JM Cardiovascular 🫀 Flashcards
Role of the CVS?
to transport or deliver substances
What 6 substances does the CV system transport?
- CO2
- O2
- nutrients
- waste
- hormones
released in bloodstream - heat
carried in circ to skin
where are hormones made and where do they travel to?
how do they travel?
from endocrine glands (production) -> where they act (tissue)
travel in bloodstream
what is delivery in blood floe generally varied according to?
needs of individual tissues
What is stroke?
loss of blood flow to the brain due to either:
- a clot
- a blood vessel rupturing
What 2 things can be caused by loss of blood supply to cardiac muscle?
- heart attack
- angina: chest pain
What can peripheral artery disease be due to? (2)
- inflammation
- atherosclerosis
cause narrowing of arterial walls
What is vasospasm and where does it occur?
narrowing/occlusion of blood vessels (arteries) - blocking blood flow.
fingers/toes
What is (pulmonary) oedema?
fluid accumulation in the interstitial fluid of cells, leading to swelling - pulmonary is when this occurs in the lungs
What is deep vein thrombois? DVT
a blood clot in the vein (typically lower limb like legs)
What is heart failure?
heart unable to pump enough blood to meet needs of rest of body
What are varicose veins?
enlarged twisted veins
What is the driver for all cardiovascular disease if untreated?
hypertension
4 drug classes that affect how blood moves around body
- diuretics
- beta blockers
- antihypertensives and HF drugs
- nitrates, Ca blockers, antianginal drugs
- lipid lowering
- antiplatelet
also treat CVD
What cardiovascular parameter contributes to arterial blood pressure (ABP)?
cardiac output - also important when considering heart failure
systemic circ (body) not pulmonary (lungs)
Factors affecting tissue blood flow will affect…
the distribution of blood flow to the coronary circulation supplying the heart
What is the cardiac output?
the amount of blood pumped by either the left or right ventricle per minute
Which 2 cardiac outputs are equal?
the left and right
What is the venous return/filling?
The amount of blood returning back to the heart
What should the venous return be equal to? If it’s not, what does it indicate?
venous return should be equal to the cardiac output otherwise it can indicate that blood is being lost or accumulating somewhere
Describe how the systemic and pulmonary circulation are in series with each other. Begin with the blood leaving the left ventricle.
- blood pumped out of LV to systemic circulation
- returns to the RV, now deoxygenated and pumped to lungs (pulmonary circ) to receive O2 and excrete CO2
- returns to LV to be pumped into systemic circulation again
What is the cardiac output normally at rest?
volume each ventricle pumps/minute =CO = 4-5L/min at rest
What does the cardiac output depend on? (2)
heart rate and stroke volume
What is the equation for cardiac output?
CO = HR x SV
cardiac output = heart rate x stroke volume (vol of blood prumped out per beat)
How could haemorrhage affect cardiac output (in terms of the equation)?
CO = HR x SV
HR increase SV decrease (as blood lost) therefore CO unchanged
whats happening in:
a) systole
b) diastole phase
a) heart pumping
b) heart relaxing- ventricles filling with blood
How does the pressure in the arteries change?
increase during systole (peak)
decrease during diastole (trough)
What exists between arteries and veins?
pressure gradient between:
arteries and veins
(arterial blood pressure/ABP) (central venous pressure/CVP)
Where is the central venous pressure measured?
from where the veins drain back into the atrium or where the veins all converge into 1
what can be deduced from the circulation having a pressure gradient between ABP and CVP? and how is it confirmed?
circ has resistance as:
you lose pressure as you go down the circulation
What blood pressure is measured clinically?
mean arterial blood pressure
What does mean arterial blood pressure (MABP) depend on?
- the volume of blood pumped per min
- the resistance of the circulation
What is the formula for systemic MABP?
systemic MABP = CO x TPR (total peripheral resistance)
i.e. BP
What is total peripheral resistance (TPR)?
resistance from all blood vessels within the systemic circulation downstream of the aorta
What is the formula for pulmonary MABP? Why is 1 parameter kept the same?
Pulmonary MABP = CO x pulmonary vascular resistance (PVR)
- it’s the same volume of blood that’s pumped out to the pulmonary circulation as that for the systemic circulation
How do the PVR and TPR compare? Why?
- TPR is approx 7x greater than the PVR
- Due to the vessels being longer and narrower in the systemic circulation
What is the consequence of TPR being greater than PVR on the systemic and pulmonary MABP?
- systemic MABP is 90mmHg
- pulmonary MABP is 15mmHg
What value is the CVP around?
0-5mmHg
pressure lost as result.
