Topic 13 - Cardiac action potential and excitation (contraction coupling)

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Last updated 12:05 AM on 4/12/26
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12 Terms

1
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every ___ in ___ must depolarize

every cell in the atria and ventricles must depolarize so the heart can beat efficeitnly

depolarization moves bw the cardiac myocytes

2
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how does depolarization travel bw cardiac myocytes

*Cardiac cells are connected by gap junction channels Present at the lateral endds of the cells to Ensure that all cardiac cells activate simultaneously

how?

1. cell 1 fires action potential causing Na+ and Ca2+ to enter cell

2. (+) ions from Cell 1 diffuse into Cell 2 through gap junctions

3. Membrane potential of Cell 2 becomes more +, triggering action potential

<p>*Cardiac cells are connected by gap junction channels Present at the lateral endds of the cells to Ensure that all cardiac cells activate simultaneously</p><p>how?</p><p>1. cell 1 fires action potential causing Na+ and Ca2+ to enter cell</p><p>2. (+) ions from Cell 1 diffuse into Cell 2 through gap junctions</p><p>3. Membrane potential of Cell 2 becomes more +, triggering action potential</p>
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what does action pentials in cardiac muscle cells look like

DIFFERENT FROM PACEMAKER CELL AP

- however also occurs without neural innervation as it gets its AP from neighboring cells thourgh gap junctions

4
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what are the 5 phases of cardiac muscle action potential

phase 4 - resting

phase 0 - depolarization

phase 1 - peak depolarization

pahse 2 - plateau

phase 3 - repolarization

5
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explain each phase of a myocyte AP

phase 4 - resting (-90mV)

- k+ channels are open --> k+ leaves cell

- Na+ from neighboring cells depolarize the cell to threshold (-70mV)

phase 0 - depolarization

- voltage gated FAST sodium channels open --> influx of Na+

phase 1 - peak depolarization (+30mV)

at peak...

- FIRST, fast Na+ channels close

phase 2 - plateau** critcal in myocytes

- instead of quicly repolarizing since the NA channels close --> L-type (long) ca+2 voltage gated chanels open (have a bit of a lag, why we see big dip after peak) --> Ca+ enters the cell

- a minimum amt of K+ is also leaving the cell at th esame time so cell deosnt get more positive

*these two togteher cause a plateau in membrane potential

phase 3 - repolarization

- L-type CA2+ channels close

- more voltage gated K+ channels open --> fast eflux of K+ out the cell --> back to -90mV

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The Electrocardiogram (ECG)

cardiac electrical activity as a function of time

- sum of all th the elextricle activites of all the cells in the heaart based on where electrodes are placed

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segments of the ECG

Pwave = atrial depolarization

QRS complex = ventricle depolarization

*atrial repolarization is also occuring here but cant see it

T wave = ventricle repolarization

flat portions: minimal electricle activity of the cells i.e.when cells are fully polarized or depolarized as it just catches deviations

- Pq segment = platue of atrial ap

- ST segment = plataeu of ventricular AP

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Abnormalitiesz in ECGs

- extrasystole = premature ventricular contraction

- ventricular fibrilation = no excitation of ventricle (no QRS complex)

- complete heart block = seperatrion bw atria and ventricel signals lead to av node acting as its own pacemakr --> dissociation bw P wave and QRS

<p>- extrasystole = premature ventricular contraction</p><p>- ventricular fibrilation = no excitation of ventricle (no QRS complex)</p><p>- complete heart block = seperatrion bw atria and ventricel signals lead to av node acting as its own pacemakr --&gt; dissociation bw P wave and QRS</p>
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cardiac myopathy ECG

myocardial infarction

- QRS blended w T wave (elevated ST segment) --> tells u theres serve cardiac problems

<p>myocardial infarction</p><p>- QRS blended w T wave (elevated ST segment) --&gt; tells u theres serve cardiac problems</p>
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Membrean depolarization of the heart triggers contraction

- contraction of the heart ocurs DURING the action potnetial (specifically the plateau phase)

- major difference to skeletal muscles which can generate greater force by fusign AP --> tetanus

why does this occur?

--> bc of Ca2+ channels that slow reploarization

--> leads to refractory period: where cell cannot be rexcited to fire a new AP

<p>- contraction of the heart ocurs DURING the action potnetial (specifically the plateau phase)</p><p>- major difference to skeletal muscles which can generate greater force by fusign AP --&gt; tetanus</p><p>why does this occur?</p><p>--&gt; bc of Ca2+ channels that slow reploarization</p><p>--&gt; leads to refractory period: where cell cannot be rexcited to fire a new AP</p>
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why is cardiac refractory period important

--> so there is NO tetanus so that heart can fill withblood in between contractions

--> to prevent RETROGRADE ACTIVATION via gap junctions: bc there are gap junctions bw myocytes so we dotn what cell 2 to re excite cell 1 which is super unregulated activity and rythym

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mechanism of excitation contraction coupling in mysocytes

1. when L-type caclium channels open --> ca2+ enters cell at t tubules

2. Ca2+ bind to calcium depended calcium channels called RYANODINE RECEPTORS in the cell on the SR

--> causes release of calcium stored in SR into cytoplasm (CALCIUM INDICED CALSIUM RELEASE)

3. Ca2+ enables contraction → Ca2+ binds troponin, allows actin/myosin cross-bridge formation

4. Ca2+ pumped back into the SR using the SERCA pump

<p>1. when L-type caclium channels open --&gt; ca2+ enters cell at t tubules</p><p>2. Ca2+ bind to calcium depended calcium channels called RYANODINE RECEPTORS in the cell on the SR</p><p>--&gt; causes release of calcium stored in SR into cytoplasm (CALCIUM INDICED CALSIUM RELEASE)</p><p>3. Ca2+ enables contraction → Ca2+ binds troponin, allows actin/myosin cross-bridge formation</p><p>4. Ca2+ pumped back into the SR using the SERCA pump</p>