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Systems Physiology > Cardiology Electrophysiology > Flashcards

Cardiology Electrophysiology Flashcards

1
Q

Describe the pressure differences in the major components of CV system.

A

pressures
Right atrial- 3 mmHg (one of lowest pressure in CV)
Right ventricle peak systolic- 25mm Hg
Left atrial- 8mm Hg
Left ventricle- 120-130-mmHg
Left ventricle generates higher pressure than any of chambers of heart

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2
Q

What is Pulmonary capillary wedge pressure? What is is used for? What is the actual pressure value?

A

Pulmonary capillary wedge pressure- 9mm Hg; pressure in left atrial measured in venous, put catheter in right side of heart, venous through RA, RV, out to pulmonary artery, inflate balloon, measure back pressure from pulmonary capillaries (clinical measure of left atrial pressure)
-used for patients with heart failure (volume of blood in left atrium)
when heart not functioning normally, volume of blood backs up in LA, pressure rises, pulmonary wedge pressure increases, indicates failure of left ventricle to pump blood.

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3
Q

What has to happen in the heart in order for contraction too occur?

A

Electrical depolarization of cardiomyocytes, cause calcium to release and allow heart muscle to contract.
-electrical activity precedes mechanical activity in CV system.

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4
Q

What is the resting membrane potential?

A

Resting Membrane potential (RMP)- electrical potential difference between inside and outside of cell (-10 mV to 100 mV)

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5
Q

What are the unique properties if electrical activity in the heart? What accounts for unequal distribution of ions across membrane? How does this affect Resting membrane potential? What is RMP in cardiac cell?

A

2 main ions:
Na and K (unequal distribution)
-Na [ ] more OUTSIDE of cell
-K+ [ ] more INSIDE cell
Na K+ pump- pumps sodium out of cell, and K+ in cell, uses ATP.
at rest- cardiac cells are 100x more permeable to K than Na+
Highest mem permeability to K+; at rest, K+ primarily determines RMP
equllibrium potential for K+ = -94 mV.
RMP for Cardiac cell is -90 (close to equilibrium potential for);
equillib potential +70 Na; Ca: +132

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6
Q

what would happen to resting membrane potential if you inhibit 50% of Na+ K+ pump

A

Inhibit 50% of Sodium-Potassium pump (Na+/K+ pump)
not as much sodium pumped out, not much K+ pumped in
ex: drugs like digitalis (block Na+K+ pump)
K+ [ ] decrease inside cell
RMP would be less negative
cell would hyperpolarize (become less excitable)

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7
Q

What three things is the magnitude of electrical potential of cardiac cell membrane based on?

A

Magnitude of electrical potential based on:

  1. pump mechanism which are operating (Na+K+ pump)
  2. relative permeability of membrane to various ions.
  3. The electrochemical gradient
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8
Q

What are the two opposing forces involved in the movement of K+ across the resting cell membrane

A

two opposing forces:

  1. chemical force (outward) based on concentration gradient
  2. electrostatic force (inward) based on positively charged K+ ions attracted by negative potential at interior of cell.
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9
Q

Describe the events during a cardiac action potential. What are the different phases that occur? What signifiant difference between nerve cell and cardiac cell.

A

phase 4- resting membrane potential (-90 mV)
when cardiac muscle cell depolarizes; have additoinal 4 phases: 0, 1, 2, 3, then goes back to phase 4.
normal cardiac action potential- long ap duration (200 ms) Membrane stays depolarized longer in cardiac muscle cell than nerve cell

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10
Q

What is gK? How do ions move across the membrane (from inside to outside) if they are not pumped?

A

gK- permeability (or conductance) of membrane to K+
ions pass through channels made of protein that spans lipid bilayer. Channels are in open (allow ions to pass) or closed confirmation (ions cannot pass through)

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11
Q

Describe the permeability of Na, K+, and Ca+ during phase 4 of action potential process.

