functioning of the heart Flashcards
what is the composition of blood vessels?
- elastin; can stretch and recoil
- collagen; tough and flexible
- endothelium - single cell layer + mainly in capillaries
- smooth muscle; contracts/reflexes and is in all blood vessels except capillaries; surrounds lumen circularly
what do the endothelium release in response to shear stress?
they will release NO or PGs to act on smooth muscle and cause tonic dilation
and they will cause inhibition of RBC, platelet and neutrophil adherence so atherosclerosis can occur
what is endothelium dysfunction?
- it is when impaired dilation can occur
- vasoconstrictor PGs, endothelin and adhesion molecules which attracts platelets and neutrophils to artery walls
- so inflammation, atherosclerosis and CV risk
what is the structure of the elastic arteries?
you have the intima, media and the adventitia
intima is endothelium, media is smooth muscle and elastin and adventitia is collagen
- the elastic arteries converts intermittent flow from heart to continuous for the rest of circulation
how do elastic arteries act in systole and diastole?
systole; elastin stretches and the systolic pressure rises in the elastic artery. valves are open
diastole; elastin recoils giving energy to blood, pressure kept high by elastic recoil and valves are closed
-collagen limits stretch of artery in systole
what is the arteriole pressure wave?
graph where at systole pressure increase until it hits a peak
then small decrease as aortic valve closes and then increases for small peak and then decrease during diastole
when it decreases to 80mmHg this is when aortic valve opens
how to calculate pulse pressure and mean ABP from SP and DP?
PP = SP- DP
mean ABP = DP + 1/3(PP)
what factors influence ABP?
- inflow into aorta during systole (CO)
- the TPR of blood leaving aorta during diastole
- composition of aorta
what happens as patients age?
they have stiffer aorta so less stretch and recoil; lose elastin
- high TPR so high DP
- higher SV so increase ventricular contractility
- high SP but lower DP
what muscles determine the TPR?
the arterioles- most pressure is lost here
muscular arteries contribute to a small extent
what are arterioles surrounded by and what do they supply?
they are surrounded by interstitial fluid and tissue cells
supply capillaries
what do arterioles regulate?
TPR, tissue blood flow and capillary pressure
- can have arteriole constriction in different tissues; increases ABP - more constriction so more resistance so can lose more pressure and tissue flow so decreased pressure in capillaries
- can have constriction and dilation of arterioles in different tissues; ABP doesn’t change much
how can you regulate arteriolar resistance?
use sympathetic noradrenergic nerve fibres
- form a network around vessels
sympathetic activity- release of Nor from nerve fibres so more intracellular Ca2+ so more vasoconstriction
when are sympathetic nerve fibres used?
- maintains TPR and ABP
- used in reflex response to correct any ABP changes
when ABP falls more sympathetic activity for vasoconstriction to increase ABP and TPR - reflex response to body temp change
- when hot less sympathetic activity so more dilation and this redistributes more blood flow to skin to cause heat loss
vice versa for cold
what is the local metabolic influence on arterioles when you have functional hyperaemia?
- arteriolar dilation occur
- substances released into interstitial space when tissue cell activity increases ; K+, adenosine, tissue specific substances
- dilation means more blood flow; increased shear stress and more release of NO and PG so more dilation
when and where does functional hyperaemia occur?
- skeletal muscle ; exercise
- cardiac muscle ; exercise and condition
- sweat glands ; body temp change
- salivary glands ; chewing
- smooth muscle and gut wall glands ; digestion
- brain ; activated neurones
how do cerebral arterioles respond when ABP rises or falls?
when ABP rises, there’s a stretch so smooth responds to this by increasing pressure ; this is auto regulation
- blood flow will remain constant
- as pressure increases you have myogenic constriction so increase resistance
too high pressure can lead to stroke and too low too much myogenic dilation so feels faint
what’s the process of cardiac conduction?
impulse generated at SA node atrai contracts impulse to AV node brief delay sweeps to bundle of his goes to left and right bundle branches conduction to purkinje fibres ventricles contract
what is sinus bradycardia?
<60/min
due to depressed SA node function
can have a vagal tone
what is sinus tachycardia?
> 100/min
accelerated SA node firing
due to exercise, stress or HF
what is first degree heart block?
greater PR interval delay
>0.2s or one big ECG block!
slow conduction in AV node so heart block
what is second degree heart block?
intermittently skipped ventricular beat
intermittent non-conducted P waves so a QRS complex absent
when fraction of impulses from atria are conducted
what is third degree heart block?
atria and ventricles depolarise independently
no association
alchemic damage in nodal tissue
what is cardiac cycle made up of?
systole and diastole
systole- ventricles contract so blood -> aorta and P arteries
diastole- relaxed ventricles
what are the phases of a cardiac cycle?
