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Cardiovascular system - Coggle Diagram
Cardiovascular system
Function
Delivery of oxygen, glucose and other nutrients to active tissues
Removal of CO2 , lactate and other waste products from active tissues
Transport metabolites and other substances to storage sites
Transport hormones, antibodies and other substances to site of action
moves blood to transport stuff in blood
Fluids
TBW: total amount of water in the body at given time (60% M | 50% F)
Intracellular fluid: fluid within cells (2/3 of TBW)
Extracellular fluid: fluid outside cells (1/3 of TBW)
Plasma, lymph (blood)
interstitial fluid: surrounds, bathes the cells and found in solid organs
Blood
fluid in blood vessel and chambers of heart
6-8% of body mass
5L of blood
55% plasma (portion of blood that remains after RBC, WBC and platelets removed)
45% cells (erythrocytes (gas transport), leukocytes (immune), platelets (blood clotting))
packed cell volume: proportion of blood made up of cells = 0.45
all cells of blood from haematopoietic stem cell in bone marrow
circulation
systemic (left side of heart)
arteries: oxygenated blood
veins: deoxygenated
pulmonary (right side of heart)
arteries: deoxygenated
veins: oxygenated
Terms
diastole: relaxation
diastolic pressure: lowest systemic arterial pressure, during diastole = 80mm Hg
systolic pressure: highest systemic arterial pressure during systole = 120mm Hg
systole: contraction
pulse pressure: difference between systolic and diastolic: 40mmHg
MAP= arterial pressure averaged over the cardiac cycle (90-95mm HG)
cardiac output: amount of blood the heart pumps each min (5l - 5.5l/ min at rest)
heart rate: number of strokes = 70 beats/ min
Stroke volume: volume per stroke 70-80ml
intrinsic control of cardiac output
venous return (ventricular filling) controls stroke volume
Frank-Starling Law: SV of heart increases in response to an increase in the volume of blood in ventricles
mechanism
Increase venous return, increases ventricular end diastolic volume and stretches the ventricles. Stretching muscle cells increase the pressure they can generate and increasing pressure increases SV
venous return: flow rate into the heart (5-5.5l/min)
factors that affect venous return and consequently CO
Veno - tone (sympathetics)
Sympathetic activation of veins decreases venous compliance, increases central venous pressure and promotes venous return indirectly by augmenting cardiac output through the Frank-Starling mechanism, which increases the total blood flow through the circulatory system.
increase ionotropy (heart contractility) - increases venous return as more blood comes out of heart/ ventricle will contract greatly
exercise: Muscle contraction. Rhythmical contraction of limb muscles occurring during normal locomotory activity (walking, running, swimming) promotes venous return by the muscle pump mechanism.
ventricular volumes
end diastolic volume: volume of blood in heart just before it contracts
end systolic volume: end of contraction
ejection fraction: fraction of blood that gets pumped out = 65%
Heart Beat
Annulus Fibrosus
Atria and ventricles are electrically isolated by the heart's fibrous skeleton
Myocardial cells (cardiac muscle cells)
myocardial contractile cells: cardiac muscle cells, do the mechanical work of pumping. These working cells normally do not initiate action potentials
connected by
gap junctions
The atria and ventricle are made of myocardial contractile cells
Gap junctions allow the cardiac action potentials to propagate from cell to cell through a low resistance pathway (low electrical resistance)
gap caused by protein channel, allowing small charged particles to flow one side to a another (electrically charged: K, Na, Cl)
use action potentials to co-ordinate contraction across the heart and activate contraction
nerves and muscle use changes in charge to send electrical signals called
Action potentials
electrically charged
Autorhythmic cells/ myocardial conductive cells
SA node: heart's natural pacemaker, situated in the upper part of the wall of the right atrium
AV node: coordinates the top of the heart. It electrically connects the atria and ventricles.
Purkinje fibres: networks of fibers that receive conductive signals originating at the atrioventricular node (AVN), and simultaneously activate the left and right ventricles by directly stimulating the ventricular myocardium.
Bundles of His
automaticity: Ability of SA node, AV node and Purkinje network to spontaneously depolarise and generate an action potential
In the pacemaking cells of the heart (e.g., the sinoatrial node), the
pacemaker potential
(also called the pacemaker current) is the slow, positive increase in voltage across the cell's membrane (the membrane potential) that occurs between the end of one action potential and the beginning of the next action potential.