A

phase 4 (during RMP):very high K+ permeability, low Na+ permeability, Low Calcium permeability

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12
Q

Describe the electrical activity that occurs in each of the phases

A

Cardiac muscle cell- starts at stable RMP of -90mV.
When propagated action potential comes, cause voltage to change and reach threshold (-60 mV) and conformation of proteins change to open.

Phase 0: conformation change in Na+ channel. membrane becomes very permeable to Na+ through fast-Sodium channels that open; mem voltage moves from -90 mV to +70 mV since membrane highly permeable to Na (seek equilibrium for Na+ ); but it stops at +20 mV (instead of +70 b/c fast Na+ channels closes/inactivates) (RAPID UPSTROKE, DEPOLARIZATION) H gate closes to end phase 0.
Phase 1: beginning of phase 1 fast sodium channels inactivated; and partial REPOLARIZATION (initial and rapid) due to K+ channels that are activated (bring mem voltage back to RMP).
Phase 2: PLATEAU phase- When membrane voltage reached between -10 and +10 voltage gated calcium channels open up, Ca+ permeability increases, Calcium move inside cell, K+ move outside of cell (voltage stays fairly constant).
As we move through Plateau phase, more K+ subtypes created, membrane voltage becomes more negative, K+ current becomes greater than calcium current
Phase 3: REPOLARIZATION phase; restored higher potassium permeability bringing voltage back to RMP in phase 4 (high K+ and low Na+)
Phase 4: Resting membrane potential,

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13
Q

Which voltage does fast-sodium channels open and close? What happens if there is a point mutation in H gate?

A

at -60mV M gate channels open, allowing sodium to move to the cell, voltage gets to 0 mV.
at 20 mV, H gate inactivates sodium channel, fast -sodium channels close. =(mark beginning of absolute refractory period)
if there is point mutation in H gate (inactivate) , the fast sodium channels may not inactivate normally, leading to arrhythmias being present.

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14
Q

What is the absolute refractory period?

A

absolute refractory period (ARP)- the whole time that fast sodium channel is inactivated
cardiac muscle has long ARP

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15
Q

Distinguish between the different calcium channels for AP activity.

A

calcium channels that open during phase 2
T-type Calcium channels- transient increase in calcium permeability; primarily present on SA nodal and AV nodal cells (not cardiac muscle)
L-type- longer duration/long lasting calcium current These L-type Ca+ channels open up during phase 2.

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16
Q

What would happen if drug Dialtiazen was given to cardiac muscle?

A

Drug Dialtizem- block L-type calcium channel (calcium channel blocking drug)
if block calcium channels: phase 2 of action potential will be SHORTER (K+ have effect earlier than normal)
normally, in plateau phase- -calcium channels were balancing out K channels.
With increasing [ ] of drug dialtizem, shorten plateau.
Phase 2 important in electrical properties of action potential and in translating the activity into contractile force.
. Calcium that enters in phase 2 of AP, is important during contraction of cardiac muscle (excitation-contraction coupling).

twitch force generated by muscle, inhibited by drug;

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17
Q

Elaborate on what happens in phase 4 of AP

A

Phase 4- RMP; membrane is most permeable to K+, low permeability to Na+ and Ca+. voltage- -90mV.

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18
Q

What happens during phase 0 of AP?

A

Phase 0: rapid upstroke, rapid depolarization due to increased membrane permeability to Na+. once voltage reaches -70 mv (threshold), Na+ conductance rises sharply due to activation of fast Na+ channels (m gate opens). This fast Na+ influx causes membrane potential to be positive by +20 or +30 mv (during phase 0, K conductance starts declining)
H gates close to end phase 0.

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19
Q

What happens during phase 1 of AP? what other structure has fast Na+ channels?

A

Phase 1: Early rapid repolarization due to H gates closing the fast Na+ channels
(purkinje fibers also have fast Na+ channels)
greater the amplitude of AP, the greater rate of change during phase 0, more rapid the conduction through the fiber.

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20
Q

What occurs in the phase 2 of Action potential? How does this phase differ in skeletal muscle vs Ventricular (cardiac) muscle?

