Control of the CVS Flashcards
describe the sympathetic nervous innervation
- though sympathetic post ganglionic fibers
- releases NA as well as A from the adrenal medulla (NA released as neurotransmitter and A as hormones)
- NA/A act on b1 receptors in SA node –> increases pacemaker potential –> increased HR
- NA/A will also act on b1 receptors on cardiac muscles itself and increase Ca2+ influx –> increased contractility (shorter and stronger contraction from more Ca2+ being used up)
- inotropic effect = increased contractility, chronotropic effect=HR
- a1 receptors at arterioles and veins –> constriction (reflex that solves immediate problem by increasing the MAP, long term will result in hypertension because you are constricting both the veins and arteries)
describe parasympathetic innervation
- done by post ganglionic fibers of the Vagus nerve
- release of Ach
- Ach acts on muscarinic receptors of the SA node –> decreases slope of pacemaker potential –> decreased HR
- vagus nerve does not really innervate cardiac muscles, no effect on contractility
difference btw nicotinic and muscarinic receptors
- nicotinic and muscarinic both bind to Ach, but nicotinic will become an ion channel while muscarinic will activate another G protein that will release second messengers
- nicotinic found in the NMJ, brain, para/sympathetic NS
- muscarinic found in the brain, heart, smooth muscles, parasympathetic NS only
preload vs afterload
preload: initial stretching or the cardiac myocytes prior to initial contraction
afterload: load against which the muscle tries to contact during ejection phase.
what is Starling’s law
the initial strength of cardiac myocytes contraction is proportional to the initial length of cardiac muscle fiber
2 things that affect EDV (which directly affects preload which affects the contractility)
- Venous return
2. size of the heart
3 things that directly affect stroke volume
- preload
- afterload
- contractility
effects of Barbituates
is a CNS depressant and slows down HR
- this can be compensated by increasing EDV
what is ejection fraction
SV/EDV: this tells us if something is wrong, sometimes just looking at the stroke volume is not enough
reduced ejection fraction = reduced exercise capacity
how does prolonged heart failure lead to cardiomegaly
kidneys notice that the heart is not pumping enough blood and will try to increase central blood volume by expanding the size of the heart
why does faster HR lead to decreased SV?
because the rapid filling phase of diastole would be cut down and you would end up with decreased EDV –> decreased SV
things that happen during exercise:
- increased HR (decreased para and increased sympathetic innervation)
- increased contractility (shorter and stronger, shortened systole)
- increased venous return (from venoconstriction and skeletal muscle pump and resp pump)
- TPR falls (reduced afterload)
- overall increased CO
things that affect the rising phase and falling phase (systolic and diastolic) arterial pressures?
- SV
- contractility
- Velocity of ejection: stronger ejection –> less time for aorta to absorb energy –> higher systolic pressure
- elasticity of arteries: little elasticity will high higher systolic pressure and lower diastolic pressure
- TPR: less TPR –> less resistance –> lower diastolic pressure
value of mean arterial pressure (at the arteries), and arterial pressure at the following places: arterioles, capillaries, venules/veins, RA
*this is for systemic circulation, pulmonary circulation is 1/5 of this
MAP: 90-95 mmHg arteries: drop from 95 --> 90 arterioles: drop from 90 --> 40 capillaries: 40 mmHg veins: 20 mmHg (systemic filling pressure) right atrium: 0 mmHg
where does blood flow faster?
blood flows faster in the veins and arteries than the capillaries. This is because although individually the capillaries have smaller diameter and therefore should have faster blood flow, capillaries overall have greater cross sectional area than arteries/veins.
5 external influences that can affect blood flow due to distensibility and flexibility of veins
- gravity
- skeletal muscle pump
- respiratory pump
- venomotor tone
- systemic filling pressure
affect of gravity on venous return?
there is no effect on the rate of venous return because gravity affects both arterial and venous blood. However, it decreases EDV, because there is more space at the bottom now less blood is going to return to the heart although the rate is still the same.
decreased EDV –> decreased preload, decreased contractility, decreased CO, decreased MAP
postural hypotension
sudden drop in blood pressure due to change in posture and standing up resulting in light-headedness.