TPR= 7 x PVR
Where is most of the pressure in the systemic circulation lost? Why?
in the arterioles, as they have the most total peripheral resistance TPR.
after this goes to capillaries then back through venous system and pressure is lost.
role of:
a) elastin
b) collagen
c) smooth muscle
a) allows vessel to recoil back to orig shape
b) strength
c) vessels to change diameter
How does the pressure change from the large arteries to the small? Why?
it decreases slightly, because there’s not a lot resistance
Which blood vessel has the most elastin and collagen?
the aorta
Which blood vessels have the most smooth muscle?
the arterioles, allowing easy change in blood vessel diameter
What is the functional importance of arterioles? (think about what they can change)
they can affect the blood pressure upstream the systemic circulation (ABP) by constricting or dilating
If many arterioles constricted, how would the arterial blood pressure change?
the ABP would go up, remembering that:
ABP = CO x TPR
constricting would cause TPR to go up
If many arterioles dilated, how would the arterial blood pressure change?
the ABP would decrease, as the TPR would go down and ABP = CO x TPR
If only some arterioles constricted while others dilatated, how would the ABP change?
it wouldn’t change much
What is the formula for blood flow?
flow = (ABP-VP)/resistance
How would the capillary pressure change due to arterioles constricting?
- arterioles constrict = increase in local resistance
- tissue blood flow decrease (because flow=ABP-VP/resistance)
- hence the capillary pressure (CHP) would decrease
How would the capillary pressure change due to arterioles dilating?
would increase as:
- decrease in local resistance
- tissue blood flow increasing (flow=ABP-VP/resistance)
- increase in CHP
How can increased pressure in the veins affect pressure in the capillaries?
also causes it to increase
What do the thin-walled venous vessels allow for?
variable filling of blood for mobilisation back to the heart
What are the 6 types of blood vessels?What are the 6 types of blood vessels?
- elastic arteries
- muscular
- arterioles
- capillaries
- venules
- veins
role of:
- elastic arteries
- muscular
- arterioles
- capillaries
- strength, recoil
- strength, distribute blood to around the body
- provide the resistance that controls ABP and tissue blood flow
- exchange of nutrients, metabolites and fluid
role of venules and veins?
- capacitance/reservoir function
- control the filling of the heart’s ventricle by variating the amount of blood carried
How can the veins cause oedema?
increase in venous pressure could = increase in capillary pressure = can leak into extracellular compartments
What is venous pooling?
gravity/standing up = reduced filling in the heart but more in the lower limbs
name a:
gram positive bacteria
gram negative bacteria
+ S. aureus, pneumonia
- E.Coli, Klebsiella, Pseudomonas, Enterobacter
consequence of untreated infective endocarditis?
Sepsis. Travels to knees, kidneys, CNS in blood
Why is drug abuse a risk factor for the development of infective endocarditis?
IV drug users: contaminated needles introduce bacteria into the bloodstream = cause of infection
- Arterial BP, vascular resistance, blood flow
What is the purpose of elastin and wheres it mainly found?
stretch + recoil
- mainly elastic arteries
elastin mainly found where?
arteries
2 properties of collagen and wheres it mainly found?
tough and flexible
for larger arteries and veins usually outside of the vessel wall
where is smooth muscle found?
in all blood vessels but capillaries
describe smooth muscle- how arranged?
circular around lumen
can contract/relax- depending on intracellular [Ca2+]
causes constriction/dilatation
how calcium and smooth muscle interacts?
increase ca++ = constriction, decrease ca++= dilation
whats endotheliuma nd where is it?
single cell layer lining all blood vessels and main constituent of capillaries
What does the endothelium of healthy blood vessels tonically release in response to shear stress?
NO and prostglandins
What is the term given to NO and prostaglandins acting on vascular smooth muscle?
tonic dilitation
List some of the things that prostaglandins and NO released from the endothelium does?
inhibit platelet, RBC and neutrophil adherence
- anti thrombotic
- anti inflammatory
- anti plaque formation
- prevents athersclerosis
what causes increase In shear stress?
increase blood flow
mech blood movement through, against walls
affect of increased shear stress?
increased release of NO and prostglandins
what else can cause NO and PGs to be released?
Some vasodilator substances such as Ach and histamine -> dilatation
what does endothelium dysfunction cause?
impaired dilation, release of vasoconstrictor PGs, adhesion molecules produced
examples of adhesion molecules that attract to the arterial walls in endothelial dysfunction?
Platelets and neutrophils and RBC’s
What can endothelial dysfunction lead to?
thrombosis, inflammation, athersclerosis and increased risk of CVD
why do we not want adhesion molecules attracted to the arteries walls
causes an inflammation response and increases sheer stress
Inside which vessel is ABP determined for the rest of circulation?
elastic arteries
- i.e. the perfusion/driving pressure
why is arterial blood pressure (ABP) important
as it controls the perfusion and driving pressure.
how does the flow from the heart to the rest of the circulation flow?
