Electrical activity of the Heart Flashcards
How does excitation contraction coupling occur in cardiac muscle
working as functional syncytium of intercalated discs
What is interlaced discs composed of and what is there individual function
electrically connected via gap junctions
physically connected by desmosomes
What does it mean is cardiac muscle is myogenic
can contract without nervous stimulation - autorhymicity
Why is there a long refractory period in cardiac muscle
Lots of calcium entry from outside the cell which does not fully saturate troponin
The Regulation of calcium from outside the cell allows control over what
Strength of heart contractions
What is the length of action potential in cardiac muscle compared to skeletal muscle
250milli seconds compared to 2mill seconds
longer
What do cells with unstable resting membrane potential acts as
Pacemaker cells
In non pacemaker cells what causes the increase in resisting membrane potential
Increased permeability of potassium
In non pacemaker cells what causes the initial slight depolarisation
An increase in sodium permeability
In non pacemaker cells what causes the the plateau in polarisation
Increase in calcium permeability
Decrease in potassium permeability
in non pacemaker cells what causes the re-polorisation
decrease in calcium permeability
Increase in potassium permeability
What causes pacemaker cells pre potential to depolarise
gradual decrease in Permeability of K+
early increase in Permeability of Na+ (= PF)
late increase in Permeability Ca2+ (T-type)
What then causes the action potential of pacemaker cells
increase in PCa2+ (L-type)
what triggers pF sodium permeability and why is that useful
Voltage dependant sodium current opened by the re-polarisation of previous channel which thens allows this early increase sodium
What is the major difference in pacemaker potential and no pacemaker potential
Pacemaker is the same as before but without fast depolarisation
what is the steps in cardiac muscle contraction
The action potential spreads from the cell membrane into the T tubules.
Calcium enters the cell from the ECF (this doesn’t happen in skeletal muscle).
This triggers the release of even more calcium from the SR.
Intracelllular calcium increases.
Calcium binds to the troponin/tropomysin complex, and tropomysin moves out of the way of the active site on the actin filament.
Actin and myosin bind, and the thick and thin filaments slide past each other
the myocyte contracts.
Relaxation occurs when calcium is actively transported back into the SR (by calcium-ATPase pump) or out of the cell into the ECF.
What is example of modulators of electrical activity of the heart
Sympathetic & parasympathetic systems Ca2+-channel blockers cardiac glycocides Temperature Hyperkalemia (high plasma K+) Hypokalemia (low plasma K+) Hypercalcemia (high plasma Ca2+) Hypocalcemia (low plasma Ca2+)
What is the effect of calcium channel blockers
decreases force of contraction
What is the effect of cardiac glycosides
Increases force of contraction
How much does 1ºC increase the heart rate
increases ~10 beats/min/ºC
What is Hyperkalemia (High K) and hypokelimia (Low K) effect on the heart
Fibriltion and heart block
What is unusual about the affect of Hyperkalemia and hypokelimia affect on the heart
should oppose each other, but don’t = anomalous
What is the affect if Hypocalcemia (low Ca) and hypercalcemia (High Ca) affect on the heart
Hyper - increase heart rate and force of contraction
Hypo - decrease heart rate and force of contraction
Why does hyerkalemia cause a heart block and fibrillation
increase potassium means heart with depolarises opening lots of channel therefore firing AP in an unorganised fashion = fibrillation
constant depolarisation than can eventual cause the heart to stop
What are the three types of cardiocytes found in the myocardium
Sinoatrial nodes
Purkinje fibres
Contractile cells
How are the SAnodes triggered to conduct
Influx of sodium makes cells more negative - pacemaker cell potential
AP threhsold is then reached
AP tiggere propagation of cells opening sodium channels, potassium channels and so-called FAST calcium channels
This causes further depolarisation of neighbouring cells
What is the annulus fibrosis and is it conducting tissue?
tough circular exterior of the intervertebral disc that surrounds the soft inner core, the nucleus pulposus
is the only non conducting part of the heart
Where is the SA node located and how long does it take to pass signal
found at the junction at the top of the right atrium
0.5m/s
What is responsible for slowing down the heart rate i.e. the delay box
Atrioventricular node
Where is the Atrioventricular node located
centre of the heart
What is the functions of the AV node
Regulates signals from the SA node
sends the electrical impulses from the atria to the ventricles - prevent rapid conduction
makes sure that the atria are empty and closed before stimulating the ventricles
How long does the function of the AV valve take
0.05 m/sec
Define fibrillation
rapid, unsynchronised contractions of muscle fibre
where is the only nonconducting part of the heart
Annulus fibrosus
What does the bundle of his allow
Signal form AV to Purkinje fibres
what is the function of Purkinje fibres
conduct APs in ventricle walls
Why is purknje fibres cause a rapid conduction, what is the time of conduction
Ð to make sure ventricles depolarise at same time
Ð ~ 5 m/sec
what rhythm does the heart beat to
The rhythm of the SA pacemakers
what does a single AP in a single myocyte evoke
a very small extracellular (cf transmembrane) electrical potential
What creates the large extracellular wave that is recorded on the periphery of an ECG
lots of small extracellular electrical potentials being evoked by many cells depolarising and repolarising at the same time and summating
Why is tetnus impossible for cardiac muscle
As the action potential lasts nearly as long as the contraction and relaxation periods, a cardiac muscle cell will have nearly completed its relaxation period before it can respond to a subsequent stimulus.
What would happen if tetnus was to occur in the heart
If tetanus could occur in cardiac muscle, it would stop the heartbeat and therefore the flow of blood
