Cardiovascular System Flashcards
1
Q
What is the role of the cardiovascular system?
A
Supplies cells in the body with their metabolic needs.
2
Q
What factors influence the exchange of substances between teh blood in cappillaries and the surrounding tissues?
A
Area (capillary density)
Diffusion resistance (difficulty of moement through the barrier)
Concentration gradient (drives diffusion)
3
Q
Why is adequate blood flow important?
A
Ensure metabolic needs for each cell is met
4
Q
What organs require a constant blood flow and what are they?
A
Brain 0.75
Kidneys 1.2
5
Q
What is the requireed blood flow to the heart?
A
0.3 - 1.2 l/min
6
Q
What is the required blood flow to the gut?
A
1.4 - 2.4 l/min
7
Q
What is the required blood flow to muscle?
A
1 - 16 l/min
8
Q
what is the required blood flow to skin?
A
0.2 - 2.5 l/min
9
Q
What is the total flow of blood around the body?
A
5 - 25 l/min
10
Q
What are the major functional components of the circulation?
A
A pump - heart
Distribution vessels - Arteries
Flow control - resistance vessels, arterioles, pre capillary sphincters
Capacitance (ability to cope with change) - veins
11
Q
Describe the distribution of blood volume over major parts of the circulation
A
11% arteries/arterioles
5% capillaries
17% heart and lungs
67% veins
12
Q
How are arteries named?
A
By the amount of elastic and smooth muscle fibres in their walls. They are named Elastic (conducting) and Muscular (distributing) arteries
13
Q
What type of arteries are usually larger?
A
Elastic - expand with each heart beat
14
Q
What is the function of arterioles?
A
REgulate the amount of blood reaching an organ or tissue and regultae blood pressure
15
Q
How is the diameter of arteries and arterioles controlled?
A
Autonomic nervous system
16
Q
Describe the structure of capillaries
A
one cell thick to allow the exchange of substances.
The wall may be continuous or fenestrated and may be surrounded partially by pericytes
17
Q
What are the structural differences between arteries and veins?
A
Veins have thinner walls and wider, more irregular lumens, usually with semilunar, paired valves.
18
Q
What is the purpose of valves?
A
Prevent blood flowing in the wrong direction. Permits blood to flow only one way.
19
Q
Below what diameter do veins no longer have valves?
A
1mm
Veins in the thoracic and abdominal cavities also do not have valves.
20
Q
How is blood flow in the veins established?
A
Muscle pump action in the leg and pressure factors in the abdominal and thoracic cavities.
21
Q
What happens if blood pressure is not maintained in the veins?
A
They collapse
22
Q
What are the 3 layers in arteries and veins?
A
Tunica intima
Tunica media
Tunica Adventitia
23
Q
Describe the histological structure of Elastic areteries
A
Tunica intima - Endothelia with long axes orientated parallel to long axis of artery, with a narrow sub-endothelium of connective tissue with discontinuous intrenal elastic lamina
Tunica media - MAIN FEATURE - 40-70 fenestrated elastic membranes with smooth muscle cells and collagen between these lamellae. Thin external elastic lamina
Tunica adventitia - The layer of fibroelastic connective tissue containing vasa vasorum, lymphatic vessels and nerve fibres
24
Q
Describe the histoogical features of muscular arteries
A
Tunica intima - Endothelium, sub-endothelial layer, thick elastic lamina
Tunica media - MAIN FEATURE - 40 layers of smooth muscle cells (connected by gap junctions), prominent external elastic lamina
Tunica adventita- Thin layer of fibroelastic connective tissue, containing vasa vasorum, lymphatic vessels and nerve fibres
25
What is the purpose of gap junctions?
Enable coordinated conduction
26
How is depolaristation of smooth muscle in blood vessels acheived?
Noradrenaline is released at the nerve endings in the adventitia and diffuses through fenestrations in the external elastic lamina into the external tunica media, where it depolarises some of the superficial smooth muscle cells. Propagated to all cells in the tunica media via gap junctions
27
What happens to the tunica media as arteries diminish in diameter?
Number of smooth muscle layers decreases
28
How do arteries differ in appearance when they are constricted?
Endothelial cells protrude into the lumen, which is narrower
29
Describe the structure of arterioles.
Thin internal elastic lamina is present in larger arterioles.
1-3 layers of smooth muscle in the tunica media - 1 layer in smaller arterioles completely encircles the endothelial cells.
External elastic lamina is absent and teh tunica adventitia is scant.
30
How do arterioles and metarterioles differ?
Metarterioles smooth muscle layer is not continuous. Rather they are spaced apart and each encircles the endothelium of a capillary arising from the metarterioles
31
What are precapillary sphincters?
The discontinuous muscle encircling the endothelium of a capillary arising from the metarteriole which controls blood flow into the capillary bed
32
How do capillaries serve as a good area for gas exchange?
Large surface area
One cell thick
Passing RBCs fill almost the entire lumen minimising the diffusion path to adjacent tissues
33
What size are capillaries?
7-10µm in diameter and usually less than 1mm long
34
What are preicytes?
Cells capable of dividing into muscle cells, or fibroblasts during angiogenesis, tumour growth and wound healing. They form a branching network on the outer surface of the endothelium.
35
What are sinusoids?
Capillaries found in the liver, spleen and bone marrow. They generally have a larger diameter, may contain special lining cells and an incomplete basal lamina.
The larger openings allow RBCs/WBCs to pass using a process aided by discontinuous basal lamina
36
What are fenestrated capillaries?
