cardiac output Flashcards
Cardiac output is the - of — ejected from a — per — (L/min)
- — circulations, both ventricles eject the — volume
* It is the product of — and the —
- volume ejected at each — x —-
- CO = – x –
* The textbook person* has a cardiac output of approximately 5 L/min
= ~70 ml x ~70 bpm = ~4,900 ml/min = ~5 L/min
* CO correlates with – , to account use the —
- CO is expressed as L/min/m? (2.5 - 4 L/min/m2)
volume
blood
venteicles
per min
closed
same time
stroke volume and heart rate
beat x number of bears per min
heart rate x stroke volume
size
cardiac index
control of cardiac output :
- its controlled by controlling either or both of —- and —
- this is regulated by —- through — , — , – reflexes
- —- regulation of —
- regulation via —
heart rate and stroke volume
autominc nevrous system
sympathetic parasymethatic and baroreceptor reflexes
intrisnic of cardiomyocytes
atrial reflexes
- SA node aka sino atrial node is the — as its — due to the —- membran , it is — to — so spontanously —
- at rest Na+ and some k+ leak into the cell and slowly — it via the —- and down its — and —
- the HCN channels are —- activated and —- gated and so — the current in the presence of —
- around — mv , slow —- channels will open and the cell —
pacemaker
unstable
leaky
leaky
cations
depolarises
depolarising it
funny HCN channels
concentration and electrical gardient
hyperpolarisation activated
cyclic nucleiotide gated
increase
cyclic nucletodie
-40 mv
voltage gated L type Ca+ channels
depolarises
the SA node action potential:
at the beging we will have – leak influx by which — channels open and then we will have — and — close with — efflux
AP is —
RP is —
na+
ca+2
k + ca+2
k+ efflux
-40mv
-55mv
PLS CHECK PHOTO SO IMPORTANT
sympthatic nervous system:
often thoight as — the SNS primarly acts via —:
- noradrenaline released from — aka —
- adrenaline from stimualtion of — aka —
- primarily bc — and — is synpthatic but –
- broadly speaking this will increase — , — , —
- they wull also act on — and chnage in the ditribution of —
fight or flight
catecholamine
nerve ending aka neurotrasmitters
adreal gland
hormone
sweating and piloerection
ACH
heart rate stroke volume and blood pressure
artries
flow
SNS action on the heart:
- SNS action is mediated via — and –
- most important adrenocrecpetor for the heart is —
- theres also a1 and b2 AR but not as important
- B-ARs are linked to – and so increase —
- these are present throughout the — as SA , AV artria and ventricles
- these are stimulated by — from —- nerves also by circualting —
- increasing the funny current through HCN channels — the rate ( HCN : hyperpoalrisation activraed and cylic nuceltoide gated )
alpha and beta adrenorecpeotr
b1 adrenorecpetors
Gs ( proteins ) and cAMP
heart
noradrenaline
sympthatic nerves
adrenaline
increase
if we increase sodium flux we will move from — to — so basically heart rate will –
slow and steady
to faster and rapid depolirisation
increase
( please check slide )
adrerngic action on the myocyte:
- the b adrenrocrepetors are found throughout the —
- in the myocyte ( atria and ventricles ) the increased — from —- activation increases the entery of — into the cells
- more === binds to — meaning more — can form and will increase the –
myocardium
cAMP/PKA
B-AR
ca+2
ca+2
troponin
cross bridge
force of contraction ( so basically stroke voulme will increase)
parasymptahtic NS:
- they act via – on — ad — receptors
–> nicotinic are — found in – and —
—> muscarnic are —
- PNS innervation of the heart is via — and —-
–> the vagus is —
—> the m2 is linked to — so — the cAMP
- the vagal innervention and recptors are mainly around the — and — so theres little if any innervention on the –
- PNS activation will — the heart rate and cardiac output
—> by – the HCN channels
ACh
muscarnic and nicotinic cholegnic receptors
ion channels
nerves and skeltal muscles
g prorein coupled receptors
vagus nerve and M2 cholingeric receptros
cranial nerve X ( CNX)
Gi
decrease
atria and S node
ventricles
decrease
closing
so basically:
- sympathetic works in — through — and — sodium entery
- paraysympthatic works in — by —
noradrenaline
b1 adrencorecptor
more
acytecholine
m2 receptor
ANS overview:
- SNS increase the — and –
since CO = HR X SV
- sympathetic agonsit are — chronotropes which basically — the — and — inotropes will – the —
- whole b-blokcers aka atenolol are — chronotropes which – the — and — inotropes which – the —
- parasymapethic nervouse systemic decreases only —
–> Ach is a – chronotropes
–> atropine ( aka – ) is a — chronotropes
heart rate and force of contraction
+ve
increase
rate aka time ( chron= time)
+ve
increases
force
-ve
decrease
rate
decrease
force
heart rate only
-ve
muscarnic antagonist
+ve
nervous control of the heart:
- both SNS and PNS innervates the — and — controlled by the — of these 2
- tachicardia is a sign of — activation through excersie , anxiety , as the SNS can increase rate to —
- both are – at rest , in normal indiviuals b blockers can drop heart rate from — to — showing — action
- the intrisic rate of SA node is about — it is – stimaultion that gives the “normal” —
–> atropine , the muscaric anatognost will cause —
SA node and heart rate
baalcne
sympthetic action
200bpm
active
7- to 60 bpm
SNS
100
vagal
70 bpm
tachycardia
intrinsic regulation:
- the cardivauclar system is a — system
- the amount of blood returning must – the amount of blood ejected so basically the — return — the 000
