Origin and Conduction of Cardiac Impulse

Question 1

describe the heart

Answer 1

electrically controlled muscular pump - sucks and pumps blood
electrical signals are generated within the heart
capable of beating rhythmically absent of external stimuli - this is called audtorhythmicity

Question 2

explain the excitation of the heart

Answer 2

normally originates in the pacemaker cells in the sinoatrial (SA) node
the cluster of specialised pacemaker cells in the SA node initiate the heart beat
SA node is located in the upper right atrium, close to where superior vena cava enters right atrium

Question 3

describe sinus rhythm

Answer 3

heart controlled by the SA node

SA node normally drives (sets pace) for entire heart

Question 4

describe generation of action potentials in SA node

Answer 4

cells in the SA node have no stable resting membrane potential
cells in SA node generate regular spontaneous pacemaker potentials
spontaneous pacemaker potential takes the membrane potential to a threshold
every time threshold is reached - action potential generated
this results in generation of regular spontaneous action potentials in SA nodal cells

Question 5

describe the routes taken for excitation to spread rapidly to ventricular muscle cells

Answer 5

across the atria mainly cell-to-cell conduction via gap junctions (intercalated disc);
from SA node through both atria
from SA node to AV node
within ventricles - there is also some internodal pathways

the bundle of His and its branches and the network of Purkinje fibres allow rapid spread of action potential to the ventricles (diagram PP)

Question 6

describe the electrical contact and conduction between atria and ventricles

Answer 6

atrioventricular (AV) node is only point of electrical contact between atria and ventricles
AV node is small bundle of specialised cardiac cells located at the base of the right atrium, just above the junction of the atria and ventricles . AV node cells are small in diameter and have slow conduction velocity
conduction is delayed in AV node - allows atrial systole (contraction) to precede ventricular systole

Question 7

describe ionic mechanisms . underlying action potentials in contractile ventricular myocytes

Answer 7

refer PP
action potential in contractile cardiac muscle cells differ from action potentials in pacemaker cells
resting membrane = -90mV until cell excited

Phase 0;
depolarisation (rising phase) caused by fast Na influx
rapidly reverses the membrane potential to +20mV

Phase 1;
closure of Na+ channels and transient K+ efflux

Phase 2 - Plateau phase;
mainly Ca2+ influx
membrane potential is maintained near peak of action potential for few hundred milliseconds
unique characteristic of contractile cardiac muscle cells and is mainly due to influx of Ca2+ through L type Ca2+ channels

Phase 3 - falling phase (repolarisation);
closure (inactivation) of Ca2+ channels and (activation of K+ channels) K+ efflux

Phase 4;
resting membrane potential

Question 8

state normal resting heart beat

Answer 8

60-100 BPM

Question 9

describe bradycardia

Answer 9

slow heart rate - below 60 BPM

Question 10

describe tachycardia

Answer 10

fast heart rate - above 100 BPM

Question 11

explain the mechanisms whereby autonomic nerve stimulation influences heart rate

Answer 11

heart rate is mainly influenced by autonomic nervous system
the vagus nerve (parasympathetic supply to heart) exerts continuous influence on SA node under resting conditions

changes in heart rate usually involve reciprocal action of sympathetics and parasympathetics

Question 12

explain the vagal tone on the heart

Answer 12

parasympathetic
dominates on the heart under resting conditions
slows the intrinsic heart rate from ~100 BPM to produce a normal resting heart rate of ~70 BPM

Question 13

describe parasympathetic stimulation on heart rate

Answer 13

causes a negative chronotropic effect to slow heart rate

cell hyperpolarises and takes longer to reach threshold => frequency of AP decreases (increase in nodal delay)
increase in pacemaker cell K+ efflux, decrease in pacemaker cell Na+ and Ca2+ influx

vagus nerve supplies SA and AV node
vagal stimulation slows heart rate and increases AV nodal delay - slope of pacemaker potential decreases
neurotransmitter is ACh acting through muscarinic M2 receptors
atropine is a competitive inhibitor of ACh used in extreme bradycardia to speed up heart rate

Question 14

describe sympathetic stimulation on heart rate

Answer 14

causes a positive chronotropic effect to speed heart rate

slope of pacemaker potential increases, pacemaker potential reaches threshold quicker
frequency of action potentials increases
decrease in pacemaker cell K+ efflux
increase in pacemaker cell Na+ and Ca2+ influx

cardiac sympathetic nerves supply SA and AV node and myocardium
sympathetic stimulation increases heart rate and decreases AV nodal delay
also increases the force of contraction
neurotransmitter is noradrenaline acting through beta1 adrenoceptors

Question 15

how is an ECG obtained

Answer 15

the spread of electrical activity (depolarisation and repolarisation) through the heart (cardiac muscle) from the skin surface is recorded

wave of depolarisation and depolarisation moves across the heart and sets up electrical currents which can detected by surface electrodes

refer PP;
P - atrial depolarisation 
QRS complex - ventricular depolarisation (masks atrial repolarisation)
T - ventricular repolarisation
PR interval - largely AV node delay 
ST segment - ventricular systole 
TP interval - diastole

Question 16

draw, label and explain the normal lead II ECG

Answer 16

refer PP
Lead I - RA - LA
Lead II - RA - LL
Lead III - LA - LL

Question 17

describe the ionic mechanisms underlying SA node pacemaker potentials and action potentials

Answer 17

PP
in pacemaker cells, the permeability to K+ does not remain constant between action potentials
pacemaker potential - slow depolarisation of membrane potential to a threshold - is due to;
decrease in K+ efflux
Na+ influx
transient Ca2+ influx (T type Ca2+ channels)

once threshold reached;
rising phase of action potential - depolarisation - is caused by activation of long lasting (L type Ca2+ channels)
results in Ca2+ influx

falling phase of action potential - repolarisation;
caused by inactivation of L type Ca2+ channels and activation of K+ channels
results in K+ efflux