CARDIO PHYSIOLOGY Flashcards
what kind of membrane potential do pace maker cells in the heart exhibit
spontaneous pacemaker potential
what gives rise to the pacemaker potential in a pacemaker cell
decrease in K+ efflux
slow Na+ and K+ influx
transient Ca2+ influx
what kind of calcium channels allow the transient Ca2+ influx in the PMP
T-type Ca2+ channels
T for transient
what gives rise to the rising phase of the pace maker action potential and what are the channels involved
(depolarisation)
opening of Ca2+ channels - Ca++ influx
L-type Ca2+ channels
what gives rise to the falling phase of pacemaker action potential (repolarisation)
opening of K+ channels - K+ efflux
inactivation of L-type calcium channels
what is the funny current
Na and K influx
why is there AV nodal delay
cells are small and slow to conduct
allows time for atrial systole to precede ventricular systole
what is the other name for phase 0 of ventricular contractile cells action potential
depolarisation / rising phase
what is responsible for phase 0 of ventricular contractile cells action potential
fast Na+ influx
what occurs in phase 0 of ventricular contractile cells action potential
reversal of resting membrane potential from -90 to +20
what occurs in phase 1 of ventricular contractile cells action potential
closure of Na+ channels and transient K+ efflux
there is some repolarisation in phase 1 of ventricular contractile cells action potential
true/false
true
what is the other name for phase 2 of ventricular contractile cells action potential
plateau phase
unique to contractile cardiac muscle cell
what occurs in phase 2/plateau phase of ventricular contractile cells action potential
Ca++ influx
K+ efflux in background causes it to balance
can an AP be generated in phase 2?
no
what channels are responsible for phase 2
L-type Ca++ voltage gated channels
what state are the sodium channels in in phase 2
closed
what is the other name for phase 3 of ventricular contractile cells action potential
falling phase / repolarisation
what causes phase 3 of ventricular contractile cells action potential
inactivation (closure) of ca++ channels
opening of K+ channels - K+ efflux
can an AP be generated during phase 3
no
what is the resting membrane potential of a ventricular cardiac muscle cell
-90
what charge is ventricular contractile cells action potential depolarised to
+20
what occurs at phase 4 of ventricular contractile cells action potential
membrane rests are membrane potential
how does vagal stimulation have a negative chronotropic effect on the heart
cell hyperpolarises - takes longer to reach threshold
slope of PMP decreases
frequency of PMP decreases
negative chronotropic effect
how does sympathetic stimulation have a positive chronotropic effect on the heart
slope of PMP increases
reaches threshold quicker
frequency of AP increases
positive chronotropic effect
what does sympathetic stimulation supply
SA node
AV node
myocardium
what does parasympathetic stimulation supply
SA and AV nodes
what neurotransmitter and receptor are working in the heart with parasympathetic stimulation
ACh on M2 receptors
what neurotransmitter and receptor are working in the heart with sympathetic stimulation
NA on B1 receptors
sympathetic stimulation decreases AV nodal delay
true/false
true
parasympathetic stimulation increases AV nodal delay
true/false
true
what does SS do to the pacemaker cell K+ efflux
decrease
what does SS do to the pacemaker cell Na+ and Ca++ influx
increase
what does PSS do to the pacemaker cell K+ efflux
increase
what does PSS do to the pacemaker cell Na+ and Ca++ influx
decreases
what is atropine
competitive inhibitor of ACh
what do hypoxia and hypercapnia do to the PMP slope
increase
–> positive chronotropic effect
what does hypokalaemia do to the PMP slope
increases
–> positive chronotropic effect
what does hyperkalaemia do to the PMP slope
decreases
–> negative chronotropic effect
what cells “provide mechanical adhesion between adjacent cardiac cells to ensure tension is developed and transmitted to the next cell”
desmosomes
where are desmosomes found
within intercalated discs
do cardiac muscle cells have neuromuscular junctions
no
is actin or myosin thick and dark
myosin (bigger word)
how do cardiac muscle cells contract
actin slides over myosin to produce muscle tension
for what 2 reasons does ATP bind to myosin heads
energise it
or breakdown cross bridge between myofibrils
if calcium is present what happens to the energised myosin
calcium switches on cross bridge formation
binds to troponin complex on myosin, causes conformational change which exposes actin binding site and cross bridge forms
what happens to the energised myosin head if no calcium is present
goes into resting state - cross bridge binding sites are covered by troponin-tropomyosin complex
what happens once myosin binds to actin
bending - myosin and actin overlap)
