Cardiac Action Potentials & Conduction (Lecture 10, Exam 2-Lecture 2)

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autorhythmic

SA node, AV node, AV bundle, & Bundle Branch cells of conducting system are ______

Autorhythmic cells (1% of cardiac muscle cells)

Type of cardiac muscle cell: -Organized into network called "conducting system of the heart" -Do NOT contract -Initiate & propagate action potentials that trigger contraction of contractile cells -pacemaker cells found in sinoatrial (SA) node of Right Atrium

Contractile Cells (99% of cardiac muscle cells)

Type of cardiac muscle cells: -respond to depolarization by contracting -do mechanical pumping activity of the heart

1. 99% are contractile muscle fibers: -respond to depolarization by contracting -do mechanical pumping activity of the heart 2. 1% are autorhythmic cells: -organized into networks called "conducting system of the heart" -Do NOT contract (no physical work) -Initiate & propagate action potentials that trigger contraction of contractile cells -pacemaker cells found in sinoatrial (SA) node or R atrium

What are the 2 major types of cardiac muscle cells?

-Conducting cells in interventricular septum are insulated from contractile cells -Purkinje fibers are electrically coupled to contractile cells

What assures that contraction of ventricle begins at apex of the heart?

1. SA node 2. AV node 3. AV bundle (Bundle of His) 4. Bundle Branch

What cells of the conducting system are autorhythmic? (4)

Action potentials generated by autorhythmic cells of the conducting system that spread through the ventricle via gap junctions

What directly initiates the action potentials in cardiac contractile cells?

1. Autonomic nervous system & hormones 2. Both sympathetic & parasympathetic fivers innervate SA node -homeostatic reflexes; constant dynamic regulation 3. Parasympathetic Fibers from Vagus Nerve release ACh at SA node (decreases heart rate) -release of ACh under Resting condition -> decreases heart rate= Vagal tone 4. Vagus nerve also innervates AV node -ACh -> decrease slope of AV node pacemaker potential which will decrease AV node conduction velocity -**IF you decrease the SA node pacemaker potential you will need to decrease the AV node potential too**

What factors regulate heart rate? (4)

Calcium Permeability

What ion permeability is depicted in this graph when generating an action potential in contractile cells?

Potassium (K+) Permeability

What ion permeability is depicted in this graph when generating an action potential in contractile cells?

Sodium (Na+) permeability

What ion permeability is depicted in this graph when generating an action potential in contractile cells?

Na+ & Ca2+

What ions flow through the gap junctions connecting autorhythmic cells & contractile cells & causes a very rapid spread of action potentials

A. (REd)= sympathetic stimulation & epinephrine depolarize the autorhythmic Cell & speed up the depolarization rate (increased heart rate) B. (Blue)= Parasympathetic stimulation hyperpolarizes the membrane potential of the autorhythmic Cell & slows depolarization (decreased heart rate)

What is happening in these 2 graphs?

Top graph (blue)=SA node cell (first to reach threshold) Middle (yellow)= Action potential spreads across right atrium and into AV node Bottom graph (green)= AV node cell (early in AV node

What is happening in these graphs?

-90 mV

What is the resting membrane potential when talking about cardiac contractile cells & action potentials

1. Action potentials generated in SA node pacemaker cells: -Right atrium near entrance of vena cava 2. Action potentials spread across walls of both atria & to atrioventricular node (AV node) -Atria depolarize & contract simultaneously -Short delay at AV node before action potential spreads to ventricles 3. Action potentials spread from AV node to apex of heat only through Bundle of His & Bundle Branches in interventricular septum 4. Action potential spread from AV node before action potential spreads to ventricles 5. Ventricle contraction begins at apex of heart, squeezing blood towards aorta or pulmonary trunk

What is the sequence of excitation in conducting system?

-40 mV

What is the threshold when talking about contractions in cardiac action potentials?

Action potential in contractile cells **Note: -Stable resting membrane potential -Time scale

What is this a graph of?

ACh decreasing heart rate (parasympathetic stimulation) Green= Hyperpolarization Blue= Parasympathetic Stimulation REd= slower depolarization

What is this a graph of? Label the colored parts

Permeability changes in Cardiac Contractile Cell Action Potential 0= Na+ channels open (cause rapid depolarization) 1= Na+ channels close 2= Ca2+ channels open, FAST K+ channels close 3= Ca2+ channels close, SLOW K+ channels open (Repolarization) 4= Resting potential (-90); FAST K+ channels reopen

What is this a graph of? List what is going on with the numbers

It is showing that the slope of the pacemaker potential in pacemaker cells sets the frequency of action potentials (heart rate) -Green line= increased slope from baseline: depolarization will happen faster and heart beats will be closer together (faster heart rate) -Brown line= decreased slope from baseline: that will push heart beats farther apart (lower heart rate)

What is this a picture of?

