The cardiac pressure volume cycle Flashcards
what are the special aspects of cerebral circulation
Brain maintains all vital functions
Constancy of flow & pressure (auto-regulation)
Circle of Willis (arteries on brains inferior surface organised into a circle, redundancy of the blood supply)
what are the special aspects of renal circulation
20-25% CO
Kidneys form only 0.5% of body weight, 50 fold over-perfused vol/weight)
Portal System
Glomerular capillaries to peritubular capillaries
Makes both ACE and Renin
Endocrine functions. Control blood vol and respond to renal pressure
what are the special aspects of skeletal muscle circulation
Adrenergic input > vasodilation Can use 80% of CO during strenuous exercise 40% adult body mass Major site of peripheral resistant Muscle pump to augment venous return
what are the special aspects of skin circulation
Role in thermo-regulation
Perfusion can increase 100X
Arterio-venous anastomoses (primary role in thermoregulation)
Sweat glands – role in thermoregulation, plasma ultrafiltrate
Response to trauma (red reaction, flare, wheal)
what is the cardiac cycle
Can be considered 4 sequential events Ventricular filling Isovolumic ventricular filling Ejection Isovolumic ventricular relaxation
how is filling and ejection shown on a pressure time graph
Sharons increase, round peak and sharp decrease for ejection and flat line for ventricular filling/ relaxation (diastolic pressure)
when does the aortic valve close
when left ventricular pressure < aortic pressure
what is isovolumic contraction
ventricles contract with no vol change as all heart valves close
what is isovolumic relaxation
ventricles relax within no volume change (ventricles empty, blood in aorta and aortic valve is closed)
how is aortic pressure shoes on a pressure time graph
slight dip at IVR, slight decrease across filling but far above diastolic pressure
how does IVR and IVC compare to S1 and S2
(mitral) S1 = IVC aortic valve opens at end, no sound
(aortic) S2 = IVR mitral valve opens at end, no sound
how do ECG waves link to ventricular pressure changes
P wave before ejection (filling)
QRS complex immediately before ejection
what is the pressure volume loop
pressure on y axis and volume on x axis IVR parallel to pressure, furthest left MO Filling along y axis, bottom MC IVC increase AO Ejection curves back to start AC
how does preload and afterload link to PV loops
IVC affected by preload
Ejection and IVR effected by after load
how do valve pathologies link to valve pathologies
Mitral stenosis _ dec in pre and afterload
Aortic stenosis - incr afterload
Mitral regurgitation - inc preload and dec after load
aortic regurgitation - inc preload
what are the valve sounds on auscultation
S1 AV valves close normally loudest
S2 SL valves close
Systole occurs between S1 and S2 (diastole has a longer duration than systole)
Murmurs are due to turbulence caused by obstacles
what causes a systolic murmur
Fluid leaves ventricle, AV regurgitation or SL stenosis
what causes a diastolic murmur
Fluid enters ventricle, AV stenosis or SL regurgitation
what causes myocytes to contract
Myosin pulling actin Sliding filament model Thin Filaments (actin) and thick filaments (myosin) Myosin – motor protein Consumes ATP Trigger is increase in free Ca2+
what is cardiac action potential
Initiated by increase in voltage (the cardiac action potential)
Cardiac action potential is longer, Ca2+ and K+ flow during plateau phase
Nodal action potential – calcium-based depolarisation
what are delayed rectifier K+ channels
Open when membrane depolarises, all gating has a delay
what are inward rectifier K+ channels
Open when Vm goes below -60mV
Very unusual, more open when cells are at rest
Functions: to clamp membrane firmly at rest
K+ channel lets K+ out of cell, repolarising it
what happens at the initial depolarisation of an AP
The cell starts at rest (-70mV)
Inward rectifier K= channels are open, k+ flowing out is dominant current
Resting membrane potential is near Ek
Something causes cell to become less negative
What is depolarisation
inside the cell the voltage becomes less negative (or more positive)
Could be nearby cell depolarising or could be a synaptic transmission where a neurotransmitter opens a ligand-gated channel
what is the positive feedback of depolarisation of an AP
The additional current of Na+ going into the cell > more depolarisation (membrane potential moves closer to 0mV)
Acts as a positive feedback loop
When the voltage goes above the threshold voltage (-50mV), the cell is committed to an AP (all or nothing)
quite positive (>+30mV)
Vm >0, period is the overshoot
What is depolarisation of an AP
voltage becomes less positive (or more negative) inside the cell
Due to the passage of time, 2 delayed-action events occur
Na+ channel inactivation > decrease Na+ current going in
