Pathophysiology of Tachy Arrhythmias - Edubirdie

University:
Camosun College
Course:
BIOL 252 | Pathophysiology for Nursing 1
Academic year:

2024
Views:

441

Pages:

1
Author:

Aysha A.

Tachyarrhythmias Pathophysiology Enhanced automaticity Triggered activity Reentry SA node, AV node, Bundle of His, Purkinje cells, Coronary sinus, Pulmonary veins are all auto-excitable cells. 1. Sympathetic activity: ↑ β1 activity → ↑ Tachy of L-type Ca2+ channels Funny channels 2. Hypokalemia, Ischemia: No extracellular fluid (ECF) [K+] ↓ Na+-K+-ATPase ↓ in repolarization → Na+ can't be thrown out. 3. Mild hyperkalemia: Leaky K+ channels → Can't throw K+ out ↑ firing rate → More +ve resting membrane potential (RMP) → K+ accumulation In severe hyperkalemia, adaptation occurs ultimately leading to cardiac arrest. 4. Warmup effect: A person is bradycardiac for a long period → Na+-K+ ATPase ↓ Na+ levels inside the cell, interfering with the current. 5. Overactive suppressions: Ectopic pacemakers & activities are formed as a result of suppression of SA node.

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