Lecture 8 - Cardiac Electrical Activity
Types of Cardiac APs
cardiac myocytes have three electrical properties:
excitability
conductivity
automaticity
cardiac cells are divided into two main types:
fast response
slow response
excitability & AP
excitability is the ability of a cell to respond to a stimulus and generate an action potential
fast response action potential
anatomical location
atrial myocytes
ventricular myocytes
cells of the fast conduction network (Purkinje fibres)
it’s a rapid depolarisation phase due to voltage-gated sodium channels
phases & ionic currents
in phase 0, a threshold stimulus opens voltage-gated Na+ channels
the rapid iNa causes a fast depolarisation
in phase 1, Na+ channels close
a brief, transient outward current of K+ (i_to) and Cl- causes a small, initial dip in voltage
plateau occurs in phase 2
there’s a balance between inward and outward currents creates a prolonged plateau
inward current: L-type voltage-gated Ca2+ channels open, allowing Ca2+ influx, which is crucial for contraction
outward current: delayed rectifier K+ channels begin to open
in phase 3, the Ca2+ channels inactivate
the delayed rectifier K+ channels become FULLY open, and iK1 channels recover from inactivation
leads to a large outward K+ current that rapidly repolarises the membrane back to the resting potential
in phase 4, the cell is at rest (~ -90 mV)
maintained by a high permeability to K+ via inward rectifier K+ channels
the Na/K ATPase and Na/Ca exchanger also contributes to maintaining the ionic gradients
refractoriness
during phases 0 to 3, the cell is refractory
unable to generate or is difficult to re-stimulate another AP
the long refractory period prevents tetanus (sustained muscle contraction), allowing the heart to relax and fill in between beats
slow response action potential (pacemaker cells)
anatomical location
SA node
AV node
parts of the His-Purkinje network (latent pacemakers)
the ability to spontaneously depolarise and generate an AP without external stimulation
phases & ionic currents
in phase 0, once the membrane potential reaches threshold, voltage-gated L-type Ca2+ channels open
influx of Ca2- causes a slow, rising upstroke
**fast Na+ channels are absent or inactive in these cells
there’s no distinct phase 1
unlike fast response APs, plateau doesn’t occur in phase 2
in phase 3, repolarisation occurs as Ca2+ channels inactivate and voltage-gated K+ channels open, allowing K+ efflux
in phase 4, the membrane potential isn’t stable
it spontaneously drifts upwards form a maximum diastolic potential towards threshold
decreasing outward current: the K+ channels that were open during repolarisation gradually closes, reducing outward K+ current
increasing inward current:
i_f (‘funny’ current): a unique, mixed Na/K current that’s activated by hyperpolarisation (becoming more negative)
provides a slow, inward, depolarising current
iCa (T-type and L-type): a small inward Ca2+ current also contributes to the latter part of the pacemaker potential
conductivity
the ability of a cell to propagate an electrical impulse to neighbouring cells. the heart is myogenic.
mechanism
cardiac muscle cells are connected by intercalated discs, which contain gap junctions (nexus junctions)
these channels allow ions to flow directly between cells, creating a function syncytium
when one cell depolarises, local currents flow through these gap junctions, depolarising the adjacent cells
factors affecting conduction velocity
cell diameter
velocity is proportional to the square root of the fibre radius
larger cells conduct faster than smaller cells
rate of depolarisation
fast response cells depolarise much faster than slow response cells, leading to faster conduction
automaticity
automaticity is the ability of a cell to spontaneously initiate an electrical impulse
mechanism
this is driven by the phase 4 diastolic depolarisation described for slow response cells
the cell with the highest intrinsic firing rate normally serves as the primary pacemaker
overdrive supression
the faster-firing SA node continuously depolarises the latent pacemakers, keeping them suppressed
if the SA node fails, the next fastest latent pacemaker will take over, establishing an ‘escape rhythm’
HR Regulation Mechanisms
HR is primarily regulated by the ANS, which modulates the slope of the pacemaker potential, the threshold potential, and the maximum diastolic potential of SA node cells
normal: 60 – 100 bpm
bradycardia: HR < 60 bpm
tachycardia: HR > 100 bpm
Cardiac Conduction Steps
the normal activation sequence ensures coordinated contraction, with atria contracting first to fill the ventricles, followed by a synchronised ventricular contraction from the apex upward to eject blood
sinoatrial (SA) Node
the impulse originates in the SA node, located in the right atrium near the opening of the superior vena cava.
tt has the fastest intrinsic rate (~70 bpm at rest).
Atrial Activation
the wave of depolarization spreads cell-to-cell through the atria via gap junctions
specialized internodal tracts conduct the impulse quickly from the SA node to the AV Node.
AV Node Delay
the impulse reaches the AV node
conduction here is very slow (0.05 m/s)
this AV delay (approx. 0.08 seconds) is crucial because it allows the atria to complete their contraction and "top up" the ventricles with blood before the ventricles begin to contract
Bundle of His (AV Bundle)
the impulse passes from the AV node into the Bundle of His, which is the only electrical connection between the atria and ventricles
Bundle Branches
the Bundle of His splits into the Right and Left Bundle Branches, which rapidly conduct the impulse down the interventricular septum.
Purkinje Fiber Network
the bundle branches ramify into a vast network of Purkinje fibers that line the endocardial (inner) surface of both ventricles
these fibers have a very fast conduction velocity (2-4 m/s), ensuring near-simultaneous activation of the entire ventricular endocardium
Ventricular Myocardium
the impulse spreads from the endocardium to the epicardium (inner to outer surface) via cell-to-cell conduction through the ventricular muscle
this pattern ensures the ventricles contract in a coordinated "wringing" motion from the apex upward, efficiently ejecting blood.
Abnormal Heart Electrical Signals
abnormal electrical activation disrupts the coordinated sequence, impairing the heart’s ability to function as an effective pump. this can range from minor to fatal
Atrial Fibrillation
is a common arrhythmia where disorganized, rapid electrical impulses originate in the atria
instead of a single, coordinated wave, the atria "fibrillate" (quiver) chaotically
This results in:
Loss of effective atrial contraction: Atria do not reliably fill the ventricles.
Irregular and often rapid ventricular response: The AV node is bombarded with impulses, leading to an irregular and sometimes dangerously fast heart rate.
Outcome: Can limit exercise capacity and increases the risk of stroke due to blood stasis in the atria. This is an example of a relatively minor (though still serious) rhythm disorder.
Ventricular Fibrillation
a life-threatening arrhythmia where the ventricular myocardium contracts in a disorganized, chaotic manner instead of a coordinated beat
there is no effective pumping of blood
this is fatal if not corrected immediately (with a defibrillator) because it leads to no cardiac output and sudden cardiac arrest.
this is an example of a fatal rhythm disorder.
Key Principle: The normal activation sequence is designed for optimal pumping. Any disruption whether it’s from a failed pacemaker (e.g., SA node dysfunction), a blocked pathway (e.g., AV block), or an ectopic focus generating abnormal impulses. It can compromise cardiac output.