Cardiovascular Pathophysiology Flashcards
what are the 2 types of circulation
pulmonary and systemic
what is the ml/beat at rest
75ml/beat
pumps in series, output must be equal
vascular beds are in parallel, some in series (gut to liver)
ff
what is the blood flow at rest? (CO)
5L/min
what is the CO equation
CO = SV x HR
what two factors affect blood flow
pressure (mean arterial pressure-central venous pressure)
resistance (radius)
what is the function of arterioles
act as ‘taps’ - resistance vessels
control regional flow of blood
narrow lumen
thick contractile wall
what is the function of veins and venules and describe them
capacitance vessels
wide lumen, distensible walls (can absorb blood)
low resistance conduit + reservoir (store blood, release when needed)
allow fractional distribution of blood between veins and rest of circulation
describe the aorta
elastic artery
wide lumen
elastic wall
damp pressure variations
describe arteries
muscular arteries
wide lumen, thick muscular wall, non-elastic, strong
low resistance conduit
what side of the myocardium on the heart is thicker
left side of heart
what are the semi lunar valves and where
pulmonary - right side to pulmonary arteries
aortic valve - left side between LV and aorta
what opens and closes valves
pressure difference
what valves are between atrium and ventricle
right - tricuspid
left - mitral
what stops valves inverting
chord tendinae
papillary muscles attaches to bottom of endocardium
what makes heart sounds
closing of valves
What’s the sarcoplasmic reticulum?
over muscle fibres, Ca2+ bind to troponin -> actin/myosin interact
whats the functional syncytium and whats in it
allow heart to act as one big muscle
- gap junctions (electrical connections) - connect individual cardia cells to allow electric current to go through
- desmosomes (physical connection)
intercalated discs (whole thing)
explain the action potential in the heart cells
longer, 200-250ml s
voltage gated Na and Ca channels (doesn’t saturate troponin)
modulate Ca coming in, to regulate strength of contraction
pacemakers explain
cells that have unstable resting membrane potentials, spontaneously fire action potential to threshold, make whole heart contract
spread AP’s through gap junctions
explain non-pacemaker cells
leaky K+ channels going out cell
cell is -90mV (resting potential)
Na, Ca channels shut
high resting permeability to K+
initial cell depolarises. Na+ flows in from channles
plateu - inc in Ca2+ (long lasting L type) + dec in K+
repolarisation - dec in Ca2+ + inc in K+
explain pacemaker activity
AP - inc in Ca2+ (L-type), slower but stay open longer Pacemaker potential (pre-potential) - gradual dec in K+ - early inc in Na+ - in in Ca2+ (T-type)
where are the pacemakers located
sinoatrial node in right atrium
whats the tissue that separates the atria and ventricles
annulus fibrosis (non-conducting)
how does the AP get from atr to ventr
atrioventricular node - conducts slowly
gives time for atria to depolarise and contract first
0.05m/s
explain the depolarisation in ventricles
fast 5m/s
bundle of His running down septum
into purkinje fibres
lots of electrical potentials, can summate to create large electrical waves
what are the ECG waves
P - atrial depolarisation
QRS complex - ventricle depolarisation
T - ventricle repolarisation
tells conduction and rhythm
what is 1st degree block
heart block
AV node slows conduction of AP
delay between P and QRS wave, more than 0.2s
whats 2nd degree block
some depolarisations don’t get through to V
missed QRS
3rd degree block heart block?
Independent P wave and QRS complex
whats atrial flutter
each depolarisation much quicker
whats atrial fibrillation
individual cells depolarising at Dif times
pacemaker not spreading wave of depolarisation across atria
occasion depolarisation getting through AV node
Ventricular fibrillation?
