Cardiac Electrical Properties part II

[FOUNDATION] What is conduction velocity?

The distance an action potential propagates per unit time

[FOUNDATION] Why is conduction velocity clinically important?

Abnormal conduction velocity can contribute to cardiac arrhythmias

What three properties influence cardiac conduction velocity?

Cell diameter, action potential amplitude, and the slope of Phase 0 depolarization

What is action potential amplitude?

The net change in membrane potential during Phase 0, measured in millivolts

What is the slope of Phase 0?

The rate of change in membrane potential during depolarization, measured in millivolts per unit time

How does increasing action potential amplitude generally affect conduction velocity?

Greater amplitude allows a larger depolarizing influence on adjacent membranes, promoting faster propagation

How does increasing the Phase 0 slope generally affect conduction velocity?

A steeper Phase 0 produces more rapid depolarization of adjacent membranes and faster conduction

Why must an action potential influence adjacent membrane regions?

Adjacent regions must be depolarized to threshold for the action potential to propagate

How does the rate of positive ion influx influence conduction velocity?

More rapid positive ion influx produces a steeper Phase 0 and generally promotes faster propagation

How does the total amount of positive charge entering during Phase 0 influence conduction velocity?

Greater inward positive charge supports a larger depolarization that can bring adjacent membranes to threshold

[DRAW/MAP] Map the relationship between Phase 0 and conduction velocity.

Greater inward positive ion current → increased Phase 0 amplitude and slope → stronger and faster depolarization of adjacent membranes → increased conduction velocity

Which ion primarily determines Phase 0 in fast-response cardiac action potentials?

Sodium entering through voltage-gated sodium channels

Which ion primarily determines Phase 0 in slow-response cardiac action potentials?

Calcium entering through voltage-gated calcium channels

How does increasing extracellular sodium affect the Phase 0 amplitude of a fast-response action potential in the lecture's model?

It increases the sodium electrochemical driving force and can increase Phase 0 amplitude

How does decreasing extracellular sodium affect fast-response action potential amplitude?

It reduces the sodium driving force and can decrease Phase 0 amplitude

How does increasing extracellular calcium affect slow-response action potential amplitude in the lecture's model?

It increases the calcium driving force and can increase Phase 0 amplitude

How does decreasing extracellular calcium affect slow-response action potential amplitude?

It reduces the calcium driving force and can decrease Phase 0 amplitude

Why does increasing extracellular sodium or calcium promote inward current through its corresponding channel?

It increases the chemical gradient favoring entry when the membrane becomes permeable to that ion

[HIGH-YIELD] Which extracellular ion primarily affects Phase 0 amplitude in fast-response cells?

Sodium

[HIGH-YIELD] Which extracellular ion primarily affects Phase 0 amplitude in slow-response cells?

Calcium

Why does the resting membrane potential affect conduction velocity?

It influences how many voltage-gated sodium or calcium channels are available to open during the next action potential

What happens to voltage-gated channels during persistent partial membrane depolarization?

A greater proportion enters or remains in an inactivated state

What is channel inactivation?

A nonconducting channel state in which the channel cannot reopen normally until sufficient repolarization allows recovery

Why do voltage-gated channels require repolarization to recover from inactivation?

Repolarization permits their inactivation gates to reset

What approximate membrane potential does the lecturer mention in discussing recovery of inactivation gates?

Approximately -50 mV, presented as an illustrative rather than universal threshold

Why does persistent partial depolarization reduce action potential amplitude?

More voltage-gated channels remain inactivated, leaving fewer available to conduct inward current during Phase 0

Why does persistent partial depolarization reduce Phase 0 slope?

Fewer available channels produce a smaller and slower inward depolarizing current

What happens to conduction velocity when Phase 0 amplitude and slope decrease?

Conduction velocity decreases

[HIGH-YIELD] What is the overall effect of persistent resting membrane depolarization on conduction velocity?

Persistent depolarization → increased channel inactivation → reduced Phase 0 amplitude and slope → slower conduction

Why is resting membrane potential especially sensitive to extracellular potassium?

The resting membrane is relatively permeable to potassium

What happens to resting membrane potential when extracellular potassium increases?

The resting membrane potential becomes less negative, or depolarized

What is hyperkalemia?

An increase in extracellular potassium concentration

How does hyperkalemia affect voltage-gated sodium and calcium channel availability?

Persistent depolarization increases channel inactivation, reducing the fraction available for subsequent activation

How does hyperkalemia affect Phase 0 amplitude?

It decreases Phase 0 amplitude when persistent depolarization causes substantial channel inactivation

How does hyperkalemia affect Phase 0 slope?