Intermittently
why Is the flow from the heart intermittent?
as its not continuous due to the aortic valve opening and closing
what happens to the aortic valve during systole and diastole?
systole - open, diastole - closed
what happens to the aorta during systole and diastole?
systole - stretched due to the elastin and limited collagen;
diastole - recoiled elastin
What is the intima of elastic arteries made up of?
endothelium
what is the media of the elastic arteries made up of?
elastin and smooth muscle
what is the adventitia made up of mainly?
collagen
what would be the effect if there was no elastin or collagen to keep the vessel stable?
leads to aneurysm
- burst if ruptured, outer-tought part
Outline what happens in systole after the aortic valve opens?
blood comes out of left ventricle into aorta
after blood fills into the aorta in systole what happens to the wall of the aorta?
elastin walls stretch against the collagen wall of the adventitia
What happens to the elastic artery in diastole?
recoils back towards blood
valve closed
What keeps the pressure high in diastole?
elastic recoil
as transfers energy back to blood again
What exists from the elastic arteries to the muscle arteries from systole and diastole?
travelling pressure wave
what limits the stretch of artery in systole?
collagen
what happens to artery pressure during systole?
increases
aortic valve opens, wall stretches
What is the equation for MABP?
CO X TPR
i.e. from graph: DP + 1/3 (SP-DP)
how is pulse pressure calculated?
SP-DP
difference
Does inflow of blood into aorta during systole (CO) influence systolic pressure or diastolic pressure?
systolic
Does resistance to blood flow out of aorta during diastole (TPR) influence systolic pressure or diastolic pressure?
diastolic
Does the composition of the aorta influence systolic or diastolic pressure?
both
characteristics of arterial pressure wave
- increase to 120mmHg- systolic pressure
- slight dip- aortic valve closes
- increase a bit and steady decrease to bottom-80mmHg= aortic valve opens- diastolic pressure
What factors affect SP/DP and therefore are measured clinically and used diagnostically in treatment?
age, co and tpr
affect composition of aorta and resistance
What effect does ageing have on the aorta?
becomes stiffer due to loss of elastin and losing elastic recoil
Why does SP go up as a patients age increases?
resistance to stretch
healthy ageing affect on pulse pressure?
SP inc
DP dec
PP inc
What effect does reduced elastic recoil and ability to give energy back to blood as age inreases have on DP?
falls
SP goes up and DP goes down during ageing. What effect does this have on pulse pressure?
increases
When stroke volume or ventricular contractility is increased, what effect does this have on SP and DP?
SP goes up and DP remains normal
What would happen to SP and DP if there was a decreased stroke volume?
SP stays normal and DP increases
Give one condition where you would expect to see a decreased stroke volume?
dec CO e.g. in haemorrhage
Increased TPR effect on diastole?
inc TPR= harder for blood to leave aorta during diastole
= diastole increases
What effect does increased TPR have on systole?
may be normal or raised
What is essential hypertension classified as in terms of DP and SP?
DP above 90 and SP above 140
affect of DECreased TPR?
-> fall in DP,
steeper rate of fall in pressure during diastole
Which blood vessels regulate TPR and therefore..?
arterioles
…and therefore regulate tissue blood flow and flow and pressure in the capillaries
In any tissues where arterioles constrict what effect does this have on:
- arteriolar resistance
- loss of pressure
- tissue flow
- flow and pressure in capillaries
- increase
- increase
- decrease- flow=(ABP-VP)/resistance
- decrease
In any tissue where arterioles dilate, what effect does this have on:
- blood flow
- pressure in capillaries
both increase
Which type of nerve fibres are present on all arterioles and regulate arteriolar resistance?
sympathetic noradrenergic
but v sparse on cerebral arterioles
CNS generates tonic sympathetic activity to…
all tissues
How does sympathetic activity lead to tonic vasoconstriction?
- ↑ released of NAd from nerve fibres
- increased stimulation of alpha adrenoreceptors on smooth muscle
- increased intracellular [Ca2+]
- leads to vasoconstriction
How does increased sympathetic activity affect vasoconstriction?
greater vasoconstriction
How does decreased sympathetic activity affect vasoconstriction?
lesser vasoconstriction and more dilation of arteries
Which nerve fibres are used to maintain normal level of TPR and ABP?
sympathetic nerve fibres
sympathetic nerve fibres work via what homeostatic reflex response and role?
baroreceptors and baroreceptor reflex to correct changes in ABP
How does a fall in ABP lead to reduced blood flow to tissues?
- generalised ↑ sympathetic nerve activity to arterioles except brain !!
- vasoconstriction -> ↑ TPR and ABP
- ↓ blood flow to tissues
What causes arteriolar dilatation when ABP rises?