Capillarries with pericytes and fenestrations in the endothelium
37
What is the diameter of postcapillary venules?
10-30µm
38
What is the purpose of postcapillary venules and how do they work?
fluid tends to drain into them because their pressure is lower than that of capillaries or the surrounding tissue. They have a similar wall to capillaries.
If an inflammatory response is operating fluid and leucocytes emigrate from them.
39
What type of vessels have the largest diameter?
Veins (generally)
40
What is the difference between artery and vein walls?
Veins are thinner with more connective tissue and fewer elastic and muscle fibres.
41
How are superficial veins in the legs different to the rest?
They have a well defined muscular wall to reesist distension due to gravity. Valves act together with muscle contraction to return blood to the heart. Most veins have a well developed adventitia
42
Describe the smooth muscle orientation in the walls of large veins.
Well developed longitudinally orientated smooth muscle in the tunica adventitia in addition to the circularly arranged smooth muscle in the tunica media
43
What properties do cardiac muscle posess that allow the heart to operate as a pump?
Striations
Branching
Centrally positioned nuclei
Intercalated discs (for electrical and mechanical coupling with adjacent cells)
Adherens-type junctions (to anchor cells and provide anchorage for actin)
Gap junctions (for electrical coupling)
44
What are T tubules in line with in cardiac muscle?
Z bands
45
Define systole
The period when the myocardium is contracting
46
Define diastole
The relaxation of the myocardium inbetween contractions
47
Describe the spread of excitation in systole
1. The SAN fires an action potential which spreads over teh atria causing atrial systole. The AP reaches the AVN where it is delayed for about 120ms
2. From the AVN excitation spreads down the septum between teh ventricles
3. Excitation spreads from the inner to outer suface
4. Ventricles contract from the apex up, forcing blood towards the outflow valves
48
What way is ventricular muscle organised?
figure of 8 bands that squeeze the ventricular chamber forcefully in a way most effective for ejection through the outflow valve.
49
How does the heart contract?
The apex contracts first and relaxes last to prevent back flow
50
Why is the left heart different to the right
Left side has thicker myocardium as it has to pump blood to the whole body, whereas the right heart only has to pump it to the lungs.
51
Where is the pacemaker?
Right atrium - Sino Atrial Node
52
What causes the mitral valves to open?
atrial pressure exceeding the interventricular pressure
53
What is the rapid filling phase?
During diastole blood flows rapidly into the ventricles from the atria as the venous return of systole causes an increased pressure in the atria which exceeds that of the ventricles.
54
What does atrial systole acheive?
Increases the pressure in the atria above the ventricles to allow more filling of the ventricles.
55
What closes valves?
Turbulence in blood flow/flowing the wrong way cause valves to shut forcibly.
56
Define isovolumetric contraction.
Contraction of the muscle causing no change in the volume of blood in the heart
57
What causes the atrial/pulmonary valves to open and when does this occur?
When the ventricular pressure exceeds the arterial pressure during ventricular contraction.
58
What is the rapid ejection period?
Blood moves out of the ventricles and into the arteries causing an increase in pressure to their maximums.
59
What is the first heart sound and what causes it?
As the AV valve closes oscillations are induced in other structures. This produces a mixed sound with a crescendo-descendo sound quality - lub
60
What is the second heart sound and what causes it?
The semi-lunar valves close and induce oscillations in other structures. This produces a shorter durateion, higher frequency and lower intensity sound than the first.
61
What is a murmur?
Extra sounds produced by the heart showing the presence of turbulent blood flow through a narrowed valve or back flow
62
When might a murmur be heard in a healthy individual?
During exercise
63
When might a 3rd heart sound be heard?
Early diastole
64
When might a 4th heart sound be heard?
associated with atrial systole
65
What is a ganglion?
A cell body in the PNS
66
What do neurones act on?
Smooth muscle
Viscera
Secretory Glands
67
What type of neurones are in the parasympathetic nervous system?
cholinergic
68
What is vascular tone and what effect does it have in the CVS?
The degree of constriction experienced by a blood vessel. It is a mechanism for controlling the total peripheral resistance
69
How is sympathetic outflow to bood vessels controlled?
From the brainstem, via vasomotor centres in the medulla oblongata which receive information from baroreceptors which are located in the arch of the aorta and carotid sinuses
70
What type of receptors are expressed in pre ganglionic neurones of the sympathetic nervous system?
Nicotinic
71
What effect does the sympathetic and parasympathetic activity have on the heart rate?
Sympatheitc speeds it up
Parasympathetic slows it down
72
What type of neurones are the post ganglion neurones of the sympathetic nervous system and what type of receptors are expressed?
noradrenergic. Two classes of receptors expressed adrenoreceptors alpha (1&2) and beta (1&2)
73
What is the heart rate if all autonomic inputs are blocked?
approx. 100bpm
74
Does the parasympathetic or sympathetic dominate at rest?
parasympathetic - reduces the heart rate to 60bpm
75
How is an increase in heart rate acheived?
Initially by a reduction in parasympathetic outflow and then an increase in sympathetic outflow
76
Where do sympathetic nerves synapse in the paravertebral chain?
At the same level as origin
At different level to the origin
May not synapse in the paravertebral chain
77
What type of outflow does the sympathetic nervous system have?
Thoraco-lumbar
Has cell bodies in all 12 thoracic sections and the first 2 lumbar sections
Short pre, long post
78
What type of outflow has the parasympathetic nervous system?
