Cardiac Electrophysiology (B 2 : W 1) Flashcards Preview

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Flashcards in Cardiac Electrophysiology (B 2 : W 1) Deck (40)

What is the resting membrane potential of a cardiac ventricle?

-90 mV


What is the significance of the shape of the action potential in a cardiac ventricle? 

The shape of the action potential has an effect on the amplitude of contraction

  • It is very long
  • One AP --> One contraction


What is the sequence of events associated with ventricular action potential? 

Electrical activity precedes physical activity

Electrical event --> chemical activity --> mechanical event

During cardiac cycle, there is a decline in ventricular pressure as AP repolarizes (T wave)


Compare action potential between nodal cells (SA and AV) and chamber action potentials (atria and ventricles) 

  • In SA and AV nodes
    • Slow upstroke velocity 
    • Depolarization is slow
    • Threshold is more positive
  • In atrial and ventricular cells
    • High amplitude 
    • Fast AP 
    • In atria: want contraction to be quick and homogenous 
    • In ventricles: endocardium is excited first, and then goes across ventricular wall
    • Slow repolarization 


What is the difference in resting potentials of SA action potentials and ventricular action potentials?

  • SA RMP sits at about -50 mV
    • Pacemaker cells have unstable resting potential that goes up and down
  • Ventricular RMP sits at -85
    • Very stable RMP
    • AP is higher than it is in SA node
    • Without impulse from SA node, it will not depolarize


Why is the SA node the dominant pacemaker over the AV node?

SA has a faster slope of depolarization than the AV node, and thus is the dominant pacemaker

  • Impulse from fast SA pacemaker reaches AV node cell and causes faster membrane depolarization 
  • If no impulse is coming to AV node, slower depolarization takes longer 
  • AV is entrained because of the impulse it receives from SA


What does the Nernst equation tell us?

Determines the energy needed to maintain ion gradient in the system.

Takes into acount chemical gradient and electrical gradient 

At equilibrium potential, there is no net flux of the ion 


How do ions particpate in the generation of a membrane potential?

Flux of ions generates membrane potential

Need ion channels to produce this flux - can't go through the lipid bilayer on their own 


What is the dominant ion to determine the membrane potential of ventricular cells and Purkinje cells?


Membrane is highly permeable to potassium


Since the resting membrane potential of most cardiac cells does not equate to Nernst potentials of any of the ions, what does this mean?

This suggests that the cardiac cell membrane is permeable to more than one type of ion.

We now know that the "resting" (diastolic) cardiac membrane is maily permeable to K, but also displays some permeability to Na.



Contrast permeability ratio of Na:K in pacemaker cells and non-pacemaker cells

  • Non-pacemaker cells (atrial, ventricular, Purkinje) exhibit a low permeability ratio of Na:K (1-3 : 100)
    • More polarized
    • More negative RMP
  • Pacemaker cells (SA and AV node) display a relatively higher permeability ratio (1 : 5-10) 


What does the GHK (Goldman-Hodgkin-Katz) equation tell us?

Takes into account the electric and chemical gradients for more than one ion in a cell



Describe the plots on this graph

  • Black: No Na permeability; linear plot 
  • Red: Relative permeability of Na is 0.02
  • When K reaches a high concentration, there is no more membrane potential - intercept 
  • K channels at rest are sensitive to the K concentration outside of the cell
    • K permeability goes down dramatically
    • Membrane potential tends to go to Na - depolarize at this point
    • Low K means danger in ventricular cells - can induce arrhythmias 


What is the function of the electrogenic Na-K pump?

  • Maintains the gradient
  • Contributes to resting membrane potential
    • By as much as -10 mV 


What is the function of the aqueous pore in a voltage-gated (dependent) ion channe?

The pore lowers the energy barrier by dissolving ion across membrane 

  • Narrow selectivity filter - only allows some through
  • Conducts millions of ions per second when they are open
  • Some are activated by depolarization, some by hyperpolarization


What is the role of voltage-gated Na and K channels in generating the action potential in axons?

Conductance = flux = channels open

  • Na conductance is low at rest
  • Na conductance increases above K during action potential
  • Na goes down on its own, K goes up and causes repolarization 


Describe the phases of typical cardiac action potentials?

  • Resting potential is phase 4
    • Excitation coming upstream from cell causes a little "foot" of an action potential
  • If it reaches threshold, it depolarizes - phase 0
    • All or none
    • Cannot be interrupted 
    • Wants to reach the ENa but K channels are opening and opposing it
  • Phase 1 - inactivation of Na channels, activation of Ca channels
  • Phase 2 is the plateau
    • Characteristic of cardiac cells
    • Ca current in matches K current out
  • Phase 3 is rapid repolarization 
    • Ca channels inactivated 


What two mechanisms are triggered by the opening of Na channels during rapid depolarization?

  • Ca channel is opened at -40 mV
    • Slow
    • Helps maintain plateau
  • K channel shuts off during action potential
    • Reopens when Na channels inactivate to repolarize


What is one important difference between action potentials in neurons and cardiac cells in regards to PK?


  • In neurons, PK goes up during the action potential
  • In cardiac cells, PK goes down

This, and the fact that cardiac cells have a prominent Ca current, is the reason for the existence of a long plateau


What is the threshold for an action potential in the SA node?

