Week #5 Flashcards
1
Q
Where are baroreceptors located?
A
- Pre-glomerular arterioles
- Responsible for releasing Renin
- Production of AngII
- Carotid sinus
- Thin walled
- Very compliant—so very sensitive
- can repsond within 1 cardiac cycle
- Highly innervated
- Internal carotid artery
- Na2+ same as a stretch receptor is also in the kidney in the distal nephron
- That is the stretch receptor in the carotid sinus
- Aortic arch
2
Q
What part of the brainstem contains the cardiovascular control centre?
A
- The medulla
- Pressure and depressor
- For high and low pressure
- Operates via sympathetic and parasympathetic nerves
3
Q
Activation of the sympathetic nervous system results in?
A
- Increased HR
- Decreases atrioventricular conduction time
- The AV conduction is between the AV and ventricle—so faster conduction.
- Increase cardiac contractility
- Greater stroke volume
- Ca2+ concentration within the cells is increased when you activate the sympathetic nervous system so you increase the activation of the actin/myosin
-
Increase total peripheral resistance
- Keep blood in arteries
- Increase venous tone
- Push on the veins and deliver more blood to the heart
4
Q
What happens when we activate the parasympathetic nervous system?
A
- Reduced heart rate
- Increase atrioventricular conduction time
- Doesn’t reduce total peripheral resistance
- There are some areas where there is vasodilation due to the parasympathetic nervous system but doesn’t really make a difference
5
Q
Summary of the autonomic nervosu system effects on controlling blood pressure
A
6
Q
What is the function of chemoreceptors?
A
- The baroreflex stops firing at 60mmHg so we use the chemical detection system
- Respond to very low O2
- Carotid and aortic bodies outside arteries
- Look like peas with nerves around them
- Are stimulated at very low MAP
- Low flow
- Low O2, high CO2, low pH
7
Q
What does high blood pressure predispose us to?
A
- Coronary disease
- Stroke
- Cardiac hypertrophy
- Heart failure
- Kidney failure
8
Q
What happens to the blood pressure in the ageing adult?
A
- Systolic BPO rises until 60 years of age
- Systolic rises after 60 years of age
- Diastolic BP rises until 60 years of age
- Diastolic pressure usually remains the same or goes down after 60
- Because we get increased pulse pressure
- Stiffening of the arteries—less compliance
- So blood vessels can no longer accommodate lower volumes of blood and blood pressure falls
- i.e. blood vessels no longer constrict as much (due to low compliance) when there is less
- So blood vessels can no longer accommodate lower volumes of blood and blood pressure falls
9
Q
What is the diurnal variation in blood pressure?
A
- Blood pressure is lower night (20mmHg)
- sympathetic action decreases-so Renin AngII system more active at night
- during the day everyday activitues increases sympathetic activity
- less variability at night
10
Q
Is blood pressure higher in summer?
A
- No it is lower
- due to the vasodilation and sweating (lose fluid-CO output drops)
*
11
Q
What is the populaiton paradox?
A
- The greatest number of deaths occur in individuals in the middle region of the blood pressure normal distribution
12
Q
The breast is from?
A
- the 2nd rib to the 6th rib
13
Q
How many ribs do we have?
A
- 12
14
Q
What is the sternum comprised of?
A
- The monubrium, sternum and xyphoid process
15
Q
Ribs artciculate with the costal cartilages and then those costal cartilages articulate?
A
- Upper 1-7 articulate with the sternal complex directly
- Costal cartilages 8,9 and 10 turn up and articulate with the costal cartilages above
- 11 and 12 costal cartilages do not articulate with anything—floating ribs
16
Q
Describe the basic anatomy of a rib
A
- Vertebral end closest to vertebral column has a head, neck and tubercle
- head has two articular facets
- Tubercle has two facets—medial facet closest to the head and lateral facet
- Medial facet is smooth—articular surface
Lateral facet is a rough lump of bone—attachment of a ligament
- Medial facet is smooth—articular surface
- Then shaft or body of the rib
- Vertically orientated with a superior and inferior edge and you can see a costal groove on the internal aspect
- Within the costal groove is where the neurovascular structures run
- Anterior or sternal end is characterised by a pit for the costal cartilage to plug into
- Vertically orientated with a superior and inferior edge and you can see a costal groove on the internal aspect
17
Q
Which ribs are described as atypical?