In normal ppl, HR would go up in response to drop in bp for a while and then return to normal, but in ppl with postural hypotension, the HR increases more than normal
describe venomotor tone
contraction of smooth muscle surrounding veins from sympathetic innervation. This is not present around arteries
anti-clotting mechs of the endothelium of blood vessels
- stop blood coming into contact with collagen to prevent platelet aggregation
- produces chemical messengers prostacyclin and NO that will inhibit platelet aggregation
- produces tissue factor pathway inihibitor (TFPI) that stops thrombin production
- expresses thrombomodulin which binds to and inactivates thrombin
- expresses heparin which also inactivates thrombin
- secretes tissue plasminogen activator (t-PA) that will be converted into enzyme plasmin that digests blood clot.
main methods to assess central arterial pressure and central venous pressure
arterial: Korotkoff sounds with sphymonometer
venous: from JVP collapse
2 nerves that carry info from baroreceptors to the brain
- gloasopharyngeal nerve
2. vagus nerve
short vs long term control of blood pressure
- arterial baroreceptors not useful in longterm because bp will eventually stabilise in longterm even without baroreceptors help
- long term is more about controlling blood volume while in short term it is more about CO and TPR
- longterm control tends to have hormonal effects
3 main systems for long term control of bp
- RAAS (renin-angiotensin-aldosterone system)
- antidiuretic factor (ADH, vasopressin)
- artrial natriuretic factor
nervous innervation of the arterial baroreflex
aortic arch baroreceptors - vagus nerve
carotid sinus baroreceptors - glossopharyngeal nerve
both heads to medullary cardiovascular centers
* if there is something wrong with MAP, the medullary center would do smth about it through sympathetic and parasympathetic NS
why does HR increase when you stand up?
drop in EDV –> decreased preload, contractility, CO, MAP –> decreased baroreceptor firing rate –> decreased vagal (parasymp) tone and increased sympathetic tone –> increased HR
describe the valsalva maneruver
- forced expiration against closed glottis: sudden rise in arterial pressure (+30 mmH) –> decreased EDV from increased thoracic pressure –> drop in MAP
- drop in MAP (bp falling) detected by baroreceptors –> increased CO and HR
- bp starts to rise again due to the reflex
- the maneuver is completed and the patient is allowed to breathe out again: sudden drop in thoracic pressure that is reflected on arterial pressure
- there is rebound increase in bp because the reflexes have not worn off yet, the buildup VR outside the heart now floods into the heart at once
define renin
photoelectric enzyme of the blood secreted by juxtaglomerular/granule cells of the glomerulus
main role is to convert angiotensinogen –> angiotensin I
3 things that trigger renin production
- sympathetic innervation of the justaglomerula apparatus
- decreased arteriole distension detected by renal baroreceptors
- decreased Na/Cl delivery detected by the muscula densa cells in the distal convoluted tubules
* all indicates decreased MAP
3 things that angiotensin II does
- stimulates aldosterone production from the adrenal cortex: increases Na+ reabsorption
- increases ADH production from pituitary gland: increases permeability of the collecting duct
- vasoconstriction: increases MAP
define ADH
antidiuretic hormone
synthesized in the hypothalamus but released from the pituitary
3 things that trigger ADH production
- decreased plasma volume (detected by baroreceptors and relayed to the medullary CVS centers)
- increased osmolarity of the interstitial fluid (detected by osmoreceptors in the hypothalamus)
- circulating angiotensin II
2 functions of ADH
- increases permeability of the collecting duct
2. vasoconstriction
ANP vs BNP
they are both found in the brain
ANP: produced and released by myocardial cells of atria
BNP: same but in ventricles
3 things that niuretic peptides do
- inhibit renin production
- increase excretion of Na+ (reduce reabsorption)
- act as neurotransmitters on the medullary CVS centers to reduce MAP
trigger of ANP and BNP production
increased distention in atria and ventricles (indicating increased MAP)
what happens to MAP in space or bedbound patients
there is no effect of gravity on EDV and therefore there is increased EDV and increased SV and MAP. Therefore, the cardiopulmonary baroreceptors are fooled into thinking that there is high MAP and triggers reduction of MAP as a reflex. When these people feel the effect of gravity again they will have low MAP because it has been repressed this whole time and may experience loss in strength in the limbs
what happens when the renal artery is blocked off?