↓ sympathetic activity
sympathetic nerve fibres respond to what? 2
baroreceptors- fall in ABP-> dec blood flow to tissues
change in body temp: hot-> more blood to skin for heat loss
How do sympathetic nerve fibres respond when the body is hot?
- reflex ↓ of sympathetic actvity to skin
- causes dilatation and ↑ sympathetic activity to muscle, intestines and kidney
- redistributes blood flow towards skin for heat loss
when the body is hot, sympathetic nerve fibres increase symp activity to where? 3
muscle, intestines, kidney
…less to skin
= redistr blood flow to skin for heat loss ☺
Name two areas where there is an ↑ sympathetic activity -> vasoconstriction during excercise and eating?
to all arterioles inc skeletal muscle and GIT
How do sympathetic nerve fibres respond when the body is COLD?
opposite…
- reflex ↑ of sympathetic actvity to skin
- causes constriction and ↓ sympaethic activity to muscle, intestines and kidney
- redistributes blood flow towards muscle,intestines, kidney for heat conservation
What is functional hyperaemia?
↑ in blood flow to an active tissue
↑ functioning
Name one muscle which experiences functional hyperaemia and in what condition?
skeletal muscle during excercise
affect of increased metabolism in functional hyperaemia, on arteriolar dilatation?
increased
What causes [arteriolar] dilatation in functional hyperaemia?
substances such as K+, adenosine, inorganic phosphate released into interstitial space when tissue cell activity increases
3 types of substances released into interstitial space when activity of tissue cells increases? -in functional hyperaemia
K+ (efflux furing APs)
adenosine, inorganic phosphate (metabolites of ATP)
tissue specific substrates
affect of dilatation on blood flow through arterioles?
increases as
- ↑ shear stress on endothelium
- ↑ release of NO and PGs- further dilatation
In functional hyperaemia what can be released to further dilate the vessels?
NO and prostaglandins
whats dilatation in functional hyperaemia impaired by?
endothelial dysfunction
- as inc blood flow thru arterioles-> inc shear stress on endothelium usually…. and NO and PGs released- more dilatation
Local hyperaemia is where nuerones are activated. Where does this occur?
brain
What effect does local hyperaemia have on total brain blood flow?
stays the sAME
What would happen without pressure autoregulation and the response of cerebral arterioles when cerebral blood flow reduces?
faint
too much dilatation
What would happen without the pressure autoregulation and the cerebral arteriolar response to increased cerebral blood flow?
stroke
too much constriction
where/when does functional hyperaemia occur?
skeletal muscle- exercise
cardiac muscle- exercise and whenever work incre
sweat glands- when activated w body temp
salivary glands- chewing
smooth musc + glands of gut wall- meal digesting
graph: how does metabolic activity compare w tissue blood flow?
directly proportional
/
/
/
/
/
whats pressure autoregulation?
smooth muscle responds to stretch… control myogenic dilatation and constriction
What does myogenic dilatation prevent when cerebral blood flow drops?
fainting
what does myogenic constriction prevent when cerebral blood flow increases?
stroke
how does brain blood flow change w diff mABPs?
remains constant
What helps to restore arteriolar co2 and o2 in the brain during moderate to severe respiratory disease?
CBF increases
..anxiety/panic attacks, CBF falls
cerebral blood flow change in
a) mild-mod resp disease
b) mod-severe?
a) no increase. brain remains hypoxic
b) increases- restore CO2 and PO2
how do arterioles affect regulation of blood flow to diff tissues? equation
major contribution
flow= ABP/ vascular resistance
how can arterioles be constricted/dilated?
by changes in symp nerve activity AND by local influences
role of arterioles?
regulate tissue blood flow and pressure in capillaries
- Capillary exchange and venous return to heart
what are capillaries and what flows through?
simple tubes of endothelial cells
RBCs flow through in single file
what 2 things exchanged via capillaries?
solutes- o2, gluc, aas… waste products and metabolites
fluid- plasma minus plasma proteins
By which process do solutes such as glucose, amino acids and oxygen pass through the endothelial cells into interstitial space?
diffusion
What does the process of fluid exchange help regulate?
circulating blood volume
what waste products pass from tissue cells -> plasma?
[capillaries solute exchange]
CO2, K+, adenosine, Pi ….
by diffusion
What is fluid exchange?
movement of plasma into interstitial space
Why are proteins not moved with the plasma in fluid exchange?
cannot cross the endothelial cells
what kind of walls do capillaries have?
endothelium, no vasc smooth muscle
3-6 uM diameter
inetrmittent blood flow- can be more/less continuous
When arterioles constrict what effect does this have on arteriolar resistance?
increases.
more pressure lost. reduced
Why are rbcs more likely to block temporarily at the opening of a capillary?
reduced pressure and rbcs close in size to capillaries
flow stops until RBC freed again
What can regulating the diameter of arterioles increase and decrease, for exchange?
capillary surface area
What happens to the velocity of blood flow as the number of branches increases?
