Seasons LG LO's Wk3 pt.1

Ions and Heart Rhythms: Ion Channels, Transport & Electrochemical Gradient

LO 1: describe how the heart muscle contracts since it cannot have multiple individual muscle cells contracting at random times

the heart must act as a single, coordinated unit.

LO 1: intercalated discs

• what they are

• what types of connections do they contain

Intercalated Discs:

• specialized junctional regions that join cardiac muscle cells (cardiomyocytes) end-to-end

• These discs contain two vital types of connections: desmosomes and gap junctions.

LO 1: desmosomes

• what they are

• their purpose in the heart muscles

• mneumonic

Physical Stability (Desmosomes):

• Think of desmosomes as "mechanical staples".

• specialized complexes that hold the cells tightly together so that when the heart contracts with great force, the cells do not pull apart or tear away from each other.

• mnuemonic: desmosomes don’t separate

LO 1: gap junctions

• what they are/function

• what are they composed of

Electrical Continuity (Gap Junctions):

• These are the true communicators.

• specialized protein channels that directly connect the cytoplasm of adjacent animal cells.

• Gap junctions are composed of proteins called connexins that form tubular channels between adjacent cells.

LO 1: ion flow

• what do ion channels create

• where do the ions flow

Ion Flow:

• These gap junction channels (formed by connexin) create a bridge of low electrical resistance, allowing ions (like Na+ and Ca2+) to flow directly from the cytoplasm of one cell into the next.

LO 1: functional syncytium

• what causes it

• what is it

• Ions move through gap junctions → this depolarizes the neighboring cardiac cell → then the signal keeps spreading to other connected cells

Functional Syncytium:

• Because ions move freely through these bridges without having to cross a cell membrane, a depolarization event in one cell triggers a chain reaction in all connected cells.

• This allows the entire myocardium to behave as a functional syncytium—a community of cells acting as a single unit.

LO 1: cardiac muscle

• describe how communication occurs

• what is the trigger & the coordination

LO 1: what happens if gap junctions are disrupted ex.) MI

• In a healthy patient, this rapid communication ensures that the atria contract first to fill the ventricles, followed by a coordinated ventricular contraction to eject blood to the body.

• If these "tunnels" (gap junctions) are disrupted—which can happen during a myocardial infarction (heart attack) or due to electrolyte imbalances—the electrical wave becomes chaotic.

• This can lead to arrhythmias, where the heart cells "wiggle" independently (fibrillation) instead of squeezing together, resulting in a failure to pump blood.

LO 1:

• __________ (_________) provide the low-resistance pathway for electrical spread.

• ________ provide the mechanical strength to prevent cell separation during contraction.

• _________is the term for the heart acting as a single unit due to these connections.

• Gap junctions (connexins) provide the low-resistance pathway for electrical spread.

• Desmosomes provide the mechanical strength to prevent cell separation during contraction.

• Functional Syncytium is the term for the heart acting as a single unit due to these connections.

LO 2: what are the 2 types of electrical signals that the heart uses

• contractile myocytes (the muscle that does the heavy lifting)

• conductible pacemaker cells (the specialized cells that set the beat).

LO 2: what are myocytes vs pacemakers designed for

• myocytes: long, powerful contractions, generate force

• pacemakers: automaticity- the ability to fire on their own without external help. initiate and distribute the impulse

LO 2: action potential phases diagram

LO 2: action potential phases 0-4 cardiomyocyte

• what they are called & what occurs

• phase 4 myocytes vs SA node/pacemaker

Phase 4 of the Sinoatrial (SA) node action potential is the spontaneous diastolic depolarization (pacemaker potential) that initiates each heartbeat. It is driven by the opening of HCN (hyperpolarization-activated cyclic nucleotide-gated) channels, which generate the "funny" current (\(I_{f}\)). This allows a slow influx of sodium and potassium ions that steadily raises the membrane potential

LO 2: what phases do myocytes vs pacemaker go though

LO 2: phase 4 myocytes vs pacemakers

Phase 4 (Resting vs. Diastolic Depolarization):

• Myocytes: Have a stable resting membrane potential (RMP) at -90 mV. They stay quiet until a signal arrives from a neighbor.

• Pacemakers: Have no stable resting potential. Instead, they use a "funny current" (If)—an inward sodium current through HCN (hyperpolarization-activated cyclic nucleotide-gated) channels, that causes the voltage to slowly "drift" upward toward the threshold automatically.

LO 2: phase 0 myocytes vs pacemakers

Phase 0 (Upstroke/Depolarization):

• Myocytes: Use fast voltage-gated sodium channels. This causes a near-vertical, lightning-fast spike in voltage.

• Pacemakers: Use slower L-type calcium channels for their upstroke. Because calcium moves slower than sodium, the upstroke is more "lazy" and slanted on a graph. Fast sodium channels are inactivated in these cells.

LO 2: phase 1&2 myocytes vs pacemakers

Phase 1 & 2 (The Plateau):

• Myocytes: Have a distinct plateau phase (Phase 2) where calcium influx perfectly balances potassium efflux. This keeps the cell depolarized (contracted) for a long time.

• Pacemakers: Completely lack Phase 1 and Phase 2. They go straight from depolarization to repolarization.