Delayed rectifier K+ channels open > increase K+ going out
These cause the membrane to be less positive and more negative inside
What is the refractory period of an AP
Period of time during which neuron is incapable of reinitiating an AP
The amount of time it takes for neuron’s membrane to be ready for a second stimulus once it returns to its resting state following an excitation
The amount of time it takes for a neuron’s membrane to be ready for a second stimulus once it returns to its resting state following an excitation
Refractory period occurs mostly during after-hyperpolarisation
what is the after-hyperpolarisation of an AP
voltage inside temporarily goes slightly more negative than at rest, followed by a return to the resting membrane potential
When the voltage goes below -60mV, the inward rectifier K+ channels open again, they stay open until next depolarisation
These normally clamp the voltage toward Ek and are responsible for maintaining the resting potential
During APH: increase the K+ permeability and decrease Na+ permeability
how do cardiac and skeletal action potentials compare
Neural action potentials: ~1 ms Always the same size In skeletal muscle Action potential completed before contraction begins short refractory period means that repeated action potentials > tetany cardiac action potentials much longer up to 500 ms varies in duration and size long refractory period, no tetany
what are the phases of cardiac action potential
0 depolarisation: Na+ gates open in response to wave of excitation from pacemaker
1 transient outward current: tiny amount of K+ leaves cell
2 plateau phase:inflow of Ca2+ about balances outflow of K+
3 rapid repolarisation phase: Vm falls as K+ leaves cell
4 back to resting potential
what is the plateau phase
Dynamic equilibrium Ca2+ current in and K+ current out Decrease Vm, decrease Ca2+ current Also for K+, but much less In decreasing Ca2+ current > positive feedback Repolarisation by K+
how does the cardiac AP vary in different regions of the heart
Vary in timing and shape, atrial AP occurs earlier also a steeper and narrower shape
what are the shape and timing of the cardiac action potentials
SA node= pacemaker Av node and Bundle of His = potential pacemakers in case of atrio-ventricular conduction failure QT interval aligns with ventricular AP QRS= ventricular depolarisation T = ventricular repolarisation
what do the ventricular myocytes do in cardiac action potential
At rest, inward rectifier K= channel > outward current stabilising membrane (phase 4)
The rapid rising phase (or upstroke) of the action potentials is, exactly as in nerve and skeletal muscle, due to transient increase in inward Na current (with positive feedback, phase 0)
Depolarisation also leads to transient opening of time and voltage dependant Ca Channels (phase 2)
The total K conductance decreases rather than increases upon depolarisation
Repolarisation delayed due to b and c
how do action potentials occur in the SA and AV node
At rest spontaneously depolarises (not stable at rest because no inward rectifier)
The upstroke of the AP is due to a transient increase in inward Ca2+ (nodal upstroke slower than in ventricular myocytes)
The K conductance increases shortly after depolarisation
Initiates repolarisation as in nerve and skeletal muscles
Duration nodal AP (phases 0-3) = ~300ms
what are the phases of the nodal AP
0 depolarisation
1 & 2 don’t exist
3 depolarisation phase
4 pacemaker potential
is the SA node automatic
SA node cells are autoarhythmic
(resting potential is unstable and close to threshold)
Cells independently beat at 100bpm
SA node is normally the pacemaker (initiation of heart beat in healthy heart as have fastest rate)
Other cardiomyocytes can be too
what is the pacemaker potential
In myocytes of SA node, AV node conduction system only
Voltage drifts positive between nodal beats
Instead of resting potential because cells lack inward rectifiers
Slope of PP determines rate of firing (aka diastolic potential)
Drifts up slowly
what is the funny current
If the funny current Makes SA node cells spontaneously active HCN channel, Not a sodium channel Autorhythmicity During pacemaker potential
what does the If current lead to
Increases upon hyperpolarisation (rather than depolarisation)
Leads to net inward current
If > Na+ inward and only tiny K+ out
Depolarises towards 0mV
Blocking Ion channels of cardiac AP
During drug therapy you only block a percentage of ion channels
(block all kill patient, eg tetrodotoxin from fugu fish)
Na+ blocked to decrease conduction velocity
Changes organisation of firing in different regions of the heart, can prevent (or sometimes cause) arrythmias
Doesn’t prevent depolarisation or affect HR
Calcium channel block can decrease heart rate and decrease contractile force