A

Phase 2: Plateau phase
plateau of ventricular AP caused by slow Na+ Ca+ influx channel
Skeletal muscle- Na+ channel closes down after depolarization, so repolarization can begin immediately
ventricular muscle AP- Na+ continues to move in slowly with Calcium (K+ conduction also decreases).
calcium is important in maintaining plateau phase and increasing intracellular calcium, which is important for contraction.

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21
Q

Explain what happens in phase 3 of action potential?

A

Phase 3: rapid repolarization
for repolarization to occur there must be a decline in Na+ and Ca+ slow channel and restoration of normal K_ efflux. This brings us back to RMP, where K+ has primary influence.

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22
Q

What is the major affect of Calcium channel blockers?

A

Calcium Channel blockers (verampil, diltiazem, nifedipine) : affects plateau phase
diltiazem shortens plateau phase, but not completely wipe it out (due to slow Na+ component)
Contractile force reduced due to reduction of inward Ca+ current by verampil

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23
Q

What is duration of action potential in ventricular muscle? What does duration of AP depend on?

A

Ventricular muscle AP: 5 phases; duration: 200-300 msec.
duration of AP depends on interbeat interval:
40 beats per min: AP duration of 500 msec
150 beats per min: AP duration of <200 msec

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24
Q

what are the drugs procaine and quinidine used for?What drug blocks fast Na+ channels?

A

Procaine (treats arrhythmias, reduces irritability of cardiac muscle) and quinidine (treat atrial fibrillation, flutter) are used to slow the opening of Na+ channels, reduce depolarization current and slowing conduction from cell to cell.
Tetrodotoxin blocks Fast Na+ channels.

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25
Q

Describe the excitability of cardiac muscle cells, including the absolute refractory period.

A

Absolute refractory period (ARP) aka Effective refractory period- no matter how strong the stimulus, cell is incapable of generating an action potential (NO AP)
heart- ARP extends from phase 0 to midpoint of phase 3 (voltage -50mV). Electrical activity is inactive during ARP. For heart to be effective pump it must contract on demand and relax on demand (pump blood).

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26
Q

What happens if tetanus is produced during AP of cardiac muscle? compare the use of tetanus in skeletal vs cardiac muscle.

A

tetanus-sustained contraction of the heart.
tetanus bad for heart (not effective pump for contracting)
Tetanus for skeletal- GOOD useful to have sustained contractions while exercising.
when you repetitively stimulate skeletal muscle cell, the action potential and refractory period are SHORT. applying another stimulus before contraction has ended will lead to increase in Calcium and force development (get sustained tetanus contraction).

27
Q

How does the Absolute refractory period in Cardiac cells differ?

A

Cardiac muscle - long ARP (absolute refractory period) ARP extends beyond max peak; so you cannot stimulate heart to contract again while still contracting
serves as electrical detector- allows heart to relax, refill with blood to be able to pump out for next heart beat.
Long ARP- important in basic function in
extends from phase 0 to phase 3.

28
Q

Differentiate between relative refractory period and supernormal period

A

Relative Refractory Period (RRP)- when an action potential can be elicited, but it requires a GREATER than normal Stimulus.
-The AP would have a lower than normal amplitude and reduced rate of rise due to not all Na+ fast channels being reset and gradients not fully established
Supernormal Period (SRP)- a stimulus of less than normal magnitude can bring the membrane to threshold and initiate an action potential
-these action potentials propagate SLOWLY (potential reached at -80-90 mV.

29
Q

What is full recovery time(FRT)? How long does FRT take in skeletal vs cardiac cells? What occurs at the end of FRT?

A

Full recovery time (FRT)- the interval between depolarization and recovery of normal resting excitability.
300-350 msec for myocardial cells
2-4 msec for mammalian skeletal muscle cells
At the end of FRT, a threshold stimulus will result in a normal action potential with normal speed of propogation.

30
Q

Describe the location and unique characteristics of SA node. What are other names used to describe RMP of SA node?

