Physiology Flashcards
what is autorhythmicity
Ability for heart to beat without external stimuli
Where do you find Pacemaker cells
SA node of heart, upper right atrium near super vena cava
A heart controlled by SA node is said to have what
Sinus rhythm
Do pacemaker cells have a resting membrane potential?
No
What do pacemakers have instead and why?
They have pacemaker potential, constantly moving towards threshold for AP. Continuous spontaneous pacemaker potentials.
What is stage 4 of pacemaker AP
decreased efflux of K, transient influx of Ca and funny current (influx of Na)
What are the phases of the AP in pacemaker cells
Stage 4: spontaneous depolarisation, stage 0: upstroke, stage 3, depolarisation
What is stage 0 of pacemaker AP
Upstroke due to Ltype Ca channels opening - influx
What happens in stage 3 of pacemaker AP
repolarisation as K channels re-open and inactivation of . ltype Ca
Myocardial cells pass the impulse from the __ node to the __ node via ___.
SA, AV, gap junctions (cell-to-cell current flow)
why is conduction delayed in AV node
so atria can fully contract
what are the structures that pass AP to ventricles (bundle + fibres)
His, left and right bundles, purkinje
what are the phases of cardiac cells (different from pacemakers)
phase 4: resting potential Phase 0: upstroke phase 1: early repolarisation, phase 2: plateau, phase 3: repolarisation
explain phase 0 of cardiac cells:
fast depolarisation by na influx
explain phase 1 of cardiac cells
closure of Na channels and transient K efflux
explain phase 2 of cardiac cells
l type calcium channels open and ca influx
explain phase 3 of cardiac cells
closure of l type ca channels and activation of k channels for an efflux
explain phase 4 of cardiac cells
resting membrane potential
what effect does sympathetic chain have on heart
speeds it up
what effect does parasympathetic chain have on heart
slows it down
what nerve has a constant effect on the SA and AV? lowering its HR from 100bpm to 70
vagus nerve exhibiting vagal tone
what is bradycardia and tachycardia
bradycardia is 60 bpm, tachycardia is 100bpm
what does the vagal nerve do
slows heartrate and increases AV node delay, slope of pacemaker potential decreases,
what is the neurotransmitter and receptor of the parasympathetic chain in the heart
M2 receptor, acetly choline (ACh)
what drug is a competitive inhibitor of acetylcholine and is used in bradycardia
atropine
what is a negative chronotropic effect
slows heart rate
which nerve branch supplies the AV, SA and myocardium of the heart
sympathetic
what effect does sympathetic have on heart
increases HR, decreases AV nodal delay, increases force of contraction (positive chronotropic effect)
what is the neurotransmitter and receptor of sympathetic in the heart
noradrenaline of B1 adrenoreceptors
describe cardiac myocytes structure
striated with central nucleusand regular arrangement of contractile proteins
what are myocytes electrically coupled with
gap junctions
what are gap junctions
protein channels that ensure excitation reaches all cardiac cells
what do desmosomes do
within intercalated discs provide adhesion
what do muscle fibres contain for contracting
myofibrils
what do myofibrils contain
thick and thin filaments, myosin and actin
describe myosin
thick and appears dark
describe actin
thin and appears light
within each myofibril, what are actin and myosin arranged into
sarcomeres
What is essential for myosin and actin contraction
ATP and calcium
what does calcium do in myosin actin activation
binds to troponin C on myosin head allowing crossbridge to form
where is calcium released from
SR
what is calcium induced calcium releases
an influx of calcium will cause calcium to be released from SR causing contraction
what is the refractory period
a short length of time following an AP where it is not possible to produce another AP
Why is the refractory period necessary
to prevent continuous (tetanic) contractions of the heart
in the plateau stage the closure of Na channels means cell cant be depolarised, and in descending phase k channels are open do cell cant be depolarised, what effect is this
refractory period
what is the stroke volume
the volume of blood ejected by the ventricles per beat
the end diastolic volume (EDV) - the end systolic volume (ESV) is equal to?
stroke volume
EDV dictates the cardiac afterload true/false
false it’s the preload.