uncoordinated depolarisation + contract of ventricle
defibrillator use to depolarise all cells and let pacemaker set rhythm again
which ecg leads look at heart in frontal plane
I, II, III, aVR, aVL, aVF
which ecg leads look at heart in horizontal plane
V1-V6 (precordial)
where does standard limb lead 1 make a recording from
Left arm w respect to right arm
where does standard limb lead 2 make a recording from
right arm wrt to left leg
where does standard limb lead 3 make a recording from
left leg wrt to left arm
a wave of approaching depolarisation causes an upward causing blip
fff
in repolarisation if approaching RI (SLL2) positive blip, why is that
the epicardium has a shorter AP than the endocardium so goes up the way
in ecg paper what is 1 large square in time
0.2 secs
how do you determine the HR on an ecg
R-R interval, count waves in 30 large boxes (=6secs)
and multiply by 10 for in a minute
what is a STEMI
ST elevation myocardial infarction - complete occlusion of arteries
what is diastole
Relaxation of the heart
fill chambers w blood
2/3 of cardiac cycle
what is systole
Contraction of the heart
heart pumps blood out
1/3 of cycle
when mitral and tricuspid valves close and aortic n pulmonary open - blood pumped out
what is systolic pressure
peak pressure of aorta (120mmHg)
what is diastolic notch
when aortic valve closes
what is diastolic pressure
minimum pressure in aorta (80mmHg)
what is pulse pressure
difference between systolic and diastolic pressure
what is mean arterial pressure (MAP)
average pressure in the arteries throughout the cardiac cycle
what is end diastolic volume (EDV)
peak volume of blood at end of filling phase
what is end systolic volume (ESV)
minimum volume of blood at end of ejection phase
what is the ejection fraction
SV/EDV
What is a phonocardiogram?
occurs due to turbulence in blood from closure of AV valves, and closure of semi-lunar valves
what are murmurs and what are they caused by
abnormal heart sounds
stenosis - narrowing of valve and cause turbulent blood flow
regurgitation - valve not shut properly
what regulates heart rate
sympathetic NS - release noradrenaline
act on B1 receptors on SA node
inc slope of pacemaker potential
inc heart rate
parasympathetic - vagus release acetylcholine
act on muscarinic receptors on SA node
hyper polarise cell + dec slope
dec HR
what regulates stroke volume
preload, contractility, afterload and neural
What is stroke volume?
volume of blood pumped out by one ventricle with each beat
what is the preload for SV
how full the ventricle is before contracting, depends on venous return
starlings law - energy of contraction proportional to how stretched the cardiac muscle is bar contracting)
(less blood back, smaller strength of contraction = smaller SV)
what is the after load for SV
load against which muscle tries to contract blood out
(TPR) how easy for blood to get away through arterioles (constricted/dilated)
(if arterioles constricted -> TPR inc and pressure will be higher at aorta -> ventricle require more pressure to open valve -> less energy to eject blood -> SV dec
how does neural affect SV
affects contractility
sympathetic NS - noradrenaline on B1 receptors inc contractility, stronger
what affects venous pressure
- gravity (standing up, more pressure in legs, lower in head)
- skeletal muscle pump
- respiratory pump
- venomotor tone (contraction of smooth muscle around veins n venules)
- systemic filling pressure (pressure difference of ventricles and veins)
what are some anticlotting mechanisms in the body
produce prostacyclin + nitric oxide (inhibit platelet aggregation)
tissue factor inhibitor (stop thrombin production)
thrombomodulin (inactivate thrombin)
heparin
tissue plasminogen activator (t-PA) (digest clot)
What is bulk flow driven by?
hydrostatic pressure and osmotic pressure (pushing water back in)
what is the equation for MAP
MAP = CO x TPR
what are the two levels of control on peripheral blood flow
local - meet selfish needs of individual tissue
central - ensure total PR (MAP) of whole body stay right
How can you measure arterial pressure
Auscultation of Korotkoff sounds using
a sphygmomanometer & stethoscope
Oscillatory blood pressure measurement
how does Oscillatory blood pressure measurement work
turbulent blood flow sets up vibrations (oscillations) in vessel wall
max vibrations at mean arterial pressure
what sounds are heard when auscultating bp
silence (above systolic pressure) tapping (blood pushing through) thumping muffled (diastolic pressure) silence
how are elastic arteries (aorta) a pressure resevoir
they damp down pressure variations
what is the pressure wave affected by
- stroke volume
- velocity of ejection
- elasticity of arteries
- total peripheral resistance
pressure falls throughout vascular tree
tt
what is the pressure drop through arteries
95 to 90mmhg
what is the pressure drop through arterioles
Large drop through arterioles (from ~ 90 to 40 mmHg)
what is the the pressure difference from capillaries to veins
20 to 5 mmHg
what is velocity related to
total cross section
how does gravity affect mean arterial pressure
causes venous distension in legs
dec EDV, dec preload, dec SV, dec CO, decreased MAP
how does gravity cause venous collapse
further up column, reduced pressure, once past 0mmHg pressure inside vessel lower than pressure out = vein get squashed flat, compressed
what are continuous capillaries
no clefts or pores e.g brain (blood brain barrier)
clefts only eg muscle
what are fenestrated capillaries
clefts and pores eg intestine and kidney, specialised for fluid exchange
what are discontinuous capillaries
clefts and massive pores eg liver
how do capillaries exchange with tissue
- diffusion
non-saturable
non-polar across memb,
polar through clefts/pores - carrier-mediated transport
e. g. glucose transporter in the brain - bulk flow
what is bulk flow
Is determined by starlings forces
capillary hydrostatic pressure vs ISF hydrostatic pressure
Plasma osmotic pressure vs ISF osmotic pressure
Hydrostatic pressure pushes fluid out through the leaky capillaries. That builds up an osmotic (oncotic) pressure which draws fluid back in.