Cranio-sacral outflow
Long pre, short post
79
What type of receptors are in the parrasympathetic nervous system?
Nicotinic pre
Muscarinic GPCR post
80
What branch of the nervous system inervates the smooth muscle of the vessel walls?
sympathetic branch of the autonomic nervous system causing constriction of the arterioles, vasoconstriction, via alpha 1 adrenorecpetors
81
What is vasomotor tone?
Constant level of nervous stimulation in muscle and blood vessels that gives it a resting level of constrction
Also a method of controlling the total peripheral resistance
82
Where is vasomotor tone high?
Skin
Skeletal muscle at rest
Gut unless a meal is consumed
83
Where is sympathetic outflow to the blood vessels controlled?
Vasomotor centres of the medula oblongata in the brainstem
84
Where are the Baroreceptors and what do they do?
In the aortic arch of the carotid sinus. Sends information to the medulla oblongata which controls sympathetic and parasympathetic outflow
85
Define flow
The volume of fluid passing a set point in a given time
86
Define velocity
Rate of movement of fluid particles along the tube
87
What is laminar flow?
There is a gradient of velocity from the middle to the edge of the vessel. Velocity is highest in the centre and fluid is stationary at the edge
88
Describe turbulent flow.
Velocity increases and the velocity gradient breaks down as layers of fluid try to move over each other faster than physics will allow. The fluid tumbles over, greatly increasing flow resistance
89
Define viscosity
The extent to which fluid layers resist flowing over each other.
Higher viscosity, slower central flow, lower av velocity
Lower viscosity, smaller difference between central and edge velocity
90
How does diameter affect flow rate?
Mean velocity is proportional to the cross sectional area of the tube. At a constant gradient, the wider the tube, the faster the middle layers move
91
Resistance =
Pressure/flow
92
How does resistance change as viscosity changes?
Resistance increases as viscocity increases. Thicker the blood, the harder it is to push around blood vessels
93
How does resistance change as the radius changes?
Resistance decreases with the 4th power of the radius. Therefore a small change in the radius makes a big change to resistance. (It is more difficult to puch blood through smaller vessels
94
If flow is fixed, how does the pressure change as resistance increases?
pressure increases from one end of the tube to another
95
If pressure is fixed, how does flow change as resistance increases?
The higher the resistance, the lower the flow
96
How will putting 2 resistances in series effect total resitance?
Add them together
97
How is the total resistance calculated when 2 resistances are combined in parallel?
Re= R1xR2/R1+R2
Effective resistance is lower
The resistance of one of the vessels in series is half of the original, as the blood has 2 paths
98
What are the high resistance vessels and what happens to pressure in them?
Arterioles. Large pressure drop
99
How does the pressure in the arterioles affect the resistance in the arteries?
Increased pressure in the arteries - difficult to push blood through.
Higher resistance in the arterioles, higher pressure in the arteries for set flow
100
What is transmural pressure?
Pressure in a cardiac chamber or blood vessel
101
How do distensible vessels cause an increase in flow?
Vessel stretches, lumen diameter increases, so resistance falls and flow increases
102
WHy does blood flow cease in distensible vessels before driving pressure reaches 0?
Walls collapse as pressure falls
103
What is capacitance?
Ability to store blood
104
How does distensibilty of a blood vessel increase capacitance?
It causes a higher transient flow into the vessel than out
105
What is systolic pressure?
Maximum arterial pressure typically 120 mmHg
106
What effects systolic pressure?
How hard the heart pumps
Total peripheral resistance
Compliance of the arteries
107
What is diastolic pressure?
Minimum arterial pressure. Typically 80mmHg
108
What affects diastolic pressure?
Systolic pressure
Total peripheral resistance
109
What is pulse pressure?
The difference between systolic and diastolic pressure
110
How is the average pulse pressure determined?
Diastolic + 1/3 pulse pressure
111
Defince total peripheral resistance
The sum of the resistance of all peripheral vasculature in the systemic circulation
112
Why is distensibility of arterial walls important?
Allows them to stretch in systole. More blood flows in than out so pressure does not rise too much. The arteries recoil in diastole and flow continues through the arterioles
113
Describe a pulse wave and where they can be found
Contraction of the ventricles generates a pulse wave, which propagates along the arteries faster than blood. This is felt at a variety of locations where arteries can be pushed against a reasonably hard surface
114
How do arterioles effect flow?
Variable flow consriction. Smooth muscle contracts to narrow lumen, reducing flow
115
What antagonises vasomotor tone?
Vasodilator factors
116
List 3 vasodilator metabolites
K+
H+
Adenosine
117
What do vasodilator metabolites do?
Cause the relaxation of local smooth muscle, lowering resistance and increasing blood flow
118
Why is blood flow so high when it is restored after it is cut off for a minute or two?
Organ or limb continues metabolising and vasodilator is still produced during the period of no circulation but there is no blood flow to remove them. When circulation is restored, the local arterioles dilate maximally and blood flow is very high
119
Describe autoregulation
At most levels of metabolic activity, most organs can automatically take the blood flow they need, as long as the pressure in the arteries supplying them is kept within a certain range
120
Define central venous pressure
The pressure in the great veins supplying the heart
121
Define venous return
The rate of flow of blood back to the heart. Limits cardiac output
122
What happens to arterial and venous pressure if TPR falls?
Arterial pressure will fall, venous pressure will rise
123
What happens to arterial and venous pressure if TPR rises?
Arterial pressure rises, venous pressure falls
124
What happens to arterial and venous pressure if CO falls at a given TPR?
