Cardiac Pressure Volume Cycle Flashcards
Cerebral Circulation
Brain maintains all vital
Constancy of flow and pressure - autoregulation
Circle of Willis - arteries on brain’s inferior surface organised into a circle - redundancy of a blood supply
Renal Circulation
20-25% of cardiac output
Portal system - glomerular capillaries to peritubular capillaries
Makes both ACE and renin - endocrine funcitons, controlling blood volume, responding to renal blood pressure
Skeletal Muscle Circulation
Adrenergic input –> 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
Skin Circulation
Role in thermoregulation (perfusion can increase 100x)
Arterio-venous anastomoses (primary role in thermoregulation)
Sweat glands (thermoregulation and plasma ultrafiltrate)
Response to trauma - red reaction, flare, wheal
The cardiac cycle
Ventricular filling
Isovolumic ventricular contraction
Ejection
Isovolumic ventricular relaxation
Auscultation: valve sounds
S1 - AV valves (mitral and tricuspid) close, normally loudest
S2 - semilunar valves close
Systole occurs between S1 nd S2
Murmur
Action potential
Depolarisation: Na+ gates open in response to a wave of excitation from pacemaker
Transient outward current - tiny amount of K+ leaves cell
Plateau phase: inflow of Ca2+ just about balances outflow of K+
Rapid repolarisation phase: Vm falls as K+ leaves cell
Back to resting potential
Comparison of action potentials
Neural: 1ms, always same size
Skeletal muscle: AP completed before contraction begins, short refractory period, tetany
Cardiac: much longer - up to 500ms, varies in duration and size, long refractory period, no tetany
Plateau Phase
Dynamic Equilibrium - Ca2+ current in, K+ current out
Decrease Vm - decreased Ca2+ current
Decrease Ca2+ current - positive feedback and repolarisation by K+
K+ channels
Delayed rectifier K+ channels: open when membrane depolarises, but all gating takes place with a delay
Inward rectifier K+ channels: open when Vm goes below -60mV, functions: to clamp membrane firmly at rest
Action Potentials in SA node and AV node
At rest spontaneously depolarises - not stable at rest because there is non inward rectifier.
The upstroke of the AP is due to a transient increase in inward Ca - nodal upstroke is slower than in ventricular myocytes.
The K conductance increases shortly after depolarisation - which initiates repolarisation, as in nerve/skeletal muscle.
Duration of nodal AP = 300ms.
Automaticity of SA node
SA node cells are autorhythmic - resting potential is unstable and close to threshold.
Cells independently bear at 100 bpm - increased/decreased by para/sympathetic activity.
SA node is normally the pacemaker - other cardiomyocytes can be too, SA nodal cells responsible for the initiation of a heart beat as they have the fastest heart rate
I(f) - funny current
I(f) makes the SA node cells spontaneously active - HCN channel (not a sodium channel), autorhythmicity during the pacemaker potential (similar but different to resting potential).
I(f) increases upon hyperpolarisation rather than depolarisation.
I(f) leads to a net inward current - leads to a lot of Na+ current inward and a tiny K+ current outward, depolarises cell towards 0mV
Blocking Ion channels of Cardiac AP
During drug therapy, you only block a percentage of the ion channels that you target - if you blocked all the Na+ channels it would kill the patient (tetrodotoxin).
Na+ channel block leads to decreased conduction velocity - changes the organisation of firing in the different regions of the heart; this can prevent or sometimes cause arrythmias; it does not prevent depolarisation of affect HR.
Calcium channel block can lead to decreased heart rate and contractile force
