Cardiac Electrical Activity and the EKG

function of the heart

pump blood to the body

order of circulation

left atrium —> left ventricle —> arteries —> veins —> right ventricle —> right atria

diastole

phase of the heartbeat when the heart muscle relaxes and allows the chambers to fill with blood

systole 

phase of the heartbeat when the heart muscle contracts and pumps blood from chambers into arteries 

excitation contraction coupling

• myocyte experiences change in transmembrane potential

• AP triggers Ca to enter cell and triggers translocation of Ca into cytosol

• Ca binds myofilaments eliciting cell contraction

properties of cardiac cells

• excitability

• automaticity

• conductivity

• ability to contract

excitability 

porperty of cells in which depolarization of the membrane above a certain threshold triggers an AP

action potential

all or nothing change in membrane potential followed by a return to resting membrane potential

resting membrane potential in cardiac cells

-88 mV

generation of action potential depends on

transmembrane ionic fluxes driven by voltage gated channels and electrochemical gradient 

Phase 0 - Rapid Depolarization

• Na channels open at -60 mV

• Na enters the cell

• fast deplarization due to rapid opening

• Na channels inactivate at 20 mV

Phase I - Partial Repolarization

• K channels open

• K moves out to make the gradient more negative

• involves transient outward K channels

Phase II - Plateau

• more K channels open 

• Ca opens and moves in

• charges entering and leaving balance each other 

• L type Ca current and delayed rectifier K current 

Phase III - Repolarization

• delayed rectifier and inward rectifier K channels

• K continues to move out

Phase IV - Resting Potential

• inward rectifier K channels remain open

• Na/K ATPase and Na/Ca exchange restore the resting membrane potential

excitability key points 

• cardiac AP results from ion currents related to voltage and time dependent channels

• upstroke in AP is due to Na channels 

• ventricular Ap exhibits plateau due to equal Ca and K flux 

• Resting Vm of myocytes is dictated by permeability of K ions due to inward rectifier channels

Slow AP

• in SA and Av node

• maximum diastolic pressure of -65 mV due to lack of Ik1

• gradual diastolic depolarization due to pacemaker currents

• low amplitude and slow depolarization due to Ica, lack of Ina

Fast AP

• in atrial and ventricular muscle, purkinje fibers

• maximu diastolic pressure of -90 mV due to Ik1

• no pacemaker currents

• large amplitude and fast depolarization due to Ina

Fast AP in Purkinje fibers 

can be converted to slow AP if Ina is blocked 

refractory period

interval during the AP in which a second or multiple APs cannot be induced

effective refractory period

phase in which a new AP cannot be induced

relative refractory period 

phase in which a new AP can be generated with a larger than normal stimulus

refractory periods prevent

tetanization

automaticity

• ability to undergo a spontaenous time dependent depolarization of cell membrane that leads to AP

• ability of self excitation

rhythmicity 

regularity of pacemaker ability 

dominant/subsidiary pacemakers

• anatomical structures that present hierarchical pacemaker activity

• Sa node is dominant

• Av node and purkinje fibers are subsidiary

pacemaker potential in nodal cells

• If contributes to diastolic depolarization by brining ions

• no Ina current for fast response AP

• Ik is responsible for repolarization

acetylcholine 

• reduces heart rate 

• reduces If and Ica

• reduce slope of diastolic depolarization and shift threshold to be more positive

• activates ligand gated K channels to promote repolarization

catecholamines 

• increase heart rate

• increase If and slope of diastolic deplarization

• increase I ca to lower AP threshold 

intrinsic heart rate

rate at which the hear beats when all cardiac, neural, and hormonal inputs are removed; approx. 110 bpm

conductivity

• ability to propogate electrical impulse from one cell to another

• special cardaic cells form the conduction system

properties of the heart 

• cells electrically coupled via gap junctions form functional syncytium

• plane of valves electrically inert except for AV node 

• normal conduction path is the same for each beat 

• conduction veolicty varies signficiantly along route 

heart conduction velocity

• is heterogeneous

• atria contract before ventricles

• Sa node is slowest to contract

functional syncytium contains

intercalated discs and gap junctions

intercalated discs 

transverse bonds that separate adjacent myocytes 

gap junctions

• intracellular communication between neighboring cells

• made of connexins

propogation of excitation

• depolarization of Cell A originiates flow of positive charge from Cell A to B vi agap junctions

• positive charges depolarize Cell B an release extracellular positive charges

• extracellular positive charges originate extracelllar current from A to B

electrocradiogram 

• formed by two electrodes placed on the patients kin and connected to a device that measures the difference of potential between the two sites when the electrodes are placed 

lead measurement equation

Vlead = Vdip cos 0 / d²

cardiac dipole

reflects at any moment, the geometric average potential difference of resting and active areas of the heart

three main deflections per cardiac cycle 

• p wave corresponds to atrial depolarization

• qrs complex corresponds to ventricular depolarization

• t wave corresponds to ventricular repolarization

atrial repolarization wave

masked by QRS complex

determinants of EKG waveform

• larger masses produce larger dipoles

• conduction velocity determines timing of occurance and duration of waveforms

• vectorial orientation

• distance between electrodes and dipole

EKG allows for determinations of 

• heart rate 

• conduction of the heart 

• direction of cardiac de/repolarization

• damage to the heart 

• arrthymias

EKGs do not provide information on

pumping or mechanical events in the heart