- 40 mV


Describe the phases of SA nodal action potentials

  • Phase 0: Ca channel produces Ca current to cause action potential
    • Channels open at - 40 mV
    • Ca channel desnity is low
    • Not much amplitude because of few Ca channels
  • Phase 3: peak of AP opens K channels - repolarization
  • If current = pacemaker current
    • Nonselective channel permeates both Na and K 
    • Pacemaker current starts to depolarize until threshold is released


Define ischemia and some of its causes

Low blood flow; happens during a heart attack (infarction)

  • Acidosis - lactic acid
  • Hypoxia (low oxygen)
  • Acummulation of potassium 


What do slow response action potentials in ventricular cells resemble?

Slow response in ventricular cells resembles action potential in SA nodal cells. 

  • More K on the outside (in ischemia) - cell is more depolarized 
    • Inactivation of Na-gated channels
  • Ca channels activate at -40 mV
    • Slow AP because they turn on slowly
  • Catecholamines stimulate these slow responses 


What is the significance of gap junctions in cardiac cells?

  • Large channels for electric conductance
  • Can be controlled by ß adrenergic stimulation
  • Low resistance pathway for passage of currents between cells 


How do local circuit currents mediate propagation?

  • Local circuit currents are transmitted across a distance
  • Can depolarize a neihboring region
    • Excite passively
    • Domino effect
  • More complicated in cardiac cells because of 3D structure than it is in nerves 
    • Same principle guiding propagation 


How does the height of an action potential affect conduction velocity?

Conduction velocity is enhanced by the height of the actionpotential

Allows for more distal downstream cells and their subsequent activation


What is the relationship between conduction velocity and the resting potential?

Conduction velocity is inversely porportional to the resting potential

Membrane depolarization reduces the availability of Na by inactivation - Reduces the rate of rise of Phase 0 in non-pacemaker cells as well as AV nodal cells


What is the impact of high K on action potentials? 

  • Slower response because of K
    • True slow response
  • Slower depolarization 
    • Slower downstream cell depolarization
    • Slower conduction velocity in general


What is the difference between the absolute/effective refractory period and the relative refractory period?

  • Absolute refractory period
    • Cannot trigger a premature contraction
  • Relative refractory period
    • Abnormal stimuls here could cause premature excitation
    • Could lead to depressed response - Na channels not fully available
    • AP will have lower response 


What controls the refractory period?

Refractory period dominated by Na channels

  • Inactivated at positive potential
  • For channels to go from inactivated (closed state) to rested and ready, there is a period of recovery
  • Need this time to go to a negative potential 


Describe the distribution of autonimic nerves in the heart

  • Sympathetic gaglionic chain feed into the heart
  • Parasympathetic Vagi feed into SA and AV nodes
    • Parasympathetic is responsible for pacemaker activity


What are the three mechanisms for altering pacemaker activity?

  1. Change the slope of phase 4 diastolic depolarization
    1. Increase - Faster AP
    2. Decrease - Slower AP
  2. Change in threshold potential
    1. Lowering threshold accelerates pacemaker activity 
  3. Change in maxium diastolic potential 


What is the effect of sympathetic stimultion on SA node?

Increases pacemaker activity

Increases heart rate


What is the effect of parasympathetic (Vagal) output on cardiac cells?

  • Atria: reduction in action potential duration
    • Receptor-modulated: ACh activation of ligand-gated K channel
  • AV Node: reduction in excitability
    • Reduces transmission through ventricles
    • Leads to ventricular escape (Purkinje fibers)
    • Slows conduction velocity and pumping
  • Ventricle
    • Little effect except for antagonizing the stimulatory effects of ß adrenergic stimulation 
    • Sympathetic effect is dominant on ventricle 


What is the effect of sympathetic ouput on cardiac cells?

  • Atria and ventricles
    • Increased contractility - due to increased Ca current
    • Has little effect on AP duration - due to activation of repolarizing K channels
  • AV node
    • Increased excitability and transmission of the impulse 
    • Increased conduction velocity


What effect does serum potassium have on pacemaker activity?

Hypokalemia: accelerates automaticity

Hyperkalemia: depresses automaticity


What happens when ventricular muscle cells experience hyperkalemia?

  • Depolarization
    • Initial excitability: decreased depolarizing stimulus necessary to cause an action potential
    • Prolonged exposure: decreased amplitude of action potential due to Na channel inactivation
  • Increased K permeability
  • Result: Decreased ventricular excitation
    • Decreased AP conduction
    • Weak ventricular contraction
    • Shorter AP


What happens when SA nodal cells experience hyperkalemia?

  • Increased potassium permeability
    • Counteracts Ifunny channel, leads to delayed depolarization
  • Result: decreased automaticity
    • Possible bradycardia


What happens when ventricular muscle cells experience hypokalemia?

  • Hyperpolarization 
  • Decreased permeability of potassium 
    • Decreased repolarization current 
  • Result: increased ventricular excitation
    • Increased number of inactivated sodium channels
    • Opportunity for reentrent arrhythmia
      • Delayed repolarization and hyperpolarization 


What happens when SA nodal cells experience hypokalemia?

  • Decreased potassium permeability 
  • Early depolarization
  • Enhanced automaticity 
    • Possible tachycardia