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Spontaneous, intrinsic rhythm generated by the AV node cells
Spontaneous, intrinsic rhythm generated by the SA node cells
The making of paces
Conduction of charge from the atria to the ventricles
Spontaneous firing of the purkinje system
If you drink a glass of milk, you'll get tacchycardias
Calcium channels, due to their fast conduction, decrease the action potential and time for repolarisation
Calcium channels, due to their slow conduction, prolong the action potential and time for repolarisation
Calcium channels decrease arrhythmias
Increased conduction capacity
Voltage dependent plasma membrane
Intracellular
Extracellular
Neurotransmitter-mediated
Pressure dependent
L-type channels, which form part of the his-purkinje system and increase transmission rate of electrical signals
B-type channels, which are important in transmission of electrical conduction and stimulation of the valves of the heart
J-type channels, which are important in working myocardium and specialised conducting regions of the heart
L-type channels, which are important in working myocardium and specialised conducting regions of the heart
B-type channels, which increase cardiac contraction and spread equally through the two sides of the heart
No more than a few milliseconds
No more than a few seconds
No more than two microseconds
No more than a minute
No more than necessary
Sodium channels open, prolonging depolarisation and causing a plateau
Calcium channels open, triggered by sodium ion depolarisation, and the slow influx maintains the plateau
Outward potassium conduction is blocked, maintaining the depolarisation
Potassium channels open, increasing the rate of depolarisation and prolonging cardiac contraction
Sodium channels close, increasing the rate of depolarisation.
Closure of calcium channels
Closure of sodium channels
Re-opening of potassium channels and efflux of ions
Closure of potassium channels
Opening of sodium channels and influx of sodium
Anatomic heart disease
Myocardial infarction
Drugs
Circulating hormones
Age
Re-entry
Electrolyte imbalance
Delayed after-depolarisation
Ectopic pacemaker activity
Heart block
Abnormally raised Na+, which causes an influx of ions and triggers abnormal action potentials, causing VT
Abnormally raised K+, which causes an influx of ions and triggers abnormal action potentials, causing VT
Abnormally raised Ca2+, which causes an influx of ions and triggers abnormal action potentials, causing VT
Abnormally low Na+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia
Abnormally low Ca2+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia
The impulse conducted to the atria doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium
The impulse in the sinoatrial node doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium
The impulse in the sinoatrial node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction
The impulse conducted to the ventricles doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium
The impulse in the atrioventricular node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction
It's a safety mechanism, so if the AV node is damaged, pacemaker activity can continue.
It's a safety mechanism, so if the SA node is damaged, pacemaker activity can continue.
It's a safety mechanism, so if the purkinje fibres are damaged, contractile activity can continue.
It's additional contractility, so if increased volume load occurs, more tissue can contract to cope with the increased demand
It's additional pacemaking, so if increased volume load occurs, more tissue can contract to cope with the increased demand
If they don't fire, can cause bradycardias
If they're inappropriately firing, can cause bradycardias
If they don't fire, can cause tacchyarrhythmias
If they're in the wrong place, can interfere with valvular function
If they're inappropriately firing, can cause tacchyarrhythmias
Fibrous or ischaemic damage to the conducting system (usually SA node)
Atria and ventricles firing independently of each other, with atria supplied by ectopic pacemakers
Fibrous or ischaemic damage to the conducting system (usually AV node)
Atria and ventricles firing independently of each other, with ventricles supplied by ectopic pacemakers
Dilatation of the chambers obliterates the conducting system, causing heart failure
SA node - atrium - AV node - purkinje fibres - ventricle
SA node - purkinje fibres - AV node - atrium - ventricle
AV node - purkinje fibres - atrium - SA node - ventricle
Ventricle - AV node - purkinje fibres - atrium - SA node
Atrium - SA node - purkinje fibres - AV node - ventricle
High calcium causes influx of ions into the cell transiently, which increases the normal after-depolarisation waves (can be seen as peaked T waves)
Can be caused by cardiac glycosides, NA or phosphodiestesterase inhibitors that increase intracellular calcium
Mediated by high levels of extracellular calcium
Increased normal after-depolarisation waves trigger a repetitive discharge and contraction that is independent of pacemaker stimulus
Can occur in the non-pacemaker cells of the heart.
Binding rates of ATP to actin and myosin fibres
Troponin, to which Ca2+ binds and triggers a conformational change