Atrial pressure falls, venous pressure rises.
125
What happens to venous and arterial pressure if CO rises at a given TPR?
arterial pressure rises, venous pressure falls
126
The cardiovascular system is demand led and stable. Explain this.
TPR changes in response to metabolic demand, altering arterial and venous pressure
127
Define end diastolic volume.
Volume of blood in the ventricle at the end of diastole
128
Define end systolic volume.
Volume of blood in the ventricle at the end of systole
129
Define stroke volume
difference between end systolic and diastolic volume
130
What are the ventricles connected to in diastole?
atria
131
What does the filling of the ventricles depend on?
Ventricular pressure. They fill until the walls stetch and there is enough blood in the ventricle to equal venous pressure
132
What is the curve showing the relationship between venous pressure and end diastolic volume?
The starling curve
133
Define pre load
The end diastolic stretch of the myocardium
134
Define after load
Force needed to expel blood into the arteries
135
How does end diastolic volume affect the force fo contraction?
The more the heart fills, the harder it contracts. The harder it contracts, the larger the stroke volume (starlings law). But there is a limit - when the heart becomes overfilled and the myocardium is overstretched
136
What does the gradient of a curve showing venous pressure against stroke volume show?
Contractility - the stroke volume you get for a given venous return
137
What do baroreceptors sense?
arterial pressure
138
How does venous return affect cardiac output?
Increase venous pressure (return) increase cardiac output
139
How does arterial pressure affect cardiac output?
Increase in arterial pressure causes a decrease in cardiac output
140
How does the cardiovascular system respond to eating a meal?
Increased gut activity causes metabolites and vasodilator to be released -\> TPR falls -\> arterial pressure falls, venous pressure rises -\> increased cardiac output and heart rate -\>Increased output increases atrial pressure and reduces venous pressure - demand met adn system stable
141
What are the risks of increased venous pressure due to exercise?
Pulmonary odema.
Venous pressure rises too much and pushes starlings curve into the flat part. The left herat cannot
142
How is the risk of pulmonary oedema reduced during exercise?
* Overfilling of the ventricles is inhibited by the increase in heart rate
* When venous pressure starts to rise, heart rate is already high
* Stroke volume kept down but CO increased
*
143
What happens to blood in the leg on standing?
* Pools in the superficial veins of the legs due to gravity
* Central venous pressure and arterial pressure fall
* Cardiac output falls (starlings law)
* Baroreceptors detect fall in arterial pressure
* HR raised
* TPR inreased to defend arterial pressure
144
What is postural hypotension?
Reduction in systolic blood pressure on standing of 20mmHg. The barroreceptor reflex does not work efficiently
145
How does the cardiovascular system initially respond to haemorrhage?
Reduced volume lowers venous pressure so cardiac output falls.
Arterial pressure falls and baroreceptors detect this
146
How does the CVS initial reaction to haemorrhage cause further probems?
Increasing the heart rate will further lower venous pressure
147
How can a haemorrhage problem be soved?
Venous pressure needs to be increased to reduce the original problem.
Veno-constriction
Blood transfusion to replace lost blood
148
What organ controls blood volume?
kidneys
149
What happens if BP rises for a few days?
* Venous pressure rises
* CO increases
* Arterial pressure rises
* More blood peruses tissues which autoregulate and increase TPR
150
What is the cardiac resting membrane potential and how is it achieved?
The potential inside a cardiac cell relative to the outside. Acheived by the selective permeability of the membrane by way of channel proteins. Mostly K+ moves out so resting value approx -90mV
151
152
How is initial depolarisation of the ventricular cells acheived?
Spread of electrical activity from the pacemaker cells
153
What happens in the ventricular cells once threshold is reached?
fast voltage gated sodium channels are opened causing depolarisation towards Na's equilibrium potential followed by repolarisation - outward flow of K
154
What does the depolarisation by Na cause?
Voltage gated Ca channels open (take longer to activate) and cause contraction
250ms later Ca channels close and K efflux returns
155
Why is the maximum -ve voltage of the pacemaker less than that of the ventricular muscle?
Fast Na channels remain inactivated
156
How is the spontaneous gradual depolarisation of pacemaker cells carried?
Carried by Na ions through slow Na channels that open during the repolarisation of the cell as it reaches it's most negative value
157
What happens to the pacemaker cells once they have reached their threshold voltage?
Ca channels open giving a relatively slow depolarisation
158
What does the size of the interval between beats depend on?
How fast the pacemaker potential repolarises.
Shortened by the action of the Sympathetic nervous system on the SAN and shortened by parasympathetic activity.
Noradrenaline speeds up the heart rate by making the pacemaker potential steeper
Acetylcholine slows the heart rate by making the potential shallower
Stretch sensitive baroreceptors
159
How might arrhythmias arise?
Ectopic pacemaker activity
After - Depolarisation
Re-entry loop
160
What is ectopic pacemaker activity?
Depolarisation and spontaneous activity causes damage to the myocardium
Latent pacemaker regioni activated due to ischaemia
Dominates over SAN
161
What is After-depolarisation?
Abnormal depolarisations following the action potential
162
What is a re-entry loop?
Conduction delay
Normal spread of excitation disrupted due to damaged area
Incomplete conduction damage (uni-directional block)
163
What are the 4 basic classes of arrhythmia drugs?
