Cardiac Electrical Activity and ECG Notes

Membrane Potentials in Cardiac Tissue

  • The potential of the SA (sinoatrial) fibre between dischargeis s -55 ext{ to } -60 ext{ mV}

  • The potential of the ventricular fibre between discharges is -85 ext{ to } -90 ext{ mV}

  • Reason for this difference: sinus fibres are naturally leaky to sodium ions (Na⁺), which affects resting potential and excitability

Pacemaker Potentials and Autonomic Modulation

  • Pacemaker cells in the sinoatrial (SA) node depolarize spontaneously (intrinsic rhythm) but the rate can be modulated

  • Epinephrine and norepinephrine increase the production of cyclic adenosine monophosphate (cAMP), which keeps cardiac pacemaker channels open and speeds up depolarization

  • Na⁺ inflow via these channels speeds heart rate

  • Parasympathetic neurons secrete acetylcholine (ACh), which opens K⁺ channels to slow the heart rate

Action Potentials in Cardiac Muscle (General)

  • Resting membrane potential of cardiac muscle: -85 ext{ to } -90 ext{ mV}

  • Ventricular membrane potential moves from -85 ext{ mV} to +20 ext{ mV} (overshoot potential)

  • The plateau phase in cardiac muscle is prolonged, lasting 3–15 times longer than the plateau phase of skeletal muscle

Prolonged Action Potential: Mechanisms (Skeletal vs Cardiac)

  • Skeletal muscle: fast Na⁺ channels open and cause rapid depolarization within about 10^{-4} ext{ s}, then repolarization occurs

  • Cardiac muscle: fast Na⁺ channels open as well as slow Ca²⁺ channels (Ca²⁺-Na⁺ channels open more slowly but remain open longer)

  • The sustained influx of both Na⁺ and Ca²⁺ causes the extended plateau phase in cardiac muscle

  • The Ca²⁺ that enters the muscle is instrumental in muscle contractility (calcium contributes to contraction strength and duration)

Onset of the Action Potential and Potassium Permeability

  • Onset of the AP decreases the muscle permeability to potassium by about a factor of ~5 (i.e., P_K ↓ by ≈ 5× during depolarization)

  • Decreased potassium permeability reduces outward K⁺ flux during the AP, preventing early repolarization

  • After the calcium and sodium influx ceases, potassium membrane permeability increases again, returning the cell to its resting potential

Excitation–Contraction Coupling in Cardiac Muscle

  • Ca²⁺-stimulated Ca²⁺ release: Ca²⁺ channels in the sarcolemma/T-tubules open upon depolarization

  • Ca²⁺ diffuses into the cytoplasm and stimulates the opening of Ca²⁺ release channels of the sarcoplasmic reticulum (SR)

  • Ca²⁺ (mostly from SR) binds to troponin to stimulate contraction

  • These events occur at signaling complexes on the sarcolemma that are closely apposed to the SR (coupling sites)

Contraction of Cardiac Muscle: Visualizing the Process

  • AP propagates along the sarcolemma and T-tubules, triggering Ca²⁺ entry

  • Ca²⁺ diffuses into the myofibrils and promotes sliding of actin and myosin filaments, resulting in contraction

  • The contraction is initiated by Ca²⁺-induced Ca²⁺ release from the SR

Repolarization and Relaxation

  • Cytoplasmic Ca²⁺ concentration is reduced by active transport back into the SR and extrusion through the plasma membrane via the Na⁺-Ca²⁺ exchanger (NCX)

  • The myocardium relaxes as Ca²⁺ is cleared from the cytoplasm

Ca²⁺ Handling and Cardiac Structure

  • Large amounts of Ca²⁺ diffuse into the sarcoplasm from the T-tubules; without this, the cardiac muscle would not contract fully

  • The sarcoplasmic reticulum (SR) in cardiac muscle is less developed than in skeletal muscle

  • T-tubule diameter in cardiac muscle is about 5 ext{ times} that of skeletal muscle, and the T-tubule system volume is about 25 ext{ times} greater than that of skeletal muscle

  • These structural differences contribute to the conduction of the AP and the Ca²⁺ handling characteristics of cardiac muscle

Electrocardiogram (ECG/EKG): What It Measures

  • An electrocardiograph records the electrical activity of the heart by detecting the movement of ions in body tissues in response to electrical activity

  • It does not record action potentials directly; instead, it records waves of depolarization

  • It does not record contraction or relaxation, but the electrical events that lead to contraction and relaxation

ECG Waves and Intervals

  • P wave: atrial depolarization

  • P–Q interval: atrial systole

  • QRS complex: ventricular depolarization

  • S–T segment: plateau phase, ventricular systole

  • T wave: ventricular repolarization

ECG Calibration and Interpretation (Typical Signals)

  • ECG trace calibration and timing:

    • Paper speed: 25 ext{ mm/s}

    • Each small box: 0.04 ext{ s}; each large box (5 small boxes): 0.2 ext{ s}

    • Amplitude scale: 1 ext{ mV} = 10 ext{ mm} (often written as 10 mm/mV)

  • Typical vertical offset examples observed on ECG diagrams include marker heights such as 5 mm and 0.5 mV, with other labels indicating P, QRS, T components and interval markers (P–R, Q–T, S–T segments, etc.)

ECG Trace Features and Key Intervals

  • P–R interval: from start of the P wave to start of the QRS complex; represents atrial depolarization and delaying conduction at the AV node

  • QRS interval: duration of ventricular depolarization

  • S–T segment: plateau phase of ventricular action during which ventricles are contracted

  • Q–T interval: total time of ventricular depolarization and repolarization

  • RR interval: time between successive R waves; relates to heart rate

  • T wave: ventricular repolarization

ECG Leads and Their Placement

  • Bipolar limb leads measure voltage between limb electrodes placed on the limbs

  • Lead I: between the right arm and left arm (often described as the electric potential difference between the left and right arms)

  • Lead II: between the right arm and left leg

  • Lead III: between the left arm and left leg

  • These leads provide different views of the heart's electrical activity and are used to assess rhythm and conduction from multiple

  • angles