INB365S: Electrical Events of the Heart

What happens where the sarcomere becomes shorter?

the whole muscle becomes shorter = contraction
contraction pulls a bone closer to another bone to create movement
= gliding door (exists in skeletal and cardiac muscle (NOT smooth muscle)

thick filaments

made of myosin (head + tail)

thin filaments

actin chain made up of tropomyosin, troponin, and g-actin molecules

tropomyosin

covers the binding sites of actin in thin filaments
= duck tape

troponin

sensor
Ca2+ binds to troponin to trigger muscle contraction

g-actin molecule

interacts with myosin
** actin and myosin naturally want to glue together

Initiation of contraction

1. Ca2+ levels increase in cytosol

2. Ca2+ binds to troponin

3. Troponin-Ca2+ complex pulls tropomyosin away from actin’s myosin-binding site

4. Myosin binds strongly to actin and completes power stroke

5. Actin filament moves

Why are dead bodies rigid?

Muscle relaxation requires ATP!!!!!!!!!!!

What happens when ATP binds to myosin?

1. Myosin releases actin.

2. Myosin hydrolyzes ATP.

3. Energy from ATP rotates the myosin head to the cocked position.

4. Myosin weakly binds to actin

Relaxation!

Where does the signal for muscle contraction come from?

Motor cortex → neurons go to spinal cord → skeletal muscle

Initiation of Muscle Action Potential

1. Somatic motor neuron releases ACh at neuromuscular junctions (nicotinic receptors = nonselective cation receptors) at motor end plate

2. Net entry of Na+ through ACh receptor-channel causes depolarization → end plate potential

3. Generates action potential through T-tubule

Muscle Action Potential in T-tubule (skeletal muscle)

Triggers DHP to open RyR Ca2+ release channels in sarcoplasmic reticulum

• Ca2+ enters cytoplasm

• Ca2+ binds to troponin, allowing actin-myosin binding

• Myosin heads execute power stroke

• Actin filament slides toward center of sarcomere

Relaxation Phase! in skeletal muscle

1. sarcoplasmic Ca2+-ATPase pumps Ca2+ back into SR

2. decrease in the free cytosol causes Ca2+ to unbind from troponin

3. Tropomyosin re-covers binding site. When myosin heads release, elastic elements pull filaments back to their relaxed position

short coming of skeletal muscle

Summation of contractions: stimuli closer together do not allow muscle to relax fully
1. Unfused tetanus: stimuli are far enough apart to allow muscle to relax slightly between stimuli (= not all Ca2+ pumped back to SR)
2. Tetanus: muscle reaches steady tension. If muscle fatigues, tension decreases rapidly

What is the force of contraction proportional to?

The force of contraction is proportional to the concentration of calcium!!!!!!!!!
Contractility in cardiac cells is graded!!!!!!!!!!!

pacemaker cells

spontaneously fire to generate action potential
do not need external stimuls to trigger action potential
depolarization of pacemaker cells spread rapidly to adjacent contractile cells through gap junctions
- note that pacemaker cells and contractile cells have different action potentials!

most famous pacemaker

SA node
right atrium

Action potential in pacemaker cells

1. Funny channels open (no stabilized resting potential) as a result of hyperpolarization

2. Net Na+ in

3. Some Ca2+ channels open, funny channels close

4. Lots of Ca2+ channels open

5. Ch2+ channels close, K+ channels open

6. K+ channels close

7. Funny channels open

Action potential in contractile cells

1. stabilized resting potential

2. signal from pacemaker cells is received

3. Na+ channels open

4. Na+ channels close

5. Ca2+ channels open; fast K+ channels close = Ca2+ plateau, which makes the action potential last longer and prevents muscle cramps (also limits how fast heart rate is)

6. Ca2+ channels close; slow K+ channels open

7. stabilized resting potential!

Muscle Action Potential in T-tubule (cardiac muscle)

1. Action potential enters from adjacent c ell

2. Voltage-gated Ca2+ channels open → depolarization

3. Ca2+ induces Ca2+ release via RyR (CARDIAC ONLY)

4. Ca2+ signal

5. Ca2+ ions bind to troponin to initiate contraction

6. Relaxation occurs when Ca2+ unbinds from troponin

7. Ca2+ is pumped back into SR for storage

Electrical pathway

SA node → internodal pathways → AV node → AV bundle → Bundle branches → purkinie fibers

It gets slower to fire as you go down…

What dominates heart rate?

SA node
this is where parasympathetic and sympathetic work

Conducting system of the heart

1. SA node depolarizes

2. Electrical activity goes rapidly to AV node via internodal pathways

3. Depolarization spreads more slowly across atria. Conduction slows through AV node. (BOOM)

   1. There are not a lot of gap junctions in the AV node → AV node delay → all 4 chambers do not fire at once → prevents accumulation of blood → prevents clot formation/platelets

4. Depolarization moves rapidly through ventricular conducting system to the apex of the heart

5. Depolarization wave spreads upward from the apex (BOOM)

ECG

3D signal to 2D surface
electrodes attached to both arms and leg form a triangle
each two-electrode pair (+ and -) constitutes one lead, an ECG is recorded one lead at a time
Lead 2 is the best one to pick up the signal!!!!!

How does an ECG correlate with electrical events in the heart?

P wave = only part from atrium
QRS, T = from ventricle

arrhythmia

abnormal/irregular intervals

heart block

“traffic jam”

partial: longer interval between P and QRS
complete: P and QRS not in synch with more P waves than QRS

atrial fibrillation

p wave different but QRS may or may not be affected

ventricular fibrillation

no QRS and T
= code blue