
1) . Funny current slowly increasing, as more HCN channels open as the membrane becomes less negative = influx of Na+
2) . Na+ influx reaches threshold and causes v-gated Ca2+ channels to open = influx and upstroke.
3) . K+ channels open and efflux allows repolarisation.
Funny current takes ~600ms
Upstroke to repolarisation takes ~200ms
32
How does the heart contract?
1). Depolarisation = opens L-type Ca2+ channels
---> Ca2+ influx
2). Ca2+ influx acts upon ryanodine receptors to open calcium induced calcium release channels
= Ca2+ release from SR.
3). Calcium binds to troponin C to cause a conformational change that reveals myosin binding site.
4). Myosin head binds to actin binding site, releasing a Pi that strengthens the bond.
5). ADP released which allows power stroke to occur
6). ATP binds to the head, allowing the head to detach from the actin binding site
7). ATP hydrolysis allows the ATP to re-cock and prepare for next stroke.
33
How does the Ca2+ in the heart return to resting levels?
1) . Pumped into SR by SERCA (high affinity, high capacity) pumping Ca2+ in using ATP
2) . Pumped out of the cell altogether by NCX (low affinity, high capacity) or PMCA (high affinity, low capacity)
34
How does vascular smooth muscle contract?
1) . Actin and myosin are bound to dense bodies in the smooth muscle cells
2) . Ca2+ influx via L type channels and via action of GalphaQ producing IP3
3) . Ca2+ binds to calmodulin to form a complex
4) . Complex acts on MLCK to activate it
5) . MLCK phosphorylates the light chain of the myosin head, so it can now bind to actin.
6) . MLCP deactivates this by dephosphorylating the head
35
Describe the activity of MLCK and MLCP.
MLCK - activated
| MLCP - constituently active
36
What does lateral folding of the embryo achieve?
It brings the cardiogenic fields and blood islands together to form the heart tube
37
What order are the parts of the embryonic heart tube?
```
Aortic roots
Truncus arteriosus
Bulbus cordis
Ventricle
Atrium
Sinus venosus
```
38
Why does looping occur?
To allow further growth of the heart into the pericardial cavity
39
What occurs in folding?
The cephalic portion moves caudally, ventrally and right.
The caudal portion moves cranially, dorsally and left.
40
What does looping achieve?
- it places the outflow section ventral to the inflow by placing atrium dorsal to bulbis cordis.
- primordium of right ventricle closest to outflow
- primordium of left ventricle closest to inflow
41
How does the transverse sinus form?
By looping, when the bulbis cordis is placed ventral to the atrium
= veins in behind arteries
42
How does the sinus venosus develop?
Initially, R and L are equal sizes.
Venous return shifts to R so L recedes
R enlarges further but is engulfed by enlarging RA
43
What does the RA develop from?
Sinus venosus
| Most of primitive atrium
44
What does LA develop from?
Absorption of proximal parts of 4 pulmonary veins
| Small part of the primitive atrium
45
What does the oblique sinus form from?
The absorption of proximal pulmonary veins by the enlarging LA.
46
What are the aortic arches?
Early arterial system of symmetrical arched vessels.
47
What does the 4th aortic arch remodel into?
Left - arch of aorta
| Right - Right subclavian
48
What does the 6th aortic arch remodel into?
Left - left pulmonary artery and ductus arteriosus
Right - right pulmonary artery
49
What do the recurrent laryngeal nerves innervate?
Intrinsic muscles of the larynx
50
How far do the recurrent laryngeal nerves descend?
Left T4/5
| Right T1/2
51
What influences the course of the recurrent laryngeal nerves and how?
1). Caudal shift of the developing heart and expansion of the developing neck region
2) . Need for ductus arteriosus
- left nerve hooks around this when heart is descending = gets "trapped" and must turn back on itself.
52
What is flow? (Definition)
The volume of fluid that passes a certain point per unit of time.
53
What is flow? (2 equations)
Flow = pressure gradient / resistance
Flow = area x velocity
54
What is velocity?
Velocity is the rate of movements fluid along a tube.