I. Drugs that block voltage gated sodium channels
II. Antagonists of beta adrenoreceptors
III. Drugs that block K channels
IV. Drugs that block Ca channels
164
Give an example of a class I arrythimic drug and explain how they work
Local annaesthetic lidocaine
Blocks open or active channels and dissociates rapidly in time for the next AP
Normal firing not blocked but but prevents AP's too close to one another
165
Give an example of a class II drug and explain how they work
Propanolol Atenolol
Block sympathetic action by blocking Beta 1 receptors in the heart, decreasing the slope of the pacemaker potential in the SAN. Inhibits adenyl cyclase decreasing inotropy
166
When are class II anti-arrythmic drugs commonly used?
After an MI to combat increases in sympathetic activity and reduce the O2 demand of the myocardium
167
How do class III anti-arrythmic drugs work?
Prolongs the action potential by blocking K channels, responsible for repolarisation. ARP is lengthened preventing another AP occuring too soon
Not generally used as they can also be pro-arrhythmic
168
Give an example of a class IV anti-arrythmic drug and explain how they work.
Verapamil
Decreases slope of pacemaker action potential at SAN
Also decreases AV nodal conduction and decreases the force of contraction.
Some coronary and vasodilation
169
How is adenosine anti-arrythmic?
Produceendogenously and acts on the A1 receptors at teh AV node. Enhances K conductance and hyperpolarises cells of conduction tissue
Resets the heart
170
What is an inotropic drug?
A drug which affects the force of contraction of the heart
171
When are negative inotropic drugs used?
Circumstances where it is beneficial to reduce workload of the heart eg after MI
172
When are positive inotropic drugs used?
When the herat needs to beat more strongly eg cardiogenic shock or acute but reversible heart failure.
Beta adrenoreceptor agonist
173
How are drugs used in heart failure?
ACE inhibitors - prevent formation of vasoconstrctor angiotensin II causing vasodilation of arterioles and venous dilation - decrease afterload and preload
Also have diuretic action - angiotensin II ususally promotes aldosterone release from zona glomerulosa which causes Na and water retention, increasing blood volume. Therefore with ACE inhibitors, the opposite occurs
174
Explain angina
O2 supply to the heart does not meet its need. Ischameia of the heart leads to chest pain, usually on exertion and relieved by rest. Due to narrowing of the coronary arteries (Atheromatous disease)
175
How is angina treated?
Reduce the work load of the heart with Beta blockers, Ca channel blockers\* and organic nitrates\*
\*also improve blood suppy to the heart
176
How do organic nitrates reduce angina?
act with thiols in vascular smooth muscle causing NO2 to be released -\> reduced to NO which is a powerful vasodilator -\>activates Guanylate cyclase, increasing cGMP and lowering intracellular Ca, causing relaxation of vascular smooth muscle
177
What is the primary action to treat angina?
Action on the venous system as a venodilator, lowering cenral venous pressure and preload. THe heart fills less thereofre force of contraction is reduced
178
What is the secondary action for treatment angina?
Acts on coronary arteries, improving O2 delivery to the ischaemic myocardium
179
Name 2 conditions which increase the risk of thrombus formation
Atrial fibrillation
valve disease
180
What is warfarin?
anti-thrombotic drug
181
What type of drug is aspirin and when is it used?
Anti-platelet drug used following MI or in coronary artery disease when there is an increased risk of MI to reduce the risk of platelet rich arterial clots forming
182
What complications can arise from hypertension?
carries the risk of developing cardiovascular disease or stroke
183
What drugs may be used to treat hypertension and how do they work?
Act to reduce cardiac output and/or peripheral resistance.
ACE inhibitors
Diuretics
Adrenoreceptor blockers
calcium channel blockers
184
What are the 2 circulations to the lungs?
Bronchial circulation - Part of the systemic circulation and meets metabolic needs of the lungs
Pulmonary circulation - Blood supply to alveoli. Required for gas exchange
185
Comment on the pressure and resistance of the pulmonary and systemic circulation
Pulmonary - Low pressure and resistance (RA 0-8mmHg, RV 15-30mmHg)
Systemic - Higher (LA 1-10mmHg, LV 100-140mmHg)
186
What are the mean pressures in vasculature of the pulmonary circulation?
arteries- 12-15mmHg
capillaries - 9-12mmHg
Veins - 5mmHg
187
How is the low resistance of the pulmonary circulation maintained?
Short, wide vessels
Lots of capillareis (many parallel elements)
arterioles have relatively little smooth muscle
188
What adaptations promote efficient gas exchange?
High density of capillaries in the alveolar walls
Short diffusion distance
Therefore high O2 and CO2 transport capacity
189
What is the optimum V/Q ratio?
0.8
190
What is the Ventilation-Perfusion ratio?
For efficient oxidation, need to match ventilation and perfusion of alveoli. Maintaining this means diverting blood from alveoli which are not well ventilated
191
How is optimal V/Q maintained?
Hypoxic pulmonary vasoconstriction - regulating vascular tone. Results in vasoconstriction.
Poorly ventilated alveoli are less well perfused
192
How does chronic hypoxia occur?
Chronic increase in vascular resistance - chronic pulmonary hypertension
Higher afterload on RV - can lead to right ventricular heart failure
At altitude or as a consequence of lung disease eg. emphysema
193
When is hydrostatic pressure greatest in the lower lung?
In upright position (orthostasis)
194
How does exercise influence the pulmonary blood flow?
Increased cardiac output
Small increase in pulmonary arterial pressure
Opens apical capillaries
Increased O2 uptake by lungs
As blood flow increases, capillary transit time is reduced (approx 1 sesc at rest, can fall to 0.3 without compromising gas exchange
195
What forces determine fluid formation?