[capillaries]
decreases
Why is velocity lowest at capillaries?
higher at arterioles and venules, then highest at arteries and veins
allows time for exchange
highest total cross sectional area.
can be inc/dec by arteriolar dilatation/ contriction
What is the equation for the rate of diffusion?
p x (c1-c2) x A
p = permeab of endothelium (c1-c2) = conc gradient across cap endothelium A = SA of capillaries, num of caps with flow
rate of diffusion…p x (c1-c2) x A
how does P change for capillaries?
Permeability of endothelium= constant for given capillary - except in inflammation
What happens to the rate of diffusion when arterioles dilate and tissue blood increases during functional hyperaemia?
increases
steeper conc gradients, esp when tissue metab increased
more caps- better perfused w blood
- blood carried quicker
What happens to the rate of diffusion when arterioles constrict and tissue blood flow decreases during sympathetic vasoconstriction in haemorrhage?
decreases
term given to the process by which fluid moves across the capillary endothelium?
filtration
Filtration depends on the balance of which two forces across the wall of the capillary?
hydrostatic and osmotic
osmotic pressure is mainly exerted by proteins and is therefore called?
oncotic pressure
hydrostatic pressure is also called…
and what is it
fluid pressure- heart pumps blood, leaves by aorta.
fluid p= whats left by time blood gets to caps
Between oncotic pressure and hydrostatic pressure which one pulls water into the capillary and which one pushes water out of the capillary?
oncotic pulls water in
hydrostatic pushes water out
starlings forces
whats changes in CHP caused by?
arterioalr dilatation/constriction
What can cutaneous dilatation lead to when a person is hot?
oedema
as arteriolar dilatation: net fluid out > net fluid in
when may arteriolar constriction (net fluid in> fluid out) opposite of oedema, occur?
e.g. in muscle, skin, GIT, during haemorrhage
How does an increase in plasma oncotic pressure help restore blood volume in states of dehydration?
increased plasma proteins so more net fluid in than net fluid out
How can malnutrition and liver failure lead to oedema?
- ↓ in plasma oncotic pressure due to less plasma proteins
- ↓ gradient between plasma oncotic pressure and tissue oncotic pressure
- ↑ net fluid out than in
- fluid accumulates in interstitium
How does inflammation or infection lead to oedema?
- ↑ in vascular permeability to protein
- protein leaks out and ↑ tissue oncotic pressure
- ↓ gradient between POP and TOP
- fluid accumulates in interstitium
How can the the importance of the lymphatic system be explained through the total amount of fluid filtered in and out of the body in 24 hrs?
capillaries
20L filtered out
16L filtered in
net loss of 4L from CVS every 24 hrs, lymphatic system returns excess fluid
What feature of lymphatic vessels increase pumping which helps fluid move along capillaries?
smooth muscle
wheres the entrance of
a) right lymphatic duct
b) left lymphatic duct
a) right subclavian vein
b) left subclavian vein
What prevents fluid going back into thoracic ducts?
valves
What is the consequence of slow drainage if outward filtration is greater than lymph drainage?
oedema
excess fluid accum in tissue space
What do the veins and venules determine the filling of in diastole?
filling of ventricle
How does the structure of veins and venules reflect their function?
thin walled, intima is made of endothelium and media has little elastin and lots of smooth muscle
how does oedema occur?
- physiologically
- pathologically?
- when out filtration> lymph drainage
e. g. hot in hands/feet/muscle during exercise - vasc perm ↑ e.g. inflamm/infection
lymphatics blocked e.g. elephantiasis, surgical removal
What material allows the veins to fill more with only small changes in venous pressure?
collagen in adventitia
what special function do venules and veins have?
advantage?
capacitance/reservoir- normally elliptical when supine (lying down)
- fill more, become circular- store blood
- determine filling of ventricle in diastole (EDV)
What effect does an increase in blood volume in systemic venous vessels have on central venous pressure?
increases
What force increases pressure in all vessels below the heart when standing?
gravity
how does pressure/vol graph differ for artery and vein?
artery= dir prop vein= small inc in pressure= large inc in volume (able to fill) up to a point then need a lot more pressure (steeper)
when collagen unfolded, furtehr changes in vol= LARGE changes in CVP
What effect does standing have on the arteries?
withstand stretch so ⬆ artery pressure
What effect does standing have on the venous vessels?
venous pooling, ⬆ leg vein pressure, venous distension and ⬇ central venous pressure
redistribution of blood volume
In HF: impaired ventricular contraction and distended ventricles and central veins when lying. What effect does heart failure have on central venous pressure?
increases
What might a person experience if they are standing for a prolonged period of time?
oedema in feet and lower legs and varicose veins excerbated
what condition might ascites, and oedema in feet and legs be indicative of?