A
- Ribs 11 and 12 and 1 are atypical
- 1st rib only articulates with T1 and do there is only one facet
- Very short and also much more curved than the other ribs and broad and almost horizontal in its orientation
18
Q
What are the costovertebral joints?
Describe their function
What are the costotransverse joints?
Describe their function
A
Costovertebral Joints
- the head of the rib articulates with the demi-facet on two consecutive vertebrae and the IV disc in between-except for T1 that does not articulate with C7
- Radiate ligament-radiates out to strengthen the joint
Constotransverse joints
- Between the transverse process of the vertebrae and the tubercle of the rib
- The medial facet of the tubercle
- Note the 3 part costotransverse ligament that holds together the neck and tubercle
- Blunt trauma will not be able to dislodge this joint
- you will break the rib first
19
Q
What are the attachments of the diaphragm?
A
- Xyphoid process attachment anteriorly
- Arcuate ligaments
- Lateral and medial
- Lateral overlies quadratis lumborum-thickening in the fascia of quadratis lumborum
- Medial arcuate ligament—psoas major-thickeing in the fascia
- Posterior attachment to the lumba vertebral column
- connects via pair of ligaments
- left crus, right crus
- connects via pair of ligaments
20
Q
The Crus originate at ___ with the right crus extending to _____ and the left crus extending to____. This could be due to diagphragm on the right being ____ than that that on the left due to the presence of the ____
A
The Crus originate at L1 with the right crus extending to L3 and the left crus extending to L2. This could be due to diagphragm on the right being higher than that that on the left due to the presence of the liver
21
Q
Where does the IVC, Oesophagus and Aorta pass through the diaphragm?
A
- We have the IVC passing through central tendon at level T8, to the right
- Oesophagus passes through muscular part of diaphragm at T10, to the left
- Aorta between the crura at T12—so not really through the diaphragm. More behind the diaphragm and medially.
22
Q
Explain the quality and direction of each of the layers of the intercostal muscles
A
External
- Front pockets muscle fibres are directed downwards and forwards—like hands in front pockets
- Brown is muscular fibres—muscle fibres form posterior and lateral parts
- And then the rest is replaced by membrane—the green—in the anterior part—external intercostal membrane
- When the external ICM contract they pull the rib below up and out. So the action is to elevate and expand rib cage and is therefore a muscle of inspiration.
Internal
- Fibres are directed downwards and backwards
- Back pockets muscle
- Membrane replaces the muscle posteriorly
- Fibres pull ribs down and in—expiration muscle ??
- But not as strong
- Probably what it does is holds the space taught rather than actually move the ribs—more of a splint rather than an expiration muscle
Innermost ICM
- Incomplete
- Direction of fibres is back pockets
- Only fills lateral part of space
- There are some muscle in the same plane
- Transversus thoracis —anterior aspect in the same plane as innermost ICM
- And
- Subcostalis —posterior aspect of the space
- But probably OK just to remember that they are discontinuous muscles
23
Q
Intercostal neurovascular bundle
A
- Each intercostal space has a bundle—vein, artery and nerve
- From top—down
- This is tucked into that costal groove
- Neurovascular plane runs between the internal and innermost ICM
- Smaller branches (collateral branches) of each of the vein, artery and nerve running in the bottom of the space—usually smaller
- So when passing a needle into the intercostal space we would put needle into bottom of the space and avoid the larger and more important bundle at the top
24
Q
Vein artery and nerve of the intercostal space
Where did they come from?
Where do they go to?
A
Intercostal nerve
- Intercostal nerve is the ventral rami of the thoracic spinal nerve
- It becomes the intercostals nerve
- And we can see that only the innermost intercostal muscle is deep to this
Arteries
- Anterior and posterior aspect of the intercostals space and the anterior and posterior arteries anastomose together. Anterior intercostal arteries come from the internal thoracic artery and the posterior come from the descending thoracic aorta.
Veins
- Veins mirror the arteries and we get them coming posteriorly and anteriorly
- Anterior intercostal veins will drain into the internal thoracic vein
- Posterior intercostal veins will drain into the azygous system of veins
25
Q
What are the movements of respiration and which muscles contribute
A
- Diaphragm is the main muscle of respiration and contracts the thorax vertically to expand it
- Intercostal muscles also contribute
- Elevation of the upper ribs (ribs 1-7) changes AP dimension of the thorax—i.e. the ribs are connected to the thorax and pulling ribs upward will expand in that direction as the ribs are not horizontal-pump hundle movements
- Lower ribs don’t articulate with the sternum so when they are elevated the middle of the shafts move laterally and expand the lateral part of the thorax—bucket handle movement
26
Q
What does the pericardium attach to and why?
