Cardiac volume-pressure cycles, ions and APs Flashcards
Cerebral circulation
Contains constant flow and pressure of blood as it is unable to store energy.
Circle of Willis- anastomosis or arteries on brain’s inferior surface
Renal circulation
Despite the kidney making 0.5% of body weight, it contributes to 20-25% of cardiac output.
Involved in the synthesis of ACE and Renin- controls blood volume in response to renal perfusion.
Contains portal system- Glomerulus and peritubular capillaries are in series- connected by efferent arteriole.
Skeletal muscle circulation
Adrenergic input causes vasodilation- sympathetic activation.
During strenuous exercise muscles can use up tp 80% of CO.
Muscle pumps facilitates venous return
Skin circulation
Thermoregulation- can increase perfusion up tp 100X.
Arteriovenous anastomoses - when arterioles join with venules.
Sweat glands- plasma ultrafiltrate and used in thermoregulation.
Trauma- Red reaction, flare wheal.
Ventricular filling and ejection
Ventricles fills when pressure is lower than atrial (and importantly aortic) pressure.
Ventricle eject blood when the pressure is higher than the aorta.
Isovolumic contraction
When the ventricle contract with no change in volume.
This occurs between the AV valves closing and the opening of the semilunar valves.
Both the AV and Semilunar valves are shut- hence pressure increases without volume change.
Isovolumic relaxation
When the ventricles relax with no change in volume.
The left ventricular pressure is lower than aortic pressure, causing the aortic valve to close.
This occurs between the closing of the semilunar valves and opening of the AV valves.
All valves are closed during this process.
Dicrotic notch
The small dip in aortic blood pressure (in the Wiggers diagram).
Occurs when the aortic valve closes, there is a slight dip in aortic pressure,
ECG waves during cardiac pressure changes
ECG waves always precede ventricular pressure changes.
Electrical changes occur before heart contractions.
Heart contractions cause the pressure changes.
P wave cause atrial contraction. P waves proceed atrial contraction and AV closing.
QRS complex precedes ventricular ejection.
Pressure volume loop
Graph that shows volume (x) against pressure (y) in the heart.
Moving in an anti-clockwise direction:
Filling—> AV valves close at the corner—-> Isovolumic contraction—> Ejection —> SL valves close —-> Isovolumic relaxation at the corner.
Preload and afterload in the pressure-volume loop
Between the mitral valve closing and the aortic valve opening- this is affected by preload. This is during isovolumic contraction.
Ejection is affected by afterload. This is between the aortic valve opening and closing.
Isovolumeric relaxation is affected by afterload. This is between the aortic valve closing and the mitral valve opening.
Low L.ventricle volume at the end of ejection
End systolic volume is low because:
Afterload was low.
Ventricles fill with less blood due to mitral stenosis.
Escape of blood back into the atrium during mitral regurgitation.
High L.ventricle volume at the end of filing
Occurs because:
Excess filling of ventricle due to high preload.
Aortic regurgitation- blood from aorta entering back into ventricle.
Mitral regurgitation- XS blood from atrium into ventricle.
High LV pressure during ejection
High levels of afterload
High LV volume at the end of ejection
Occurs when ejectio is incomplete:
- Myocardial weakness/damage, thus less contractile force
- High after load
Aortic stenosis pressure-volume loop
There is an increase in afterload.
The loop will show a narrower loop on the right hand side.
Mitral stenosis pressure-volume loop
There is a decrease in preload and afterload:
Less volume of blood enters the ventricle and aorta.
This shifts the loop to the left, from the normal loop.
Mitral regurgitation pressure-volume loop
There is an increase in preload BUT decrease in afterload:
There is more blood escaping into the ventricles but it also leaves back into the atrium during ejection, decreasing afterload.
Therefore the loop forms an oval shape- widens at the right and left.
Aortic regurgitation pressure-volume loop
There is an increase in preload: blood from aorta leaks into the ventricle.
Isovolumic relaxation doesn’t really happen because the aortic valve is never close so blood from aorta leaks into the ventricle.
