Home > Flashcards > Print Preview
The flashcards below were created by user
on FreezingBlue Flashcards. What would you like to do?
Lecture 13 - Heart Electrophysiology
Pacemaker Myocardial Cell RMP
- have a resting membrane potential (Em) that periodically & spontaneously shifts toward 0
- have a max resting potential less than that seen in non–pacemaker cells (-60 to –70 mV vs. -90 mV in non- pacemaker cells)
- such cells are located in the sinoatrial node (SA node), atrioventricular (AV node), & in other parts of the specialized conduction system of the heart
What is the threshold potential in pacemaker cells?
- about –50 mV
- pacemaker cells slowly & automatically depolarize to the level of the threshold potential
- when threshold is reached, voltage dependent cation channels open → triggering an AP
Phase 4 Depolarization (pacemaker potential)
- characterized by an increase in membrane resistance due to decreased permeability to K+
- RMP exists b/c of a high level of K+ permeability, so the reduction of K+ permeability → depolarization
- the resting phase in cardiac cells = phase 4 (doesn't last long - as soon as Em is reached, K+ channels begin to close)
What determines a pacemaker cell's RATE of firing?
- its phase 4 slope (*)
if (funny inward current)
- helps produce depolarization during phase 4
- Na+ channels open when the voltage is more negative, immediately after the end of a previous action potential (contrary to what usually happens in other cells)
What is the dominant inward current during an action potential in pacemaker cells?
a Ca2+ current (in contrast to non-pacemaker cells of the myocardium)
SA (sinoatrial) Node
- the heart's natural pacemaker - SA node cells normally lead the others & controls heart rate
- pacemaker cells in the SA node depolarize at a faster rate during phase 4 than pacemaker cells in other parts of the conducting system
- nodal cells are autorhythmic - can contract without innervation
Order of Electrical Conduction
SA Node pacemaker cells generate action potentials which are rapidly conducted through the atria to the AV node → His Bundle → RBB & LBB → Purkinje Fibers
also septum → apex → base
& endocardium → epicardium
AP normally arrive in these later tissues before their slowly depolarizing pacemaker potentials have had time to reach threshold
small fibers in the thick part of the ventricles' wall designed to rapidly take a signal once it enters the ventricle & spread it in a coordinated way through the ventricle muscles
when AV node pacemaker cells take over control of the ventricular beat at an abnormally slow rate if for some reason the SA node cell firing rate decreases to a level slower than the rate of depolarization in the area around the AV node
Which corresponds to sympathetic, normal, & parasympathetic stimulation?
- a: SNS (catecholamines)
- b: normal stimulation
- c: PNS stimulation (acetylcholine)
Effect of NE on Pacemaker Potentials
- sympathetic stimulation causes a release of NE which binds to β1 receptors on the pacemaker cells (+ other myocardial cells)
- adenylate cyclase is activated & causes a local increases in intracellular Ca2+ which decreases conductance in Ca2+ sensitive K+ channels
- result = ↑ depolarization rate during phase 4 & thus ↑ heart rate
Effect of ACh on Pacemaker Potentials
- acetylcholine released during parasympathetic stimulation increases K+ conductance leading to hyperpolarization
- in this state it takes longer for the phase 4 depolarization to reach threshold → heart rate is slowed
Non-pacemaker Myocardial Cell RMP
- resting membrane potential (RMP) in non-pacemaker myocardial cells is identical to that described previously for neurons & skeletal muscle (i.e. the RMP is very close to the equilibrium potential for K+, being determined almost entirely by the concentration gradient for K+ across the cell membrane)
How are tetanic contractions of cardiac muscle prevented?
- are prevented by the long duration cardiac action potentials (~200 miliseconds in humans) which result in long refractory periods during which further stimulation of the cells is not possible
- such fused strong contractions produced by skeletal muscle at high frequencies of stimulation would be detrimental to cardiac function
- the rising phase of the cardiac AP
- is caused by an inward Na+ current once threshold is reached and causes a rapid increase in Na+ conductance
- the membrane depolarizes to an overshoot of +20-30 mV during this phase as Em approaches ENa (Na+ equilibrium potential)
- a short period of partial repolarization after Na+ channels quickly inactivate
- in addition, a particular type of K+ channel (ito1) opens which contributes to the slight repolarization during phase 1 [some K+ is able to leave the cell, making the Em more negative]
- the membrane potential stays at ~0 mV for a prolonged period of time called the “plateau”
- it results from a combination of
- 1. closing of K+ channels (iK1) which prevents further repolarization &
- 2. opening of voltage-gated Ca2+ channels (slow channels)
- when repolarization occurs after a plateau period of 100-200 milliseconds
- repolarization is mediated by Ca2+ channels closing & K+ channels (iKr) & iKs) opening
- Em approaches EK
- when the resting potential is maintained by open K+ channels at a highly negative membrane potential
- the channels are called inward rectifying K+ channels b/c as the membrane is depolarized, they do not permit outward movement of K+
- it is this property that facilitates rapid depolarization during phase 0
What purpose does the order in which an action potential propogates through different points in the heart serve?