Starling forces
Hydrostatic pressure of blood within the capillary (pushes fluid out of the capillary)
Oncotic pressure - pressure exerted by large molecules such as plasma proteins (draws fluid intot he capillary)
196
How is the formation of lung lymph minimised?
Low capillary pressure
197
What does increased capillary pressure cause/
More fluid filters out -\> oedema
filtration \> reabsorption
198
What effects does pulmonary oedema have and how is it treated?
impairs gas exchange - affected by posture, mainly at base when upright, throughout lung when lying down
Use diuretics to relieve symptoms and treat underlying cause
199
What % of the cardiac output supplies the brain?
15% (although only acounts for 2% of body mass)
20% of total body O2 consumption by brain grey matter
Must be a secure supply
200
How does the cerebral circulation meet the high demand for O2?
High capillary density
High bassal flow rate (x10 of av body)
High o2 extraction (35% above av)
201
Why is constant and stable O2 supply to the brain vital?
Neurones are very sensitive to hypoxia
Loss of consciousness after a ffew seconds of cerebral ischaemia
Begin to get irreversible damage to neurones in approx 4 mins
Interuption to blood suppy causes neuronal death
202
How is a secure blood supply ensured?
Structurally - anastomoses between basilar and internal carotid arteries
Functionally - brainstem regulates other circulations, myogenic autoregulation maintains perfusion during hypotension, metabolic factors control bloodfow
203
How is myogenic autoregulation acheived?
Cerebral resistance vessels have well developed myogenic response, responds to changes in transmural pressure
Maintains cerebral blood flow when BP changes
Fails below 50mmHg
204
What does panic hyperventilationi cause?
hypocapnia nad cerebral vasoconstriction leading to dizziness or fainting
205
What is cushings reflex?
Rigid cranium protects the brain but does not allow for volume expansion
Increase in intracranial pressure impairs cerebral blood flow (tumour/haemorrhage)
Impaired blood flow to vasomotor control regions of the brainstem increases sympathetic vasomotor activity (increase arterial BP and helps maintain cerebral blood flow)
206
What type of molecules readily diffuse across the blood brain barrier?
Lipid soluble molecules eg O2 and CO2
Lipid insoluble solutes such as K and catecholamines can't diffuse freely
207
How is the high required basal rate of O2 facilitated?
High capillary density
Diffusion distance \<9micro-m
Continuous production of NO by coronary endothelium maintains a high basal flow
208
Describe the realtionship between required O2 and blood flow.
Linear until very high O2 demand
Vasodilation due to metabolic hyperaemia
209
What type of arteries are coronary arteries and how does this affect them?
Functional end arteries:
Few aterio-arterial anastomoses
Prone to atheroma
Narrowed coronary arteries leads to angina on exercise
Sudden obstruction by thrombus causes myocardial infarction
210
How does exercise effect blood flow to skeletal muscle?
Must increase O2 and nutrient delivery and remove metabolites during exercise - increased vasodilation and blood flow to muscle
211
What role does skeletal muscle have in blood pressure?
Important in helping regulate arterial blood pressure - 40% of adult body mass is muscle
212
Describe the features of the skeletal muscle circulation
Capillary density is dependent on muscle type - postural muscle has higher density
Very high vascular tone - permits lots of dilation, flow can increase \>x20 in active muscle
At rest only about half of capillaries are perfused at any one time
213
What effect does the opening of capillaries have on the skeletal system?
Increase blood flow and reduces diffusion distance
214
Name some vasodilators
Potassium
Increasing osmolarity
Inorganic phosphates
Adenosine
Hydrogen ions
Adrenaline
215
How does Adrenaline act as a vasodilator at arterioles in skeletal muscle?
Acts through Beta 2 receptors
Vasoconstriction by noradrenaline acting on Alpha 1 receptors
216
What role does the cutaneous circulation have in the body?
Temperature regulation - core temp usually maintained around 37 degrees. Balance between heat production and loss. Skin is the main heat dissipating surface and this is regulated by cutaneous blood flow
Role in blood pressure maintainance
217
What are artereovenous anastomoses (AVAs)?
communication between an artery and vein by collaterol channels
218
How do AVAs in the skin affect heat loss from apical skin?
Apical skin have a high surface area to volume ratio
AVAs are under neural control not local metabolites
Decrease in core temp increases sympathetic tone in AVAs - decrease blood flow to apical skin
Increased core temp opens AVAs...
219
How do AVAs prevent blood entering capillaries?
Low resistance shunt to venous plexus
220
221
What is the primary cause of Heart Failure?
Ischaemic Heart Disease
222
List a few other causes of Heart Failure.
Hypertension
Dilated Cardiomyopathy
Valvular heart disease/congenital
Restrictive cardiomyopathy
Pericardal disease
High-output Heart Failure
Arrythmias
223
What is Class I Heart Failure?
No symptomatic limitatino of physical activity
224
What is class II HF?
Slight limitation of physical activity
Ordinary physical activity results in symptoms
No symptoms at rest
225
What is class III HF?
Marked limitation of physical activity
Less than ordinary physical activity results in symptoms
Mo symptoms at rest
226
What is class IV heart failure?
Inabilityto carry out any physical activity without symptoms
May have symptoms at rest
Discomfort increases with any degree of physical activity
227
What is the cardiac output?
5l/min
228
What is the average stroke volume?
75 ml/beat
229
What factors effects cardiac output?