A

Sinoatrial (SA) Node- displays highest order of rhythmicity
location- SA node consists of a bundle of neuromuscular tissue. SA node located on endocardial surface of RIGHT ATRIUM and junction of Superior Vena Cava and right atrial appendage
cells in SA node have UNSTABLE RESTING MEMBRANE POTENTIAL- responsible for PACEMAKER activity.
unstable RMP aka prepotential, pacemaker potential, diastolic depolarization.

31
Q

Compare and contrast the characteristics of Ventricular muscle and SA node

A 
Ventricular Muscle: 
-stable RMP (phase 4)
RMP voltage:-90 mV
very rapid Phase 0
max membrane potential during AP: +20 mV
Sharp peak in phase 1
plateau- phase 2
rapid decline to RMP in phase 3
SA Node:
UNSTABLE RMP (phase 4)
RMP voltage: -70 mV
gradual upstroke for phase 0
Max membrane potential during AP: 0 mV
No Phase 1
NO phase 2
Gradual decline to RMP in phase 3.
32
Q

What is the basis for pacemaker potential? how does this relate to firing rate?

A

The pacemaker potential is due to fact that cells are more permeable to Na+ at rest (RMP) and have gradual decline in K+ conductance through their cell membranes
K+ efflux keeps RMP negative
The gradual closing of K+ conduction channel has a variable slope from tissue to tissue.
The tissue with steepest slope (greatest rate of decay K+ conductance has the most RAPID firing rate.
in mammalian hearts, the region with the most rapid rate of decay K+ conductance is the SA node.

33
Q

What three factors all contribute to produce SA nodal prepotential? Why is Slow Calcium influx important?

A

Three factors that contribute to SA nodal prepotential:
1. Increased Na+ conductance at rest
2. gradually decreasing K+ conductance
3. Slow calcium influx (Verapamil inhibits prepotential)
Slow Ca+ influx is very important for pacemaker potential in nodal cells
verapamil or decreased Calcium can inhibit spontaneous pacemaker activity

34
Q

Describe the phase 0 of SA node action potential? What do SA node and AV nodes have in common?

A

Phase 0 of SA node Action potential;
-upstroke of AP in SA nodal tissue is due to slow influx of Na Calcium. Fast Na+ channels NOT activated.
SA and AV nodes are both SLOW response tissues with NO Fast Na+ channels.

35
Q

What are the three natural pacemakers in the heart?

A

3 natural pacemakers in the heart with each having its own intrinsic rate of firing:
1. SA node- 60-100 times /minute
2. atrioventricular (AV) node - 40-55 times/min
3. idioventricular pacemaker (purkinje fiber)- 25-40 times/min
the difference in these cells is the difference in rate of decay of K+ conductance during phase 4.

36
Q

What happens to firing activity if SA node is destroyed?

A

If the SA nodal tissue is destroyed, the pacemaker of the cell with the next highest rate of firing will take over (AV node).
With AV node as pacemaker, the heart rate would drop to 40-55 beats/min
if AV node junctional area does not initiate impulse, then the idioventricular pacemaker will take over at a rate of 20-40 beats/min.
i

37
Q

How does the frequency of discharge of the pacemaker cells vary?

A

Frequency of discharge of pacemaker cells vary:

  1. changing the rate of diastolic depolarization (slope of prepotential -phase 4)
  2. changing resting membrane potential
  3. changing threshold potential.
38
Q

How can you slow down the pacemaker discharge?

A

Slow down pacemaker discharge:

  1. decrease rate of depolarization
  2. hyperpolarize the cell
  3. change threshold potential
39
Q

What factors alter pacemaker activity?

A

Sympathetic and parasympathetic stimulation alter pacemaker activity.
Sympathetic stimulation (Norepinephrine) or increased circulating catecholamines (epinephrine) INCREASES the slope of prepotential
Parasympathetic stimulation (acetylcholine)- HYPERPOLARIZATION DECREASES the slope of prepotential- decreased heart rate
when all innervation is removed, SA nodal discharge is approx 100 beats/min
-SA node is under tonic parasympathetic inhibitory influence
TEMPERATURE also affects prepotential
-FEVER increases slope of prepotential- INCREASES HR.