after bending, what happens if ATP is present
ATP breaks down the cross bridge and cycle starts again
after bending what happens if ATP isn’t present
rigor complex formed
what is calcium usually stored
in the sarcoplasmic reticulum in lateral sacs
what is the release of calcium from SR dependent on
presence of extracellular Ca++
explain calcium induced calcium release
Ca++ influx during plateau phase of AP causes Ca++ to be released from SR to cause contraction
how is relaxation achieved in cardiac muscle cell
removal of ca++ back into SR or out of cell
what is the optimal fibre length of cardiac muscle cells
stretching
as opposed to skeletal which is the resting muscle length
what does the refractory period prevent happening
tetanic contractions (continuous)
what is the EDV
end diastolic volume
volume of blood remaining in each ventricle following diastole
what is the determining factor of EDV
VR
what is the equation for SV
EDV - ESV
what is SV
volume of blood ejected by each ventricle per heart beat
what is the preload
volume of blood in each ventricle before contraction
what is the afterload
resistance against which the heart has to pump after contraction
what does an increased EDV do to the force of contraction and why
increased EDV increases force of contraction
stretch increases troponin affinity for calcium
how does VR affect SV
VR increases
EDV increases
stretch increases
SV increases
what is the frank starling law
the greater the EDV the greater the SV during systole
how does FS compensate for increased afterload
increased after load decreased SV increased EDV increased stretch increased contractile force SV returns to normal
what way does sympathetic stimulation shift the FS curve
to the left - increased SV
Frank Starling’s Law states that the more the ventricles are filled with blood/ the greater the EDV - the greater the systolic contractions. Sympathetic simulation increases systolic contraction and shifts the curve to the left.
what way does shock shift the FS curve
to the right
what way does exercise shift the FS curve
to the left
what is the equation and definition of CO
CO = SV x HR
volume of blood pumped out by each ventricle per minute
what is the average CO in a resting adult
5L
with a HR of 75 what would diastole equal and what would systole equal
D - 0.5s
S - 0.3s
what is the pulse pressure and what is it normally
systolic - diastolic BP
30-50
what are the 5 stages of the cardiac cycle
passing filling atrial contraction isovolumetric ventricular contraction ventricular ejection isovolumetric ventricular relaxation
what occurs during passive filling
AV valves open
blood flows into ventricles
pressures in atria and ventricles close to 0
what happens during atrial contraction
remaining atrial volume fills ventricles by atrial systole completing EDV
what on the ECG represents atrial depolarisation
and what represents atrial contraction
atrial depolarisation - p wave
atrial contraction - P - QRS
what occurs during isovolumetric ventricular contraction
AV valves shut as Pa < Pv
what happens during ventricular ejection
aortic/pulmonary valves open and Pv > Parteries SV ejected ESV left ventricular pressure falls aortic and pulmonary valves shut S2
what does dicrotic notch represent
aortic valve closing
what does s2 signal
the start of isovolumetric ventricular relaxation (diastole)
ventricle again a closed box
when ventricular pressure falls below Pa AV valves open
- Pa increasing as it fills with blood (VR)
- Pv decreasing due to relaxation
when is S1 in cardiac cycle
isovolumetric ventricular contraction
when do the aortic and pulmonary valves open
ventricular ejection
what does the QRS complex represent
ventricular depolarisation
what is blood pressure
outward force exerted by blood on blood vessel walls
when is turbulent blood flow heard through a stethoscope
when external pressure is between S and D pressure
what is the 1st Korotkoff sound
peak systolic pressure
what is the 5th korotkoff sound
no sound - diastolic pressure
measurement taken after last sound
what is MAP
average arterial BP during a single cycle
what is the nucleus tractus solitarius
1st synapse of all CVS afferents in medulla
give 5 different equations for MAP
DP + 1/3 (SP - DP)
[(2 x DP) + SP]/2
DP + [SP - DP]/3
CO x TPR
SV x HR x TPR
diastolic portion is twice as long as systolic portion
true/false
true
what is the main way of controlling resistance to blood flow
changes to blood vessel radius
resistance to blood flow is directly proportional to what
thickness and length of vessel
how is resistance linked to radius
directly proportional to 1/radius^4
how is NO produced
by vascular endothelium
from AA L-arginine
through enzymatic action of NO synthase (NOS)
what is flow dependent nitric oxide formation
sheer stress on vascular endothelium due to increased blood flow causes release of calcium in endothelial cells and subsequent activation of NOS