LO 2: phase 3 myocytes vs pacemakers

Phase 3 (Repolarization):

• Both cells use potassium (K+) exit to return the cell to its negative starting voltage.

LO 2:

• __________ is due to the unstable Phase 4 funny current in pacemaker cells.

• Myocytes use ______ _______channels for depolarization; pacemakers use ______ _____

• The _____ (Phase ___) only exists in myocytes to ensure a long contraction.

• Automaticity is due to the unstable Phase 4 funny current in pacemaker cells.

• Myocytes use fast sodium channels for depolarization; pacemakers use slow calcium channels.

• The plateau (Phase 2) only exists in myocytes to ensure a long contraction.

LO 3:

• why can’t heart cells stay continuously contracted like neurons

• what phase helps this

• the heart must contract → relax → refill → contract again

• A neuron just needs to send a quick "zap," but a heart cell needs to squeeze and stay squeezed to push blood out.

• phase 2: heart cells add a massive calcium-driven plateau to slow everything down by keeping depolarization for longer and delaying repolarization

  
  

LO 3: duration of action potential neurons vs cardiomyocytes and why

Duration:

• Neurons: The signal is incredibly brief, lasting only 1–2 milliseconds.

• Cardiomyocytes: The action potential is "marathon-length," lasting 200–300 milliseconds.

LO 3: plateau neurons vs cardiomyocytes

The "Why" Behind the Plateau:

• Neurons: No plateau. They fire and reset instantly.

• Cardiomyocytes: The Phase 2 plateau is caused by calcium entering while potassium leaves. This long duration creates a long refractory period, meaning the heart cell cannot be shocked again until it has finished its current contraction.

LO 3: tetanus neurons vs cardiomyocytes

• tetanus: sustained contraction

Tetanus (The Safety Switch):

• Neurons/Skeletal Muscle: Can be stimulated repeatedly and very fast, leading to tetanus (a sustained, frozen contraction).

• Cardiomyocytes: Because the action potential lasts as long as the contraction itself, tetanus is impossible. This is vital—if your heart had a tetanic contraction, it would stay frozen in a squeeze and never refill with blood.

• The heart’s contraction is triggered by an action potential, but because the plateau creates a long refractory period, another action potential cannot occur before the muscle relaxes, preventing tetanus.

LO 3:

• Plateau (Phase 2) : ion & function

• The long cardiac action potential ensures the heart has time to ______ and ______.

• Tetanus can happen in ________/______ muscle but is impossible in the______.

• Plateau (Phase 2) : Ca²⁺ influx keeps ventricular myocytes depolarized longer.

• The long cardiac action potential ensures the heart has time to relax and refill.

• Tetanus can happen in neurons/skeletal muscle but is impossible in the heart.

LO 4:

• what is excitation-contraction coupling in simple terms

• what is the essential messenger

• Excitation-contraction (E-C) coupling = how a cardiac action potential (electrical signal) causes the heart muscle to contract (physical squeeze).

• calcium is the essential messenger

LO 4: the signal

• what does the action potential travel down in cardiac muscle cells

The Signal:

• The action potential travels down T-tubules, which are tunnels that bring the electrical signal deep into the center of the cell.

LO 4: trigger calcium

• what phase, what channels, & what occurs

Trigger Calcium:

• During the Phase 2 plateau, L-type calcium channels open in the T-tubule membrane, letting a small amount of extracellular calcium into the cell.

LO 4: calcium-induced calcium release

• what does the calcium from the trigger bind [receptors] and where

• what does the sarcoplasmic reticulum do & what is this process called

(CICR):

• This small "trigger" calcium binds to Ryanodine receptors (RyR2) on the Sarcoplasmic Reticulum (SR).

• This causes the SR to dump a massive amount of stored calcium into the cytoplasm—a process called Calcium-Induced Calcium Release (CICR).

LO 4: contraction

• what does calcium bind

• what does this lead to

• what then leads to muscle contraction

Contraction:

• Calcium binds to Troponin C. This causes tropomyosin to move out of the way, exposing binding sites on actin. Myosin heads then grab actin and pull, shortening the muscle (contraction).

• Ca²⁺ binds troponin C → tropomyosin moves → myosin binding sites on actin exposed → myosin heads bind to actin & pull

LO 4: relaxation

• what must occur for the muscles to relax

• what 2 options can accomplish this

Relaxation:

• To relax, calcium must be sucked back into the SR by the SERCA pump or pushed out of the cell by the NCX (Sodium-Calcium Exchanger).

• SERCA: Sarcoplasmic/Endoplasmic Reticulum Ca²⁺-ATPase

• NCX: Na⁺/Ca²⁺ Exchanger

LO 4:

• _________________: A small amount of extracellular calcium triggers a large release from the SR.

• _______ channels provide the trigger; ________ receptors provide the large release of calcium.

• ___________is the specific protein calcium binds to initiate contraction.

• CICR (Calcium-Induced Calcium Release): A small amount of extracellular calcium triggers a large release from the SR.

• L-type channels provide the trigger; Ryanodine receptors provide the large release of calcium.

• Troponin C is the specific protein calcium binds to initiate contraction.