Module 3.2 - Cardiovascular Physiology Flashcards
initiation of heart beat
heart has an intrinsic beat (ability to beat on its own)
=> auto-rhythmicity
- can beat outside body
coordination of contraction
of myocardial cells of atria/ventricles through specialised conducting tissue
AP of ventricular contractile fibre
- rapid depolarisation as fast as nerve AP due to being Na+ driven
- contraction whenever there is Ca2+ => length of contraction is determined by width of plateau
electrocardiogram - Pwave
atrial depolarisation
=> atrial contraction
electrocardiogram - QRS complex
- onset of ventricular depolarisation
- atrial repolarisation (but wave is lost within much bigger QRS complex => shape doesn’t represent)
- spread of activation through ventricles
- shape of wave due to direction of spread
electrocardiogram - S-T segment
when whole ventricle is depolarised (extended plateau of AP)
=> electrical balance
=> no voltage change
elevation/depression if abnormalities in ventricular wall => chest pain
electrocardiogram - Twave
- ventricular repolarisation (not as rapid)
=> relaxation / start of diastole
electrocardiogram - T-P segment
when all cardiac myocytes are at RMP
chronotrope
something that changes heart beat
- positive chronotrope: increase heart rate
inotrope
something that changes in contractility/contraction power
- positive => increase, negative => decrease
regulation of heart rate
(autonomic) nervous system regulation of heart rate originates in the cardiovascular centre of medulla oblongata
input to cardiovascular centre
from higher brain centres (forebrain) + receptors (proprio, baro, chemo)
output to effectors
parasympathetic (vagus) / sympathetic nerves to heart+ vasomotor nerves (sympathetic) to blood vessels for vasoconstriction
sympathetic / parasympathetic balance at rest
SA node is dominated by vagal activity at rest (50-70 bpm)
regulation of blood pressure
ANS (autonomic nervous system) innervation of heart/baroreceptor complexes that help regulate BP
regulation of BP - nerve direction
- baroreceptors -> cardiovascular centre in medulla
- cardiovascular centre ->
1) SA/AV node - parasympathetic
2) spinal cord - cardiac accelerator nerves -> spinal cord (thoracic level) -> sympathetic trunk ganglion -> SA/AV node, ventricular myocardium (sympathetic)
BP hormones
circulating hormones
- adrenalin/noradrenalin
- ion concentrations
etc.
proprioceptor input
major stimulus that accounts for rapid rise in HR at onset of physical activity
hyperthermia
increases HR
sympathetic nervous system increases
- HR
- SV
- spontaneous depolarisation of SA/AV nodes
- contractility of ventricles/atria
parasympathetic nervous system decreases
- HR
- rate of spontaneous depolarisation of SA/AV nodes
dicrotic wave
rebound from aortic valve closing
can you have negative blood pressure
yes
cardiac output
amount/volume of blood ejected into aorta per minute
cardiac output unit
mL/min
L/min
average cardiac output
5 L/min
- between 4-7 L/min at rest
- can go up to 5x e.g during exercise
- 40 L/min for athletes
cardiac output equation
= HR x SV
cardiac reserve
difference between max. cardiac output and cardiac output at rest (rates at which heart pumps blood)
- shows maximum capacity of heart to pump blood
normal heart rate
normal = 60-100 bpm
- controlled by SA node (sympathetic/parasympathetic activity)
normal stroke volume
50-100 mL per beat
stroke volume equation
= end diastolic volume (EDV) - end systolic volume (ESV)
EDV
max. volume (most full)
- 120-140 mL
ESV
min. volume
- 50-70 mL
frank-starling law of heart
in stable system, venous return (diastole) = cardiac output (systole)
- increased return => heart works harder => stretch of myocytes => energy of ventricular contraction => forcefulness of contraction => SV increases
- greater force of contraction can occur if the heart muscle is stretched first
factors determining SV
1) preload
2) contractility
3) afterload
preload
force that stretches cardiac muscle prior to contraction
- increased diastolic filling => increase EDV => increased SV
factors changing diastolic filling
- ∆venous return
- ∆blood volume (more blood in system => more blood to heart)
- ∆filling time (duration of ventricular diastole)
- ∆respiratory pump (inhaling => negative pressure around lungs and heart shares same space => also affected - decreased diastolic filling)
- ∆compliance (MI - myocardial infarction damage - becoming stiffer, can’t contract as well due to scarred tissue, attack, disease etc.)