how much fluid is lost and regained each day
20L lost
17L regained into circulation
3L to lymphatic system
what is oedema
accumulation of excess fluid
lose balance of starlings forces
what can oedema be caused by
lymphatic obstruction
rasied CVP
hypoproteinemia
increased capillary permeability
what is the purpose of the blood brain barrier
The blood-brain barrier prevents toxic substances, large molecules, and neurotransmitters released in the blood from entering the brain
what is Poiseuille’s law
varying radius of resistance vessels is used to control
- blood flow
- TPR and regulate MAP
- redirect blood
what is the MAP equation
MAP = CO x TPR
Reducing resistance of a vascular bed increases flow through that vascular bed
But, reducing total peripheral resistance also reduces mean arterial pressure
To keep the blood flow to each vascular bed sufficient, and keep mean arterial pressure in the right range, you have to engage in some resistance juggling.
what does arteriolar radius affect
affects flow through individual vascular beds, and mean arterial pressure
why do you have to control the radius of arterioles
to keep blood flow to each vascular bed sufficient and keep MAP in right range
how do you control the TPR of arterioles
2 levels of control over smooth muscle around arterioles
- Local (intrinsic) mechanisms - concerned with meeting the selfish needs of each individual tissue
- Central (extrinsic) mechanisms – concerned with ensuring that the total peripheral resistance (and therefore MAP) of the whole body stays right
what is active (metabolic) hyperaemia
a local control
- trigger - inc in metabolic activity
- inc local metabolites
- release paracrine signal (EDRF)
- inc flow to wash out metabolites
what is pressure (flow) autoregulation
Local (intrinsic) control
trigger = dec perfusion pressure
- dec MAP, dec flow
- paracrine signal cos metabolites conc inc
- arterioles dilate, washes out metabolites
what is reactive hyperaemia
Local (intrinsic) control
trigger = occlusion (blocked) of blood supply
- inc in blood flow
- extreme version of pressure autoregulation
what central controls are there for TPR
sympathetic
parasympathetic
hormonal
what effect does sympathetic nerves have on TPR
release noradrenaline binds to a1-receptors causes arteriolar constriction therefore dec flow through that tissue inc TPR
what effect do parasympathetic nerves have on TPR
usually no effect
genitalia and salivary glands are the exception
how does adrenaline (hormonal) affect TPR
released from adrenal medulla
binds to a1-receptors
causes arteriolar constriction
therefore dec flow through that tissue, inc TPR
in some tissues - B2-receptor
arteriolar dilation
inc flow = dec TPR
explain the coronary circulation
blood supply interrupted by systole
active hyperaemia - arteriolar dilation (inc in local metabolism)
B2-receptors
explain cerebral circulation
needs to be stable
has pressure autoregulation (if decrease in perfusion pressure)
explain pulmonary circulation
dec O2 causes arteriolar constriction
ensure blood is directed to the best ventilated parts of the lung
explain renal circulation
main function is filtration which depends on pressure
changes in MAP would have big effects on blood volume
pressure autoregulation
what is late diastole
both chambers relaxed, start filling w blood
what is atrial systole
atrial contraction, slight delay, blood into ventricles
what is isovolumic ventricular contraction
pushes AV valves closed
what is ventricular ejection
ventric pressure rises, exceeds pressure in arteries
semilunar valves open, blood ejected
isovolumic ventricular relaxation
pressure falls, semilunar valves close
why does MAP need to be regulated
MAP is the driving force pushing blood through the circulation
cant be too low - fainting
too high - hypertension
what are arterial baroreflex
and what 2 types are there
sensors that detect changes in bp
aortic arch - vagus nerve to brain
carotid sinus - glossopharyngeal nerve
stretch receptors, will signal by increase in firing APs
what does a high firing rate of APs from arterial baroreflex receptors mean
high firing rate = high pressure
what nerve goes up to the brain from the aortic arch baroreflex and where in the brain?