Cardiac pacemakers
SA node = fastest = 90-100 beats/ min
AV node = 40-60 beats /min
Bundles of his = 15-30 beats/ min
Fastest pacemaker normally drives the heart and suppresses other pacemakers
Ectopic beat
: beat generated outside the normal pacemaker and site that generates an ectopic beat is
ectopic focus or ectopic pacemaker
QRS opp direction and different shape
beat would not eject blood
produce no pulse, but picked up in ECG
Ventricular extra systole
Neuronal control of HR
chronotropic: agents that alter heart rate
positive: (increase HR) = Adr/ NA act on b-adrenergic receptors
negative : (slow the heart)= Ach acts on M-cholinergic (muscarinic) receptors
at rest = parasympathetic tone = slows natural rhythm
Heart block
failure of AV node, so no connection between atria and ventricles anymore
Regular rhythm of P waves - different QRS complex (upside down) and T wave is irregular
Direction of AP changed
Beat occurring outside SA node, somewhere in the purkinje fibres or Bundle of His
Ventricular fibrillation: heart rhythm problem that occurs when the heart beats with rapid, erratic electrical impulses.
no contracting together, cause not getting an electrical signal
different parts of the heart, depolarising at different times
no pumping = no systole/ diastole and need paddles to electrocute someone
Atrioventricular valves: between atria and ventricles
Right AV valve: tricuspid vale
left AV Valve: mitral valve
produce S1 loudest heart sound
semilunar valves: between ventricles and arteries
Pulmonary and aortic valve
closure produces second sound
Vascular system: organ system that allows blood to circulate and transport nutrients
Blood vessels
Lined with endothelium: stops clot formation
Elastic tissue: maintain pressure alongside connective tissue
Connective tissue: maintain pressure alongside elastic tissue
no parasympathetic nerves
Smooth muscle
contractions changes vessel size
sympathetic nerves: Adr/ NA contract blood vessels via a-receptors
Arteries
connective tissue
thick walls: contain high pressure to prevent rupture
elastic tissue
diastole: maintain arterial pressure and blood flow
systole: stretches
maintains blood flow during diastole
store elastic potential energy
Systole: Heart contracts => blood pushed out => arteries expand => stretch walls => stores elastic potential energy
Diastole: valves closed => one way to flow/ pressure maintained as elastic potential energy will slowly convert to kinetic energy, during elastic recoil of arteries and pushes blood against resistance
Resistance = opposition to blood flow
Flow (Q
) depends on pressure difference and resistance of vessel [Q
= Pa - Pv/ R]
high resistance = low flow
small vessels have more resistance than large vessels
Total peripheral resistance: resistance of arteries to blood flow (systemic circulation)
Mean arterial pressure: average pressure driving blood forward into tissues throughout cardiac cycle
Venous pressure is quite low, so MAP is usually arterial pressure (Pa - Pv) ===> Pa-Pv = Q* x R ===> MAP = CO X R
MAP is closer to diastolic (2/3) than systolic (1/3)
MAP = DP + 1/3 Pulse Pressure
Factors regulating MAP
Cardiac output
Cardiac output determined by product of SV (determined by inotropy and ventricular preload (altered by changes in venous compliance and blood volume) [Frank-Starling mechanism]) and HR
Increase cardiac output, pressure will increase until the flow rate out of arteries = flow rate in arteries
Arteries expand due to increase CO (increase pressure), so arterial venous pressure will increase leading to increase flow out of arteries
Increase veno-constriction will increase blood volume and therefore increase venous return and consequently stroke volume (and increases CO, which increases MAP)
Total peripheral resistance
Increase TPR, harder for blood to flow out (increase resistance and tube gets narrower), so flow rate will go down initially. As there's more flow in than flow out, the volume in arteries will increase over a few heartbeats making the pressure in the arteries to increase. Once the venous and arterial pressure Is high enough, the flow rate out will increase again. As long as the CO is constant, it will increase the flow in at a higher pressure difference {Pa-Pv}
Increase vasoconstriction (constriction of arterioles ) will increase TPR, but not capacitance since blood volume is small
Arterioles
most of the resistance to blood flow in arterioles
smooth muscle
control diameter
vasoconstriction: active control of diameter (when smooth muscle contracts, the vessel's circumference becomes smaller and increases resistance and consequently decreases flow)
At rest: sympathetic tone at rest
Decrease sympathetic tone = decrease resistance
Decrease global sympathetic tone = Increase TPR = Decrease MAP