55
If cross sectional area of a tube increases, how does this affect velocity and why?
Velocity decreases.
To counter the change and maintain the flow at the same rate along the vessel.
56
Name and describe the 2 types of flow?
1) . Laminar - the usual one where velocity and cell content is highest in the centre, as plasma on edges forms H bonds with vessel walls.
2) . Turbulent - often caused by exceeding the critical velocity n a laminar vessel, where liquid tumbles over itself = resistance and sound.
57
What ultimately determines flow?
1) . Viscosity - the extent to which fluid layers resist sliding over each other
2) . Tube radius - wider it is, the faster the middle layers can move.
58
How is resistance of vessels calculated in series?
Resistance of the vessels are added together.
59
How is resistance of vessels on parallel calculated?
1/Rof1 + 1/Rof2
60
What is the pressure of arteries like and why?
High to force blood from them into the much narrower arterioles.
61
What is the resistance of capillaries like?
Individually high, but they are in parallel, so altogether much lower due to high cross sectional area.
62
What is pressure like in circulation?
```
Heart --> Arteries 100
Arteries --> Arterioles 100
Arterioles --> Capillaries 35
Capillaries --> Venules 10
Venules --> Veins 8
Veins --> Heart 3
```
63
How can blood flow become turbulent?
If a vessel narrows (e.g. Atherosclerosis) the velocity will increase and may exceed critical level = turbulence.
64
What occurs if pressure increases in a distensible vessel and why?
It increases the lumen of the vessel (distensibility) and as a result, area increases and resistance falls, maintaining flow.
More blood is flowing in than out of the vessel = storing blood = capacitance.
65
What happens if pressure falls in a distensible vessel?
Before pressure reaches 0, the vessel will collapse because pressure outside the tube will be greater than that inside.
66
What is capacitance and its purpose?
It is the ability of a vessel to store blood and allows us t change the blood flow in the body.
67
What is cardiac output?
Stroke volume x heart rate
68
What is the resistance of the vessels in circulation?
All are low except arterioles
| Capillaries are low together, individually high
69
When is pulsatile flow at its min and max?
Max in systole
| Min in diastole
70
What affects systolic pressure?
How hard the heart pumps
How hard it is to push the blood into the aorta (TPR)
Stretchiness of arteries
71
What pulse pressure?
Difference between diastolic and systolic.
72
What is average pressure?
Diastolic + 1/3 of the pulse pressure
73
How is blood distribution controlled?
Via action of sphincters in arterioles increasing and decreasing TPR.
74
What is vasomotor tone produced and antagonised by?
Produced by sympathetic action on the vessels.
| Antagonised by vasodilator metabolites.
75
How does reactive hyperaemia occur?
When blood flow is cut off, vasodilating metabolites are produced by respiring tissues (K+, adenosine, H+).
When flow is returning these act to relax smooth muscle = increased flow to provide what's needed until metabolites are washed away.
76
What does reactive hyperaemia allow for?
Autoregulation - tissues can signal via metabolites to arterioles if it needs more blood flow
= change in blood supply pressure causes a change in flow (lower pressure, lowers flow)
= change in metabolite levels
= change in arterioles resistance
77
What is pressure of veins determined by and what is that determined by?
The volume of blood stored in them rather than the pressure of that pushing through.
The volume of blood stored is determined by the volume of blood being returned to the vein from the body, and the volume being taken out via the heart.
78
What does central venous pressure depend on?
Return of blood from the body (by gravity and muscle pumping)
Pumping of the heart.
79
What do tissues rely on to take the blood they need, and what organ is the exception to this?
They rely on pressure remaining within set limits.
The brain is an exception as it is already affected by gravity, so pressure is lower. This decreases the brains capacity for autoregulation as pressure fall results in fall in flow.
80
What are the main factors in ensuring tissues receive the supply they need?
Arterial pressure high enough to push into arterioles
Total peripheral resistance altering with need
Central venous pressure high enough to fill heart
81
What is arterial pressure determined by?
CO
| TPR
82
What is venous pressure determined by?
Rate the blood enters them
| Rate the heart pumps
83
What is stroke volume?
