Week 8 Notes 1/3 - Feb 23

Introduction and Course Announcements

• Professor Haas introduces himself and welcomes students back after a break.

• Reminders about contact information:

  • Administration issues should be directed to email k3012.

  • Content-related queries are to be sent to k3012_questions, not the personal email.

• Office hours:

  • Not specifically scheduled, but Professor Haas is happy to arrange time to discuss concepts at students' convenience via email or after class.

• Midterm Exam review:

  • Midterm one marks are posted.

  • Scheduled exam review will take place next Monday as per the posted time and location.

  • This is the only scheduled review; additional reviews will be arranged if demand exceeds capacity.

• Importance of midterm performance:

  • Discussion encouraged for improvement strategies and studying habits before the second midterm in two weeks.

• Recording changes:

  • Transitioning from Zoom to Panopto for lecture recordings.

  • Each lecture will feature one recording for the two morning sessions, available via a box on the right side of the screen.

  • Recording access will be posted later that day.

Heart Depolarization Overview

• Introduction of the heart's electrical activity as central to planned discussion.

• Recap from previous lectures on depolarization mechanics in the heart:

  • Focus on the Sinoatrial (S.A.) node as the heart’s pacemaker, initiating depolarization.

  • Spread of electrical activity via the AV node, Bundle of His, and Purkinje fibers to ventricular myocytes.

Pacemaker Action Potential

• Explanation of unique pacemaker action potential:

  • Key feature: Pacemaker cells' ability to spontaneously depolarize is due to unique leaky or funny sodium channels.

  • Mechanism of depolarization:

  • Sodium ions are the most abundant positively charged ions outside the cell, contributing to depolarization.

  • A trickle of sodium enters the cells at negative membrane potential, gradually increasing membrane potential until reaching the threshold.

  • Threshold potential significance: Crossing leads to full depolarization where voltage-gated calcium channels open, allowing calcium ions into the cell, driving complete depolarization.

  • Repolarization mechanism:

  • Potassium ions exit as the voltage-gated channels open, restoring negative membrane potential.

  • This characteristic is common to all excitable cells.

• Spontaneous depolarization rate:

  • The intrinsic rate of pacemaker cells is approximately 100 beats per minute (bpm) without neural influence.

  • Understanding this rate is critical as adjustments are made in live settings based on physiological demand.

Unified Depolarization in the Heart

• Importance of coordinated electrical activity among all cardiac cells:

  • Every atrial and ventricular cell must depolarize simultaneously for effective heart function.

  • Gap junction channels facilitate direct ion movement between adjacent cells, crucial for synchronization of depolarization.

  • Ions move from one cell to another due to concentration gradients, further facilitating the depolarization wave.

Ventricular Action Potential Phases

1. **Resting Phase:

   • Resting membrane potential of ventricular myocytes is approximately -90 millivolts (mV).

   • Predominantly influenced by open potassium channels that allow potassium ions to exit.

   • Minor influx of sodium due to adjacent cells depolarizing through gap junctions raises the potential towards the threshold.

2. Depolarization Phase (Phase 0):

   • When the membrane reaches approximately -70 mV, fast sodium channels open, resulting in a rapid influx of sodium ions leading to a spike in membrane potential.

3. Initial Repolarization/Plateau Phase (Phase 2):

   • Fast sodium channels close quickly after depolarization.

   • The influx of calcium ions through L-type calcium channels sustains a plateau in membrane potential, lasting around 250 to 300 milliseconds.

   • Potassium channels also activate but only moderately contribute to the state due to the overpowering influx of calcium ions.

4. Final Repolarization Phase (Phase 3):

   • The closure of L-type calcium channels and increase in potassium efflux restore the negative membrane potential.

   • Return to the resting potential of approximately -90 mV indicates readiness for subsequent cardiac cycles.

Electrocardiogram (ECG) Overview

• Description of the ECG:

  • Plots electrical activity over time, with time represented on the x-axis and electrical activity on the y-axis.

  • Important to understand that positive deflection does not strictly indicate depolarization; the measurement reflects the presence of significant electrical activity.

• P wave: Atrial depolarization occurs after S.A. node fires, indicating action potential spreading through the atria.

• QRS complex: Represents ventricular depolarization; the complexities arise from the directional flows of ions and differences in cell sizes impacting readings.

• T wave: Indicates ventricular repolarization.

Ecg Abnormalities and Clinical Implications

• Common abnormalities detected in ECG:

  • Extrasystole: Occurs when ventricular depolarization fires out of sequence, potentially due to stress; this represents disordered electrical activation.

  • Ventricular Fibrillation: Lack of any QRS complex due to chaotic electrical activity preventing effective contractions.

  • Heart Block: Acknowledges isolation between atrial and ventricular conduction—often indicated by dissociation of P waves and QRS complex, demonstrating different pacing rates.

  • Elevated ST segment: Often signifying potential heart attack or serious cardiac issues that need immediate attention.

Excitation-Contraction Coupling

• The link from electrical activity to contraction involves:

  • The influx of calcium ions facilitating contraction through the action potential and T-tubule interactions with the sarcoplasmic reticulum (SR).

  • Calcium-induced calcium release allows bound calcium to trigger the cross-bridge cycle necessary for muscle contraction via actin-myosin interactions.

• Refractory Period: This prevents sustained contractions by ensuring the heart fills properly between beats, essential for proper blood flow

• Relaxation involves:

  • Closure of calcium channels and reuptake of calcium back into the SR via SERCA pumps, preparing the cell for the next excitation-contraction cycle.

Conclusion

• Transition to upcoming lectures.

• Flowchart summarizing cardiac physiology and electrical conduction will be presented in the next class to aid understanding.

• Anticipation of practical engagements in recording ECGs as part of laboratory work in subsequent sessions.

• Professor Haas concludes by thanking the students and encouraging questions for clarity on the material covered.