Six Flashcards

1
Q

What are the two primary types of cells (types of conduction) in the heart? Where does each occur?

A

} Two primary types of cells in the heart } Calcium based conduction (Sinoatrial node, AV node) } Sodium based conduction (His-Purkinje network, myocardial tissue)

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2
Q

What are the 5 phases of cardiac conduction (sodium based)? Describe what occurs in each and how it occurs in detail.

A

Phase 0: Depolarization } Rapid upswing of action potential } Voltage activated sodium channels allow influx (positive ions) causing potential to rapidly change from negative to positive (-92 mV to +20 mV). Phase 1: Initial repolarization } Rapid inactivation of sodium channels } Voltage dependent potassium channels (ITO) open allowing potassium (positive charge) to leave cell, making it more negative Phase 2: Plateau } Complex phase with multiple channels involved } L-type calcium channel (voltage activated) allows calcium (positive ion) to influx making cell more positive }Calcium also needed for muscle contraction electromechanical coupling) } Sodium-Calcium pump increases positive charge in cell (three sodium ions in for every calcium ion out) } This is somewhat balanced by potassium efflux from cell Phase 3: Final repolarization } Potassium efflux from cell making cell more negative } Leads to a return to the resting potential Phase 4: Resting potential } High component of leak type potassium channels } Membrane resting potential very close to potassium Nernst potential (-92 mV)

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3
Q

Where does the calcium based AP occur? What are 3 major differences compared to sodium based AP?

A

} Sinoatrial node and AV node } Major differences compared to sodium based AP } Slower conduction properties } Resting potential gradient leads to Auto-activation } High input from Autonomic nervous system

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4
Q

What are the phases of calcium based AP? Describe what occurs in each and how it occurs in detail.

A

Phase 0 } Depolarization } Voltage activated calcium channels allow calcium influx into cell leading to a positive membrane potential Phase 3 } There is no phase 1 or 2 in calcium based cardiac cells } Repolarization } Potassium efflux from cell, similar to myocardial cells Phase 4 } Resting potential } “Funny current” (If) is a mixed sodium and potassium inward current and causes a slow rise (depolarization) in the resting potential

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5
Q

Explain why there has to be two different cardiac cells with different conduction mechanisms.

A

} Pacemaker cells need to auto-activate or else there would be no way for the heart to continue to contract } AV nodal cells are important to slow conduction to allow for atrial contraction prior to ventricular activation to allow A-V synchrony in contraction } “Hierarchy of Cardiac Conduction” } Myocardial cells and the His-Purkinje system need to have rapid conduction properties to allow muscle contraction to rapidly flow through the heart chambers to create a strong, efficient contraction to pump blood to the body

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6
Q

What are refractory periods? How are they caused on a cellular level? On a cellular level, describe the two parts of a refractory period. Describe the differences in refractory period between the two types of cardiac cells.

A

} Defined as the time that a cell or tissue can not be re-excited } On a cellular level, related to channel properties (open/closed) that block ion transport into the cell as the cell reestablishes its resting potential (repolarization) } Cardiac tissue has a long refractory period due to plateau phase (phase 2) that prolongs depolarization period } In fast response (sodium based) cells, refractory period is from phase 0 to late phase 3 } Based on recovery of fast sodium channels (occurs at about -50 mV) } In slow response (calcium based) cells, refractory period extends beyond period that full repolarization has been restored (post repolarization refractoriness) } On a cellular level, broken into two parts: } Absolute refractory period } No stimulus is capable of evoking a depolarization } Relative refractory period } Only stimuli that exceed the normal threshold can initiate a depolarization } Depolarization generally slower and of lower amplitude compared to normal cellular depolarization

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7
Q

What kinds of things will alter the refractory period? In what ways? How are refractory period and HR related in sodium based cells, especially purkinje cells? In AV nodal cells?

A

} Changes in cycle length will alter action potential duration and change the refractory period } Autonomic inputs also alter action potential duration and refractory periods } Sodium based cells, especially Purkinje cells, have an inverse relationship between refractory period and heart rate } AV nodal cells have an increase in refractory period with increase in heart rate

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8
Q

What are two ways in which cell to cell conduction occurs? Which is faster?

A

} Longitudinal and Transverse } Longitudinal conduction much faster } Intercalated discs

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9
Q

What do intercalated discs? What allows them to contribute to cell to cell connectivity? What do they contain? What do they create?