40
Q

Describe the components of the conduction system.

What determines the conduction velocities?

A

Conduction system:
1.Begins at SA node
2. Atrial internodal pathways (3 fiber groups)
3. Atrioventricular node (AV node)- 3 zones; AN, N and NH
4. Bundle of His or AV Bundle
5. Bundle Branches (right and left)
6. Purkinje system
7. Ventricular Muscle
Fast Na+ channels important in determining conduction velocities, since greater the amplitude of AP, and greater the rate of change during phase 0, the more rapid the conduction velocity.

41
Q

Describe the Refractory period and Supernormal potential. May be deleted

A

Relative refractory period- stimulus of greater than normal magnitude can generate action potential.
b/c when you get past ARP, Fast Sodium channels reset to normal confirmation, allows m gate to open. Stimulate muscle to depolarize. At end or RRP, normal AP, because high percentage of Na+ channels are reset
-80-90mV- supernormal potential: where all fast Na+ channels reset to normal active confirmation, membrane potential is closer to threshold (AP will be normal, stimulus of less than normal magnitude for AP,).more excitable.

42
Q

What defines the excitability of cardiac muscle?

A

Absolute refractory period, relative refractory period and supernormal potential define excitability of cardiac muscle.

43
Q

What are the two major types of channels in the heart? What do nodal cells have that allow for unstable RMP?

A

Fast response fiber- atrioventricular muscle and purkinje, fast Na+ channels that rapidly permit the polarization of membrane from mem potential to rapid phase 0. STABLE RMP (constant value)

slow response fiber- nodal tissue (SA node and AV node); No Fast Na+ channel protein, no typical rapid upstroke. RMP is unstable due to K+ permeability decreasing over time and because SA nodal channel has funny channel IFc that allows Na+ to come into channel during phase 4 (RMP less negative).
Also have Ca+ leak channel that allows Calcium to come in
Funny Na+ leak channel (IFc), Ca+ leak channel, and decrease in K+ permeability all contribute to unstable RMP for slow-response fibers.
phase 0 for slow fibers- caused by voltage gated Calcium

44
Q

How do impulses move from the SA node to the AV node? What must the impulse go through and why?
What zone causes the main delay in conduction?

A

Impulses move out of SA node via internodal pathways to AV nodal area, where there is a DELAY in conduction due to slow conduction velocity (0.02 msec)
-the depolarization wave cannot just jump from atria to ventricles due to fibrous Atrioventricular ring which serves as an insulator.
The impulses can only go through at AV nodal area (3 zones):
-AN zone- transitional zone: cell types in this region are Mixture of atrial and nodal fibers interspersed with connective tissue.
N zone- middle portion of AV node
NH zone- transitional zone; nodal fibers gradually merge with fibers from bundle of His
The N zone is actually the slowest conduction velocity, but it has less tissue in its region, than AN zone, so main delay occurs in AN zone of AV node.

45
Q

Describe the conduction velocity of AV node? Why is AV node so important for cardiac cells?

A

The average conduction velocity through AV node is 0.02 msec, which is SLOWER than the rest of conduction pathway.
This produces a delay in ventricular excitation and makes it possible for atria to contract and contribute 10-20% of their ventricular volume prior to ventricular depolarization and contraction
AV node is important region for development of HEART BLOCKS; because AV node is the only region (under normal conditions) where impulses from atria can get to the ventricles.

46
Q

Explain how the autonomic nervous system plays an important role in regulating AV node conduction.