Decrease local sympathetic tone = decrease resistance = increase blood flow
control total peripheral resistance
Redirect CO and control where flow goes
most of blood flow goes through whichever organs have the lowest resistance (vasodilated)
Differences in flow determines extent of vascuarization and differences in resistance offered by arterioles supplying each organ
differentially adjusting arteriolar resistance in various vascular beds and therefore controlling flow
Veins
blood storage vessels
floppy
volume depends on pressure in vessel and the vessel stiffness
blood volume in veins regulated by veno-constriction
contraction of veins reduces capacitance, therefore veins hold less blood and increases venous return , consequently increasing CO
sympathetic stimulation = increases venous return and increases CO from increasing SV
resistance of veins is small so veno-constriction does not change TPR as much
vaso-constriction cannot regulate blood volume due to less blood in arterioles (however regulates TPR)
capacitance: how much blood a vessel can hold
Stiff vessels = low capacitance = less blood
floppy vessels = high capacitance (AT rest) = more blood stored
Venous valves
valves prevent back flow
combine with skeletal muscle to assist pumping of venous blood
thin walls
2/3 blood volume in veins
low pressure - central venous pressure (pressure measured in the central veins close to the heart.), 10mmHg
Systemic blood pressure: 120/80 mmHG and pulmonary blood pressure: 22/8 mmHg
pulmonary BP much less
CO of left and right heart are on average same
lower total resistance in pulmonary circuit
Microcirculation and blood flow
Component vessels of microcirculation
Arterioles
Smallest
layer of endothelial cells, elastic/connective tissue >> thin wall
True capillaries coming off them
blood flows from arterioles to metarterioles
venules
endothelial cells/ fibrous tissue (no smooth muscle to elastic tissue)
exchange
Metarterioles
Bigger = smooth muscle (can narrow and contract)
true capillaries come off metarterioles
capillaries
can't control capillary diameter and they come off metarterioles
Pre-capillary sphincter: when capillary comes off arteriole/ met arteriole the smooth muscle around them. These can close capillaries
Atrioventricular shunts
larger than true capillaries/ smooth muscle in wall and can close off
Hot weather -> skin -> close bypass circuits and sends blood to surface
Cold weather --> relax/ open circuits --> send less blood
Transport across capillary wall
Lipid soluble substances
Pass straight across lipid membrane (Plasma)
Diffusion
Eg: oxygen, carbon dioxide, anaesthetics and ethanol
Large substances
Exocytosis/ endocytosis (pinocytosis)
Vesicular transport
Lipoprotein
Small / medium sized water soluble molecules
diffuse between endothelial cells
Eg: water, sodium, chloride, calcium, urea, lactate, glucose, insulin, ADHD
Cells
Migrate through endothelium gaps called fenestrations
Eg: leukocytes
endothelial produce chemokines that attract cells and the cells can bind onto capillary wall/ endothelium >> crawl out and extend pseudopods to crawl out
note: albumin cannot cross capillary walls
Starling equilibrium
fluid movement due to plasma filtration across capillary wall
Hydrostatic vs colloidal osmotic pressure
How changes in plasma protein, BP, vasoconstriction tone alter plasma and interstitial volume?
Changes in filtration (volume of fluid leaving capillary) [increase filtration = oedema]
Factors
Vasodilation = increase blood flow >> increase pressure in capillaries and increase filtration
Arterial/ venous hypertension >> increase in venous pressure >> increase filtration
Increase plasma leakage
endothelial cells do not keep albumin in and plasma has protein deficiency = Increase filtration
Changes in absorption (inward movement of fluid [in capillaries] (increase)
Vasoconstriction
Decrease blood flow out of capillaries and into arteries
decrease capillary hydrostatic pressure
fluid in
Atrial/ venous hypotension
BP decreases
less fluid out of capillaries
colloidal osmotic pressure > capillary hydrostatic pressure = reabsorption
increase plasma volume = increase blood volume
Dehydration
lost water/ retained salts
blood volume doesn't fall as much as IF
Haemorrhage
loss of BP/ loss of venous hypotension (reabsorption/ dehydration)
Colloidal osmotic pressure increases
reabsorption increases plasma volume
Functional role of lymphatic system
Primary function: transport lymph (fluid containing infection/ fights WBC)
Lymphatic transport
peristaltic contraction of smooth muscle
lymph vessel wall
valves
to thoracic duct
smooth muscle cell around them = contract >> push fluid upwards to thoracic duct
How changes in arteriolar resistance distribute CO?