what is receptor stimulated nitric oxide formation
vasoactive substances act as chemical stimuli to induce NO formation
what does NO do when released from vascular endothelium
diffuses into adjacent SMCs where it activated cGMP which stimulates smooth muscle relaxation
what are baroreceptors
mechanoreceptors sensitive to stretch
what happens when there is higher BP re baroreceptor
higher BP
greater the firing of baroreceptors in afferent neurones
where are carotid baroreceptors found and what nerve do they fire through
carotid sinus CN IX (glossopharyngeal)
where are aortic baroreceptors found and what nerve do they fire through
aortic arch CN X (vagus nerve)
what happens in high BP is sustained
firing decreases and is reset to a higher steady level
where is CV control centre in brain
medulla
how does decreased firing of baroreceptors increase BP
decreased firing decreased parasympathetic activity increased sympathetic activity increased vasoconstriction increased SVR and tone in veins increases VR and SV increased BP
what is postural hypotension
failure of BRR to adjust to gravitational shifts in blood
how do proteins move across vascular bed into interstitial fluid
vesicular transport
where is renin released from
juxtapulmonary apparatus in kidney
where is angiotensinogen produced
liver
where is ACE produced
pulmonary vascular endothelium
where is aldosterone released from
adrenal cortex
what does aldosterone do
increases thirst and acts on kidneys to increase ADH - Na+ and water retention
systemic vasoconstriction - endothelia produced - increases SVR
what cells release secrete renal tubular fluid
macula densa - specialised cells of kidney tubules
where is ANP synthesised and stored
atrial myocytes
what does ANP do and how
decreases BP
causes excretion of Na+ and water
decreases renin release, vasodilates
what is ANP released in response to
atrial distension - hypervolaemic state
or neurohormonal stimuli
is there is high serum BNP and N-terminal piece of pro-BNP what should you suspect
heart failure
what is ADH release monitored by
osmoreceptors in brain close to hypothalamus
where does ADH act
kidney tubules
ADH causes a small degree of vasoconstriction due to endothelin production
true/false
true
what is the vasomotor tone
vascular smooth muscle is partially constricted at rest due to tonic discharge of sympathetic system
what is the neurotransmitter and receptor in vasomotor tone
NA
alpha-1 adrenoreceptors
where is adrenaline released from
adrenal medulla
what does adrenaline on alpha receptors cause
vasoconstriction
what does adrenaline on beta receptors cause
vasodilation
where are beta receptors mainly found
skeletal and cardiac muscle arterioles
what does vasomotor tone do to the SVR and MAP
increases
what is the venomotor tone
stimulation of sympathetic nerve fibres in venous smooth muscle causing venous constriction
what does venomotor tone do to the VR, MAP and SV
increases
local metabolic conditions can override extrinsic control of vascular smooth muscle
true/false
true
does decreased local PO2 cause systemic vasodilation?
yes
does increased local PCO2 cause systemic vasodilation?
yes
does decreased osmolarity of ECF cause systemic vasodilation?
no
increased osmolarity of of ECF causes vasodilation
does adenosine release cause systemic vasodilation?
yes
does increased local H+ cause systemic vasodilation?
yes
does decreased local K+ cause systemic vasodilation?
no
increased local K+ causes systemic vasodilation
what happens to resistance vessels in the brain and kidney when MAP falls
resistance vessels dilate to increase flow
how does muscle activity increase VR to heart
large veins lie in limbs between skeletal muscle
contraction of muscle aids VR
prothrombotic, pro-inflammatory and pro-oxidant agents are all endothelial produced vasoconstrictors or vasodilators
vasoconstrictors
which cause vasoconstriction and which cause vasodilation -
endothelin histamine serotonin bradykinin prostaglandins thromboxane A2 leukotrienes nitric oxide
vasodilators - histamine bradykinin prostaglandins nitric oxide
vasoconstrictors - serotonin thromboxane A2 leukotrienes endothelin
during exercise what happens to blood flow to kidneys and gut
decreases due to vasomotor tone causing vasoconstriction in this areas
during exercise what happens to blood flow to skeletal and cardiac muscle
increases - vasodilation in these areas due to metabolic hyperaemia which overrides sympathetic effects
when does physiological splitting of S2 occur
where is this heard
INspiration (INnocent) pulmonary area (left 2nd ICS at sternal border)
what is shock
abnormality in the circulatory system resulting in inadequate tissue perfusion and oxygenation –> anaerobic metabolism –> accumulation of waste –> cellular failure
what kind of pulse is seen in hypovolaemic shock
