Cardiac Electrophysiology Lecture Powerpoint Flashcards
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How does the wave of electrical current generated in the heart spread to adjoining cells?
gap junctions allow ions to pass freely from cell to cell
During depolarziation of the cardiac cells ___ occurs in the cardiac myocytes, during repolarization ___ occurs
Contraction, relaxation
In cell, for depolarization of resting membrane potential must become less ____
negative
At resting state, what ion is found in higher conc inside the cardiac muscle cell?
K+
Where are the 3 normal areas of the heart to have automaticity?
- SA node
- AV nde
- Bundle of His/purkinje fibers
The pacemaker cell with the ___ rate will over ride the others
highest
At rest, Na+ conc. is higher ___ the cell. K+ conc. is higher ___ cell, Ca2+ is at higher conc. ___ cell
outside, inside, outside
Threshold value to initiate an AP in a pacemaker cell
-40 mV
Cardiac muscle AP is much ____ than skeletal muscle because of a longer ____
Slower, refractory period
Skeletal vs cardiac muscle differences (4)
- intrinsic impulse generation in cardiac
- plateau phase in cardiac
- longer refractory period in cardiac
- summation not possible in cardiac
There are NO _____ channels operating in the SA node, but they are present in the cardiac muscle
fast Na+
Action potential generation in autorhythmic cell mech of action
- autorhythmic cells begin depolarizing (becomes less negative) due to slow continuous inward movement of Na+ and reduced outward movement of K+ from -60mV approx resting potential
- upon reaching threshold -40mV, Ca2+ channels open and Ca2+ rushes into cell making cell much less negative, depolarization occurs
- K+ channels are triggered at -10mV and opened and Ca2+ channels close resulting in K+ flow out of the cell (repolarization)
- Ion pumps use ATP to move Ca2+ back to extracellular space and Na/K ATPase pumps Na+ out of cell and K+ back into cell
Action potential generation in cardiac myocyte mech of action
- -90mv is resting potential for the cardiac myocyte
- Positive ions moving thru gap junctions create small voltage change initiating depolarization
- this stimulates opening of fast Na+ cells at -70mV, begins depolarization
- myocyte contraction begins here
- Depolarization to +20mV triggers opening of slow Ca2+ channels, allowing Ca2+ entry from extracellular space
- At same time, depolarization to +20mV triggers K+ channels to allow K+ to begin leaving the cell
- This generates the plateau phase
- Ca2+ channels close and more K+ channels open causing cell to become less positive (repolarization)
- myocyte relaxation begins here
- simultaneously, ions pump Ca2+ out to extracellular space and Na+/K+ATPase pumps Na+ out and K+ back in
Effective/Absolute refractory period
Protective mech by limiting frequency of APs preventing tetany, period where 2nd AP cannot be initiated occurring during the majority of the AP cycle
Relative refractory period
Period following the effective/absolute refractory period where a 2nd AP is inhibited but not impossible, requiring supra threshold stimulation to elicit AP, they tend to be slower and wider since not all Na+ channels have had time to recover
Primary pacemaker of heart normally and where is it located anatomically?
SA node, posterior wall of right atrium
Intrinsic rate of the heart of the SA node
100-110 BPM
Vagal tone
Sympathetic nervous influence that slows the heart rate from its intrinsic beat at rest (100-110 bpm) to 60-80bpm in healthy patient
Internodal tracks
Speed up conduction thru gap junctions to spread an AP thru the atrium quickly, alongside nonconductive tissue that insulates the atrium from the ventricles
AV node function and intrinsic rate
Slows signal from SA node down by 120 msec allowing ventricles to fill allowing for complete atrial depolarization, contraction, and emptying of blood into ventricle prior to ventricular contraction, intrinsic rate is 40-60bpm
Bundle of His
High speed conduction network that forms the narrow QRS complex allowing for ventricular contraction, receives signal (delayed by) the AV node and transmits signal to rest of heart
Premature ventricular contraction/extra systole
Extra abnormal heartbeats that begin in the ventricle and can give the sensation of a skipped beat in chest, normal in moderation but if continuous could indicate a problem
How does a PVC/extra systole appear on the EKG?
As an extra, often widened and inverted QRS complex with an absence of a P wave preceding the contraction
4 big classes of drugs that we can use to alter AP in the heart
- Na+ channel blockers
- B blockers
- K+ channel blockers
- Ca2+ channel blockers
How does a drug that partially inactivates fast Na+channels impact AP in ventricular myocyte and thus conduction veolcity in the ventricle?
It decreases conduction velocity
Example of when there is increased vagal tone and decreased vagal tone
- sleeping causes increased vagal tone
- being startled can decrease vagal tone
When heart cells lack O2 they become ___. This makes the resting membrane potential ___, therefore many….
depolarized, less neg (-75mV vs -90mV)
…many Na+ channels are inactivated leading to altered impulse formation and conduction decreasing contractility and increasing arrhythmia
AV block
Occurs when an impulse starting in SA node cannot enter the ventricle because of block at AV node causing increased PR interval (ventricular bradycardia)
1st degree vs 2nd and 3rd degree AV block
Depends on the ratio of how many p waves occur without ventricular contraction on the EKG
Bundle branch block
Occurs when either right or left bundle branch is blocked, impulses are still fired from atria to ventricles and SA node is still origination, it will take longer to depolarize the ventricles tho manifesting as an extended QRS complex that is misshapen
Hemiblock
Occurs when the left anterior or posterior fascicle of the left bundle branch becomes blocked (more often anterior than posterior) resulting in left axis deviation on EKG
Voltage gated channel definition
Ion specific channels that open in response to a particular potential gradient across the cell membrane (in mV) being achieved, with them closing at a particular voltage as well
K+ leakage current and Na+ leakage current
Refers to tendency for K+ ions at resting potential in a pacemaker cell to be driven outside the cell by the slight permeability of the cell membrane to K+ slowly changing the voltage until reaching threshold, and Na+ ions in resting potential in pacemaker cell to be driven inside the cell by slight permeability of the cell membrane to Na+ slowly changing the vooltage until reaching threshold
Resting membrane potential is negative because…
…there are more positive ions outside the cell than inside, making the cell relatively more negative inside
Ectopic foci
Sites that spontaneously depolarize and produce AP independent of SA node (normally overridden by SA node), occurs anytime the pacemaker of the heart is not the SA node, acts as a protective mechanism to ensure the heart still beats even in the absence of the SA node
Purkinje fibers
Network of conducting cells that receive a signal from the bundle of His and spread the AP fastest to the rest of the heart activating the ventricles from the apex upwards
A lack of a p wave on an EKG would indiacte…
…no SA node activity
Intrinsic ventricular rhythm range
20-40 bpm (too slow to sustain life?)
Sometimes nonpacemaker cells after becoming hypoxic will…
…change into pacemaker cells that then depolarize spontanously and demonstrate automaticity resulting in irregular beats and arrhythmia
Reentry mechanisms
Refers to how ischemia can cause a block in conduction but partial retrograde conduction occurs setting up a circus rhythm allowing for reentry of the signal
Global reentry
Occurs between the atria and ventricles and often involves abnormal accessory pathways such as the bundle of kent
Wolff-parkinson-white syndrome mech of action
-Due to presence of bundle of kent episodes of tachycardia occur via AP traveling via bundle of kent to the ventricle then retrograde to the AV node
Local reentry
Sites within the atria or ventricles that often involve abnormal accessory pathways resulting in tachyarrhythmias
