Anatomy & Physiology
Active Transport in the Heart
Electrical Signals, Sodium-Potassium Pumps,
and Refractory Periods
2

What Does the Heart Do?

  • The heart is a muscular pump that circulates blood throughout the entire body
  • Blood delivers oxygen and nutrients to every tissue and organ
  • Blood carries carbon dioxide and waste products away from tissues
  • The heart must contract in a coordinated, rhythmic pattern — the right sequence at the right time
  • An average adult heart beats 60–100 times per minute, pumping ~5 L of blood per minute at rest
Both sides of the heart work together: the right side sends blood to the lungs; the left side sends oxygenated blood to the body.
Right Atrium Left Atrium Right Ventricle Left Ventricle ↑ O₂-rich to body ↓ O₂-poor from body
Source: Tortora & Derrickson, Principles of Anatomy and Physiology, 15th ed.
3

How Does the Heart Know When to Beat?

  • Each heartbeat is triggered by an electrical signal — no external nerve is required
  • The sinoatrial (SA) node acts as the heart's natural pacemaker, firing 60–100 times/min
  • Signal spreads through both atria, causing them to contract
  • Signal reaches the atrioventricular (AV) node, which adds a brief delay
  • Signal travels through the Bundle of His → Bundle Branches → Purkinje fibers to contract both ventricles
The AV node delay (~0.1 s) lets the atria finish emptying into the ventricles before ventricular contraction begins.
SA Node (Pacemaker) AV Node (Delay) Bundle of His L Branch R Branch Purkinje Fibers
Source: American Heart Association; Guyton & Hall, Medical Physiology, 14th ed.
4

Electrical Activity in Cardiac Cells

  • Cardiac cells generate electrical signals by moving charged particles (ions) across their membranes
  • The resting membrane voltage is about −90 mV — the inside is more negative than the outside
  • When ion channels open, ions flow along their gradients, changing membrane voltage
  • This voltage change is called an action potential
Na⁺ Sodium K⁺ Potassium Ca²⁺ Calcium
Na⁺ — high outside, flows IN → causes depolarization
K⁺ — high inside, flows OUT → causes repolarization
Ca²⁺ — triggers muscle contraction during the plateau phase
OUTSIDE CELL INSIDE CELL Channel Na⁺ Na⁺ K⁺ K⁺ Ca²⁺ −90 mV Phospholipid bilayer (cell membrane)
Source: Costanzo, Physiology, 6th ed.; NIH National Heart, Lung, and Blood Institute
5

What Is Active Transport?

  • Passive transport: substances move from high to low concentration — no energy required (e.g., simple diffusion)
  • Active transport: substances are moved from low to high concentration — requires cellular energy (ATP)
  • Active transport uses protein pumps embedded in the cell membrane
  • These pumps allow cells to maintain specific ion concentrations on each side of the membrane
  • Without active transport, ion gradients would gradually disappear
Passive
High → Low concentration
No ATP needed
Active
Low → High concentration
ATP required
PASSIVE ACTIVE PUMP ATP cell membrane
Source: Silverthorn, Human Physiology, 8th ed.; Khan Academy Biology
6

Active Transport in the Heart

  • Active transport maintains the correct concentrations of Na⁺, K⁺, and Ca²⁺ inside and outside cardiac cells
  • These ion gradients are essential for:
Establishing the resting membrane potential (−90 mV)
Creating electrical impulses (action potentials)
Allowing cardiac muscle contraction
Resetting the cell after each heartbeat
Without active transport, ion gradients disappear → cardiac cells cannot generate normal electrical signals
Nucleus Mitoch. ATP → High Na⁺ outside Low K⁺ outside High K⁺ inside Low Na⁺ inside Na/K pump
Source: Guyton & Hall, Medical Physiology, 14th ed.; NIH NHLBI
7

The Sodium-Potassium Pump (Na⁺/K⁺ ATPase)

  1. 1
    Three Na⁺ ions inside the cell bind to the pump protein
  2. 2
    ATP provides energy, causing the pump to change shape
  3. 3
    The three Na⁺ ions are released outside the cell
  4. 4
    Two K⁺ ions from outside the cell bind to the pump
  5. 5
    The pump returns to its original shape
  6. 6
    The two K⁺ ions are released inside the cell
3 Na⁺ OUT  |  2 K⁺ IN  |  1 ATP used per cycle
This pump is electrogenic — moving more positive charges out than in creates a net negative charge inside the cell.
Na⁺/K⁺ ATPase ATP Na⁺ Na⁺ Na⁺ Na⁺ K⁺ K⁺ K⁺ K⁺ — OUTSIDE CELL — — INSIDE CELL —
Source: Alberts et al., Molecular Biology of the Cell, 7th ed.; Guyton & Hall, Medical Physiology
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Why Is the Na⁺/K⁺ Pump Important?

