The Cardiac pressure

Question 1

Describe the cerebral circulation

Answer 1

Requires a constant flow and pressure which is autoregulated
Circle of Willis includes arteries anterior on brains inferior surface organised into a circle which function as a redundant blood supply

Question 2

Describe the renal circulation

Answer 2

20-25% of cardiac output goes to kidneys even though they only account for 0.5% of body mass (50x over-refused vol/weight)

Portal system linked by efferent arteriole connects glomerulus and peritubular capillaries

Makes both ACE & renin
Has endocrine function, controls blood volume, responds to renal bp.

Question 3

Describe skeletal muscle circulation

Answer 3

Adrenergic input leads to vasodilation
Can use up to 80% of CO during strenuous exercise
Major sight of peripheral resistance
Muscle pump augments venous return

Question 4

Describe skin circulation

Answer 4

Has a roel in thermo-regulation
Arteriovenous anastomoses (primary role in thermoregulation)
Sweat glands play a role in thermo-regulation, plasma ultrafiltration
Response to trauma includes: red near cut, flare, wheal (inflammation)

Question 5

What does isovolumeric mean?

Answer 5

A change that occurs while the volume of the ventricle remains almost constant

Question 6

Outline the cardiac cycle from Ventricular filling

Answer 6

Ventricles fill when ventricular pressure is less than atrial pressure. AV valves that are non-stenotic won’t make a sound

Isovolumeric ventricular contraction occurs whereby there is no change in ventricle volume but the pressure is increasing. This is affected by preload, if preload is heigh PV loop will move to the right.

Ejection

Isovolumeric ventricular relaxation

Question 7

Consider PV loops. How would it appear in the case of mitral stenosis?

Answer 7

Decreased preload
Decreased after load
PV loop shifts to left

Question 8

Consider PV loops. How would it appear in the case of mitral regurgitation?

Answer 8

Increased preload
Decreased after load
Eliptical shape

Question 9

Consider PV loops. How would it appear in the case of aortic stenosis?

Answer 9

Increased afterload

Tall rectangle to right, point superior in place of normal AO

Question 10

Consider PV loops. How would it appear in the case of aortic regurgitation?

Answer 10

Increase preload
Large eliptical shape with projection to right
Sharp curve in place of mitral opening corner

Question 11

Describe what is heard during auscultation

Answer 11

S1- AV valves close, normally loudest
Systole (shorter than diastole as it is a high pressure event)
S2- Semilunar valves close

Obstacles cause turbulence which is heard as a murmur

Systolic murmur is heard as fluid leaves ventricle. AV regurgitation or semi-lunar stenosis

Diastolic murmur is heard as fluid enters ventricle. AV stenosis or SL regurgitation

Question 12

What is the difference between delayed rectifier K+ channels and inward rectifier K+ channels?

Describe their responsibility in an action potential

Answer 12

Delayed rectifiers open when membrane depolarise but all gating takes place with a delay.

Inward rectifiers open when Vm goes below -60mv (unusual- more open when cells are at rest). Their function is to clamp membrane firmly at rest (K+ channel lets K+ out of cell, depolarising it)

Inward rectifiers maintain the cells membrane potential by opening K+ channels which means that the membrane is most permeable to K+ at rest so Vm tends towards Ek

Delayed rectifiers are employed during repolarisation to increase K+ permeability OUT of cell

Question 13

How does contraction of myocytes differ to that of skeletal contraction?

Answer 13

It is much longer

Long refractory period, no tetany

Varies in size and duration

Question 14

Describe the phases involved in contraction of a cardiomyocyte.

Answer 14

Phase 0- Depolarisation: Na+ gates open in response to wave of excitation from pacemaker

Phase 1- Transient outward current: tiny amount of K+ leaves cell

Phase 2- Plateau phase: inflow of Ca2+ just about balances outflow of K+. This is the dynamic equilibrium between Ca2+ current in K+ current out. The membrane potential decreases leading to decreased ca2+ current also delayed rectifiers increase K+ out, but much less

Phase 3- Rapid repolarisation: Vm falls as K+ leave cell

Phase 4- Back to resting potential
Associated with inwards rectifier K+ channel

Question 15

Describe the automaticity of the SAN

Answer 15

SAN cells are auto rhythmic
Their resting potential is unstable and is close to threshold
Indepenedently beat at 100bpm (increased by sympathetic and descreased by parasympathetic)
They have the fastest rate of contraction in heart.

Question 16

What is meant by pacemaker potential?

Answer 16

Voltage drifts positively between nodal beats instead of resting potential
This is because they lack inward rectifiers

Question 17

Describe action potentials in SAN and AVN

Answer 17

At rest spontaneously depolarises due to funny current (If)

Phase 0 is due to increase in Ca2+ not Na+. Nodal upstroke is slower than in ventricular myocytes

The K conductance increases. shortly after depolarisation which initiates depolarisation as in nerve and skeletal muscle

Question 18

Outline the phases of nodal action potential

Answer 18

0= depolarisation phase
1= doesn't exist 
2= doesn't exist
3= repolarisation phase
4= pacemaker potential

Question 19

Describe the funny current (If)

Answer 19

Based on HCN channel during phase 4
Increases upon hyper polarisation rather than depolarisation

Leads to a net inward current
If causes a lot of Na+ current inward and a tiny amount of K+ current outward. In other wards, depolarises cell toward 0mV

Question 20

What is the effect of drug therapy on AP

Answer 20

During drug therapy only a percentage of ion channels are blocked.

Na+ channel block leads to decreased conduction velocity ; changes organisation of firing in different regions of heart; can prevent arrhythmia but DOESNT prevent depolarisation or affect HR. (Only blocked Ca2+ decrease HR and contractile force)