A
- The pericardium is connected to the central tendon of the diaphragm
- When the diaphragm contracts on inspiration this pericardial sac can stop the diaphragm from descending.
- Pericardial sac is positioned in the middle mediastinum
27
Q
What are the devisions of the pericardium?
A
- Outer fibrous pericardium
- And inner serous pericardium
- Parietal layer lines internal aspect of the fibrous pericardium
- And then the visceral layer lining surface of the heart
- Arrangement creates pericardial cavity between these two layers—visceral and parietal
- Potential space only—couple of mls—not a large volume
- Friction free surface for the heart to move
- Friction free glide
28
Q
Describe the internal features of the right atrium
A
- atria are thin walled receiving chambers
- internal aspect of the anterior part of the right atrium are lined with ridges—musculi pectinati
- posterior surface is smooth—sinus venarum
- Crista terminalis—clear defined point where the musculi pectinati end and the sinus venarum starts.
- Superior Vena cava returns blood from head, neck and upper thorax—no valve
- And the inferior Vena cava—returns through the central tendon—remember it goes through the diaphragm at T8
- Remember that the central tendon is adherent with the pericardium so the moment the IVC pierces the diaphragm it empties into the atrium
- Rudimentary valve associated with the IVC opening
- This will lead us to the fossa ovalis
- Which in utero would have opened into the left atrium because the baby is not breathing air—i.e. blood is already oxygenated so we bypass the pulmonary circulation and just pump through the body
- Eventually this seals off—can see it in left and right atrium.
- This will lead us to the fossa ovalis
- Coronary Sinus is the venous drainage form the heart itself.
29
Q
Describe the internal features of the right ventricle
A
- Anterior wall has been flapped down
- Thicker walls
- Large number of muscular ridging—trabeculae carnae
- At the outflow tract just before the pulmonary trunk begins is a smooth area that does not have the trabeculae carnae and this area is the conus arteriosus/infundibulum. (note every other area has trabeculae carnae, posteriorly and anteriorly.
- Three specialised (atypical) trabeculae carnae are called papillary muscles where their base is connected to the wall but apex projects into the centre
- From the apex of each we have a series of chordae tendinae which connect the apex of the papillary muscles with the tricuspid valve
- Remember that the papillary muscle are just an extension of the trabeculae carnae—i.e. contract together
30
Q
Decribe the features of the left atrium and the left ventricle
A
- Looking into left ventricle on left and left atrium on right
- Left ventricle has the thickest wall overall—pumping into systemic—higher pressure than pulmonary circulation
- Bi-cuspid atrioventricular valve—mitral valve—mostly cut away—has the chordae tendinae and papillary muscles
- Left atrium simply thin walled and smooth with 4 openings for the 4 pulmonary veins
- Ear like appendage heading around to anterior surface of the heart
31
Q
What is the function of the fibrous skeletocn of the heart and where is it found?
A
- Pair of atrioventricular valves
- Rings surrounding
- And pair of lunar valves
- Coronets surround pulmonary and aortic valves
- This structure anchors atria and ventricular muscles separately.
- 2 separate muscle masses—separated in their attachment to the fibrous skeleton. Atrial muscle mass forming the atrial chamber and the ventricle muscle mass—separated by fibrous and so are separated from AP passing between them—need something to jump this gap
32
Q
Decribe the atrioventricular valves
on left and right
A
- Tricuspid on right and bicuspid (mitral) on left
- 3 cusps
- anterior
- posterior
- septal
- Ventricular surface is rough and has attachment of the chordae tendinae
- The chordae tendinae connects to two adjacent cusps separately and the pulls them together to close the valve
33
Q
Describe the semi-lunar valves
A
- Base is attached to internal surface of the wall of the vessel and the apices meet in the centre
- Anterior, posterior, and left and right (aortic is labelled correctly)
- When ventricle contracts blood is pushed through the pulmonary and aortic valve when the pressure increases to above the pressure in the vessels. And then when we get a decrease in pressure in the ventricles then the valves just close off.
