Origin and conduction of cardiac impulse (CVS2&3) Flashcards
autorythmicity
- the heart is an electrically controlled muscular pump
- the electrical signals which control the heart are generated within the heart itself
- the heart is capable of beating rhythmically in the absence of external stimuli, this is called autorythmicity
how is an ECG (electrocardiogram) obtained
it is possible to record the spread of electrical activity through the heart from the skin surface to obtain an ECG
normal origin of excitation within the heart
in the pacemaker cells in the sinoatrial node/SA node
how is heart beat initiated
by the cluster of specialized pacemaker cells in the sinoatrial node
location of sinoatrial node
in the upper right atrium close to where the superior vena cava enters the right atrium
tricuspid valve
between right atrium and right ventrical
mitral valve
between left atrium and left ventricle
what drives/sets the pace for the entire heart
sinoatrial node
what does it mean if a heart is said to be in sinus rhythm
it is controlled by the sinoatrial node
properties of cells in the sinoatrial node
- they do not have a stable resting membrane potential
- they exhibit spontaneous pacemaker potential
function of spontaneous pacemaker potential exhibited by cells within sinoatrial node
takes the membrane potential to a threshold to generate an action potential in the SA nodal cells
pacemaker potential
- slow depolarization of membrane potential to a threshold, due to a decrease in K+ efflux superimposed on a slow Na+ influx (funny current)
- the permeability to K+ within the pacemaker cells does not remain constant between action potentials
efflux
inside to outside
influx
outside to inside
what causes the rising phase of the action potential/depolarization in pacemaker cells
activation of voltage gated calcium ion channels, resulting in calcium(Ca++) influx
depolarization
rising phase of action potential
what causes the falling phase of the action potential/repolarization in pacemaker cells
activation of K+ channels, resulting in K+ efflux
intracellular recording from SA node cell/graph of action potential
- pacemaker potential causes slow depolarization of membrane potential to a threshold (from -60 to -40)due to a decrease in K+ efflux superimposed on a slow Na+ influx
- once the threshold is reached, activation of voltage gated calcium ion channels, resulting in calcium(Ca++) influx causes the rising phase of the action potential/depolarization (from-40 to 0)
- the activation of K+ channels, resulting in K+ efflux which is responsible for the falling phase of the action potential/repolarization (from 0 to -60)
how does cardiac excitation normally spread across the heart
- from SA node to AV node via cell-cell conduction (from one myocardial cell to another myocardial cell and so on and so on)
- through SA node through both atria via gap junctions
- and within ventricles via gap junctions
atrioventricular node
- small bundle of specialized cardiac cells (AV node cells are small in diameter and have slow conduction velocity which allows for delay of action potentials, allowing heart to conduct in contracted manner- atria first then ventricles)
- ONLY point of electrical contact between atria and ventricles
pathway through heart that the spread of excitation follows
-originate in sinoatrial node, travel to atrioventricular node via cell-cell conduction, then to the bundle of His conductive pathways and down their divided left and right branches, before reaching purkinje fibres and spreading through out ventricle
gap junctions
- part of intercalated discs (a specialized intercellular attachment of cardiac muscle cells comprising gap junctions, fascia adherens, and occasionally desmosomes)
- cell-cell current flow
- allow action potentials to spread from cell-cell
how do action potentials spread from cell-cell
cell-cell conduction via action potentials
location of AV node
base of right atrium, just above the junction of atria and ventricles
systole
contraction
dyastole
relaxation
spread of excitation across atria
mainly cell-cell conduction via gap junctions
spread of excitation from SA node to AV node
mainly cell-cell conduction via gap junctions but there is also some internodal pathways
why is the conduction delayed in the AV node
allows atrial systole (contraction) to precede ventricular systole (spreads in contracted manner)
role of bundle of His and its branches (right and left) and the network of purkinje fibres
allow rapid spread of action potential to the ventricles
spread of excitation through ventricular muscle
via cell-cell conduction