- chronology of signal generation: septum→apex→base
- because contraction occurs in the apex (bottom the heart) before traveling up to the base (top of the heart), it ensures that blood sitting at the bottom of a ventricle is squeezed up and out of it so a maximum cardiac output exits the heart during systole
What purpose do the small small diameter junctional fibers of the AV node serve in contraction of the heart?
- b/c of their small diameter, they DELAY the transfer of electrical signals from the atria → ventricles
- this ensures complete atrial depolarization before the ventricles may be depolarization
- aka ensures atrial SYSTOLE occurs before ventricular systole does → topping off the ventricles & maximizing cardiac output
AV (atrioventricular) Node
- located in the atrial septum (junction)
- contains small diameter junctional fibers through which an action potential must pass from the SA node to be further propagated from the atria through the rest of the heart
- the slow conduction velocity at the atrial junction where the AV node is causes an important delay (PR interval) between atrial & ventricular depolarization
AP Durations in Different Myocardium Regions
- AV node has slowest conduction velocity
- bundle branches have the longest phase 2
What is the order of repolarization in the heart after blood has been pumped from the ventricles?
- base → apex → septum → His Bundle → AV node
- (Purkinje Fibers → RBB & LBB)
- essentially the REVERSE of depolarization
Which of the three cells is activated?
- the leftmost positive on the inside one
- other ones are inactive b/c they're at a negative resting potential
- AP will spread via gap junctions between myocardial cells
- when one part of the tissue is activated (has an AP moving through it causing a positive Em) juxtaposed with an inactive (negative Em) portion of the tissue
- can measure the dipole using a voltmeter
Lecture 14 - Electrocardiography
- meter & 2 electrodes
- one is the plus/positive (measuring) electrode & the other is the negative (null) electrode; is set to 0
- when the 2 electrodes are put on something that has an electrical difference, will be able to read the amplitude of that electrical difference in volts
- depending on which end the + electrode is on, the polarity of the system can also be determined
- when both electrodes see the same charge (eg. 0) the signal reads as 0
- the positive end of the dipole is indicated by the vector arrow
- the negative end of the dipole is indicated by the tail
- the depolarized portion constitutes the negative side, & the yet-to be depolarized portion constitutes the positive side of the dipole
A wave of depolarization moving away from the negative electrode toward the positive electrode is recorded as what type of voltage?
- a positive voltage
- a depolarization toward the - electrode results in a downward signal
A wave of repolarization moving away from the positive electrode toward the negative electrode is recorded as what type of voltage?
- a positive voltage
- a repolarization toward the + electrode results in a downward signal
Mean Vector of Atrial Depolarization
- equals the sum of the individual vectors that originate in the SA node - has to do with the location of the SA node
- depolarization begins in the SA node located in the right atrium
- the wave of depolarization emerges from cells of the SA node & moves through atrial myocardium generating the P WAVE of an EKG
When does atrial repolarization take place?
- during ventricular DEpolarization & is obscured by the QRS complex
- there is normally no direct connection between the atrial & ventricular myocardium b/c the fibrous tissue of the AV groove serves as a barrier to conduction
- normally depolarization only travels through the AV node & His bundle → ventricles
Where is conduction fast, along the left bundle branch or along the right bundle branch?
- conduction into & along the left bundle branch is normally faster than in the right bundle branch
- means the 1st portion of the ventricles to be depolarized is the left ventricular side of the septum just under the endocardium
- P wave: atrial depolarization
- QRS: ventricular depolarization
- T wave: ventricular repolarization
What happens when a dipole is oriented perpendicularly to the angle of the voltmeter electrodes?
- the voltmeter reads 0 Volts
What happens when a dipole is rotated so that its axis is parallel to the axis of the voltmeter electrodes?
- the maximum possible voltage is measured
In any position, what happens when the magnitude of a dipole is decreased?
- there is a proportional decrease in measured voltage
Measuring Myocardial Dipoles
- at rest myocardial cells have a negative charge inside & a positive charge outside
- as cells depolarize, the depolarized segments become - outside & + inside
- depolarized segments are adjacent to segments that've not yet depolarized & so still bear a + charge outside/ - inside
- it is this situation that creates a series of dipoles w/in EXTRAcellular fluid of a depolarizing tissue at an instant in time
- basically direction/arrow of dipole is in reference to outside the cell
Why aren't intracellular dipoles measured?
dipoles are also set up in the intracellular fluid, but because of the high resistance of the cell membranes they cannot be measured by electrodes in the extracellular fluid or on the surface of the body
In which order to cells repolarize?
- the last cells to be depolarized are the 1st to repolarize
- this means that the + end & - end of the dipole (and the orientation of the vector arrow) are in the same direction as they were during depolarization EVEN THOUGH a very different process is occurring
Atrial Depolarization (P) Vector
• atrial depolarization originates in the SA node & spreads from R → L & inferiorly over both atria
• head of the arrow points toward the + end of the dipole where the atrial muscle has not yet depolarized (+ outside, - inside)
• - end of the dipole is at the tail of the arrow where depolarization has already occurred (- outside, + inside)
• point A is + relative to point B & → causing an upward (“positive”) deflection of the EKG; P wave
• at the mid-point of atrial depolarization the net dipole vector is oriented from R → L, down, & has a magnitude proportional to the mass of the atrial muscle involved
What happens to the P wave once the atria are completely depolarized?