Heart rate
Venous capacity (LV preload)
Aortic and peripheral impedance (after load)
Myocardial contractility
230
What is starlings law?
The force developed in a muscle fibre depends on the degree to which the fibre is stretched
231
What happens in systolic dysfunction?
Increased LV capacity
REduced LV cardiac output
Thinning of the myocardial wall - fibrosis and necrosis of themyocardium, activity of matrix proteinases
Mitral valve incompetence
Neuro-hormonal activation
Cardiac arrhythmias
232
What are the structural changes of the heart in systolic dysfunction?
Loss of muscle
Uncoordinated or abnormal myocardial contraction
Changes to ECM - increased collagen (III\>I), slippage of myocardial fibre orientation
Change of cellular structure and function
233
What are the long term deleterious effects of the Sympathetic nervous system?
Beta adrenergic receptors are down regulated/uncoupled
Noradrenaline induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha receptors. Induces up regulationi of the RAAS
Reduction in heart rate variability (reduced paraSNS, increased SNS)
234
WHat happens to the RAAS in HF?
Commonly activated reducing renal blood flow and SNS induction of renin from macula densa
Elevated Angiotensin II:
- Potent vasoconstrictor
- Promotes aldosterone release
- Promotes NA/H2O retention
- Stimulates thirst by central action
235
What do Natriuretic Hormones do?
Cause Atrial stretch:
* Predominant renal action - constricts afferent and vasodilates efferent arterioles
* Decreases Na reabsorption in the collecting duct
* Inhibits secretion of renin and aldosterone
* Systemic arterial adn venous vasodilation
Balance the effects of the RAAS on vascular tone and Na/H2O balance
236
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What are common causes of chest pain from the heart and great vessels?
Myocardium- Angina, MI
Pericardium- Pericarditis
Aorta- Aortic dissection
238
What are common causes of chest pain from the lungs and Pleura?
Pulmonary embolism
Spontaneous Pneumothorax
Pneumonia
239
How do you determine what system chest pain is related to?
Circulatory- Central pain
Respiratory- Lateral chest pain, on inspiration, associated respiratory symptoms
GI- Often also epigastric pain
Chest wall- Often localised pain, movements may inc pain, history of trauma/use
240
What are common causes of chest pain due to GI problems?
Oesophagus- Gastro oesophageal reflux disease (GORD)
Peptic ulcer disease
GB- Biliary colic, cholecystitis
241
What are common causes of chest pain due to problems in the chest wall?
Ribs- fractures, bone metastases
Costo-chondral joints
Muscles
Skin
242
Describe coronary blood flow.
in systole small intramuscular vessels are compressedby forces generated in the cardiac muscle; coronary flow through LV muscle decreases to a minimum
Coronary flow occurs during diastole when the heart muscle is relaxed
Shortening of diastole (rapid heart rates) reduces time for this flow
243
What area of the heart is most vulnerable to ischaemia and why?
Subendocardial area. Heart muscle is perfused from the epicardial surface to endocardial surface. Myocardial wall pressure is greatest in the sub-endothelial area which is closest to LV cavity
244
Describe the collaterals in the myocardium
No collateral vessels between major arteries on the epicardial surface
Collateral vessels present between smaller arteries and arterioles
Expansion of existing collaterals and development of new ones occur whenischaemic but takes time
245
When does ischaemia occur?
When supply of oxygen cannot meet demand
Atheromatous Coronary artery disease is the most common cause
246
What are the modifiable risk factors for IHD?
Important 4:
Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus - doubles risk
Also:
Lack of exercise, obesity, stress, age , gender, family history etc...
247
What is the structure of an atheromatous plaque?
Necrotic centre
Fibrous cap
248
How does coronary atheroma occur?
Fibrous cap of plaque can undergo erosion or fissuring
Exposes blood to thrombogenic material in the necrotic core
Platelet clot followed by fibrin thrombus
249
What are the clinical syndromes of IHD?
Chronic stable angina
Acute coronary syndrome
250
What is chronic stable angina?
Stable plaque therefore coronary artery narrowing
Moderate reduction in flow
Blood flow sufficient to meet needs at rest
Ischaemia only whenoxygen demand increases
Relieved when demand ceases
Angina reproducible with the same amount of exertion
251
What is acute coronary syndrome?
Plaque fissure with thrombus formation at the site
acute, severe reduction in blood flow
252
What is STEMI?
ST elevation MI
90% of cases have total occlusion of coronary artery
extensive ischaemic injury involving full thickness of myocardium
K leak from injured sub epicardial myocytes causes depolarisation. Manifested as ST elevation
Proved benefit from emergency re-opening artery by PCI or Thrombolysis by Fibrinolytic drug
253
What is the difference between partial occlusion and total occlusion STEMI?
Only more vulnerable subendocardial areas are affected in partial.
K leak in partial causes depolarisation of subendocardial cells, manifested as ST depression. K leak in total occlusion causes K leak from subepicardial myocytes and the depolarisation is manifested as sST segment elevation
254
What is ischaemic chest pain like?
Site - sentral, or left sided diffuse pain
Typical pattern of radiation of the pain - arms and shoulders (one or both), neck, jaw, epigastrium, back. May present with isolated pain at these sites without chest pain
'Tightening' 'heavy' 'crushing' 'constricting' 'pressure'
Occasionally burning epigastric pain particularly in inferior MI
255
What is chest pain in angina like?
Brief episodes of ischaemic pain brought on by exertion/emotion and relieved by rest or nitrates within about 5 mins
Pain is often predictable ie reproducible
256
How is a diagnosis of stable angina made?