It decreases Phase 0 slope when fewer channels remain available to carry inward current

How does hyperkalemia affect conduction velocity in the mechanism emphasized by the lecturer?

It decreases conduction velocity

[HIGH-YIELD] Map the effect of hyperkalemia on cardiac conduction.

Increased extracellular K+ → resting membrane depolarization → increased voltage-gated channel inactivation → reduced Phase 0 amplitude and slope → decreased conduction velocity → increased arrhythmia risk

Can localized hyperkalemia develop in cardiac tissue without systemic hyperkalemia?

Yes. Ischemia or infarction can increase extracellular potassium locally even without an overall serum potassium elevation

What is ischemia?

A reduction in blood flow to tissue

How can cardiac ischemia promote localized hyperkalemia?

Ischemia alters sodium-potassium pump activity and ATP-sensitive potassium channel function, producing local extracellular potassium accumulation

Does the lecturer require memorization of the detailed potassium transport mechanisms during ischemia?

No. The emphasized outcome is that ischemia can produce localized hyperkalemia

How can myocardial infarction increase extracellular potassium?

Damaged or dead cardiomyocytes release intracellular potassium into the surrounding extracellular space

Why can myocardial infarction reduce conduction velocity in nearby myocardium?

Local extracellular potassium accumulation can depolarize membranes, increase channel inactivation, and reduce Phase 0 amplitude and slope

[CLINICAL] A patient experiences myocardial ischemia and develops slowed conduction near the affected region. Which local electrolyte change helps explain this?

Localized hyperkalemia

[CLINICAL] A patient has elevated extracellular potassium and a less negative resting membrane potential. Why might conduction slow?

Persistent depolarization inactivates voltage-gated channels, reducing Phase 0 amplitude and slope

[CLINICAL] A myocardial infarction releases intracellular potassium from damaged cells. What electrical consequence is expected in surrounding tissue?

Local membrane depolarization and potentially reduced conduction velocity

[DRAW/MAP] Map myocardial ischemia to arrhythmia risk.

Reduced coronary blood flow → local potassium accumulation → resting membrane depolarization → channel inactivation → reduced Phase 0 amplitude and slope → slower conduction → increased arrhythmia susceptibility

[FOUNDATION] What is a refractory period?

A period after an action potential during which a cardiac cell cannot be excited normally or has reduced excitability

Why are refractory periods important in the heart?

They prevent sustained tetanic contraction, limit excessive excitation, and influence abnormal conduction patterns

Why must cardiac muscle avoid tetanus?

The heart must alternate contraction and relaxation to permit ventricular filling and blood ejection

What is tetanus in muscle physiology?

A sustained contraction produced by summation of repeated contractions

Why does the long cardiac refractory period prevent twitch summation?

The myocardium remains refractory during most of its contraction, preventing another action potential from initiating an additional contraction before relaxation

What is the relationship between cardiac relaxation and the end of the absolute refractory period?

Relaxation is largely complete before another normal action potential can initiate

Why would sustained tetanic contraction be incompatible with effective cardiac pumping?

The heart would be unable to undergo normal cycles of diastolic filling and systolic ejection

How do refractory periods help limit ectopic pacemaker activity?

They restrict how soon cardiac tissue can respond to another impulse, placing limits on abnormal repetitive excitation

Why can very high heart rates reduce cardiac output?

Insufficient ventricular filling time reduces effective blood ejection

What are the two major refractory periods discussed in the lecture?

Absolute or effective refractory period and relative refractory period

What is the absolute refractory period?

The period during which a cardiac cell cannot generate another normally propagated action potential regardless of stimulus strength

What alternative term does the lecturer use for the absolute refractory period?

Effective refractory period

Approximately when does the absolute refractory period end?

Around the middle of Phase 3 repolarization in the lecture's schematic

Why can a cell not generate another normal action potential during the absolute refractory period?

A large proportion of voltage-gated channels remains inactivated

What is the role of channel inactivation in the absolute refractory period?

It prevents sufficient inward depolarizing current from being generated for another normal action potential

What is the activation gate of a voltage-gated sodium channel called in the lecture?

The M gate

What is the inactivation gate of a voltage-gated sodium channel called in the lecture?

The H gate

What happens to the sodium channel M gate when threshold is reached?

It opens rapidly, permitting sodium influx

What happens to the sodium channel H gate after depolarization begins?

It closes more slowly, producing channel inactivation

Why does sodium influx occur before the sodium channel becomes inactivated?

The M activation gate opens faster than the H inactivation gate closes

What happens to the sodium channel H gate during sufficient repolarization?

It resets, allowing recovery from inactivation

[DRAW/MAP] Map the sodium channel gating cycle.