vagus nerve, medullary cardiovascular centres
what nerve goes up to the brain from the carotid sinus baroreflex and where in the brain?
glossopharyngeal nerve, medullary cardiovascular centres
what effect will parasympathetic nerves have on the heart from the medullary cardiovascular centres
release acetylcholine
act on muscarinic receptors
hyperpolarized pacemaker cells will make them depolarise slower.
Reach threshold later and slow down your heart rate
what will sympathetic nerves do to the heart from the medullary cardiovascular centres
release noradrenaline
B1-receptors in pacemakers
depolarise faster, inc HR
adrenal medulla
also innervate ventricle muscles
inc Ca released in cells
more cross bridges a greater excitation contraction coupling
increase the strength volume
venoconstriction (squeeze blood back to heart, inc preload, inc CO) + arteriolarconstriction (inc TPR, inc MAP)
what are other inputs to the medullary cardiovascular centres
- cardiopulmonary baroreceptors, sensing central blood volume
- Central chemoreceptors, sensing arterial pCO2
- Chemoreceptors in muscle, sensing metabolite concentrations
- Joint receptors
- Higher centres, hypothalamus and cerebral cortex
what is the Valsalva manoeuvre
forced expiration against a closed glottis
what effect does the vasalva manoeuvre have on the cvs
Increased thoracic pressure is transmitted through to aorta
Increased thoracic pressure reduces the filling pressure from the veins, which therefore dec VR, dec EDV, dec SV, dec CO, dec MAP
detected by baroreceptors which initiate a reflex increase in CO and TPR
the decrease in thoracic pressure is transmitted through to the aorta
VR is restored so SV
kidneys regulate plasma volume
controlling plasma volume is used to regulate MAP
- long term control of BP
gg ff
what determines how big the osmotic gradient will be in the kidneys
Na+ transport
kidney collecting ducts have control of permeability of ducts to water
hh
what happens if the collecting duct is very permeable to water
collecting duct very permeable to water will result in lots of water reabsorption, little urine, and conserve plasma volume
what happens if the collecting duct is very impermeable to water
result in little reabsorption (back into circulation), lots of urine (= diuresis), and a reduction in plasma volume, goes out body
what hormone systems regulate the process of water reabsorption
Renin-angiotensin-aldosterone system Antidiuretic factor (ADH, vasopressin) Atrial natriuretic peptide (factor) & brain natriuretic peptide (factor)
Where is renin produced?
From the juxtaglomerular (= granule cells) of the kidney
What triggers renin production?
- Activation of sympathetic nerves due to reduced MAP
- Decreased distension of afferent arterioles
- Macula densa, decreased delivery of Na+/Cl- through the tubule
all signal reduced MAP
What does renin do?
Converts inactive angiotensinogen to angiotensin I
Which is in turn converted by angiotensin converting enzyme to angiotensin II
what does angiotensin II do?
- Stimulates release of aldosterone from the adrenal cortex, inc plasma vol = inc MAP
- Increases release of ADH from the pituitary, inc water permeability, inc plasma vol
- vasoconstrictor, inc TPR
Where is antidiuretic hormone (ADH) produced
Synthesised in the hypothalamus
Released from the posterior pituitary
What triggers ADH release?
- A decrease in blood volume (sensed by cardiopulmonary baroreceptors)
- An increase in osmolarity of interstitial fluid
- Circulating angiotensin II
What does ADH do
- Increases the permeability of the collecting duct to H2O, therefore reduces diuresis and increases plasma volume
- Causes vasoconstriction, inc MAP
where are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) produced
myocardial cells in the atria & the ventricles respectively
What triggers ANP & BNP release?
Increased distension of the atria & ventricles (sign of increased MAP)
What do ANP & BNP do?
Increase excretion of Na+ (natriuresis)
Inhibit the release of renin
Act on medullary CV centres to reduce MAP