muscula densa cells and renal baroreceptors tricked into thinking that there is low MAP and trigger increase in MAP even though the MAP elsewhere is normal, resulting in hypertension
drugs that reduce hypertensino
- Ca2+ channels antagonist (reduces CO in cardiac muscles and decreases TPR in muscles - both reduce bp)
- bata adrenoreceptor antagonist
- thiazide diuretics (reduces osmotic Na+ gradient in kidneys)
- angiotensin converting enzyme inhibitors (inhibits conversion of angiotensin I –> II)
- angiotensin II antagonist (blocks angiotensin II receptors)
purpose of blood brain barrier
prevent diffusion of polar hydrophilic molecules like glucose from crossing over without a transport protein
You know that the main exchange method in blood is diffusion. What are the 4 main benefits of diffusion?
- self-regulating: since it follows a gradient, the more is used the more will be supplied
- no saturation: unlike proteins that have saturation points, diffusion does not
- polar substances will diffuse through clefts and channels
- nonpolar substances diffuse right though the membrane
Hydrostatic vs Osmotic/onconic pressure
hydrostatic pressure (arterial pressure): pressure that pushes fluids out of the vessels, resulting in increased solute concentration within the plasma (20L per day) osmotic/oncotic pressure: gradient that draws water back into the blood due to increased solute concentration in the plasma. Works opposed to the hydrostatic pressure to keep things in balance. (17L)
the excess 3L will get reabsorbed through lymphatics, if this system fails, it will result in edema
4 main causes of edema
- lymphatic obstruction/removal: surgery, parasitic worms (filariasis)
- raised central venous pressure: due to backed up blood from ventricular failure
- hypoproteinaemia: decreased oncotic pressure resulting in less reabsorption of water in the plasma and excess water in the extracellular space –> edema
- increased capillary permeability: leads to hypoprotenaemia and too much fluid leaking out. Caused by inflammatory response in diseases like rheumatism
describe resistance juggling
if you dilate some vessels, you will need to constrict others in order to keep the TPR and thus the MAP constant.
If you dilate the vessels without constricting others, it will result in the overall TPR to decrease without the CO increasing and the reservoir of blood would be drained faster (MAP also decreases) –> the areas where vessels are not dilated will not get enough perfusion.
2 main mechs of extrinsic control of blood flow
- neural control (sympathetic and parasympathetic)
2. hormonal control
describe the neural extrinsic control of blood flow
sympathetic:
- NA released from post ganglionic sympathetic fibers (also A released from adrenal medulla, but that is hormonal)
- acts on a1 receptors
- vasoconstriction (only in parts of the body where a1 receptors is predominant, dilation in other areas, this is how TPR is kept constant)
- results in increased MAP
parasympathetic:
- not much effect, not much parasympathetic fibers around blood vessels
describe the hormonal extrinsic control of blood flow
- adrenaline:
- released from adrenal medulla
- acts on a1 receptors –> vasoconstriction
- acts on b2 receptors in the heart and skeletal muscles –> vasodilation (TPR constant) - ADH
- Angiotensin II
- Atrial nitriuretic factor
what are the 4 main mechs of intrinsic control of blood pressure
- active (metabolic) hyperaemia
- pressure autoregulation
- reactive hyperaemia
- injury response (pain signal and substance p neurotransmitter released from c fibers –> substance P activates mast cells to produce histamine –> vasodilation, increased permeability, lymphocytes recruitment)
* main factor used is EDRF (endothelium derived relaxing factor –> vasodilation)
examples of reactive hyperamia?
how coronary arteries get occluded during systole
- a1 receptors in the heart muscles and SA node that responds to sympathetic innervation
- b2 receptors in the coronary arteries that that will respond and dilate the arteries to provide more blood during exercise while the heart beats faster and harder (apparently the b2 thing is parasympathetic innervation overwhelming sympathetic innervation, but I am confused because b2 is a sympathetic receptor)
main differences between intrinsic and extrinsic control of blood flow
intrinsic control responds to selfish need of tissues, the factor released is local and has local effect.
Extrinsic control has systemic effect on MAP and TPR and the factors are released somewhere else, not local
