Cardiac output (Pt1): Electrical events and heart rate Flashcards
CO =
HR x SV
Heart rate is driven by
waves of electrical activity that induce cardiac muscles to contract
2 types of pacemaker cells
ones in the AV node and SA node
AV node
connects atria and ventricles and delays the signal for 0.1ms- allows atria to contract before ventricles
Bundle of His
Fast conducting myocytes that connnect to the Purkinje fibres, only way activity can pass to the ventricles
Myocyte
cardiac muscle cell
Purkinje fibres- why are they wide
Wide allowing rapid conduction throughout the ventricle and simultaneous contraction of ventricles
Purkinje fibres are
nerves
Atrial excitation involves
SA node
ventricular excitation involves
AV node
what causes pacemaker cells of the SA node to trigger an AP
Low RMP
Na+ leakage, leading to depolarisation
Mechanism for APs in pacemaker cells of the SA node
sodium ions leaking in through the F type channels and calcium ions moving in through the T type (transient) channels cause a threshold graded depolarisation.
Rapid opening of calcium L-type channels responsible for rapid depolarisation
Reopening of K+ channels and closing o calcium channels responsible for repolarisation.
What is the overall driver of heart rate
SA node, overrides AV and purkinje fibres
Mechanism for contraction of ventricular myocytes
Rapid opening of VGNC responsible for rapid depolarisation phase
Prolonged ‘plateau’ of depolarisation (contraction) due to slow but prolonged opening of VGCCs and closure of K+ channels
Opening of K+ results in repolarisation
How does calcium produce contraction of cardiac muscle
excitation-contraction coupling
Entry of extracellular ca ions causes release of Ca from sarcoplasmic reticulum by binding to ryanodine receptors
Why does cardiac muscle have a long refractory period
Allows ventricles to fill prior to pumping
vagus nerve (parasympathetic)
decr heartbeat
Innervates just SA and AV nodes
Sympathetic ganglia
incr heartbeat (also regulate force/SV) Innervates whole heart
What do parasympathetic and sympathetic nervous system regulate
rate of depolarisation in the SA node
At rest which one dominates
Parasympathetic
Parasympathetic mechanism
Parasympthetic neurones release Ach
acts upon m2 muscarinic receptors of SA node
Incr K+ efflux, decr Ca influx
Hyperpolarises cell and decr rate of depolarisation
decr HR - bradycardia
Sympathetic mechanism
Release noradrenaline acts upon B1 adrenergic receptors of SA node Incr NA+ and Ca2+ influx Incr rate of depolarisation Incr heart rate Tachycardia
ECG
measures electrical activity of the heart
Summation of the spread of APs throughout the heart
P
atrial depolarisation
QRS
ventricular depolarisation
T
ventricular repolarisation
PQ
length of atrial contraction
QT
length of ventricular contraction
ECG provides info on
HR rhythm disturbances of rhythm and conduction (arrhythmia, pacemaker) conduction velocity orientation of heart relative size of chambers Condition of tissue within the heart Damage to myocardium Drugs
Inspiration
faster
PQRST closer together
decr in vagal parasympathetic activity> incr in heart rate
Expiration
Slower
PQRST further apart
Vagal paraympathetic activity increase> heart rate decrease
sinus arrythmia
bnormal heart rhythms that start at the sinus node
Third degree
complete failure of conduction atria to ventricles
beat independently
Ventricular etopic beat
Aberrant firing of myocytes in ventricles-ill synchronised and fails to eject blood
Common after heart attacks
ventricular fibrillation result
Random firing
Fibrillating ventricles can’t pump blood
Fatal
Ventricular fibrillation caused by
Myocardial infarction
Electric shock
Drug intoxication
Impaired cardiac metabolism