Resting state: M gate closed and H gate available → threshold: M gate opens rapidly → Na+ influx → H gate closes more slowly → channel inactivated → repolarization → H gate resets and channel becomes available again

[HIGH-YIELD] Why does an extremely strong stimulus fail to initiate a normal action potential during the absolute refractory period?

Most relevant voltage-gated channels remain inactivated and unavailable for activation

What is the relative refractory period?

The period during which another action potential may occur if the stimulus is sufficiently strong

Approximately when does the relative refractory period begin?

Around the middle of Phase 3 repolarization

Approximately when does the relative refractory period end?

When the membrane returns to its resting or maximum diastolic potential

Why can a sufficiently strong stimulus initiate an action potential during the relative refractory period?

Enough voltage-gated channels have recovered from inactivation to permit excitation

Why is excitability reduced during the relative refractory period?

Some channels remain inactivated, so fewer are available than after complete recovery

How does channel availability change as Phase 3 progresses?

More channels recover from inactivation as the membrane repolarizes

[HIGH-YIELD] Compare the absolute and relative refractory periods.

Absolute: another normal AP cannot occur regardless of stimulus strength. Relative: another AP can occur if the stimulus is sufficiently strong

[DRAW/MAP] Map refractory periods onto the cardiac action potential.

Phase 0 → Phase 1 → Phase 2 → early/mid Phase 3: absolute refractory period → mid/late Phase 3: relative refractory period → Phase 4: recovery of normal excitability

What is post-repolarization refractoriness as discussed in the lecture?

The lecture uses this term while comparing abnormal action potentials initiated at different points during recovery in the relative refractory period

How does an action potential initiated early in the relative refractory period differ from one initiated later?

It generally has lower amplitude and a shallower Phase 0 slope

Why does an early relative-refractory action potential have reduced amplitude?

Fewer voltage-gated channels have recovered from inactivation

Why does an early relative-refractory action potential have a reduced Phase 0 slope?

Reduced channel availability limits the rate of inward depolarizing current

How does conduction velocity differ between action potentials initiated early and late in the relative refractory period?

Early impulses generally conduct more slowly because they have reduced Phase 0 amplitude and slope

What can result from the slow propagation of an abnormally early action potential?

Conduction delay or conduction block

[HIGH-YIELD] Why is the timing of an abnormal impulse during the relative refractory period clinically important?

Earlier impulses may have reduced amplitude and slope, producing slower conduction and increasing the possibility of conduction abnormalities

[CLINICAL] A premature stimulus occurs early in Phase 3 and generates a weak action potential. Why might conduction be delayed?

Many voltage-gated channels remain inactivated, reducing Phase 0 amplitude and slope

[CLINICAL] Two premature impulses occur during the relative refractory period, one early and one late. Which is expected to conduct more slowly?

The earlier impulse

[DRAW/MAP] Map recovery of excitability during Phase 3.

Early Phase 3: many channels inactivated → absolute refractoriness → mid/late Phase 3: partial recovery → relative refractoriness → progressively greater amplitude and Phase 0 slope → full repolarization and restored excitability

[FOUNDATION] What is an ectopic focus?

A site other than the normal SA node that initiates an action potential

Where can ectopic foci occur?

At abnormal pacemaker sites throughout the atria or ventricles

What can an ectopic focus cause?

Premature contractions or abnormal cardiac rhythms

Why can ectopic impulses propagate abnormally through the heart?

They may spread through myocardium without following the normal sequence of the cardiac conduction system

Why is direct cell-to-cell conduction generally slower than normal His-Purkinje conduction?

Ordinary myocardial propagation is slower than rapid conduction through specialized Purkinje fibers

What ECG change may indicate abnormal ventricular conduction from an ectopic ventricular focus?

A widened QRS complex

Why may a premature ventricular contraction produce a wide QRS complex?

Ventricular depolarization spreads more slowly through myocardium instead of following the normal rapid conduction pathway

[CLINICAL] A patient develops an early ventricular beat followed by a widened QRS complex. What abnormal electrical source is suggested?

A ventricular ectopic focus

[CLINICAL] Why can an ectopic focus become clinically important even if its initial impulse is small?

Once sufficient tissue is excited, the impulse can propagate and produce premature contraction or an arrhythmia

[FOUNDATION] What are afterdepolarizations?

Abnormal depolarizing electrical events arising after an initial action potential and potentially producing triggered activity

What is triggered activity?

Abnormal electrical activity initiated by a preceding action potential that can produce additional depolarizations

What is the general electrical pattern of afterdepolarization-associated triggered activity?

Abnormal oscillations of depolarization and repolarization following an initiating action potential