What is EDV determined by
venous return
what is the frank-starling curve
the relationship between EDV, SV and venous return
what does the frank-stirling curve mean
the greater the EDV, the greater the SV and therefore venous return
what is the optimal length for energy in cardiac muscle
stretching (for increases EDV)
what and when is afterload?
resistance the heart pumps into? after heart contracts
how does sympathetic control of the heart have a positive inotropic effect
greater activation of ca channels in SR, reduces duration of systole and diastole
does the parasympathetic nerves cause a inotropic (contractility effect)
no
where are adrenaline and noradrenaline released from to have a inotropic and chronotropic effect
adrenal medulla
what is cardiac output and equation
volume of blood pumped by ventricles per min CO = SV x HR
what is the cardiac cycle
the events occurring from the beginning of one heartbeat to the next
what is diastole
ventricles relax and fill with blood from atria
what is systole
ventricles contract and pump blood to aorta and pulmonary artery
what is the order of events in cardiac cycle
passive filling, atrial contraction, isovolumetric ventricle contraction, ventricular ejection, isovolumetric ventricular relaxation
what are the steps in passive filling (valves, pressures, % full)
AV valves open, pressure in atria and ventricles close to 0, aortic valves close and aortic pressure is around 80, ventricles become 80% full
what are the steps in atrial contraction (ECG)
P wave in ECG shows atrial depolarisation, contraction occurs between p and QRS. when atria finish contraction = EDV
steps of isovolumetric ventricular contraction (ECG, pressure, valves, heart sounds)
contraction is after QRS, the ventricular pressure rises, when it exceeds atrial pressure AV valves shut producing first heart sound, pressure rises around closed space
steps of ventricular ejection? pressure, valves, SV, ECG, heart soundsSS
when pressure exceeds aortic/ pulmonary, the valves open, SV is ejected leaving ESV, T wave shows repolarisation, pressure falls, when below aortic/ pulmonary valves close to produce 2nd heart sound, vibration is dichroitic nothc
isovolumetric ventricular relaxation (sound, pressure, valves)
2nd heart sound signals start, the pressure falls, when below atrial pressure the AV valves open again
when do the heart sounds occur
during ventricular contraction, mitral valve (S1), and at the start of ventricular relaxation, aortic valve (S2)
why does the pressure of the heart and aorta never return to 0
due to elastic properties of arteries, would have too much pressure exerted on them and collapse and recoil
what is the JVP and what can it be used to identify
indirect measure of central venous pressure, shows right sided heart failure.
what is BP
the outwards hydrostatic pressure exerted by the blood on vessel walls
what is systolic BP (and normal range)
pressure exerted on aorta when heart contracts >120
what is diastolic BP (and normal range)
pressure on aorta when heart relaxes >80
what are the values for hypertension
140/90
what is pulse pressure? normal ranges
difference between diastolic and systolic 30-50mmHg.
in what fashion does blood flow in the arteries
laminar
what pressures do BP cuffs exert and how do they work
external exceeds internal so no sound, if external between systolic and diastolic can here turbulent flow.
peak systolic pressure reveals what sound
1st korotkoff (first sound heard when checking BP)
what is heard in the 2nd and 3rd korotkoff sounds
intermittent sounds due to turbulent flow
when is diastolic ‘heard’?
When the sounds dissapears, 5th korotkoff sound.
the pressure gradient between the ___ and the ___ ___, drives ____ circulation
aorta, right atrium, systemic
pressure gradient = ___ - ____
MAP - central venous pressure (right atrium) which is close to 0.
what is the mean arterial blood pressure?