A

AV nodes receives fibers from sympathetic and parasympathetic nerves.
Sympathetic- INCREASES AV node conduction velocity
Parasympathetic- DECREASES AV node conduction velocity

47
Q

Describe the conduction pathway after stimulus reaches AV node

A

once impulse passes through AV node, it is conducted along common Bundle of His (AV bundle). The conduction velocity along AV node is 1-2msec. From the AV bundle, conduction occurs along through bundle branches and Purkinje fibers (2-4 msec). Cells in Purkinje fibers conduct impulses more rapidly than myocardial cells (0.3 msec)
once, impulses leave the Purkinje system, its transmission through muscle fiber of ventricular wall greatly aided by system of T-tubules (transverse) and intercalated disks

48
Q

What is the role of intercalated disks? What are gap junctions? How are they formed?

A

Intercalated disks- located between where two myocardial cells join end to end and consist of an extensive series of folds in cell membrane of both cells
these folds create more contact area and stronger cell to cell adhesion
Within intercalated disks- are GAP JUNCTIONS- low resistance channels that aid the spread of excitation from cell to cell.
Gap junctions formed from alignment of two transmembrane CONNEXON units from adjacent myocytes that form intracellular channel.
connexon- have 6 membrane spanning connexon protein subunits that open and close based on pH and calcium concentration (high Ca+, low pH, pores open; low Ca+, normal pH: pores close)

49
Q

What is the main role of intercalated disks in cardiac muscle cells?

A

Intercalated disks- to serve as low resistance bridges, allows for more rapid spread of electrical activity between cells and facilitates transmural propagation of excitatory impulse from endocardium to epicardium.

50
Q

Describe what happens during Reentry. What must happen for reentry to occur?

A

Reentry occurs when an excitation wave reexcites some region through which it has recently passed.
These reentry circuits can either be random or ordered.
UNIDIRECTIONAL BLOCK must happen for reentry to occur. Also, for reentry to occur, the effective refractory period (ARP) of the reentered region must be shorter than propagation time around the loop.
unidirectional block- basis for other arrhythmias.

51
Q

What are the three things the ECG is based on?

A

The principle of ECG is based on 3 suppositions:

  1. body is a conduction medium with heart in the center
  2. myocardial depolarization generates a flow of ions throughout the extracellular space of body.
  3. electrodes placed on the body surface can detect this ionic flow.
52
Q

What are the main differences between ventricular muscle AP and SA nodal AP?

A

SA nodal -
As time passes, the Na+ and Ca+ leak in, and K+ permeability decreases, cells spontaneously reach threshold and fire AP on their own
cells located on two places (slow-resposne fibers)
SA nodal cells-are between node and superior vena cava joins right atrium
AV node (atrioventricular) - between atria and ventricles
SA nodal and AV node- pacemaker cell (can spontanenously depolarize and determine rate of contraction of heart).

53
Q

What are two pacemaker cells and their roles in the heart? Which is the dominant pacemaker cell?

A

Two pacemaker cells:
-SA nodal and AV node: which both can spontaneously depolarize and determine the rate of contraction of the heart.
SA node- DOMINANT pacemaker b/c of its intrinsic rate of depolarization is faster than AV node (60-100 x for depolarizing)

54
Q

What is overdrive suppression? which pacemaker undergoes this process? What happens if SA node is damaged?

A

SA nodal- dominant pacemaker because of overdrive suppression
Overdrive suppression: 2 pacemaker tissues, one is driven to depolarize at rate faster than its intrinsic rate, it becomes hyperpolarized and suppresses that pacemaker (good thing)
if SA node damaged, have another pacemaker ; AV node, that depolarize at slower rate (40-50 times)

55
Q

What is the role of calcium in the depolarization of SA nodal cells?

A

if you reduce calcium level, AV nodal AP suppressed, prepotential flattened,
AP in SA nodal is due to Calcium-voltage gated channel.
use a drug like Nifedipine (ca+ channel blocker)
Ca+ lowers depolarization, because if Ca+ channel blocked, less AP result.