fast pulse
what are 3 causes of non-hemorrhagic hypovolaemic shock
vomiting
diarrhoea
excessive sweating
what is the 3 end stages common to all shock
DECREASED SV
DECREASED CO AND BP
LOW PERFUSION AND OXYGENATION
what is hypovolaemic shock
loss of blood volume
what is cardiogenic shock
sustained hypotension due to decreased cardiac contractility
what is an example of obstructive shock
tension pneumothorax
what happens in obstructive shock
increased intrathoracic pressure decreased VR (reduced gradient) reduced EDV
what is neurogenic shock
loss of sympathetic tone (vasomotor) so increased vasodilation
what kind of pulse is seen in septic shock
bounding
what is an example of vasoactive shock
anaphylaxis
what is an example of disruptive shock
septic shock
what happens in vasoactive/disruptive shock
release of vasoactive mediators/abnormal distribution of BF in smallest BVs
increased vasodilation and increased capillary permeability
until what point can compensatory mechanisms (baroreceptors/chemoreceptors) work with BV loss
up until 30% is lost
what is the treatment for shock
ABCDE
1) high flow oxygen
2) volume replacement
3) shock specific treatment
what is given for obstructive shock
immediate chest drain for tension pneumothorax
what is given for septic shock
vasopressors
what is given for cardiogenic shock
inotropes
how does heart increase oxygenation
increase coronary flow
already has 75% oxygen extraction so this can’t be increased - organ of highest O2 demand
when is the peak coronary flow
diastole
what 2 arteries supply the brain
internal carotid arteries
vertebral arteries
is grey or white matter more sensitive to hypoxia in the brain
grey
what artery is formed from the joining of the 2 vertebra arteries
basilar artery
how is the circle of willis formed
basilar artery anastomoses with internal carotids
where do cerebral arteries arise from
circle of willis
when does auto regulation of cerebral flood flow fail
MAP <60 or >100
what does decreased PCO2 cause in the brain
cerebral vasoconstriction
why does hyperventilation lead to fainting
decreased PCO2 causes cerebral vasoconstriction
what is the equation for CPP
MAP - ICP
which end are the forces for filtration greater than forces for absorption and vice versa
forces for filtration - greater at arterial end
forces for absorption - greater at venule end
capillary hydrostatic pressure and interstitial fluid osmotic pressure are forces for
filtration
capillary osmotic pressure and interstitial fluid hydrostatic pressure are forces for
absorption
what is NET filtration
forces for filtration - forces for absorption
why does reduced capillary osmotic pressure cause oedema
reduced driving force driving blood back into capillary
what is the JVP a wave
Atrial contraction
what is the JVP c wave
bulging of tricuspid valve into atrium during ventricular Contraction
what is the JVP v wave
rise of atrial pressure during atrial filling
true / false
JVP waves occur before RA pressure waves
false
JVP waves occur after RA pressure waves
what does exercise do to the SBP / DBP / PP
SBP increases
DBP decreases
Pulse pressure increases
what is ischaemic stroke
obstruction due to emboli or atherothrombosis causing interrupted blood supply to brain
what is haemorrhage stroke
rupture of damaged artery causing interrupted blood supply to brain
what are varicose veins
do they cause a reduction in CO
pooling of blood in lower limbs due to incompetent valve
no - due to chronic compensatory mechanism of increasing BV
LDL is taken up from blood into where
intimate of artery
what is LDL oxidised to
atherogenic OXLDL
what role do monocytes play in atherosclerosis disease progression
migrate across endothelium into intima where they become macrophages and take up OXLDL
what are macrophages converted to when they take up OXLDL and what does this form
foam cells –> fatty streak
what does the release of inflammatory substances cause
division and proliferation of SMCs into the intima
what does an atheromatous plaque consist of
lipid core (dead foam cells) and fibrous cap (SMCs and connective tissue)
what % of total body fluid is made up by ECF
1/3
which one of the following does not stimulate endothelin production ADH Angiotensin II mechanical shearing force prostacyclin
prostacyclin
what germ layer is the heart derived from
mesoderm
what is involved in primary haemostasis
the formation of a soft clot - platelets bind to fibrinogen to form a soft clot
what is involved in coagulation
formation of a solid clot by the end process or propagation when thrombin cleaves fibrinogen to form fibrin.
how many branches of the aorta are there during embryological development
6
what is the function of the vitelline veins
drain the yolk sac
Which layer of a blood vessel contains endothelial cells, basal lamina and connective tissue?
tunica intima
umbilical veins carry…
oxygenated blood