- because no voltage difference exists between points A and B the voltage recording returns to zero (baseline)
- in this situation the EKG is isoelectric: there is no deflection above or below zero
What shows up on an EKG as depolarization moves through the AV node & His (AV) bundle?
- nothing - dipoles generated by depolarization of these structures are too small to be measurable from the surface of the body
- after the P wave depolarization moves slowly through the AV node, the His (AV) bundle, & is on its way to the R & L bundle branches
Bundle Branch Depolarization
• action potentials enter the fibers of the bundle branches, & depolarize the L bundle branch & left side of the septum 1st b/c conduction here is slightly faster than conduction in the R bundle branch
• at this time electrode B is + with respect to electrode A (closer to the depolarized LBB)
• the dipole vector has its + end closer to the - electrode → downward deflection, the Q wave
RBB Depolarization Quickly Follows Q Wave
- RBB depolarizes soon after the L & now the entire septum is depolarized
- as this happens the tracing returns to an isoelectric (zero)
Purkinje System Depolarization
- from the BBs the depolarization quickly spreads via the Purkinje fibers across the walls from apex → base of both ventricles
- this generates a net dipole with its + end oriented toward the L ventricle b/c individual dipoles there are larger than those in the R ventricle due to the larger muscle mass of the L ventricle
What dipole is generated by the last portions of the ventricles to depolarize?
- one w/ its + arrow head oriented toward the - electrode, generating a negative or downward deflection in the EKG, the S wave
- the period between the end of the S wave & the beginning of the T wave
- is normally isoelectric b/c no dipoles large enough to influence the EKG are present since all ventricular myocardium is depolarized (phase 2 plateaued)
- begins in the subepicardial cells in the base of both ventricles (APs are shortest here)
- b/c of the larger muscle mass of the L ventricle repolarization generates a net dipole w/ its + end toward the left
- the T wave deflection is upward
- place electrodes on 3 points that roughly produce an equilateral triangle around the heart
- when leads are dialed in, looking at the same electrical events from 3 different axis (provides more information)
• they measure voltage differences between 2 discrete positions on the body
• Lead I records the potentials induced at any instant in time between the right shoulder or arm (negative terminal) & the left shoulder or arm (positive terminal)
• Lead II records the potential differences between the right shoulder (negative) & the junction of the left leg with the torso (positive)
- • Lead III records potential differences between the left leg (positive) & the left shoulder or arm (negative)
- come from using one of the bipolar lead electrodes as a measuring (+) electrode & using the 2 other bipolar leads grounded together as a minus (-) electrode
- the minus electrode therefore is physically located half-way between the 2 electrodes not being used as the measuring electrode
- gives 6 instead of 3 electrical axis to measure dipoles on
left arm is the measuring (+) electrode vs other two leads grounded together
right arm is the measuring (+) electrode vs other two leads grounded together
- left foot is the measuring (+) electrode vs other two leads grounded together
- aVF is perpendicular (90 degrees) to Lead I
precordial (V) leads
- measure dipoles in a horizontal plane at the level of the heart at the angles shown in the diagram
- limb leads are grounded together so that voltage differences between a “neutral” point at the center of Einthoven’s triangle and points on the anterior & left side of the chest wall can be measured
- V leads detect dipoles oriented from the heart toward each of the electrodes place on the chest wall anterior of the heart
- V lead deflections sare generally larger than those seen in the limb leads because the V electrodes are close to the heart and there is little resistance between them and the origin of the cardiac dipole
Mean Cardiac Vector (Ventricular Axis)
a single vector that represents the mean magnitude & direction of ventricular depolarization, the QRS
How to computing a mean cardiac vector from the bipolar leads:
1. determine the net amplitudes of the deflections in the QRS of at least two bipolar leads (count up the squares the peak reaches up to)
2. transfer the values to the appropriate axes on a graph
3. draw lines perpendicular to vector intersecting at the vector tip
- 4. draw the resultant vector from the origin to the point where the perpendiculars cross
How can the mean cardiac vector (ventricular axis) be estimated?
- by examining the limb lead tracings to find the lead whose positive & negative deflections sum to 0
- In the EKG above the sum of + & - deflections in lead aVF is 0, therefore the mean cardiac vector line is drawn perpendicular to aVF
- this line runs along Lead I
- to determine whether the vector is in the positive or negative direction along Lead I, you can look at other leads
- in both Leads I & II the deflections sum to a net positive value so we know that the mean vector is in the positive direction on Lead I
What is the normal range of the mean electrical axis?
- from -30 → +90 degrees
- less than -30 (more negative) is considered a left axis deviation
- more than +90 (more positive) is considered a right axis deviation