- In the aortic valve the coronary arteries arise and then these arteries deliver blood to the heart
34
Q
Describe the conduction system of the heart
A
- SA node in the right atrium and right at the top of the crista terminalis
- The AV node is also in the right atrium
- The bundle of His is what allows the conduction system to bridge across the fibrous skeleton and then bundled branches (purkinje fibres) take the AP down to the ventricles
35
Q
What is the nervous supply of the heart?
A
- The cardiac plexus is situated at the base of the heart and is divided into a superficial and deep part. It receives branches from the vagus and sympathetic trunk
36
Q
Describe the coronary arteries, draw them
A
- The very first branches of the aorta
- They emerge onto the anterior surface of the heart either side of pulmonary trunk
- Right coronary artery descends in the anterior atrioventricular groove (coronary groove)
- There is a marginal branch that comes of the right coronary artery which runs along inferior border of the anterior portion of the hear
- And the right coronary artery will give off another branch that leads to the left coronary artery and runs along the posterior interventricular groove
- In 60% of cases we will see a branch come off the start of the right coronary artery and then run between ascending aorta and right atrial appendage to supply the SA node and in 90% of cases the right coronary artery will also supply the AV node
- Left coronary artery also starts at the anterior of the heart but then splits into circumflex branch and an anterior interventricular branch.
- The circumflex branch moves posteriorly and then meets with the right coronary artery in the posterior atrioventricular groove
- May be other branches also
37
Q
What is the parasympathetic control of the heart?
When are the parasympathetics exerting control over the heart?
A
- Two fibre system
- pre-ganglionic and post ganglionic
- Pre-ganglionic neurons release ACh which acts on the post ganglionic neurons and this results in ACh release and action on MuscR which result in slowing of HR, through action on the SA node and AV node
- The parasympathetic nervous sytem is constently acting upon the heart slow HR-evident through the application of “atropine” a parasympathetic blocker
38
Q
What is the sympathetic control of the heart?
When does this system act on the heart?
A
- two fibre system
- pre ganglionic fibres release ACh which acts on Nicotinic receptors, they then act to release NA which acts on Beta and alpha adrenoceptors
- Innervates the SA node, conducting tiussue and myocardial cells
- Increase HR and increase contractile force (positive ionotrope)
- When blocked by propranolol the HR decreases a bit indicatign that sympathetic fibres are not that actie at rest
39
Q
Which fibres (sympathetic or parasympathetic) have more of an effect on HR at rest?
A
- The parasympathetic nervous system
40
Q
Describe the phases of an Action potential in the spontaneously depolarising SA node
A
- The SA node is the key cell type that regulate rate and if we block the autonomic nerved the cells will depolerise at 100bpm
- Resting membrane potential of -60
- At resting there is a bit of Na and a bit of Ca leaking down an electrochemical gradient (i.e. the cell is negatively charged compared to the extracellular environment)
- Eventualy the Na and Ca leaking reaches a threshold and Ca then floods in.
- And then we get repolerisation–i.e. opening of the pottasium channel
41
Q
How do the parasympathetics actually slow the HR?
A
- ACh acts on muscurinic M2 receptors (G-protein coupled)
- decreases cAMP leading to opening K+ channels
- leads to hyperpolarisation K+ leaves and slows Na and Ca influx
- So now it takes longer for the cells to reach threshold (phase 4)
42
Q
How does the sympathetic nervous system result in increased HR?
A
- Acitavation of Beta1 Adrenoceptors (G-protein coupled) increases cAMP production leads to opening of Ca channels
- Ca entry speeds up rate of firing
- Increases the slope of phase 4 depolarisation
- increases rate of firing of SA node and more rapid conduction AV node
- can trigger dysrythmia if pushed too hard
43
Q
Describe the ventricular action potential?
A
- The ventricular myocyte AP has a stable resting membrane potential.
- Phase 0-depolerization-Na in
- Phase 1-rapid repolerisation-K out
- Phase 2 plateu-Ca in K out
- Phase 3-repolerisation K out
- Phase 4-stable membrane potential
44
Q
What are the common symptoms of dysrythmia?
A
- Shortness of breath, fainting, fatigue, chest pain
45
Q
What are some of the possible mechanisms for dysrythmias?
A
- Altered impulse formation
- Automaticity of pacemaker cells
- Abnormal generation of action potentials at sites other than the SA node
- Altered impulse conduction
- Conduction block
- Ventricles adopt own slower rate
- Re-entry
- Extra beats increase rate
- Conduction block
- Triggered activity
- Early or late after-depolarisations
- Excess sympathetic activation
- Early or late after-depolarisations
46
Q
What are the four main types of antidysrhythmics drugs?
