the cardiac pressure and volume cycle Flashcards
explain the special aspects of the cerebral circulation? 3
- brain maintains all vital functions
- constancy of flow and pressure
- circle of Willis= arteries on the brains inferior surface organised into a circle, this means there is a redundancy of blood supply, so if one bridge of the circle is blocked, it can be supplied through another
what are the special aspects of renal circulation? 4
- 20-25% of cardiac output when body is a rest
- kidneys only form a 0.5% of body weight
- portal system where glomerular capillaries join to peritubular capillaries
- makes both ACE and renin, which have endocrine functions, control blood volume and respond to renal blood pressure
what are the special aspects of skeletal muscle circulation? 5
- androgenic input leads to vasodilation
- can use 80% of cardiac output during strenuous exercise
- 40% of adult body mass
- major site of peripheral resistance
- muscle pump augments venous return
what are the special aspects of skin circulation? 4
- role in thermoregulation- perfusion can increase 100x
- arteriovenous anastomoses have a primary role in thermoregulation
- sweat glands have a role in thermoregulation, and produce plasma ultrafiltrate
- response to trauma= red reaction, flare, wheal
what are the events in the cardiac cycle? 4
- ventricular filling
- isovolumic ventricular contraction
- ejection
- isovolumic ventricular relaxation
what does isovolumic mean?
the volume of the ventricle doesn’t actually change
where do the ECG waves come in relation to the ventricular pressure changes?
- precede them
what is the isovolumic ventricular contraction affected by?
preload
what is the ejection affected by?
afterload
what is the isovolumetric ventricular relaxation affected by?
afterload
what happens to the cardiac cycle during mitral stenosis? 2
- decreased preload
- decreased afterload
what happens to the cardiac cycle during aortic stenosis?
- increased afterload
what happens to the cardiac cycle during mitral regurgitation?
- increased preload
- decreased afterload
what happens to the cardiac cycle during aortic regurgitation?
- increased preload
what is the general rule for a systolic murmur? 2
- fluid leaves the ventricle
- AV regurgitation or SL (semilunar) stenosis
what is the general rule for a diastolic murmur? 2
- fluid enters the ventricle
- AV stenosis, Sl regurgitation
name 2 types of K+ channels? 3
- delayed rectifier K+ channels = open when the membrane depolarises, but all gating takes place without a delay
- inward rectifier K+ channels= open when Vm goes below -60mV, clamps the membrane firmly at rest
explain the initial depolarisation of an AP? 2
- inward rectifier K channels open, K flows out
something causes the cell to become less negative
explain the positive feedback of depolarisation? 4
- causes a few Na+ channels to open
- the additional current of Na+ leads to more depolarisation
- positive feedback loop
- once the voltage goes above the threshold (-50mV) the cell is committed to an AP
explain repolarisation? 4
- voltage becomes less positive on the inside of the cell
- delayer NA+ channel inactivation
- Delayed rectifier K+ channels open
- this causes the membrane to be less positive and more negative inside
explain the refractory period? 3
- period of time when the neuron is incapable of retaining an AP
- occurs mostly during hyperpolarization
- if a functional description
explain hyperpolarisation? 2
- at the end of an AP, the voltage inside temporarily goes more negative than at rest followed by a return to the resting membrane potential
- when the voltage goes below -60mV, the inwards rectifier K channels open again and stay open until the next depolarisation
describe the phases of the ventricular myocyte action potential? 5
- phase 0= depolarisation: Na+ gates open in response to a wave of excitation from the pacemaker
- phase 1= transient outward current: tiny amount of K+ leaves the cell
- phase 2=plateau phase: inflow of Ca2+ just about balances outflow of K+
- phase 3= rapid repolarization phase: Vm falls as K+ leaves the cell
- phase 4= back to resting potential
compare neuron, skeletal muscle and cardiac action potentials? 3
- neurons= 1ms, always the same
- skeletal= AP completed before contraction begins, short refractory period means that repeated AP can cause tetany
- cardiac= much longer, up to 500ms, varies in duration and size, long refractory period so no tetany
describe the plateau phase? 3
- dynamic equilibrium of Ca2+ in and K+ out
- decreased Vm leads to decreased ca2+ current, not as much decrease for K+
- as there is a decrease in Ca2+ current, positive feedback causes repolarization by K+
what determines the ECG recording?
- the cardiac AP varies in timing and shape in different regions of the heart
describe the shape and timing of cardiac action potentials? 5
- SA node= pacemaker
- AV node and bundle of His= potential pacemakers in case of atrioventricular conduction failure
- QT interval aligns with ventricular AP
- QRS= ventricular depression
- T= ventricular repolarization
describe the ionic basis for an action potential in ventricular myocytes? 4
- at rest, the inward rectifier K+ channel has an outward current which stabilizes the membrane (phase 4)
- the rapid rising phase of the action potential is, exactly as in the nerve and skeletal muscle, due to a transient increase in inward Na current (with positive feedback- phase 0)
- depolarisation also leads to transient opening of time and voltage dependent CA2+ channels (phase 2)
- the total K+ conductance decreases rather than increases upon depolarisation
explain AP in the SA node and the AV node? 4
- at rest it spontaneously depolarises, not stable at rest because there is no inward rectifier
- the upstroke of the AP is due to a transient increase in inward CA2+, not due to NA+. nodal upstroke is slower than ventricular myocytes
- the K+ conductance increases shortly after depolarisation which initiates repolarization
- duration of nodal AP is around 300ms
explain the automaticity of the SA node? 3
- the SA cells are autorhythmic, so resting potential is unstable and close to the threshold
- cells independently beat at 100bpm, which can be increased by symp activity and decreased by parasymp
- SA node is normally the pacemaker as it has the fastest rate
explain pacemaker potential? 4
- in myocytes of the SA node, AV node and conduction system only
- voltage drifts positive between nodal beats instead of resting potential because the cells lack inward rectifiers
- the slope of the PP determines the rate of this firing
- also called the diastolic potential
explain the If (funny current)?5
- If makes the SA node cells spontaneously active
- driven by HCN channel (responsible for Na+ in and K+ out)
- increases upon hyperpolarization rather than depolarisation
- leads to ent inward current, a lot of Na+ inwards
- depolarises cell towards mV
explain blocking ion channels of the cardiac AP? 3
- only block a % of channels otherwise you would kill the patient
- Na+ channel block leads to a decrease in conduction velocity, changing the organisation fo firing in different regions of the heart, preventing arrhythmias, does not prevent depolarization of decrease HR
- Ca2+ channel block can decrease the heart rate and contractile force
