Cardiac action potential and ECC

What does it mean that the heart is autonomous?

The heart can generate and conduct its own electrical impulses without external stimulation.

What is the excitation pathway of the heart?

SA node → AV node → bundle of His → right and left bundle branches → Purkinje fibres.

What is the role of the SA node?

It initiates the electrical impulse that triggers each heartbeat.

What is the role of the AV node?

It delays the impulse from the atria before transmitting it to the ventricles.

What does the bundle of His do?

It conducts impulses from the AV node to the bundle branches.

What is the role of Purkinje fibres?

They rapidly distribute the electrical impulse through the ventricles for coordinated contraction.

What do the P, QRS, and T waves represent on an ECG?

P wave = atrial depolarization, QRS complex = ventricular depolarization, T wave = ventricular repolarization.

What does an electrocardiogram (ECG) measure?

The summed electrical activity of the heart over time, recorded from the body surface.

What ion is most critical for cardiac contraction?

Calcium (Ca2+).

How is cardiac contraction visualized at the cellular level?

Through fluorescent reporters showing synchronized calcium release across the cell.

Why do human embryonic stem-cell derived cardiomyocytes not contract end-to-end?

Because they lack mature intercellular coupling found in adult cardiac tissue.

What determines the resting membrane potential (RMP) of cardiac cells?

The selective movement of ions, mainly K+, across the sarcolemma and the activity of the Na+/K+ ATPase.

What is the approximate resting membrane potential of cardiac cells?

About -90 mV.

What does the Na+/K+ ATPase do?

It pumps 3 Na+ out and 2 K+ into the cell using ATP, maintaining ion gradients and the RMP.

What is the role of the Na+/Ca2+ exchanger?

It removes one Ca2+ from the cell in exchange for bringing in three Na+ ions.

What causes depolarization in the cardiac action potential?

Rapid influx of Na+ through voltage-gated sodium channels.

What causes the plateau phase (phase 2) of the cardiac action potential?

Ca2+ influx through voltage-gated L-type calcium channels (LTCC).

What causes repolarization in the cardiac action potential?

Efflux of K+ ions restoring the negative membrane potential.

What maintains the resting potential during diastole (phase 4)?

The Na+/K+ pump and K+ efflux through open K+ channels.

What is the difference between ECG and an action potential recording?

ECG records the summed electrical activity of the whole heart; an action potential records the ion flux of one cell.

How do nodal cells differ from atrial and ventricular cells in their action potentials?

Their phase 4 is unstable due to spontaneous depolarization.

What is the funny current (If)?

A slow inward Na+/K+ current through HCN4 channels responsible for spontaneous depolarization in SA node cells.

What is the role of HCN4 channels?

They generate the pacemaker current that initiates heartbeats.

What is the target of the drug Ivabradine?

The HCN4-mediated funny current (If) in SA node cells to reduce heart rate.

What proteins are involved in the cardiac contractile apparatus?

Actin, myosin, tropomyosin, and troponin.

What happens when Ca2+ binds to troponin C?

It shifts tropomyosin, exposing binding sites on actin for myosin to attach.

What is the 'power stroke' in muscle contraction?

The movement of the myosin head that pulls actin filaments, powered by ATP hydrolysis.

What triggers contraction in cardiac muscle?

Ca2+ entry through L-type Ca2+ channels during the action potential plateau.

What is excitation–contraction coupling (ECC)?

The process linking electrical excitation of the sarcolemma to the mechanical contraction of the myofilaments.

What is calcium-induced calcium release (CICR)?

The process by which Ca2+ entry through LTCC triggers further Ca2+ release from the sarcoplasmic reticulum (SR).

Which channels mediate Ca2+ release from the SR?

Ryanodine receptor 2 (RyR2) channels.

What is the main intracellular store of Ca2+ in cardiac cells?

The sarcoplasmic reticulum (SR).

How is relaxation of cardiac muscle initiated?

By removing cytosolic Ca2+ through reuptake into the SR and efflux from the cell.

Which transporter reuptakes Ca2+ into the SR?

SR Ca2+-ATPase (SERCA).

What regulates SERCA activity?

Phospholamban (PLB), which inhibits SERCA when unphosphorylated.

How is Ca2+ removed from the cytosol during relaxation?

By SERCA reuptake, Na+/Ca2+ exchange (NCX), and the sarcolemmal Ca2+ ATPase.

What are the main steps in excitation–contraction coupling (ECC)?

LTCC Ca2+ entry → RyR2 Ca2+ release → binding to troponin C → contraction → Ca2+ removal by SERCA, NCX, and SL Ca2+-ATPase.

What happens during cellular depolarization?

Na+ influx depolarizes the membrane, triggering Ca2+ entry.

What happens during repolarization?

K+ efflux restores the resting membrane potential and ends contraction.

What ensures synchronization of cardiac contraction?

Tight coupling of electrical excitation, Ca2+ signaling, and myofilament activation.

Why is ECC considered a homeostatic system?

Because total Ca2+ entering and leaving the cell remains balanced over each cycle.

What are the main routes of Ca2+ removal from cardiac cells?

SERCA (major route), NCX, and SL Ca2+ ATPase.

How does Ca2+ handling differ between humans and rodents?

Humans rely more on NCX for Ca2+ removal, while rodents rely more on SERCA.

Why do species differences in Ca2+ handling matter?

They influence cardiac performance, including contraction rate and strength.