A
- Na+ channel blockers-reduce phase 0 slope and peak of ventricular action potential:
- 1a moderate block
- 1b weak block
- 1c strong block
- Beta-adrencoceptor antagonism-decrease rate and conduction (SA node)
- K+ channel blockade-delay phase 3 of ventricular action potnetial and prolong APD
- Ca2+ channel blockade-most effective at SA and AV nodes-reduce rate and conduction
47
Q
What are the effects of the different Na+ channel blockers?
What can be the side effects of these drugs?
A
- Predominatly used for ventricle arrythmias
- Class 1a lengthens the repoleraisation and so lengthens the effective refactory period-this class is probably the one that is most effective at the SA node AV node dysrythmias but they are all mostly for ventricular AP modification
- Can get many different side effects at different doses
- effective does is 2-3 ug/ml
- Na+ channel blockers will have many systemic effects
- 4ug/ml Lip and tongue numbness
5ug/ml Light headedness
7ug/ml Visual disturbance
8ug/ml Muscular twitching
10ug/ml Convulsions
15ug/ml Coma
20ug/ml Respiratory arrest
25ug/ml Cardiovascular depression
48
Q
What are the main effects of the Beta adrenoceptor antagonists? how do they exert their anti-dysrhthmic action?
Adverse effects?
A
- Prevent β1-adrenoceptor effects on SA & AV nodes
- Decrease sinus rate, conduction velocity & aberrant pacemaker activity
- Also have membrane satbilising effects on the Purkinje fibres and so they can also block sodium channels
- Adverse effects
- Bradycardia, reduced exercise capacity, AV conduction block, hypotension
- Bronchoconstriction(poor selectivity?), Hypoglycaemia
49
Q
What are the main effects of the K+ channel inhibitors? how do they exert their anti-dysrhthmic action?
Adverse effects?
A
- prolong cardiac action potnetial
- slow phase 3 repolarisation
- decrease incidnece of re-entry
- increase risk of triggered events
- So mainly used for ventricular re-entry dysrythmias but may also trigger these events too
- Amiodarone is also shown to block Na+, Ca2+ and B-adrenoceptors
- reversible photosensitisation, skin discolouration and hypothyroidism
- pulmonary fibrosis with long term use
50
Q
What are the main effects of the Ca2+ channel blockers? how do they exert their anti-dysrhthmic action?
Adverse effects?
A
- Cardioselective-act preferentialy on SA and AV node and have effects on the initiation of AP.
- Can also slow connduction and increase refactory period
- Facial flushing, peripheral oedema, dizziness,bradycardia, headache, nausea
51
Q
What is Hypertension?
A
- BP> than 140/90 mmHg
- risk factor for
- stroke, TIA
- MI, Ischaemic heart disease, CHF
- aortic aneurism, retinal heamorrhage
- renal failure
- death
- Multifactorial disease
- often no known cause
- Risk factors
- smoking, diet, weight, stress
- Treatment benefirs are unequivocal
- less morbidity
- fewer deaths
53
Q
Describe the neural and hormonal regulation of blood pressure?
A
- Baroreceptors sense the pressure change and signals to the brainstem.
- Sympathetic nervous activation
- Noradrenaline is released which can act on alpha1 adrenoceptors to constrict blood vessels, increase cardiac output with B1 adrenoceptors.
- NA also acts on B1 adrenoceptors in the kidney which secretes Renin
- Activates AngII and causes increased constriction of blood vessels though AT1 receptors.
- AngII also works on kidney to conserve water and perhaps direct effects on the heart too
55
Q
How do ACE inhibitors work to reduce blood pressure?
What are the adverse effects?