Action potentials generated by autorhythmic cells of SA node; action potentials are the heart contracting Blue= pacemaker potential (generated by autorhythmic cells of SA node) Green= Action potentials

What is this a picture of? Label the colored parts

It's a graph showing the relative membrane permeability of the ions forming an action potential in contractile cells Green= PNa+ (sodium channels) Red= PCa2+ (L-type calcium channels) Brown= PK+ (Potassium channels) -2 in this case: Fast K+ channels & slow K+ channels

What is this a picture of? Label the colored parts

Ionic basis of pacemaker potential generating an action potential: Steps= 1. (Blue) If channels (Na+ funny channels) open- causes depolarization 2. (Green) Some Ca2+ channels open at threshold, If (Na+ funny channels) close 3. (Yellow) A lot f Ca2+ channels are open 4. (Red) Ca2+ channels close, K+ channels open (Repolarization occurs) 5. (Purple) K+ channels close 6. (Orange) If (Na+ funny channels) open in response to Hyperpolarization 7. The cycle continues

What is this a picture of? What are the steps? (Colored parts)

Calcium potential (Ca2+) **Action potentials are caused by Ca2+ influx

What kind of ion permeability is this a graph of in regards to pacemaker potential when generating an action potential?

Potassium Potential (K+)

What kind of ion permeability is this a graph of in regards to pacemaker potential?

Sodium potential (Na+)

What kind of ion permeability is this a graph of in regards to pacemaker potential?

1. Atria cells are insulated from ventricle cells 2. All current to ventricles MUST PASS THROUGH AV NODE & BUNDLE OF HIS 3. Spread of depolarization is delayed at the AV node ~100msec -Intrinsic property of AV node cells lead to slow conduction velocity -small cell diameter -slow response cardiac with long refractory period limit the maximal rate at which atria can drive ventricles -Regulated by parasympathetic fibers

What prevents ventricles from contracting at the same time as the Atria? (3 things)

Parasympathetic fibers

What regulates AV node delay?

Slope of pacemaker potential in pacemaker cells sets frequency of action potentials (heart rate) -in absence of hormonal or neural input: SA node can be upwards of 200 beats/min -vs. normal heart rate which is around 60-140 beats per minute -If slope increases= depolarization is faster & heart beats are closer together (faster heart rate) -If slope decreases= this will push heart beats farther apart (slower heart rate)

What sets the heart rate?

Sympathetic fibers

What stimulates epinephrine (EPI) or norepinephrine (NE) release at SA node?

Apex of the heart

Where does contraction of the ventricle begin?

It allows the atria to contract & empty their contents into the ventricles before the ventricles contract

Why is AV node delay important?

It has the fastest rhythm

Why is SA node the pacemaker?

To ensure the maximal contractile strength can be generated to ensure the maximum amount of blood can be ejected out of the ventricle per beat

Why is a long refractory period important in cardiac muscle?

Plateau corresponds roughly to refractory period: interval in which second muscle contraction cannot occur

Why the plateau in cardiac muscle action potential?

Purkinje Fibers

____ arranged so that papillary muscles contract just prior to remainder of ventricle

Pacemaker potential

____ has NO stable Vm (resting membrane potential) -spontaneous, rhythmic self-excitation

AV node *AV node acts as an auxiliary pacemaker

____ spontaneously depolarizes to act as an auxiliary pacemaker, but slower than SA node depolarization rate

Autonomic input

_____ alters slope & extent of Repolarization of pacemaker potential

Action potentials

______ generated by autorhythmic cells of SA node free heart from regulation by motor neurons -automaticity

1. AV Block: signal coming from the atria dos NOT get transmitted though the AV ode, so SA node is no longer driving the system -The SA node can be working just fine but if the signal doesn't get to the AV node the conduction is stopped there & the endogenous scythe is being driven somewhere else, this is slowing down the heart rate 2. Sick sinus syndrome: when the SA node doesn't work correctly & the AV node is driving the system

2 things could be wrong, What are they?

Motor neurons

Action potentials generated by autorhythmic cells of SA node free heart from regulation by ______

Calcium (Ca2+) influx

Action potentials in contraction are caused by

Slope & extent of Repolarization

Autonomic input alters ____ & ____ of pacemaker potential

Gap junctions -Na+ & Ca2+ flows through these gap junctions and causes a very rapid spread of action potentials

Autorhythmic cells are electrically coupled to each other & to some contractile cells by _____

Sick Sinus Syndrome

Condition when the SA node doesn't work correctly & the AV node is driving the system

AV Block

Condition where the signal coming from the atria dos NOT get transmitted though the AV ode, so SA node is no longer driving the system -The SA node can be working just fine but if the signal doesn't get to the AV node the conduction is stopped there & the endogenous scythe is being driven somewhere else, this is slowing down the heart rate

SA node (blue) -> VERY FAST conduction via internodal pathway (yellow) -> *Delay at AV node (green); depolarization must pass though AV node bundle (red) -> Bundle Branches (purple) -> Purkinje Fibers (orange)