Two types of K+ channels in cardiomyocytes
Both channels let K+ out of the cells.
Delayed rectifier K+ channels:
Only opens when membrane depolarises but does so in a slow fashion.
Inward rectifier K+ channels:
Opens when membrane potential is below -60 mV
This clamps membrane firmly at rest towards the equilibrium potential for K+.
After hyperpolarisation.
The stage at the end of the AP where the Vm gets more negative than resting potential.
The voltage goes below -60mV due to opening of inward rectifier K+ channels- which stay opened until depolarisation.
The membrane becomes less permeable to Na+ and more permeable to K+. This pushes the Vm closer to K+ equilibrium potential.
Phases of ventricular myocyte action potential
0= Always depolarisation
1- Transient outward current: small amount of K+ leaves the cell.
2= Plateau phase: dynamic equilibrium b/w K+ and Ca2+.
3- Rapid repolarisation
4- Back to resting potential. The current is maintained by inward rectifier K+ opened.
Action potentials in skeletal muscle
ALWAYS occurs before contraction begins.
Contains a short refractory period- repeated APs causes tetany.
Cardiac action potentials
Length: up to 500ms
Always varies in duration and size
Contains a long refractory period- no tetany can occurs. This prevents fibrillation.
The plateau phase
Phase 2 of ventricular myocytes action potential.
Ca2+ channels open when membrane is depolarisation.
This is when there is a dynamic equilibrium between the Ca2+ going in and K+ going out of the cell.
- This causes the voltage to become depolarised VERY slowly due to K+ current slightly outweighing the Ca2+ current.
The more negative the membrane goes, the more Ca2+ channels close- positive feedback mechanism.
Atrial vs Ventricular AP
Atrial AP occurs earlier than ventricular AP- The P wave on the ECG.
Ventricular AP aligns with QT interval.
Automaticity of SAN
SAN cells are autorhythmic:
Resting potential is unstable and close to threshold potential (-40mV).
The cells always independently beat at 100 bpm if not affected by autonomic system.
SAN cells initiate the heartbeat as it has the fastest rate- even though other cardiomyocytes can initiate it.
Pacemaker potential/ Diastolic potential
Pacemaker cells lack inward rectifier cells so it drifts towards the positive between nodal beats- instead of the resting potential (-40mV).
The slope of this diastolic potentials determines rate of firing.
AP in SAN and AVN
There is no inward rectifier so it spontaneously depolarises at rest- the resting Vm is not stable.
The nodal upstroke is slower than in ventricular myocytes - when Ca2+ flows inwards.
K+ conductance increases after depolarisation which initiates repolarisation.
Phases of nodal AP
0= depolarisation phase
1+2= does not exist. There is no transient outflow of K+ and plateau phase.
3- repolarisation- after K+ conductance increases.
4- return to pacemaker potential.
The funny current (If)
In SAN- this is maintained by the hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. channel which makes the nodal cells spontaneous.
This leads to a net INWARD current- a lot of Na+ inward, with small K+ outward. This causes the cell to depolarise towards 0 mV.
This current increases during hyperpolarisation.
Tetrodotoxin
A toxin found in fugu fish that blocks all the Na+ channels.
This causes DEATH.
Blocking K+ channels
This decreases conduction velocity- changes organisation of firing in the heart.
This can be used to prevent arrhythmias.
Does not prevent depolarisation of affect HR.
Blocking Ca2+ channels
This can decrease heart rate and contractile force.
This is because the SAN is dependant on Ca2+ channels.
Diminishing Ca2+ influx decreases the rate of voltage depolarisation (Phase 0)
Dihydropyridine
Drugs that targets Ca2+ channels in the blood vessels more than the heart.
They are used as anti-hypertensives.
Example: Amlodipine
Amlodipine
A dihydropyridine that is used as an anti-hypertensives.
The drug blocks Ca2+ channels in the blood vessel.
Diltiazem
Anti-anginal drug that lowers heart contractility.
Does so by blocking Ca2+ channels.
Verapamil
Antiarrhythmic agent in the heart that blocks Ca2+ channels.