A
- Renin works on angiotensinogen which makes angiotensin I and then ACE converts to AngII and then that acts on AT1 receptors and causes vasoconstriction and release of aldesterone which acts on the kidney and casue salt and water retention
- AngII also causes increase of Sympathetic nerve activity-positive feedback
- ACE inhibitors are called “prils”
- prevent conversion of AngI to AngII
- Reduce vascular tone
- Reduce aldosterone production
- Reduce cardiac hypertrophy
- through reducing further sympathetic nerve activation
- prevent conversion of AngI to AngII
Adverse effects
- Most of the side effects due to the fact that ACE inhibitors also prevent the breackdown of bradykinin by ACE (ACE is a kininase) (bradykinin is a vasodilator and also involvged in the pain responses)
- First-dose hypotension
- Dry cough
- Loss of taste
- Hyperkalaemia (+ thiazide diuretic)
- always prescribed with a diuretic to control hyperkaaemia
- Acute renal failure
- Itching, rash, angio-oedema
- Foetal malformations
62
Q
Lable the Heart tissue
A
63
Q
What are the histological features of a cardiac muscle cell
A
- Cells are small
- They have a central nucleus
- Form branching fibres
- Joined by intercalated discs
64
Q
What is the role of gap jucntions in cardiac muscle cells?
A
- Gap junctions are at intercalted discs are there to electrically connect the cells and coordiante beating.
- However, the gap junctions only co-ordinate electrical activity on a local level
- To co-ordinate contraction of different chambers a separate conducting system is needed – Purkinje fibres
74
Q
Describe thr composition and function of the capillaries
A
- Capillaries arfe often thinner then the diameter of a RBC and so force contact between the vessel wall and the RBCs
- capillaries only have a single smooth muscle cell controlling blood flow associated with it
- may be a meta arteriole between the arterioles and the smooth muscles
- capillaries are formed by a single endoothelail cell wrapping around to form a thin tube and sealed with tight junctions
- sitting on a basal lamina
- sometimes has a pericyte (media)
- a few collagen fibres surround the vessel (adventitia)
*
81
Q
What is Arteriolosclerosis?
What are some of the resulting sequale?
A
- intimal damamge and thickening of the arterioles
- Smooth muscles have produced too musch matrix and proteins from blood (albumin, Immunoglobulins) can leak across damaged endothelium
- known as hylanine arteriolosclerosis
Sequale
- poor blood supply to tissues (ischeamia)
- benign nephrosclerosis-ischaemia of the functional units of the kidney due to narrowed arterioles
- possibility of microaneurysms and then bleeding
- cerebral heamorrhage
*
- cerebral heamorrhage
84
Q
A
93
Q
Diagram of atherosclerosis
A
94
Q
What is an Aneurysm?
A
- Abnormal dilation of a blood vessel
- can also get them in heart
- Can get true aneurysm or a false aneurysm
- True aneurysm is when the whole wall stretches out-without bursting
- can be saccular-one side
- fusiform-both sides
- False aneurysm is where it has ruptured
- dissection
- heamatoma
- True aneurysm is when the whole wall stretches out-without bursting
- Weak media-lack of blood supply due to inflammation due to atherosclerosis or congenital etc
- weak media due to intimal thickening
- risk is that the aneurysm can rupture and blood will leak out
100
Q
What are the two different types of LV hypertrophy?
describe what actually happens in each and some of the common causes
A
- Concentric hypertrophy
- increase LV mass
- Increase wall thickness
- often due to pressure overload
- more sarcomers in parallel
- Eccentric Hypertrophy
- increase LV mass
- Normal relative to wall thickness
- often due to volume overload
- myocyte stretching-more sarcomeres in series
- Remodelling
- Normal LV mass
- Increase in relative wall thickness
112
Q
How do we measure right ventricle pressure?
How do we measure left ventricle pressure?
A
- Use JVP as a indirect measure
- Use pulmonary artery wedge pressure
- Catheter wedged into pulmonary artery will measure the pulmonary venous pressure
- so occlude the pulmonary artery and we can measure the left ventricle pressure indirectly
113
Q
What are the pressures acting across the capillary wall?
What pressure predominates at the arterial end and what pressure predominates at the venous end of the capillary?
A
- Hydrostatic pressure pushing out
- pressure of the fluid pushing non the capillary wall
- osmotic pressure pushing in
- Hydrostatic pressure dominates at the arterial end so fluid is pushed out of the capillary
- at the venous end osmotic pressure dominates and so fluid is pushed back in
- So most of the arterial pressure is lost across the cappilaries
118
Q
What does the body do when we get cardiac failure (i.e. the heart contracility decreases) to compensate
A
- The body must retain fluid and increase venous return and increase LV end diastolic pressure.
- But if the LVEDP increases too much (i.e. above 20-25mmHg) than the CO does increase but at the expense of the lungs and fluid will build up and leak into the alveoli and patients will present with shortness of breath