average arterial BP during single cardiac cycle
how long is diastole compared to systole
twice as long
what are the 2 equations for MABP
MABP = [(2 x diastolic) + systolic]/3 MABP = DBP + 1/3 pulse pressure
what re the ranges of normal for MABP
70-105
what MABP is needed to perfuse major organs
at least 60
what happens if MABP too high
damage blood vessels and extra strain on heart
what is the relationship between MABP, CO and SVR
MABP = CO x SVR (CO = HR x SV)
what do baroreceptors detect
changes in BP
where do baroreceptors send signals too
medulla
what are the effectors of baroreceptor
heart and blood vessels
in what loop do baroreceptors work
negative feedback
where do you have baroreceptors
carotid and aortic
what happens if baroreceptors detect too low BP
carotid baroreceptors decrease firing, vagal activity decreases, sympathetic increases, vasoconstriction
what happens if baroreceptors detect too high BP
carotid baroreceptors increases firing, vagal activity increases, sympathetic decreases, vasoconstriction decreases
what is postural hypotension
when someone stands from lying quickly and BP rapidly drops
how is postural hypotension corrected in a healthy person
venous return rapidly drops, MAP decreases so baroreceptors decrease rapidly
in a person with diagnosed postural hypotension what does there body do? (baroreceptors)
baroreceptors fail to respond to gravitational shifts
what are risk factors for postural hypotension
age, meds, disease, reduced blood volume, prolonged bed rest
what is a positive test for postural hypotension
drop within 3 mins of lying to standing: systolic at least 20, diastolic at least 10
symptoms of postural hypotension
light headedness, dizziness, blurred vision, faints and falls
baroreceptors can detect chronic hypertension? true/false
false, they can only detect acute changes
the total body fluid is made of ICF and ECF in what ratios
2/3 ICF, 1/3 ECF
what is ECF composed of
plasma volume and interstitial fluid volume
what happens if plasma volume falls
fluid is moved from interstitial compartment
___ is controlled if ECFV is controlled
MABP
hormones that regulate ECFV generally regular what 2 substances
salt and water
what 3 hormones mainly control ECFV
renin-angiotensin-aldosterone system (RAAS), natriuretic peptides NP, antidiuretic hormone (ADH)
if there is low BP in the kidney (low Na in renal tubular fluid), what is released
renin
renin converts ___ produced in the ___ to ____
angiotensinogen produced in liver to angiotensin I
what is angiotensin I converted too
angiotensin II
what enzyme converts angiotensin I to angiotensin II and where is it produced
ACE in the lungs
angiotensin II stimulates the adrenal cortex to release what
aldosterone
what does aldosterone do
retain water and sodium from kidneys
apart from stimulate the release of aldosterone, what else does angiotensin II do?
causes vasoconstriction and increases the release of ADH
what do natriuretic peptides do?
cause excretion of salt and water in kidneys and decreases renin release. (decrease BP).
what are the 2 types of NP
atrial NP and brain-type NP
where is ANP stored and when is it released
atrial myocytes, in response to atrial distension
where is BNP synthesised and what is it cleaved to?
synthesised in brain, ventricles and other, pre-BNP –> postBNP –> BNP.
where is the precursor of ADH stored and where is it synthesised
posterior pituitary and hypothalamus
what stimulates the release of ADH
it increases BP, low ECFV and high plasma osmolality
what are the main resistance vessels
arterioles
what type of vessels hold the most blood at rest
veins
what is the stroke volume influenced by
Preload, afterload and contractility
what is the relationship for MAP
MAP = CO (HR x SV) x SVR
resistance is directly proportional to what 2 things, and inversely to what 1 thing
vessel length and viscosity, and radius (mainly controls it)
what type of nerve supply acts on arterial smooth muscle
sympathetic
artery smooth muscles are partially constricted at rest by sympathetic nerves, what is this called?
vasomotor tone
where is adrenaline produced
adrenal medulla
where are alpha receptors found
skin, gut kidney
where are beta receptors found
cardiac and skeletal
can intrinsic controls override extrinsic ones?
yes, to match their perfusion needs
name some metabolites that cause relaxation and hyperaemia (6) - opposites cause constriction
decreased PO2, increased CO2, decreased pH (acid), increases EC K, increases osmolality, adenosine
name some local humoral agents that are dilators, often released in injury
histamine, bradykinin, NO
where is NO produced, what is it’s precursor and enzyme
vascular endothelium, amino acid l-argine –> NO by NOS
how is NO production stimulated
stress on endothelium causes it’s release for vasodilation.