The difference between the end systolic volume and end diastolic volume of the heart.
84
How is intraventricular pressure created?
Stretching of the ventricular walls due to filling in diastole
85
What rule does the ventricular compliance curve follow?
The more the heart fills, the greater the intraventricular pressure.
86
Why does the ventricular compliance curve not increase much at the start?
Because pressure doesn't increase too much until the heart fills enough that it expands and is pushing against the pericardium, which is when the pressure begins to shoot up.
87
When does the heart stop filling in diastole?
When ventricular pressure reaches venous pressure.
88
What is starlings law?
Rise in stroke volume increases venous pressure until the point where the heart can expand no further.
At this point, if the heart fills more it begins to compress its own arteries and its contractility decreases.
89
What is the curve on a starlings law graph representitative of and when is it reduced or increased?
Contractility of the ventricles
Reduced in heart failure and increased in periods of sympathetic activity.
90
What is ventricular emptying dependant on?
Force of contraction of the heart (therefore ejection)
TPR
91
How are falls in arterial pressure dealt with?
Receptors in the carotid sinus detect this.
Send signals to medulla of brain.
Increases sympathetic activity of the heart = increased HR and force of contraction.
92
How are rises in venous pressure dealt with?
Brain bridge reflex.
Detected by baroreceptors in the RA and vena cava.
Sends info to medulla of brain
Reduced parasympathetic activity to vessels = increased HR
93
What occurs if the heart rate changes with no increase in demand for blood and when may this happen?
```
CO rises
Arterial pressure increases
Venous pressure falls
Stroke volume falls
Heart fills less
CO falls
```
Post op in those with pacemakers
94
What would occur if exercise was begun with no change in HR?
Enormous increase in demand.
Venous pressure would increase greatly as muscle pumping drives a greater volume of blood from its fibres' capillaries to the heart.
Arterial pressure would therefore fall.
95
Why is a rise in venous pressure dangerous?
It can overfill the heart, pushing it to the flat part of the contractility slope =
Blood would arrive at the RH faster than at the LH.
Therefore RH must pump faster to deal with increasing venous pressure.
LH doesn't keep up and therefore they uncouple
Blood therefore accumulates in lungs = pulmonary oedema
96
Why would the RH and LH uncouple if exercise was not met with an increase in HR beforehand?
Because the venous pressure increases greatly so the right heart is pushed off of starlings curve
= usually only stay coupled due to reliance on starlings curve effect, which gives them a shared stroke volume. The starlings curve is no longer functional so the stroke volumes now can differ = uncoupling.
97
How is uncoupling of the left and right heart in exercise prevented?
HR increases before exercise so when venous pressure increases, the heart can cope with the increase in cardiac output.
98
Why is standing a problem for circulation?
Upon standing, blood pools in superficial veins of the legs = CVP falls greatly.
Arterial pressure remains high initially but then begins to fall (fall in venous pressure decreases cardiac output, decreasing arterial pressure)
= VENOUS AND ARTERIAL PRESSURE NO LONGER OPPOSE
99
How is the challenge of standing overcome by the circulation?
Baroreceptors detect fall in arterial pressure and increase sympathetic activity to increase HR
TPR increased to increase and maintain arterial pressure
100
Why is haemorrhage dangerous to the circulation?
70% blood is kept in veins so haemorrhage = massive decrease in venous pressure.
This decreases input to the heart and as a result, CO also falls.
This causes arterial pressure to fall, so the TPR and HR is increased BUT this worsens venous pressure as it is very low to start with.
101
How does the body respond to haemorrhage?
Venoconstriction to try and increase venous pressure.
Autotransfusion (water moves from the tissues into circulation to increase pressure due to a fall in hydrostatic pressure)
102
Why is an increase in long term blood dangerous?
Because it increases venous pressure and therefore diastolic filling and CO.
This increases arterial pressure as TPR is unchanged.
The body doesn't need this extra blood so TPR increases to restrict it
= increased arterial pressure
= hypertension
103
How can a long term increase in blood volume be dealt with?
Loop diuretics if caught early.