venous return
amount of blood returning to heart each min from venous system
contractility
performance (forcefulness of contraction) of heart (esp left ventricle) at a given preload/afterload
- aka inotropy
- increased contractility => decreased ESV => increased SV
factors changing contractility
- autonomic nervous system (increased sympathetic => increased contractility)
- venous return (increased preload => increased contractility)
- [Ca2+] (all factors affecting contractility act by changing [Ca2+])
- drugs (inotropes) - target contractility not longetivity as it doesn’t address underlying conditions
- ion balances
- circulating levels of various hormones
afterload
amount of pressure that the heart needs to exert to eject blood during ventricular contraction (what heart works against)
- increased afterload => increased ESV => decreased SV
factors affecting afterload
- hypertension - high blood pressure
- valve pathologies
- aortic plaques - constriction in aorta
ventricular pressure-volume relationship
A: mitral valve opens
B: mitral valve closes
C: aortic valve opens
D: aortic valve closes
ventricular pressure-volume relationship - A-B
ventricular filling
- first: pressure decreased due to suction effects of relaxing muscle
- later: pressure rises passively as volume increases
ventricular pressure-volume relationship - B-C
isovolumetric contraction
- pressure increases steeply
- no change in volume as aortic valve closed
ventricular pressure-volume relationship - C-D
blood ejection
ventricular pressure-volume relationship - D-A
isovolumetric relaxation
stroke work
heart’s pumping action is achieved by mechanical work of myocardium
= area of pressure-volume curve of ventricular contraction (total external work carried out by ventricles during one cardiac cycle)
stroke work equation
work done = ∆pressure x ∆volume
blood volume distribution
1) systemic veins and venules (blood reservoirs) - 64%
2) systemic arteries and arterioles - 13%
3) pulmonary veins - 9%
4) heart - 7%
5) systemic capillaries - 7%
blood pressure
pressure of circulating blood against vessel walls which can vary throughout cardiac cycle
mean arterial pressure (MAP) equation
cardiac output (CO) x total peripheral resistance (TPR)
total peripheral resistance
amount of force affecting resistance of blood flow through circulatory system
poiseuille’s law
describes flow is related to factors such as velocity
if CO decreases while MAP constant
TPR increases by sympathetic stimulation of smooth muscles => reduce diameter (vasoconstriction) => increase resistance
blood hydrostatic pressure (BHP)
force exerted by blood confined within vessels
- arterial: ~35 mm Hg
- venous: ~16 mm Hg
blood colloid osmotic pressure (BCOP)
- aka oncotic pressure
form of osmotic pressure induced by proteins in blood - ~26 mm Hg
decreasing BCOP
deficiency/low plasma protein level
hemorrhage
release of blood from broken blood vessel
interstitial fluid hydrostatic pressure (IFHP)
mechanical pressure exerted on interstitial fluid by elastic recoil of tissues in any region of body
- ~0 mm Hg
interstitial fluid osmotic pressure (IFOP)
osmotic force which is the result of differences in water conc. between plasma and interstitial fluid
- ~1 mm Hg
capillary exchange
exchange/movement of material between blood and interstitial tissue/fluid across capillary wall
ways of capillary exchange
1) diffusion
2) trancytosis
3) bulk flow/filtration
diffusion
solute exchange, down conc grad
trancytosis
vesicles (contents wrapped in membrane) of large, lipid-soluble (insoluble in H2O/blood)
e.g insulin
bulk flow/filtration
- passive movement of flow + substances
- faster than diffusion alone
- net flow is driven by difference between balance of hydrostatic pressure / osmotic pressure gradients (starling’s law of capillaries)
net filtration - favours filtration
BHP + IFOP
- arterial: 35 + 1
- venous: 16 + 1
net filtration - favours reabsorption
BCOP + IFH
- arterial and venous: 26 + 0
pressures
(BHP + IFOP) - (BCOP + IFHP)
- arterial: +10 mm Hg
- venous: -9 mm Hg
negative pressure means
favours reabsorption
organ without lymph vessels
brain - glymphatic system
oedema/edema
accumulation of fluid outside vessels
- common symptom of many conditions
- most obvious in legs due to gravity
hypertension =>
arterial BHP increases
- vasoconstriction
- increased arterial tone
arterial tone
degree of constriction relative to maximally dilated state
kidney disease =>
loss of blood proteins (more in urine) => BCOP decreases => low capillary reabsorption
heart failure =>
venous BHP increases
long-haul travel =>