HF
increased sympathetic activity leads to venoconstriction. What effect does this have on CVP?
increases
decreased sympathetic actvity leads to venodilatation. What effect does this have on CVP?
decreases
symp NAd-renergic nerve fibres. where foes NAd act on?
alpha adrenoreceptors
the skeletal muscle pump causes the contraction of leg muscles to push blood in the veins towards the heart. What effect does this have on CVP?
increases
the respiratory pump involves inspiration to pull blood in the veins towards the heart. What effect does this have on CVP?
increases
skeletal muscle pump and resp pump (roles in CVV and CVP) are accentuated and impaired when?
acc in exercise
impaired in sick and elderly
what does filling of central veins determine?
filling of R ventricle, EDV, SV therefore. by starlinngs law
what do changes in SV contribute to?
changes in CO
CO= HR x SV
thus in ABP
ABP= CO x TPR
- physiological regulation of BP and BV
what affects ABP ACUTELY?
ABP= CO x TPR
- changes in HR, SV and/or TPR
change in autonomic nerve activity/ local influences on heart + blood vessels
what affects ABP CHRONICALLY?
healthy aging- lose elasticity/inc stiffness of larger arteries
- inc SP, dec DP, mABP may not change
essential hypertension: maintained inc TPR-> inc ABP
renal disease: similar effects
changes to ABP- acutely
when may ABP
- increase
- decrease
- cough/sneeze/ response to pain/alerting stimuli/stressors
exercise-static (weightlifting, carrying, pushing) - cutaneous vasodilatation when hot
when standing (venoud pooling, dec CVP,EDV, SV, CO, ABP)
haemorrhage, dehydration, dec BV, dec CVP…
changes in ABP- effect on tissue blood flow?
flow = ABP- VP/R
low ABP= low flow= low O2 delivery
dec ABP faint
inc ABP stroke
requirement of ABP for tissues to receive O2?
needs to be raised
HF= dec CO= dec ABP= dec tissue blood flow
why does inc ABP inc workload for heart- afterload?
heart must inc force of contraction to maintain SV
important in coronary artery disease-> angina-> infarction
chronically raised ABP(hypertension)
what affect blood volume ACUTELY?
balance in
- fluid intake (drinking/transfusion)
- fluid loss (sweating)
what affect blood volume CHRONICally?
what reduces and what increases?
fluid loss from gut- diarrhoea, vomiying- redu BV
poor renal func- fluid retained- inc BV
HF- fluid retained and distends ventricle- inc BV
affect of distribution of body fluid between CNS and interstitium affect BV?
supine v standing- venous pooling- oedema in lower limbs
between CNA and tissue fluid- oedema assoc with inflamm, low plasma protein, impaired lymoh drainage
what do factors affecting BV specifically affect?
venous capacitance vessels
in a healthy person, why do we need to correct INC/REDUCED central blood volume?
increased CBV: inc CVP
raises CO and ABP
excess fluid needs to be lost via kidney
reduced CBV: dec CVP
reduces CO and ABP
HF and oedema affect on blood volume?
inc (inc CVP)
adds to filling + distension of vent and exacerbates problems
swelling impairs normal tissue func- reduces BV and ABP, exacerbates problems
what does the baroreceptor reflex do?
homestatically regulates ABP
i.e. pressure in elastic and large arteries
how do baroreceptors respond to inc ABP and dec ABP?
inc: inc afferent activity
dec: dec afferent activity
baroreceptor reflex
look at diagram page 10 s1w8
role of baroreceptors?
constantly monitoring ABP and correcting it
dampens changes in ABP
when is baroreceptor reflec sensitivity reduced?
when does it have higher set point?
reduced in anxiety/stress= allows ABP to reach higher values
higher set point (resting level of ABP) in hypertension
baroreceptor reflex- what does it do in HF?
MAINTAINS ABP in HF
volume receptor reflex- what are volume receptors and what affect them?
stretch receptors in right atrium…
changes in CVP (filling of veins)
-REAL changes in BV
-changes in distr of BV- posture
homeostatically regulate BV!!
volume receptor reflex- affect of…
- inc stretch
- dec stretch
- inc afferent activity
- dec afferent activity
afferents-> via vagus (X) to CNS
volume receptor reflex- affect of DEC BV?
