Lecture 8 - Cardiac Electrical Activity

what are the three key electrical properties of cardiac myocytes?

• excitability

• conductivity

• automaticity

what are the two main types of cardiac cells based on electrical behaviour?

• fast response cells

• slow response cells

where are fast response cells found?

SA node, AV node, latent pacemakers

what ion causes the rapid upstroke in fast response cells?

Na⁺ influx

what ion causes the upstroke in slow response cells?

Ca²⁺ influx

L-type Ca²⁺ channels

what’s the key difference between fast and slow response phase 0?

• fast = Na⁺ mediated (rapid)

• slow = Ca²⁺ mediated (slow)

in the fast response, phase 4 resting potential (~ -90 mV) is maintained mainly by

K⁺ permeability via iK1 channels

what happens during phase 0 in fast response AP?

rapid Na⁺ influx → depolarisation

what causes phase 1 in fast response AP?

transient outward K⁺ current (i_to)

what creates the plateau in fast response AP?

balance between Ca²⁺ influx and K⁺ efflux

why is Ca²⁺ influx in phase 2 (fast AP) important?

triggers cardiac contraction

what causes phase 3 repolarisation in (fast AP)?

K⁺ efflux via delayed rectifier K⁺ channels

why is the refractory period (fast AP) important in cardiac muscle?

prevents tetanus (sustained muscle contraction) and allows filling between beats

what is automaticity?

ability to spontaneously generate APs

pacemaker potential is driven by

i_f

Ca²⁺ influx

decreasing K⁺ efflux

what’s the funny current (i_f)?

mixed Na⁺/K⁺ inward current activated by hyperpolarisation

threshold for pacemaker cells?

approximately -40 mV

why do pacemaker cells not have a stable resting potential?

continuous slow depolarisation

why is there no plateau phase in slow response cells?

lack of sustained Ca²⁺/K⁺ balance like in fast cells

what structures allow electrical coupling between cardiac cells?

gap junctions in intercalated discs

what is a functional syncytium?

cardiac cells acting as a single electrical unit

how does depolarisation spread between cells?

local current flow through gap junctions

how does cell size affect conduction velocity?

larger cells → faster conduction

why do fast response cells conduct faster?

faster depolarisation (Na⁺ vs Ca²⁺)

primary pacemaker of the heart?

SA node (60 – 100 bpm)

whats the intrinsic rate of the AV node?

40 – 55 bpm

what’s the intrinsic rate of His–Purkinje system?

25 – 40 bpm

what’s overdrive suppression?

faster pacemaker suppresses slower ones

what happens if the SA node fails?

latent pacemaker takes over

what primarily regulates HR?

ANS

normal resting HR?

60 – 100 bpm

define bradycardia

HR < 60 bpm

define tachycardia

HR > 100 bpm

what three properties of SA node cells does the ANS modify to regulate HR?

• slope of pacemaker potential

• threshold potential

• maximum diastolic potential

an increase in the slop of the pacemaker potential will

increase HR

a more negative maximum diastolic potential will

decrease HR

main neurotransmitter of the parasympathetic system in the heart?

acetylcholine (ACh)

what ion channel does ACh open in SA node cells?

ACh—sensitive K⁺ channels (iK_ACh)

parasympathetic stimulation _____ SA node cells

hyperpolarises

how does parasympathetic stimulation affect pacemaker slope?

decreases it

effect of parasympathetic stimulation on HR?

decreases HR (negative chronotropy)

effect of parasympathetic activity on AV node conduction?

slows conduction

main neurotransmitter of the sympathetic system in the heart?

noradrenaline (NA)

what ion channel activity is increased by sympathetic stimulation?

L-type Ca²⁺ channels

sympathetic stimulation _____ the slope of the pacemaker potential

increases

effect of sympathetic stimulation on HR?

increases HR (positive chronotropy)

addition effects of sympathetic stimulation on the heart?

increases contractility and relaxation rate

opposite effects of PNS vs SNS on pacemaker slope?

• PNS: decreases slope → ↓ HR

• SNS: increases slope → ↑ HR

opposite effects of PNS vs SNS on membrane potential?

• PNS: hyperpolarises

• SNS: depolarises faster

what’s the correct sequence of electrical conduction through the heart?

SA node → atria → AV node → Bundle of His → bundle branches → Purkinje fibres → ventricular myocardium

why do the atria contract before the ventricles?

to allow ventricular filling before contraction

why do ventricles contract from apex upward?

to efficiently eject blood out of the heart

where’s the SA node located?

right atrium near the superior vena cava

what’s the role of the SA node?

primary pacemaker; initiates electrical impulse

why does the SA node control heart rhythm?

it has the fastest intrinsic firing rate

how does depolarisation spread through the atria?

cell-to-cell via gap junctions

what structures speed conduction from SA node to AV node?

internodal pathways

what’s the main function of the AV node?

delay electrical conduction

duration of AV nodal delay?

~0.08 seconds

why is the AV delay important?

allows ventricles to fill before contraction

the AV node has _____ to allow time for ventricular filling

slow conduction velocity

what’s unique about the Bundle of His?

only electrical connection between atria and ventricles

why is the Bundle of His necessary?

fibrous skeleton electrically insulates atria from ventricles

what’s the function of bundle branches?

rapidly conduct impulse down interventricular septum

what’s the function of Purkinje fibres?

distributes impulse rapidly throughout ventricles

why’s Purkinje conduction so fast?

ensures near-simultaneous ventricular activation

in which direction does ventricular depolarisation spread?

endocardium → epicardium

what type of contraction does this create?

coordinated ‘wringing’ motion

where’s conduction slowest in the heart?

AV node

where’s conduction fastest in the heart?

Purkinje fibres

why is slow conduction in AV node beneficial?

allows time for ventricular filling

why’s fast conduction in Purkinje fibres important?

ensures synchronised ventricular contraction

what’s the consequence of abnormal electrical activation in the heart?

disrupted coordination → impaired pumping (decreased CO)

what’s an arrhythmia?

abnormal heart rhythm due to disordered electrical activity

what characterises atrial fibrillation?

chaotic

rapid electrical activity in the atria

what happens to atrial contraction in atrial fibrillation?

lost (atria quiver instead of contracting)

how does atrial fibrillation affect ventricular rhythm?

irregular and often rapid

atrial fibrillation increases risk of _____ due to blood stasis

stroke

why does blood stasis occur in atrial fibrillation?

atria don’t contract effectively

is atrial fibrillation immediately fatal?

no, but it’s serious

what characterises ventricular fibrillation?

chaotic electrical activity in ventricles → no coordinated contraction

what’s the effect of ventricular fibrillation on CO?

no effective CO

why is ventricular fibrillation fatal?

no blood is pumped → cardiac arrest

immediate treatment for ventricular fibrillation?

defibrillation

ventricular fibrillation leads to _____ if untreated

sudden cardiac arrest

key difference between atrial fibrillation and ventricular fibrillation?

• atrial : atria affected, not immediately fatal

• ventricular : ventricles affected, fatal

which arrhythmia is more dangerous: atrial or ventricular fibrillation?

ventricular fibrillation

name three causes of abnormal electrical activation

• failed pacemaker (SA node dysfunction)

• blocked pathway (AV block)

• ectopic focus

what’s an ectopic focus?

abnormal site generating electrical impulses