Phase 1= atrial contraction Phase 2= isovolumetric contraction Phase 3 = rapid ejection Phase 4 = reduced ejection Phase 5 = isovolumetric reflex Phase 6 = rapid filling Phase 7 = reduced filling
how does para/sympathetic activity affect HR?
parasympathetic = decrease HR sympathetic = increased HR
what does the autonomic nervous system do?
it modifies HR
contains parasympathetic centre; SA node firing is less so lower HR
sympathetic centre; more depolarisation occurs so HR increases as more pacing of SA node
what are chronotropic agents?
they influence the currents and alter slope of pacemaker and so the heart rate
e.g. noradrenaline
what is positive inotropic agents related and what is negative inotropic agents related to?
+ve agents are related to sympathetic; release Nor and activate the adrenergic receptors which increase myocyte contraction and so heart rate
-ve agents release Ach and binds on to muscarinic receptors which attenuates contract so less binding of calcium to myofilament so decreased HR
what does contraction of myocyte happen because of?
calcium binding to myofilament
how is cAMP produced?
hormones cause beta receptors to make adenylcyclase change ATP to form cAMP
cAMP allows phosphorylation to occur and troponin to be produced
so contractions can occur
how to calculate SV?
SV = EDV - ESV
EDV should usually be 120ml
ESV should usually be 50ml
what is the usual atrial and ventricular pressure and aortic pressure?
atrial = 0-10mmHg ventricular = 0-120 mmHg aortic = 80-120 mmHg
how does preload and afterload influence SV?
preload - filling of ventricles
- pressure increases
- initial stretching of myocytes before contraction
afterload - resistance of blood leaving ventricles into arteries
- aortic pressure must be overcome to eject blood
- higher AP so higher afterload
when does afterload and preload increase?
pre load increases in hypovolemia- high venous pressure and low heart rate
after load increases in hypertension
what is the Frank Starling mechanisms?
- muscle stretching increases calcium sensitivity
- due to ATP energy heart muscles contract more forcefully when muscle fibres stretch
a higher EDV means more muscle fibre length so more cross bridges can be formed between actin and myosin -> more ventricular contractility
how does heart failure affect EDV?
heart failure increases EDV and so decreases SV as less contractility
what does having a myocardial injury lead to?
- reduced CO
- less renal perfusion
- activates RAAS and SNS
- increase HR and myocardial toxicity
- vasoconstriction occurs so more afterload
- this worsens LV function when inhibited by BB, ace inhibitors, aldosterone antagonists
- can all lead to HF symptoms
how does exercise effect CO?
central command -> medulla -> more sympathetic outflow and more vagal tone -> higher HR and more contractility -> more venoconstriction and more blood supply and oxygen to working muscles -> release of vasodilation metabolites so vasodilation -> increase in CVP -> more cardiac work and more CO
what exchange occurs in the capillaries?
- solutes such as oxygen, glucose and amino acids enter interstitial space via diffusion and waste products pass to plasma by diffusion
- fluid - plasma without proteins will go across endothelial cells to IF and back in opposite direction by filtration
what are the characteristics of capillaries?
- endothelium
- 3-6mm
- intermittent blood flow; can become continuous so allows easier exchange
- has large SA
- low speed of blood flow to allow exchange to occur
how does arteriolar constriction affect capillaries?
pressure at capillary opening decreases
no flow
RBC block flow
so capillary SA for exchange is reduced
when does diffusion rate increase?
arterioles dilate and tissue blood flow increases
- functional hyperaemia
and vice versa for diffusion rate decreasing
what is filtration?
when fluid moves across capillary endothelium
depends on:
balance between hydrostatic and osmotic forces across wall of capillary
- measured in mmHg
what does oncotic and hydrostatic pressure do?
oncotic pulls water into arteriolar and hydrostatic pressure pushes water out down a gradient
how is oedema caused?
when there is net fluid out > net fluid in
increase in vascular permeability and lymphatics are blocked
protein leaks out - so tissue OP increases
POP and TOP gradient reduced
outwards filtration > lymph drainage
so oedema
where do right lymphatic duct and thoracic duct enter?
right lymphatic duct enters into right subclavian vein
thoracic duct enters into left subclavian vein
what kind of shape are venules/veins and how do they change?
they are supine usually but can become circular as they fill with blood more
determine EDV in diastole
when you stand how does this affect ur pressure?
when you stand gravity will increase pressure in all vessels below heart
arteries can withstand stretch due to strong muscle
but venous vessels will have venous pooling -> leg vein pressure increases so venous distension; decrease CVP so redistribution of blood vol.
how can heart failure affect CVP?
impaired ventricular contraction
- distended ventricles and central veins
so high increase of CVP
how does skeletal muscle pump and respiratory pump increase CVP?
skeletal muscle pump- contraction of leg muscles pushes blood in veins toward heart
respiratory pump - inspirations pulls blood in veins towards heart so high CVP