⬇ afferent activity-> medulla
⬆ symp activity to kidney-> vasoconstriction
⬇ renal perfusion… flow=ABP-VP/R
⬆ renin release, ⬆ AngII…. renal tubules absorb more Na+
⬆ ADH release…. renal tubules absorb more water
⬇ urine vol helps ⬆ BV
volume receptor reflex- affect of INC BV?
opposite effects on kidney…. reabsorbs less Na+ and water
opposite to
[⬇ afferent activity-> medulla
⬆ symp activity to kidney-> vasoconstriction
⬇ renal perfusion… flow=ABP-VP/R
⬆ renin release, ⬆ AngII…. renal tubules absorb more Na+
⬆ ADH release…. renal tubules absorb more water
⬇ urine vol helps ⬆ BV]
how long to get volume receptor reflex-> effect?
continually monitoring central BV and correcting it…
20-30 min for effect
when is volume receptor reflec sensitivity reduced?
when does it have higher set point?
reduced in HF, renal failure- allowing BV to get higher values
higher set point (level of CVP) in HF, renal failure
speed difference in affects of baroreceptor and volume rec?
BRR effects on ABP FASTER than VRR effects on BV
reflexes keep ABP and BV at rest, lower than what they would otherwise be
what do BR and VR continuously monitor and adjust?
ABP and CVP to persons own set points (good or bad)
- Integration of the CVS physiology-> pathology
baroreceptor and volume reflex when ABP/BV falls…. look at diagrams s1w9
Essential hypertension- how diagnosed?
chronically raised ABP (>140/90)
no known cause
whats hypertension associated w?
ageing stress obesity high salt intake insulin resistance sentariness genetics
hypertension is a major risk factor for….
stroke MI peripheral vasc disease CKD HF!!
hypertension may be w increased TPR… whats this mean/indicate?
increased symp nerve activity
hypertension is associated with what in terms of vasodilatation?
blunted endothelium-dependant vasodilatation
whys symp outflow to CVS INCreased in essential hypertension?
increased descending excitatory activity down SC.. neurodriven
resting ABP increased and TPR inc from inc renal constriction, muscle+ splanchnic vasoconstriction, HR, contractility
affect of hypertension development on symp nerve activity to muscle, splanchnic circulation and kidney
increases
hat causes symp nerve activity to further increase (after essential hypertension develops)?
obesity obstructive sleep apnea (snoring and stop breathing) congestive HF metabolic syndrome renal failure
how does symp activation in hypertension and associated disorders –> further CVD development?
has adverse CV and metabolic effects
- vasoconstriction (hypert)
- tachycardia
- large artery stiffening+remodelling (hypert)
- insulin resistance (metab)
- inc coagulation
- cardiac electrical instability
how is baroreceptor reflex different in hypertnension?
still corrects changees in ABP…
set point is ⬆, i.e. correct ABP to new higher level of resting BP
how does cerebral autoregulatory range change as hypertension develops?
increases-
helps protect against strokes
eventually, at risk of stroke, HF, renal disease etc as ⬆ stress on organs
b) Haemorrhage-> irreversible shock
when will it occur?
when aortic BP < 45% (even at 60% with transfusion)
= decompensated!! = irreversible shock
6 hours
what will BRR and VRR do to respond to haemorrhage?
inc symp activity: arterioles, constric(actually will cause the problems not solve), dec cap HP, inc TPR
⬆ ADH, ⬆renin, AngII…. vasoconstriction, ⬆water, Na+ retention by kidney
how is mild-mod haemorrhage (10-35% BV) compensated for?
reflex:
- ⬆HR, ⬆vent contractility
- venous +arteriolar vasoconstriction
- ⬆filtration fluid INTO caps from tissue spaces
- water, Na+ retention by kidney
over 2-3wks
- ⬆RBC aynth (EPO)
- ⬆plasma protein synth
how is more sever haemorrhage (>35%) treated?
without transfusion?
BR and VR CANNOT correct ABP
strong reflec vasocons in:
- kidney -> renal failure
- GIT -> liver failure
ABP< cerebral autoreg range: dec brain blood flow- unconscoius- coma!!!
what mechanisms involved during multiple organ failure- irreversible shock?
neutrophils activate, inflamm mediators release
endothelial dysfunction,
vasc smooth muscle= unresponsibe to vasoconstrictors
myocardium depressed as cytokines around bloodstream
ABP dec more-> DEATH
c) resp-cardiovasc interactions
2 types of resp influences on heart?
mechanical interaction
neural interaction
describe mechanical interaction- resp influence on heart
inspiration->…
⬆ venous return to RV
⬆ right SV (starlings law)
⬆ left EDV and SV
describe neural interaction- resp influence on heart
inspiration->…
⬆ HR
respiratory sinus arrhythmia
resp sinus arrhythmia (neural interaction resp influence on heart) how is it done? (2)
central resp neurones and pulmonary stretch receptors
- inhibit cardiac vagal neurones
voluntary hyperventilation metal stress/anxiety systemic hypoxia-periph chemorec input systemic hypercapnia- central chemorec input exercise muscle+ joint recs input ... CNS.... to ⬆HR!!
pic on p20 s1w9
exercise in health- effects of exercise in a healthy person?
image also on p24 s1w9
⬆ resp (maintain PaO2, remove CO2)
⬆ HR and contractility (⬆CO)
vasoconstriction in splanchnic circ + kidney… balanced by
vasodilatation in exercising and cardiac muscle
= ⬆ O2 delivery to working muscles and away from other tissues
ABP maintained/increased
cerebral blood flow maintained by autoregn
hows cerebral blood flow maintained by autoregn in exercise? 2
- exercise reflex- sensory receptors in muscles
- functional hyperaemiain working muscles, depends on endothelium dependant dilatation- locally released metabolites and shear stress acting on endothelium: NO, PGs
effects of exercise on ventricular function in a healthy person?