Clinical diagnosis based on history
Examination: no specific signs. Look for signs of related risk factors, LV dysfunction, evidence of atheroma elsewhere
Resting ECG usually normal
Exercise ECG stress test - positive if ECG shows ST depressions \>=1mm (horizontal/down sloping). Strongly positive test indicates stenosis
257
How is stable angina treated?
Nitrates decrease preload by venodilation, Cal CB decreases afterload by peripheral vasodilation, ACEI decreaes afterload. This reduces wall tension
Beta blockers decrease heart rate and contractility
Aspirin decreases platelet aggregation, hence decreasing thrombus formation if plaques disrupted
Statins decrease LDL cholesterol, decreasing progression of atherosclerosis, increasing plaque stability
Revascularisation mechanically restores blood flow
Sub lingual nitrate spray/tablet
258
When is angiography used?
To study coronary artery anatomy when revascularisation is planned
259
What are the 2 main types of revascularisation?
Percutaneous Coronary intervention (PCI)
Coronary artery bypass (CABG)
260
When is CABG used?
Internal mammary artery (internal thoracic artery) grafts
Radial artry grafts
Saphenous vein grafts (using reverse segment of vein
261
How does acute coronary syndrome present?
Recurrent chest pain
Occuring frequently and with little or no exertion and with episodes often lasting longer than 15 mins is suggestive.
Priority is to differentiate into STEMI/NSTEMI becasue the treatment is different
262
What are the symptoms of an MI?
Ischaemic chest pain
Severe pain, patient distressed
Persistant pain
Pain at rest, often no precipitant (50%)
Not relieved by rest/nitrate spray
Autonomic features - Sweating, pallor
Nausea, vomitting
Breathlessness (due to LV dysfunction)
Faint
263
What are the symptoms of unstable angina?
Acute worsening of stable angina - more frequent, severe, longer duration
Angina at rest
Recent onset of new effort limiting angina
Presence of risk factors
264
What is looked for in an examination for MI?
Patient anxious, distressed
Sweating, pallor
Cold, clammy skin
Tachycardia/arrhythmias +/-
Low BP +/-
Signs of heart failure
Crackles in lung bases (LVF)
265
What initial investigations are carried out for ACS?
ECG
Cardiac Biomarkers
266
What is the difference in ECGs of STEMI and NSTEMI?
STEMI: ST elevationin\>=2 leads facing same area 1mm limb leads, 2mm chest leads
NSTEMI: ST segment depression, T wave inversion or no ECG change
267
Why is cardiac troponin I (cTnI) and T (cTnT) used as a biochemical marker of myocyte damage?
It is a protein important in actin/myosin interaction which is released in myocyte death
Very sensitive and specific marker
Rise 3-4 hours after onset of pain
Peak at 18-36 hrs
Decline slowly upto 10-14 days
268
What is CK and why can it be used as a biochemical marker?
Enzyme present in skeletal muscle, heart and brain
3 iso enzymes
CK-MB is the cardiac iso enzyme
rise 3-8 hrs after onset
Peak at 24hrs
Back to normal 48-72 hrs
269
What is the treatment of STEMI?
Anti platelet agents
Reperfusion
Anti ischaemic therapy
ACEI esp if LV dysfunction
Statins
Revscularisation
270
What is the treatment of unstable angina?
Anti thrombotic therapy - anti platlet agents, antic coagulants
Restore perfusion of partially occluded vessel(s)
Risk stratification
General measures - Pain control, O2
Anti ischaemic therapy - IV nitrates, Beta blockers
Statins, ACEI
271
What is the long term treatment of an MI?
Aspirin
Beta Blocker
ACEI
Statin
Manage risk factors
272
What are some complications of MI?
Sudden cardiac death
Arrhythmias
Heart block
Ventricular tachycardia/Ventricular fibrillation
Atrial fibrillation
Heart failure
Cardiogenic shock
273
What causes pericarditis?
Infections- viral
Post MI/cardiac surgery
Autoimmune
Ureamia
Malignant deposits
274
What are the symptoms of pericarditis?
Central/left sided chest pain
Sharp, worse with inspiration
Improved by leaning forward
275
What is looked for on examination for pericarditis?
Pericardial rub
Signs of pericardial effusion
276
What investigations would you undergo to diagnose pericarditis?
ECG - ST elevation with upward concavity, in all the leads
Echocardiogram - diagnosis of pericardial effusion
277
How do you treat pericarditis?
Treat cause
If effusion causing tamponade - pericardiocentesis
278
What can cause tearing of the aorta?
Hypertension
Trauma
Iatrogenic - cardiac catheterisation
Inherited defects of collagen
Age
279
What are the symptoms of aortic dissection?
Severe tearing type chest pain
Which radiates to the back to between teh shoulder blades
Very abrupt onset
280
What are the signs of an aortic dissection?
unequal pulses in the 2 arms
Signs of aortic regurg
Occlusion of aortic branches may cause a variety of complications
281
What are the effects of aortic dissection?
Aortic ring dilation - acute aortic regurg = new AR murmur
Obstruction of branches of aorta
Rupture of aorta
Compression - Trachea/oesophagus/SVC
Double-barrelled lumen (if re-enters lumen through another intimal tear)
282
What are the 3 clinical features an acute aortic dissection can generally be identified by?
Immediate onset of aortic pain with a tearing and or ripping
Variation inpulse and/or blood pressure between the right and left arm
Mediastinal and/or aortic widening on chest radiograph
