Control of CV Flashcards
function
transport nutrients, transfer heat, buffer pH, transport hormone, respond to infection and urine filtration
cardiac cycle
consists of systole and diastole of atria then ventricles
direction of blood flow
high to low pressure
starlings law
CO = SV x HR
initiate impulse
an action potential is created in the SA node which spread to atria then ventricles.
AV node
slows conduction and acts as secondary pacemaker
EC coupling
purkinje fibresn interdigitate with myocytes to spread impulse across ventricles
ECG
detects phasic change in potential difference between two electrodes and is recorded on paper, computer or oscilloscope
sequence of cardiac cycle
atrial and ventricular diastole: AV open and SL closed
atrial systole and ventricular diastole: AV open and SL closed
atrial diastole and ventricular diastole: AV closed and SL open
automaticity
that it fires spontaneously controlled by autonomic nervous system
SA Node
fastest intrinsic rate so determine heart rate
Lub
closure of the AV (ventricular systole)
Dup
SL and AV valves closing (atrial systole)
ESV (end systolic volume)
ventricles not completely emptied during systole: allows to increase stroke volume under certain circumstances (exercise) 50mL
SV (stroke volume)
blood ejected per beat which is 70mL (values change during exercise)
conduction
very rapid and co-ordinated which results in rise and fall of BP
arrhythmias
irregular heart beat
Order on ECG
atrial depolarisation
ventricular depolarisation
ventricular repolarisation
delay through AV node (PR interval) then
Plateau phase of AP (ST interval)
SA node action potential
Phase 0 - slow depolarisation due to inward calcium
No phase 1/2 - no Na+ current
Phase 3 - repolarisation due to inward Ca2+ current counterbalanced by outward K+
Phase 4 - pacemaker potential - slow spontaneous depolarisation due to activated cAMP channels and transient Ca2+ channels
nodal tissue
there is a lack Na+ channels
K+ permeability increases
longer time to reach threshold resulting in fewer BPM and reduced HR
ACh
released from vagus nerve - parasympathetic
Ca2+ permeability increases
shorter time to reach action potential - higher BPM and increased HR
noradrenaline
sympathetic innervation
purkinje action potential
Phase 0: rapid depolarisation due to inward Na+
Phase 1: partial repolarisation occurs as Na+ current is inactivated
Phase 2: plateau results from inward Ca2+ current counterbalanced by outward K+ currents
Phase 3: repolarisation due Ca2+ current inactivating and delayed rectifier K+ channel activate
Phase 4: resting state of the cell membrane potential (no pacemaker potential)
calcium enter cardiac muscle cells
trigger contraction - allows for greater contraction for a small movement of calcium (amplify)
adrenoceptors
alpha and beta subtypes
adrenoceptors in heart
beta1 in nodal tissue, conducting system and myocardium - binds noradrenaline and circulating adrenaline
effects of noradrenaline
-positive inotropy
-positive chronotropy
-positive lusitropy
-positive dromotropy
vagus nerve
terminated in nodal tissue
- right vagus supplys SA node
- left vagus supplys AV node
Release of ACh from nerve terminals (vagus nerve)
activates muscarinic (M2) receptors which reduces HR due to increase K+ permeability