what can cause damage to endothelium
high BP, high cholesterol, diabetes, smoking
what humoral agents causes constriction
serotonin, thromboxane, leukotrienes, endothelin
what physical intrinsic controls apply
temp and myogenic response
what 4 factors affect venous return
venomotor tone, blood volume, resp pump and skeletal pump
what nerves supply venous smooth muscle
sympathetic
where are large veins situated and what type of valves are in place
in-between skeletal muscle, one way valves
during exercise sympathetic nerve activity increases to cause increases HR and SV, this causes reduced flow to what areas
kidney and gut
during exercise, what type of muscles metabolic needs override vasomotor drive
skeletal and cardiac, ie increased blood flow
what is ‘shock’
an abnormality of the circulatory system resulting in inadequate tissue perfusion
what are the 4 types of shock
hypovolaemic, cardiogenic, obstructive and disruptive
what is hypovolaemic shock and what can cause it
loss of blood volume, haemorrhage, vomiting and diarrhoea
what is cardiogenic shock and what can cause it
heart muscle has decreased contractility, MI can cause it
what is disruptive shock and what can cause it
loss of sympathetic tone to blood vessels, can be from neurogenic shock (trauma) and sepsis
what is obstructive shock and what can cause it
increases pressure in thoracic cavity which decreases venous return, can be caused by pneumothorax, cardiac tamponade
how do you treat shock (generally)
ABCDE, O2, volume replacement (except cardiogenic)
how does vasoactive shock arise
release of vasoactive mediators causes vasodilation
in hypovolaemic shock there are compensatory mechanisms until what % of blood loss
30%.
where do the right and left coronaries arise from
base of the aorta
where does most of the coronary venous blood drain too
coronary sinus right atrium
what is the only way to increase o2 in the heart? (what doesn’t work)
increase flow, O2 extraction is not possible
what effects does low PO2 have on coronary arterioles
vasodilation
what effect does sympathetic nerves have on coronary arteries
dilate it to increase SV and HR
when does peak coronary flow occur
diastole
which arteries supply cerebral circulation
internal carotids and vertebral
what arteries anastomose to form the circle of willis, what arises from this
basilar and carotid, major cerebral arteries
if one artery is obstructed can cerebral perfusion be maintained? what if a smaller branch is blocked?
Yes perfusion can be maintained, deprive small region of the brain = stroke
how does the brain respond to decreases PCO2
vasoconstriction, why hyperventilating leads to fainting
how does autoregulation in cerebral circulation work?
increased MAP causes constriction, decreased MAP causes dilation. only works between 60-160 mmHg
how does increases intracranial pressure affect blood flow? what can cause this?
increased cranial pressure decreases flow so as not to damage brain, can happen in trauma (swelling) and tumours
in the pulmonary circulation, why do the absorption forces exceed filtration
to prevent oedema
why does hypoxia in lungs cause vasoconstriction
to prevent blood from going to poorly ventilated areas of the lungs
in exercise, what overcomes the sympathetic vasoconstrictor tone in skeletal muscle
local hyperaemia and adrenaline
what is interstitial fluid
extracellular fluid, the space between cells and blood
how does gas, exchangeable proteins, soluble substances and plasma proteins cross capillary walls
diffusion, vesicular transport, pores and they don’t
how is capillary fluid driven
pressure gradients
what is the NET filtration pressure
forces favouring filtration - forces favouring reabsorption
where do forces favouring filtration occur
capillaries
where do forces favouring reabsorption occur
venules
where does excess fluid drain
lymphatic system
what factors affect filtration in capillaries
capillary hydrostatic pressure and interstitial fluid osmotic pressure
what factors affect reabsorption in venules
capillary osmotic pressure and interstitial hydrostatic pressure
what is oedema?
an accumulation of fluid in the interstitial space, can compromised gas exchange in lungs
what can raised capillary hydrostatic pressure (reduced filtration) that can cause pulmonary oedema
raised venous pressure, LV failure, prolonged standing
how does left ventricular failure cause pulmonary oedema
raised pressure in LA which increases pulmonary pressure and capillary pressure.