56
Q

How to alter slope of prepotential

A

alter slope of prepotential - autonomic nervous system
slope- how quickly membrane depolarizes and reaches threshold.
HR can be increased or decreased
Sympathetic
Norepinephrine binds to Beta 1 receptor in SA nodal cells, slope of prepotential steeper, reaches threshold more quickly; decreases potassium permeability, enhance sodium and calcium permeability.
stimulate sympathetic nerves, SA nodal cells reach threshold more quickly, fire AP more sooner, to increase HR.
parasympathetic stimulation: postganglionic neurotransmitter: Ach binds to muscarinic receptor. When AcH binds to receptor, slope of prepotential moves from A to C
-takes longer to reach threhshold
increases K+, decrese Na+ and Calcium permeability (opposite of sympathetic). both sympathetic and parasympathetic can alter heart rate
if cut parasymp and sympathetic innervation to the heart;
The heart would not stop beating (intrinsic stabilization of HR
intrinsinc depolarization of SA node- causes the heart beat

57
Q

What happens to HR during parasympathetic and sympathetic stimulation?

A

stimulate parasympathetic nerves- reduce HR to 30 (ACh bind to muscarinic receptors)
stimulate sympathetic raise HR to 75-125 or higher due to norepinephrine increasing Na+/Ca+ permeability (beta-1 receptors)
release of norepinephrine bind to Beta 1 receptors.
both sympathetic and parasympathetic can stimulate HR. cut all
cut sympathetic nerve, HR drives
parasympathtic has greater effect on baseline HR than sympathetic.
either affect HR by affecting membrane permeablity.

58
Q

What causes the cardiac ventricular muscles to be depolarized

A

AP propogated across atria through atrial nodal phases,
atria-1st part to contract
AP can only pass Atria to ventricles through AV node
conduction velocity through AV node is slow.
rapid conduction velocity, distributed change in electron potential.
conduction system- rapidly distribute AP that starts in SA node to all of myocytes in heart for organized contraction

59
Q

What causes arhytmias?

A

Reentry causes rapid arrhythmias
requirements for reentry:
unidirectional block in conduction pathway
-ARP of reentered must be shorten than propagation time around reentry lop

60
Q

Why should AV node have a slow conduction velocity?

A

AV node-
when atria contract, they force blood into ventricle (last part of volume added in ventricle ,before blood pumped out). electrical AV nodal delay ensures that you have maximum filling of ventricle prior to each heart beat.
(ensure maximum volume in ventricle prior to contraction)

61
Q

What leads to Arrhythmias? Why do they occur? What are the requirements for reentry?

A

disruption of normal activation/conduction sequences cause arrhythmias
reentry cause rapid arrhythmias
requirements for reentry:
-unidirectional block in conduction pathway
-ARP of reentered tissue must be SHORTER than propagation loop
any branchpoint for conduction and communicating branch in purkinje fiber- has potential for reentry to occur.

62
Q

What happens when two action potentials meet in communicating branch? What happens with AP’s in reentry? What disease can cause reentry?

A

when 2 AP meet and move in opposite directions in communicating branch, the right conduction and left conduction fibers are in ARP, the AP’s CANCEL OUT and APs stop.
Reentry- injury called unidirectional block- conduction tissue is damaged so AP is damaged when it moves in anterograde or retrograde path. When AP comes through communicating branch,
AP in unidirectional block {blocked in one direction) but can be conducted in retrograde direction.
if reentered tissue passes ARP, it will be in retrograde direction (it will initiate rapid rhythm like atrial flutter, fibrillation) leading to arrhythmias.
Ischemia (lack of blood flow) can cause reentry
reduction of blood flow, conduction pathway injured, conducting AP in one direction.

63
Q

What are the major electrical waves in EKG? What parts of AP correlate to the waves? What does P wave represent?

A

AP has relationship to normal EKG
P, QRS complex, T waves are in EKG.
QRS complex correlates to phase 0 of cardiac AP (what causes QRS complex is depolarization of all cardiac myocytes spontaneously)
T wave corresponds with phase 3- repolarization phase of cardiac myocytes.
P wave- does NOT correspond with any ventricular electrical activity.
P wave represents Atrial depolarization (occurs before ventricle contraction)

Systems Physiology (19 decks)

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