In this video, we dive into Second-Degree AV Block Type I (Mobitz I or Wenckebach), focusing specifically on how cardiac ischemia leads to AV nodal dysfunction. Through detailed ECG interpretation of an inferior myocardial infarction (MI) example, we'll highlight the key features—such as the progressively lengthening PR interval and dropped beats.
You’ll also gain a clear understanding of the pathophysiology behind ischemia-induced conduction issues, including:
How ischemia reduces ATP, impairing Na⁺/K⁺ pumps and Na⁺/Ca²⁺ exchangers.
Why L-Type Calcium Channels become decrementally fatigued, causing progressive conduction delays.
The cellular impact, including cell swelling, altered resting membrane potentials, and impaired conduction through the AV node.
Ideal for medical students, cardiology fellows, nurses, and anyone looking to deepen their understanding of heart block physiology.
⏱ Timestamps:
00:00 – Introduction: Mobitz I and Cardiac Ischemia
00:08 – ECG Example: Inferior MI with Right Coronary Artery (RCA) Involvement
00:38 – Identifying Regularly Irregular Rhythm (Mobitz I)
01:07 – Finding Hidden P-Waves in Prominent T-Waves
02:03 – Analyzing PR Interval: Progressive Lengthening
02:41 – Confirming Mobitz I: Drop Beats & Narrow QRS Complexes
03:21 – Pathophysiology: Why Ischemia Causes AV Node Dysfunction
03:46 – AV Node Action Potential & Role of L-Type Calcium Channels
05:47 – Decremental Fatigue of Calcium Channels & Progressive PR Interval Prolongation
06:44 – Why Ischemia Impairs the Na⁺/K⁺ ATPase Pump
08:01 – Consequences of Sodium-Potassium Pump Failure & Ion Imbalance
09:35 – Reversal of Na⁺/Ca²⁺ Exchanger (NCX): Cellular Consequences
11:01 – Impact on Resting Membrane Potential & Conduction
12:45 – How Cellular Dysfunction Leads to Progressive AV Node Fatigue & Dropped Beats
13:32 – Additional Complications: Cell Swelling & Channel Dysfunction
14:30 – Clinical Implications & Why Mobitz I Can Indicate Serious Underlying Ischemia
15:03 – Key Takeaways & Summary of Pathophysiology
You’ll also gain a clear understanding of the pathophysiology behind ischemia-induced conduction issues, including:
How ischemia reduces ATP, impairing Na⁺/K⁺ pumps and Na⁺/Ca²⁺ exchangers.
Why L-Type Calcium Channels become decrementally fatigued, causing progressive conduction delays.
The cellular impact, including cell swelling, altered resting membrane potentials, and impaired conduction through the AV node.
Ideal for medical students, cardiology fellows, nurses, and anyone looking to deepen their understanding of heart block physiology.
⏱ Timestamps:
00:00 – Introduction: Mobitz I and Cardiac Ischemia
00:08 – ECG Example: Inferior MI with Right Coronary Artery (RCA) Involvement
00:38 – Identifying Regularly Irregular Rhythm (Mobitz I)
01:07 – Finding Hidden P-Waves in Prominent T-Waves
02:03 – Analyzing PR Interval: Progressive Lengthening
02:41 – Confirming Mobitz I: Drop Beats & Narrow QRS Complexes
03:21 – Pathophysiology: Why Ischemia Causes AV Node Dysfunction
03:46 – AV Node Action Potential & Role of L-Type Calcium Channels
05:47 – Decremental Fatigue of Calcium Channels & Progressive PR Interval Prolongation
06:44 – Why Ischemia Impairs the Na⁺/K⁺ ATPase Pump
08:01 – Consequences of Sodium-Potassium Pump Failure & Ion Imbalance
09:35 – Reversal of Na⁺/Ca²⁺ Exchanger (NCX): Cellular Consequences
11:01 – Impact on Resting Membrane Potential & Conduction
12:45 – How Cellular Dysfunction Leads to Progressive AV Node Fatigue & Dropped Beats
13:32 – Additional Complications: Cell Swelling & Channel Dysfunction
14:30 – Clinical Implications & Why Mobitz I Can Indicate Serious Underlying Ischemia
15:03 – Key Takeaways & Summary of Pathophysiology
- Category
- Cardiology

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