A

} Intercalated discs } Separate cardiac myocytes } Contain the gap junction which is characterized by nonselective channels that have pores } Pores create low electrical resistance channels (V=IR) that allow rapid longitudinal conduction

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10
Q

What else do gap junctions accomplish?

A

} In addition to allowing for rapid conduction, gap junctions are protective for cardiac myocytes } Low pH, high calcium closes connexon channels } Protects against calcium influx from adjacent cell death } Work like the bulkhead doors in boats to prevent flow of water from one compartment to the next

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11
Q

How do intercalated discs differ from cell to cell both generally and specifically? What allows them to do so?

A

} Density and type of intercalated discs vary in cardiac tissue } Higher density, faster conduction in His-Purkinje system } Low density, slower conduction in AV node } Gap junctions contain connexon proteins (multiple isoforms). Isoforms determine conduction properties of connexons

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12
Q

What are the components of the cardiac conduction system?

A

} Sinoatrial node (SA node) } Atrial myocardium } Bachmann’s bundle } Atrioventricular node (AV node) } Bundle of His } Bundle branches/ Purkinje network } Ventricular myocardium

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13
Q

What is the SA node? Location? Function? Activation?

A

} Cardiac Pacemaker } Located on epicardial surface of right atrium near the SVC junction } Surrounds the sinoatrial artery } Sinus rhythm originates here } Calcium type activation } (If) (sodium based ‘funny’ current) also plays a role } High level of sympathetic and parasympathetic inputs

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14
Q

What is Bachmanns bundle?

A

} Main pathway of intra-atrial conduction } Parallel aligned myocardial strands that cross superiorly through the intra-atrial septum

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15
Q

What is the AV node? Location? Function? Activation?

A

} Specialized compact area of cells that transmit conduction from atrium to ventricle } In a normal heart, this is the only way electrical conduction can pass from atrium to ventricle } Calcium type activation properties } “Electrical speedbump” slows conduction to allow atrial contraction to complete prior to ventricular activation } Important protective properties for atrial tachyarrhythmias } Large input from sympatheticand parasympathetic nervous system allow for modification of conduction properties

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16
Q

Waht is the HIS bundle? How does it work? Where is it located? What does it do?

A

} Located in the central

fibrous body of the

ventricular septum

} Sodium type activation

} Rapidly transmits

conduction from the

AV node to the bundle

branches

17
Q

Waht are the bundle branches/purkinje network? How does it work? Where is it located? What does it do?

A

} Carries electrical

impulses rapidly from

the AV junction through

the septum and to the

ventricular myocardium

} Divided into left and right

bundles

} Left bundle further divided

into anterior and posterior

fascicles

} Sodium type activation

properties

} Purkinje fibers are large

and have the greatest conduction velocity

18
Q

In what direction does activation/contraction flow?

A

} Flow of electrical activity

from right to left and

superior to inferior

through the atrium

} Activation in ventricle

is endocardial to

epicardial, apex to base

} Repolarization tends to

follow depolarization

19
Q

What are the symp. effects on conductivity?

A

} Sympathetic Effects

} Release of

norepinephrine

} Acceleration of diastolic

depolarization

} Shortening of action

potential duration

} Increase inward current

(Phase 0 activation)

20
Q

What are the parasypm effects on conduction?

A

} Parasympathetic Effects

} Acetylcholine release

} Muscarinic receptors

activate potassium

channels and diminish

ionic currents of If

} Increases maximum

negativity of cells

} Reduces the slope of

diastolic depolarization

and ICa

21
Q

What is meant by automaticity? How does it work?

A

} All cardiac cells have a slight positive deflection to

the resting potential

} This leads to the property of automaticity

} Automatic activation of cardiac cells at the resting

potential becomes more positive over time

} Eventually this leads to phase 0 activation of the cells

with the activation of voltage gated sodium or calcium

channels

} Electrical activation in the heart is determined by the

quickest cells to fire; normally this is the sinoatrial

node

} So what happens if the sinoatrial node does not

22
Q

What is meant by the hierarchy of cardiac conduction? How does it work? What escape rhythms are there?

A

} If the dominant pacemaker is lost (sinoatrial node),

automaticity will occur in the next most dominant

cluster of cells (AV node)

} If the AV node is not capable of activating, then the

bundle branches/Purkinje network will become the

pacemaker for the cell

} Because each of these cell types have different

resting potential gradients, there is a slowing of the

heart rate with each subsequent cell type becoming

the pacemaker for the heart

} Junctional (from AV node): 40-60 bpm

} Ventricular (from His-Purkinje network): 20-40 bpm