⬆SV x ⬆HR = ⬆CO
SV ⬆ by reflex ⬆ in symp activity to vent muscle, at given EDV
EDV ⬆ by skeletal muscle, resp pump and symp vasoconstr= ⬆venous return to heart
graph on p25 s1w9
why CVD patients cant do dynamic exercise (cardio) but can do static (weights)?
cardio: inc O2 consumption, HR and ABP ⬆ and remain high for longer.
muscles in action, BV cant dilate (diastolic)
d) HF and exercise intolerance
signs + symptoms of HF?
tired cough shortness of breath pulmonary oedema: compromised by poor CO and pleural effusion (around lungs) pumping action of heart=weaker ascited: ⬆ fluid from circ, in tummy oedema in ankles, legs
CHF- 50-60% people will die within 5 yrs of diagnosis
avg age= 76 yrs
a risk factor for young ppl developing CHF?
coronary artery disease
2 types of CHF?
HFrEF: reduced ejection fraction (<50% EDV-ESV)
- systolic dysfunction- dilated vent- IMPAIRED CONTRACTION
HFpEF: preserved ejection fraction (>50% EDV-ESV)
- diastolic dysfunction- still vent wall- LIMITED FILLING
three common links/ risk factors with HFrEF and HFpEF?
aging
obesity
NT-proBNP
different characteristics of HFrEF and HFpEF?
HFrEF
- men
- MI
- smoking
- myocardial cell death
HFpEF
- women
- AF
- renal dysfunction
- urinary albumin loss
NYHA classification of CHF categories?
I: no limit of physical activity
II: slight limit. dyspnoea and fatigue w mod activity
III: marked limit. dyspnoea with minimal activity
IV: severe limit of activity. symptoms at rest
hows starlings relationshiop (SV/EDV graph) different for
- HFrEF
- HFpEF
- ⬆EDV and ⬇ capacity to maintain normal SV… to the right and flat
- normal SV, little ability to ⬆SV further by ⬆ing EDV… same but lower
affect of low SV on ABP?
become low too….
CO=HR x SV
ABP= CO x TPR
LINKED
affect of compensatory mechanisms on primary condition i.e. HF?
worsen it!
decompensation
- ⬆overfilling of heart and veins- ⬆ preload
- ⬆afterload (arteriolar constriction)
- blunting of endothelium dependant dilatation
- need therapeutic treatment: vasodilators, diuretics, B blockers, inotropes
consequence: HF accompanied by exercise intolerance
p34!!!
..
General cause of myocardial infarction
Blockage of coronary artery, which is caused by clot.
Infarction: region of cell death/necrosis
What does Peripheral Oedema refer to?
fluid accumulation in tissue spaces i.e. outside of systemic circulation
Pulmonary Oedema
Fluid accumulation in lungs
Prevalence:
proportion of people with given disease
Incidence:
number of new cases over period of time, usually per year
Relation of
Systemic vascular resistance (total peripheral resistance (TPR)) to pulmonary vascular resistance
Systemic vascular resistance (total peripheral resistance (TPR)) is ~7 times greater than pulmonary vascular resistance.
As consequence: left ventricular wall much thicker than right ventricle as it has to do more work, and pressures developed in systemic arteries higher than pulmonary
Systole and Diastole:
Systole: contracting phase of cardiac cycle. highest pressure in aorta
Diastole: Filling phase. Lowest pressure in aorta
What is TPR (Totalperipheral resistance) mainly due to in systemic circulation?
Resistance of arterioles (the major resistance vessels of whole system. circ) where most pressure is lost = high resistance to blood flow: energy lost
If vascular resistance in particular tissue increases:
Pressure in the capillaries of that tissue would be expected to decrease
because:
resistance of arterioles must’ve increased as they’re main site of vasc resistance in each tissue, same as whole circ.
If arteriolar resistance increases, more pressure lost in going through them, reduced in capillaries.
then, venous pressure also falls.
Describe large veins
Distensible and can be elliptical/ circular in shape
However, when blood volume increases they begin to fill - become more circular. A similar change happens in the veins of the lower limbs when you move from supine to standing because of the effects on gravity. The veins below heart levels become distended. This is known as venous pooling.
