Term 2 Lecture 1: Cardiovasc Physiology Overview

Question 1

Purpose

Answer 1

Transport system for materials on which the cells of the body depend : O2 CO2, hormones, heat.
By these processes homeostasis is maintained allowing survival

Question 2

Components of blood

Answer 2

Plasma- fluid in which cells and platelets are suspended; contains various solutes including electrolytes and proteins

Erythrocytes (RBC): contain haemoglobin (Hb) which carries O2 and CO2

Leukocytes (WBC): participate in immune and defence functions

Platelets: participate in clotting

Question 3

Types of blood vess l

Answer 3

Arteries: carry blood away from heart

Arterioles: carry blood to capillaries and regulate blood flow

Capillaries: allow exchange of material between blood and interstitial fluid

Venules: carry blood away from capillaries - participate in some exchange of materials

Veins: carry blood to the heart

Question 4

Heart: functional regions

Answer 4

Right atrium: receives blood from systemic circuit (deoxy)
Right ventricle: pumps blood to pulmonary circuit.

Left atrium: receives blood returning from pulmonary circuit (Oxy)
Left ventricle: pumps blood to systemic circuit

Question 5

How blood enters/leaves the heart

Answer 5

Enters right atrium from superior (head) and inferior (body) Vena Cava through right AV valve to right ventricle through pulmonary semilunar valve and out through left/right pulmonary artery

Enters left atrium from left & right pulmonary vein flows through left atrioventricular valve into left ventricle then to aorta through aortic semilunar valve.

• Left ventricular wall is thicker to generate blood pressure to push blood around the body

Question 6

Origin of the heart beat

Answer 6

The heart beats from a few days after conception until death.

In an average human lifespan the heart contracts about 3 billion times

Never stopping except for a fraction of a second to fill up between beats

Action potential is generated intrinsically by pacemaker cells

Direction of wave of excitation: Conduction system transfers signal from SAN to AVN to bundles of his to Purkinje fibres

Question 7

Ionic basis of SAN generated AP

Answer 7

SAN cells are fast firing. They are impacted by the autonomic nervous system - parasymp slows beat and symp speeds up beat.

Cardiac autorhythmic cells display pacemaker activity
Membrane potential slowly depolarises or drifts between AP until threshold is reached
Cyclic process determines basic heart rate
Absence of nervous stimulation
(Autonomic control)
Nerve and skeletal muscle cells have constant RMP unless cell is stimulated

Question 8

Ionic basis of SAN generated AP: steps 1-3

Answer 8

Ionic mechanism responsible for pacemaker:

1) increased Na+ potential current
2) decreased K+ current
3) increased inward Ca²+ current

Question 9

1) initial slow depolarisation to threshhold

Answer 9

• Na+ enters through voyage gated Na channels only found in cardiac pacemaker cells
• IF (funny) channels open when membrane is hyper polarised at the end of repolarisation from the previous AP allowing in Na+
• Net inward Na+ current so membrane potential moves towards threshold
• (Normally voltage gated channels open when membrane depolarises)

Question 10

2) progressive reduction in passive outflux of K+ ions

Answer 10

• cardiac pacemaker cells K+ permeability doesn’t remain constant between AP (it does in nerves and skeletal muscle though)
  -K+ channels open at the end of preceding AP and slowly close at neg. Potential.
• rate of K+ efflux reduced at same time as slow inward leak of Na+ occurs
• net drift towards threshold

Question 11

3) Ca²+ entry (2nd half of AP generation)

Answer 11

• If channels close
• Transient Ca²+ channels open (T-type)
  before membrane reaches threshold
• Brief influx of Ca²+ further depolarises membrane bringing it to threshold
• T-type Ca2+ channels close

Rising phase: L type Ca²+ channels open, large Ca²+ influx (nerve, muscle, Ca²+)

Filling phase: L type Ca²+ channels close voltage gated K+ channels open. end of AP, slow closure of K+ channels contributes to next AP generation

Question 12

Steps AP takes

Answer 12

1) see points 1,2,3 previous
2) Atria contract and push blood into ventricles ventricular contraction is delayed 0.1 seconds by AVN giving time for atria to empty into the ventricles.
3) AVN to bundle of His
4) Bundle of H to left/right bundle branches
5) Purkinje fibres spread AP throughout ventricular myocardium

Question 13

Spontaneous AP generation

Answer 13

-SAN triggers HR (AP per min 70-80)*
- AVN rarely initiates HR (AP per min 40-60)*
- As SAN had higher AP generation it drives HR if SAN becomes dysfunctional AVN drives HR - but this is not a long term solution

• In presence of parasympathetic tone

Question 14

If Ap conduction blocked between atria and ventricles:

Answer 14

Then atria beat ~70/min & ventricles assume slower rate of contraction ~30/ min determined by Purkinje fibres
(Idioventricular pacemakers)

Ventricular rate of 30/min requires a very sedentary existence - patient becomes comatosed and requires an artificial pacemaker

Question 15

Complete heart block

Answer 15

Occurs when conduction tissue between atria and ventricles is damaged aka heart attack. The heart becomes non-functional.

Question 16

Cardiac AP diff to SAN AP

Answer 16

Diff in Ionic mechanism and shape. RMP 90mv constant until excited by electrical activity propagated by SAN

Question 17

AP of cardiac muscle shows a characteristic plateau

Answer 17

RMP, K+ channels open and leaky

1) rising phase - membrane potential reversal ~ +20mV+30mV due to increase in Na+ permeability (activation of voltage gated Na+ channels) then peak potential of Na+ permeability decreases as high influx causes channels to close

2) peak potential, K+ channels open (transient) allow fast limited efflux to give brief small repolarisation

3) plateau phase, membrane potential maintained close to peak positive level ~100ms activation “slow” L-type Ca²+ channels and K+ channels close (transient/leaky)

4) Rapid falling phase, “slow” L type Ca²+ channels close “ordinary” voltage gated K+ channels open

The action potential brings about cardiac muscle contraction because the L type Ca²+ channels in the T (transverse) tubules initiate a much larger Ca²+ release from SR (sarcoplasmic reticulum)

Question 18

How AP leads to contraction in cardiac cell

Answer 18

AP travels down T tubules
>Small amount of Ca²+ enters from ECF (extracellular fluid) enter through L type Ca²+ channels inducing release of lots of Ca²+ from SR through ryanodine Ca²+ release channels
> Leads to cytosolic Ca²+ in cardiac cells
>Causing troponin-tropomyosin complex in thin filament to be pulled aside
> Cross-bridge cycling between thick and thin filaments
> Thin filaments slide inwards between thick filaments
> Contraction

Question 19

Long refractory period

Answer 19

Prevents tetanus of cardiac muscle - second AP cannot be triggered until excitable membrane has recovered from preceding AP thus no summation or tetani occurs ( that occurs in skeletal muscle)

Plateau phase lasts 250ms
Contraction lasts 300ms

Inactivation of Na+ channels prevents AP

Question 20

Summary

Answer 20

Circulatory system is heart, blood vessels and blood
Blood flow from heart to end organ is brought about by generation of coordinated contraction of the heart muscle.
Autorhythmic cells in SAN determine basal heart rate
SAN and cardiac muscle cell AP generation relies on diff ionic mechanisms