venous volume increases as heart tries to hold volume (more filled up) => SV increases
venous BHP increases
how does long-haul travel increase BHP
- gravity
- leg swelling => venous compression
=> blood pools in venous sytem
=> BHP increased without changing overall blood volume
venous volume increases =>
capillary permeability increases => IFOP increases
nervous control effect on TPR
decreased frequency of sympathetic nerve activity => vasodilation in systemic blood vessels => increased radius of vessel lumen => decreased resistance to blood flow => decreased total peripheral resistance
effect of blood volume on nerve activity
decreased blood volume
=> decreased EDV => decreased SV
and
=> decreased BP => baroreceptors sense => increase sympathetic activity to heart + decreased parasympathetic / vagal
(reflex neural mechanisms that respond to change in arterial pressure)
reason for having parallel structure of circulatory structure
allows same hydrostatic gradient at each organ
relationship between bloodflow and total cross-sectional area in different blood vessel types
velocity is inversely proportional to cross-sectional area (of all of that type of blood vessel)
to increase blood flow
1) increase cardiac output (increase HR and/or SV)
2) redirect existing cardiac output/blood flow to organs that need it (vasoconstriction)
what control direction of bloodflow
precapillary sphincters
coping with haemorrhage - challenge to homeostasis
- vasoconstriction
- increase HR (need CO to maintain blood)
- clotting to stop bleeding (+ maintain BP)
- redirection
- increase SV by increasing contractility (not much by venous return as blood is being lost
baroreceptors
- respond to ‘stretch’ in arterial wall
- signals connect up to brain via cranial nerves
baroreceptors and tonicity
tonically active
- can respond to increases/decreases in BP (not on/off)
baroreceptor location
- carotid sinus
- aortic arch
carotid sinuses
sits above bifurcation of carotid artery (into two other arteries) along with carotid body
- one of smallest organs
vascular tone - increased electrical signals from neuron =>
norepinephrine release onto receptors increases => vasoconstriction / increased HR => increased BP
vascular tone and blood vessel size
effect of hormones in response to electrical signals is esp prominent in small arteries/arterioles due to ratio of muscle
- bigger change is required for bigger arteries to cause change
total spinal anesthesia
block transmission across neurons in spinal cord from a specific point (below level of heart) down
muscle activity in veins and BP
there is smooth muscle in veins but this has a smaller effect on BP due to low pressure, instead affects venous return
what increases BP
increased:
- HR
- TPR
- VR (venous return)
possible stimuli of change in BP
- haemorrhage
- drinks (1L of water/energy drink)
- standing up quickly
- temperature (hot day => peripheral vasodilation)
resistance and radius
resistance is inversely proportional to radius^4
redundant physiology
multiple systems that overlap in different ways to affect same variable
slow response to increased blood volume
blood volume homeostasis (decreasing) via compensation by kidneys
- need to solve fundamental issue
angiotensin II
vasoconstrictor peptide
- increased as a result of low BP (not affected by cardiac sympathetic activity)
glossopharyngeal nerves
from carotid sinus -> cardiovascular centre
vascular resistance is
1) size of lumen
- inversely proportional to radius^4
2) viscosity
- directly proportional
3) (total) length of blood vessel
- directly proportional
alpha receptors
- skeletal muscle
- smooth muscle (blood vessels - arteries/arterioles)
beta receptors
- cardiac muscle (myocardium): ventricular muscles, SA/AV nodes
Starling’s Law of the Capillaries
the volume of fluid reabsorbed at the venous end of a capillary is nearly equal to the volume of fluid filtered out at the arterial end
vagus nerve
only affects heart rate
- NOT contractility/inotropy or vasomotor
right subclavian vein
behind collar bone
superior sagittal sinus
runs above longitudinal fissure
long haul flights
decreased skeletal muscle action => decreased venous return (preload => SV => CO) => increased venous volume => increased venous BHP => stretched pores => increased capillary permeability (large solutes exit vessel) => IFOP increases => NFP increased => interstitial fluid increased => oedema (lymphatic can drain)
lactic acid
- causes vasodilation => decrease in BP
- NOT produced when standing still
proprioceptive input
does NOT affect HR
- only sends info about location/orientation of joints etc.
