Term 2 Lecture 1: Cardiovasc Physiology Overview Flashcards
Purpose
Transport system for materials on which the cells of the body depend : O2 CO2, hormones, heat.
By these processes homeostasis is maintained allowing survival
Components of blood
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
Types of blood vess l
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
Heart: functional regions
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
How blood enters/leaves the heart
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
Origin of the heart beat
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
Ionic basis of SAN generated AP
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
Ionic basis of SAN generated AP: steps 1-3
Ionic mechanism responsible for pacemaker:
1) increased Na+ potential current
2) decreased K+ current
3) increased inward Ca²+ current
1) initial slow depolarisation to threshhold
- 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)
2) progressive reduction in passive outflux of K+ ions
- 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
3) Ca²+ entry (2nd half of AP generation)
- 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
Steps AP takes
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
Spontaneous AP generation
-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
If Ap conduction blocked between atria and ventricles:
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
Complete heart block
Occurs when conduction tissue between atria and ventricles is damaged aka heart attack. The heart becomes non-functional.
Cardiac AP diff to SAN AP
Diff in Ionic mechanism and shape. RMP 90mv constant until excited by electrical activity propagated by SAN
AP of cardiac muscle shows a characteristic plateau
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)
How AP leads to contraction in cardiac cell
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
Long refractory period
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
Summary
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