Distribution: dilation/ contraction of blood vessels
Arteriolar resistance
Determines perfusion = total perfusion = CO
Parallel systemic vascular beds determines BF
Top capillary dilated + rest constrict , so BF through dilated vessel determines distribution of blood flow through organs
Cannot increase CO because increase work done to heart and cause heart failure
Terms
Hyperaemia: increase blood flow (increase BF)
Active hyperaemia: Increase metabolic rate
Reactive hyperaemia: flow re-established (reaction to loss of blood = overshoots)
Ischaemia: loss of BF to tissues (magnitude/ duration of hyperaemia is proportional to duration of ischaemia
remodelling: increase in vessel diameter, if perfusion decreases = metabolic rate increases
Angiogenesis
produce new blood vessels/ triggered by changes in oxygen tension/ express growth factors = promote vascular remodelling
ECGF/FGF and androgen - likely mediators
Role of local metabolites in regulation of blood flow (arteriolar radius) [note: metabolites alter smooth muscle tone]
Increase metabolic activity
Oxygen decrease (vasoconstrictor) = metabolising cells use up more Oxygen to support oxidative phosphorylation for ATP production
Carbon dioxide [vasodilation] = by-product of oxidative phosphorylation
increase acid: more carbonic/ lactic acid
Increase potassium: restore resting concentration gradient and increase K+ in IF of active tissues
Increase osmolarity [conc. of osmotically active tissues]
adenosine release: response to increase metabolism/ oxygen deprivation (increases cAMP), as can't keep up with ATP demands
arteriolar dilation by relaxing arteriolar smooth muscle will increase blood flow
decrease metabolic activity
increase oxygen
decrease CO2, acid, K+, osmolarity and adenosine release (vasodilators reduced in order to reduce blood flow)
Control of blood pressure
control of systemic arterial pressure (depends on CO and TPR = work load)
Increase muscle work (no parasympathetic)
Increase local products/ reduces local nutrients
local metabolite changes will dilate smooth arteriolar muscle increase blood flow
Blood flow increased to working tissue
due to low TPR, there will be changes to MAP
Control blood vessels
carbon dioxide
Increase adenosine (vasodilator)
Decrease oxygen (vasoconstrictor)
circulating hormones
Decrease adrenaline (vasodilator)
increase adrenaline (vasoconstrictor)
sympathetic nerve activity
increase -- vasoconstrictor SM and release Adrenaline/ NA
vaso-constriction = TPR/ stop MAP decreasing and reduces flow to tissues
Veno-constriction: venous return = Increase CO
Who win? vasodilators (local metabolites)/ constriction (sympathetic nerves)?
During exercise sympathetic nerves and circulating Adr vaso-constrict arterioles, which reduces blood flow but increases BP
Local metabolites produce vaso-dilation but only in the active tissue. Blood flow goes up though the active tissue but down through other tissue.. CP redistributed to active tissue. But if lots of tissue is working arterial pressure will still drop unless cardiac output increases
Extrinsic regulation
depends on hormones, autonomic nerves and drugs that alter force of contraction
Intrinsic regulation
venous return and regulate contraction without external factors
ionotropy - alter contractility
sympathetic nerve and adrenaline is ionotropy
Baroreceptor reflex
- changes in central arterial pressure detected by baroreceptors
located in carotid and aortic arteries
cardiac baroreceptor reflex
decrease arterial BP
decrease baroreceptor activity which increases CO/ BP
decreases parasympathetic tone and increases HR
Increase sympathetic tone, heart rate, contractility and stroke volume
vascular baroreceptor reflex
Decrease in arterial BP will decrease baroreceptor activity
increase vaso-tone and TPR, which will increase CO
Increases veno tone, venous return and stoke volume, which will ultimately increase CO
haemorrhage
decrease blood volume/ BP activates baroreceptors
Increases HR and force (chronotropy/ ionotropy) will increase CO and MAP and consequently increase BP
increase vaso-tone (not useful), will increase BP by increasing TPR but doesn't decrease CO and consequently increase BP
Increase veno- tone, which will increase venous return, increase SV + CO and reverse the drop in CO, which will increase BP
standing
standing shifts blood volume away from the heart and brain towards the feet/ Increase filtration = swelling
reduces CO and BP
fall In BP detected by baroreceptors
Baroreceptor reflex stimulates HR and contractility, increasing CO and BP
vascular component of the reflex increases total resistance, increasing BP and redistributing flow to heart and brain
venoconstriction redistributes blood pooling in veins increases venous return
ADH hormone and it's effect on BP (renal topic)
central ischemic response
reduced blood supply to the brain produces the central ischemic response (CIR)
BP below 60mmHg will initiate CIR
mimics baroreceptor reflex but much more potent
can elevate BP above 200mm Hg and block blood flow to all tissues except the heart, lungs and brain
Regulation of ECF
long term control of BP is control of blood volume
changes in blood volume alter venous return, SV and CO
Blood volume controls BP
ECF volume controls BP
Blood/ ECF volume depends on fluid intake and loss - kidneys control loss by changing urine volume and concentration/ osmolarity