System physiology ch 10

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Last updated 2:36 AM on 3/27/26
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23 Terms

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Pacemaker cells

Start the heart beat

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Contractile cells

Pump the blood

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EKG

Records electrical activity

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2 types of Cardiac cells

A. pacemaker cells (autorhythmic)- Do not contract, set the rhythm, found in the conduction system (~ 1% of cells): self-excitable (no nervous system needed)

B. Contractile cells- make up most of the heart, responsible for pumping blood

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Analogy for 2 types of Cardiac cells

Pacemakers =”set” and Contractile = “squeeze”

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Conduction pathway (very high yield)

SA node→ AV node→ AV bundle (Bundle of His)→ Bundle branches → Purkinje fibers

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Analogy for Conduction pathway

SA→AV→Bundle→Branch→Purkinje or Start At A Very Big Bridge Path

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SA node key function

main pacemaker (~75 bpm)

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AV node key function

Delay (0.1 sec) → allows atria to contract first

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Bundle/Purkinje key function

spread signal to ventricles; whole process takes ~0.22 sec

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<p>Pacemaker cells: Action Potential (3 steps)</p>

Pacemaker cells: Action Potential (3 steps)

  1. Pacemaker potential- Na+ slowly enters→ K⁺ channels close→gradual rise

  2. Depolarization - Ca2+ enters→spike

  3. Repomarization - k+ leaves → back to negative

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<p>Contractile Cell Action Potential (Different) </p>

Contractile Cell Action Potential (Different)

  1. Depolarization → Na+ IN (fast)

  2. Plateau→ Ca2+ IN (keeps contraction going)

  3. Repolarization → K+ OUT

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Differences between Cardiac and skeletal AP

Cardiac AP lasts ~200 ms

Skeletal AP lasts 1–2 ms

Important because: Prevents tetany → ensures proper pumping

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EKG Waves (critical)

P Wave - Atrial depolarization

QRS Complex - Ventricular depolarization (Atrial repolarization hidden)

T Wave - Ventricular repolarization

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Important Intervals

P-R interval: atria → ventricles delay

S-T segment: ventricles fully depolarized

Q-T interval: total ventricular activity

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Clinical connections (common Exam points)

Abnormalities:

  • Ectopic focus → abnormal pacemaker

  • Heart block → AV node fails

  • Extrasystole → premature beat (caffeine/nicotine)

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EKG Clues:

  • Large R wave → enlarged ventricles

  • ST elevation/depression → ischemia

  • Long QT → arrhythmia risk

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Pacemaker Problems (Rhythm Origin Issues)

A. Ectopic Focus

Mechanism: Abnormal region starts firing instead of SA node

Effect: Irregular or premature beats

B. Junctional Rhythm (AV node takeover)

Cause: SA node fails

Rate: 40–60 bpm (slower than normal)

EKG:

No P waves (atria not properly activated)

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Conduction Problems (Signal Transmission Issues)

Heart Block (AV Node Dysfunction)

Mechanism:

Signal from atria → ventricles is delayed or blocked

Types:

Partial block: some signals pass

Complete block: no signals pass

Effect:

Atria and ventricles beat independently

Ventricles default to slow intrinsic rhythm (~30 bpm)

Treatment:

Artificial pacemaker

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Premature Beats (Extrasystole)

Mechanism:

Early depolarization from ectopic focus

Causes:

Caffeine

Nicotine

Effect:

Skipped beat sensation

Next beat feels stronger (“thud”)

Why?

More filling time → stronger contraction

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4. Dangerous Rhythm Disorder

Ventricular Fibrillation

Mechanism:

Chaotic, disorganized electrical activity

Effect:

No effective pumping → life-threatening

Causes:

Heart attack

Electrical shock

EKG:

Completely irregular, chaotic waves

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EKG Clinical Interpretation

A. Enlarged Ventricles

Finding: Large R waves

Meaning: Hypertrophy

B. Ischemia (low oxygen)

Finding:

ST segment ↑ or ↓

“ST = Stress Trouble”

C. Long QT Interval

Problem: Delayed repolarization

Risk: Dangerous arrhythmias

“Long QT = Quivering Threat”

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Homeostatic imbalance

Rhythm Problems:

Ectopic focus → abnormal beats

SA failure → AV takes over (no P waves)

Conduction Problems:

Heart block → atria & ventricles disconnected

Severe → needs pacemaker

EKG Red Flags:

Big R → enlarged heart

ST changes → ischemia

Long QT → arrhythmia risk

Emergency:

Ventricular fibrillation → no effective pumping

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