Describe the pathway action potentials take to get a contraction

1. Action potentials generated in SA node pacemaker cells: -Right atrium near entrance of vena cava 2. Action potentials spread across walls of both atria & to atrioventricular node (AV node) -Atria depolarize & contract simultaneously -Short delay at AV node before action potential spreads to ventricles 3. Action potentials spread from AV node to apex of heat only through Bundle of His & Bundle Branches in interventricular septum 4. Action potential spread from AV node before action potential spreads to ventricles 5. Ventricle contraction begins at apex of heart, squeezing blood towards aorta or pulmonary trunk

Describe the sequence of excitation in conducting system

Blue= SA node drives the train because it has the fastest rhythm Green= AV node has faster endogenous rhythm that bundle cells Red= Bundle cells have slow endogenous rhythm **The SA node is "driving" the train ***-If SA node fails, then AV node drives it. If AV node fails then the Bundle Cells drive it

Describe this picture & label the colored parts

Papillary muscles

Function is to make sure the valves stay shut & aren't pushed back open by the pressures in the heart

By gap junctions -Autorhythmic cells are electrically coupled to each other & to some contractile cells by gap junctions (Na+ & Ca2+ flow through gap junctions)-> causes a very rapid spread of action potentials

How do Autorhythmic Cells communicate with contractile cells?

-Cardiac refractory period ~300msec (0.3 sec) -Skeletal muscle refractory period only 1-2 msec -summation & tetanus are important in skeletal muscle, NOT in cardiac muscle

How do electrical & mechanical events in cardiac muscle differ from skeletal muscle?

1. ACh binds to M2 muscarinic receptors on SA & AV node cells -Gi-alpha -> decrease adenylate cyclase -> decreases cAMP -> decreases Na+ funny current -> decreases the slope of pacemaker potential -Gi-beta-gamma activates K+ channels -> grater Hyperpolarization -Also increases duration of AV node delay

How does Acetylcholine (ACh) decrease Heart Rate?

1. Norepinepherine can affect contractile cells by binding to beta-Receptors that increase the # of open L-Type Ca2+ channels raising the plateau & shortening the plateau 2. Shortening the action potential by causing the potassium channels to reopen sooner in response to elevated plateau 3. Overall, action potentials are taller & shorter causing faster conduction, shorter refractory periods, & increased contraction strength 4. Calcium pump (SERCA pump) speeds up also in response to speed up return of calcium to the sarcoplasmic reticulum

How does norepinepherine affect the cardiac system? (4 steps)

1. Sympathetic fibers release norepinephrine (NE) at SA node -increases heart rate during exercise, stress, emergency, ect. 2. Norepinephrine (NE) binds to Beta1-adrenergic receptors on SA node cell increasing cAMP -this increases activity of funny (If) Na+ channels -> decreases Hyperpolarization between action potentials & increase the slope of pacemaker potentials in SA node **Epinephrine (EPI), hormone released from adrenal medulla into bloodstream, usually has similar cardiac actions as NE -sympathetic fibers stimulate EPI release

How does the sympathetic nervous system increase heart rate? (2 steps)

Hyperpolarization

If channels (Na+ funny channels) open in response to

Refractory period

Interval in which second muscle contraction cannot occur

Yes! 1. Slow depolarization to threshold primarily due to Na+ "leak" via F-type (funny) channels -voltage & time dependent currents -channels open in response to membrane Hyperpolarization -channel opening regulated by cAMP directly 2. At Threshold: Voltage-gated L-Type Calcium (Ca2+) channels (L= long lasting) open & If (Na+ funny) channels are closed 3. Repolarization: Ca2+ channels close & voltage-gated K+ channels open 4. Hyperpolarization: K+ channels close & If (Na+ funny) channels reopen -If (Na+ funny) channels open in due to Hyperpolarization

Is ionic basis of pacemaker potential slow? List the steps:

Red= Action potential in cardiac contractile cells Brown= Ventricular contractile cell muscle tension Blue= Refractory period

LAbel the colored parts

Blue= sinoatrial (SA) node Green= Atrioventricular (AV) node Yellow=Bundle of His Orange= Bundle Branches in interventricular septum Red= Purkinje Fibers Purple= apex

LAbel the colored parts of the heart

Green= Threshold (-40) Blue= Action Potential Red= Pacemaker potential

Label the colored parts of the graph

Green= during sympathetic stimulation Purple= during parasympathetic stimulation

Label the colored parts of the graph

BLue= sinoatrial (SA) node Green= Atrioventricular (AV) node Yellow= AV Bundle (Bundle of His) Red= Purkinje Fibers Purple= Left/Right bundle branches

Label the colored parts of the heart

1. Na+ channels open (cause rapid depolarization) 2. Na+ channels close 3. Ca2+ channels open, FAST K+ channels close 4. Ca2+ channels close, SLOW K+ channels open (Repolarization) 5. Resting potential (-90); FAST K+ channels reopen

List the steps of Ion permeability changes in cardiac contractile cell action potential


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