- the heart has the — ability to adapt to changed in blood volume ( intrisnic in that its not dependent on — regulation as nerves )
- this is a —- of the heart
closed
equal
venous return
cardiac output (VR =CO )
intrisinc
external
frank starling law
the frank starling law:
- named after otto frank and erest h starling
- they independley did experiments investigating the effect of the filling pressure of on the stroke volume
- the greater the degree of — the grater the — of the contraction of the myocyte
- increasinf the – increases the —-
degree of stretch
force of contraction
preload
stroke volume
mechanics of starling law:
- actin and myosin are brought together as myocardium — this leads to increased — and increased —
- the increased overlap allows for more — to form and greater — to be generated , which mat involve in increased sensiitvity to —
- this is not a — relationsjop , if the muscle is stretched too much the number of cross bridge formed — and so does the force generated
- this is the same idea as the lenght tension rs
stretched
filling
stretch
cross bridges
force
ca+2
linear
falls
basis of the length tesion rs :
- at low stretch , the area of the thin filmanets are — for cross bridge formation
—> the z discs are – together
—> minimal room for—
- as preload is — more binding sites of action becomes —
–> so a — contraction is possible
- as the stretching continues beyond the optimal stretch , the overlap between the filments begin to —
- fewer cross bridges mean – force and eventuallu overlap will cease togther
unavailable
close
shorteing
increased
actin
available
stronger
decrease
less
factors affecting preload:
- preload is an umberlla term to describe — during —
- so basically its a term that describes —
- ventricullar filling is affected by many things such as — of the atria , — pressure , — and the — of the blood in the cirulation
- each of these will impact n ventricular filling and so in return the stroke volume and cardiac output
ventriucllar filling
disastole
end diastiolic volume
pressure
venous
gravity and filling volume
blood volume and venous tone:
- the great veins act as capactance vesseles for — of the blood
—> viens contain — of total blood volume at any given time
- an increase in blood volume results in increased — and hence increased –
–> equally an increased — will also increase the —
- it follow then that low blood volume ( dehydration or haemorrage ) will — preload
storage
60-70%
central venous pressure
preload
venous tone
central venous pressure
decrease
- blood returning to the heart has to work – gravity
—> this is also true for atrial blood going to the –
– > giraffes have blood pressure of ~260 mmHg (3.5 m of h20 ) - when upright , this is a – factor for venous return
–> this is basis of postural hypotesnion on standing
–> this is especially true if – is suppressed or struggling - in supine ( lying flat) position the venous return is —
–> this also contribute to pulmonary congestion sand othopenea
–> breathlessness when lying glat as can occur in heart failure
against
brain
-ve
ANS
increased
the muscle pump ( it bascially helps blood get back to the heart from ur feet) :
- veins have — that prevents back flow and only permit blood to move towards the heart
- in limbs large veins pass between — and are compressed as —-
–> to a lesser extent this happens an adjacent artery pulsates
- this compression displaces the blood and the presence of the valves mean it must go back towards the heart
- the pump is activity related , increased activity causes — venous return
valves
muscle blocks
muscle contraction
increased
thoracic pump:
- the flattening of the — on — , – the abdominal pressure and — the thoracic pressure
– > blood moves from the — into the —
—> or stays below — in the –
- the reversal of this is — which — the abdonomal pressure and — the thoracic pressure
–> the blood moves from the– into the –
–> thus will move – during the next —
diaphram
inspiration
raises
lowers
abdomen
thorax
abdomen
legs
expiration
lowers
raises
legs
abdomen
up
inspiration
brainbridge or atrial reflex:
- the other link between preload and cardiac output is — which is also known as brainbridge reflex after work of arthur brainbridge
- — right atrial pressure when preload is increased will activate the — receptors in the –
- these afferent signals are processed in the —
–> the cardiovasuclar centre
—> similar to barorecpetor reflex
- will increase the atrial stretch so theres is an increase of — output and —
atrial reflex
increased
stretch
atria
medulla oblongata
sympthetic
heart rate
starling vs contracility:
- the starling law of the heart increases the — by changing the — of the —
- +ve inotropes like sns — contracility by changing —
- these are 2 independent mechanisms so their effects are —
- an inotrope will increase the — for any give preload
stroke volume
orientation
fibres
increase
ca+2 signilling
additive
force of contraction
( check slide pls)
afterload and stroke volume:
- changes in preload affects the — of the ventricules as the – increases so does the —
- the pressure in the atriel system the blood is ejected into also affects —
- an — afterload will — the cardiac output in the short term
filling
preload
filling
cardiac output
increased
decreased
- as the stroke volume – the end of systolic volume –
-> atrial filling remains —
-> the end of diastolic volume is — - increased end diastolic pressure ad increased stretch of the ventricles leading to more —-
–> cardiac output is mainated at greater work
drops
raises
unchanged
increased
forceful contraction