  • High Na⁺ concentration outside → drives Na⁺ influx during depolarization
  • High K⁺ concentration inside → drives K⁺ efflux during repolarization
  • The negative resting membrane potential (−90 mV) of cardiac cells
  • The ion gradients needed for repeated action potentials
  • Enables the cycle: depolarize → contract → repolarize → relax → repeat
Clinical Note: Abnormal Na⁺/K⁺ pump function can interfere with cardiac electrical activity and contribute to cardiac arrhythmias (irregular heartbeats).
Example: Digoxin inhibits this pump and is used carefully to treat heart failure — but overdose can trigger dangerous arrhythmias.
Depolarize Contract Repolarize Reset Na⁺/K⁺ Pump ATP
Source: Rang & Dale's Pharmacology, 9th ed.; American Heart Association
9

Cardiac Action Potential

Phase 0 — Depolarization: Na⁺ channels open → Na⁺ rushes in → voltage rapidly rises
Phase 1 — Early Repolarization: Na⁺ channels close; some K⁺ channels briefly open
Phase 2 — Plateau: Ca²⁺ channels open → Ca²⁺ enters; triggers muscle contraction
Phase 3 — Repolarization: K⁺ channels open → K⁺ leaves → voltage falls
Phase 4 — Resting Potential: Na⁺/K⁺ pump restores ion balance (−90 mV)
+30 0 −90 0 1 2 3 4 Membrane Voltage Time → Na⁺ in Ca²⁺ in K⁺ out
Source: Costanzo, Physiology, 6th ed.; Guyton & Hall, Medical Physiology, 14th ed.
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What Is a Refractory Period?

  • A refractory period is the time after an action potential during which the cell is unable — or less able — to respond to another stimulus
  • Refractory periods prevent cardiac cells from being continuously stimulated
  • The heart must have time to contract, relax, and refill with blood before the next beat
  • The cardiac refractory period lasts ~200–300 milliseconds — almost as long as the contraction itself
  • There are two types: Absolute Refractory Period and Relative Refractory Period
Absolute
No new AP possible
Relative
AP possible with stronger stimulus
Unlike skeletal muscle, the heart cannot tetanize (sustain constant contraction). Refractory periods make this impossible — protecting the heart.
Source: Silverthorn, Human Physiology, 8th ed.; Berne & Levy Physiology, 7th ed.
11

Absolute Refractory Period

  • The cell cannot produce another action potential, regardless of stimulus strength
  • Most fast Na⁺ channels are inactivated (closed and unable to reopen immediately)
  • Corresponds to Phases 0, 1, 2, and early Phase 3 of the action potential
  • Duration: approximately 200–250 ms in ventricular muscle
Prevents another contraction from starting too soon
Prevents cardiac tetanus (sustained contraction)
Ensures the heart has time to relax and fill before next contraction
Maintains a coordinated, rhythmic heartbeat
+30 0 −90 ABSOLUTE REFRACTORY PERIOD 0 1 2 3 4 Time →
Source: Guyton & Hall, Medical Physiology, 14th ed.; Costanzo, Physiology, 6th ed.
12

Relative Refractory Period

  • A new action potential may occur, but requires a stronger-than-normal stimulus
  • Some Na⁺ channels have recovered; the membrane is partially repolarized
  • Corresponds to late Phase 3 of the action potential
  • The resulting action potential may be smaller or abnormal
An unusually strong stimulus during this period may cause an early (premature) or abnormal heartbeat
Clinical: the "R-on-T phenomenon" — a premature beat landing on the T wave — can trigger ventricular fibrillation
+30 0 −90 RELATIVE REFRAC. Absolute Refractory 0 1 2 3 4 Time →
Source: Guyton & Hall, Medical Physiology, 14th ed.; American Heart Association
13

Absolute vs. Relative Refractory Period

Feature Absolute Refractory Period Relative Refractory Period
New Action Potential? No — impossible Possible with stronger stimulus
Stimulus Required None can trigger AP Supranormal (stronger than normal)
Na⁺ Channel State Open or inactivated — cannot reopen Some channels have recovered
Phase of AP Phases 0, 1, 2, early Phase 3 Late Phase 3
Duration (approx.) ~200–250 ms ~50–75 ms
Primary Function Prevents premature contractions; protects from tetanus Transition back to excitability
Risk Low — heart is fully protected Higher — vulnerable to premature beats
Source: Costanzo, Physiology, 6th ed.; Silverthorn, Human Physiology, 8th ed.
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Why Refractory Periods Are Important

  • Prevent continuous cardiac muscle contraction — the heart needs to relax to refill with blood
  • Allow the chambers to relax and fill between beats (diastole)
  • Separate contractions — keeping each beat distinct and effective
  • Support coordinated electrical conduction through the heart
  • Reduce the chance of dangerously rapid stimulation and life-threatening arrhythmias
The relative refractory period is a window of vulnerability — stimulation here may cause premature beats or abnormal rhythms (e.g., the R-on-T phenomenon).
AEDs work in part by resetting refractory periods across all cardiac cells — restoring synchronized rhythm from fibrillation.
Refractory Relative Premature? Beat 1 Refrac. Beat 2 ECG-like Waveform Refractory zones separate each beat Absolute Relative
Source: American Heart Association; Guyton & Hall, Medical Physiology, 14th ed.
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Summary

The heart uses electrical signals to coordinate each heartbeat
Ion movement across cardiac membranes creates these electrical signals
Active transport uses ATP to maintain critical ion gradients
The Na⁺/K⁺ pump moves 3 Na⁺ out and 2 K⁺ in per ATP molecule
The absolute refractory period prevents any new action potential from occurring
The relative refractory period allows AP only with a supranormal stimulus
Ion Gradients
Na⁺/K⁺ pump
Electrical Signal
Action Potential
Heart
Contraction
Refractory
Period
Cell
Recovery
Next
Heartbeat
References: Tortora & Derrickson, Principles of Anatomy & Physiology, 15th ed. | Guyton & Hall, Medical Physiology, 14th ed. | Costanzo, Physiology, 6th ed. | Silverthorn, Human Physiology, 8th ed. | Alberts et al., Molecular Biology of the Cell, 7th ed. | American Heart Association (heart.org) | NIH National Heart, Lung, and Blood Institute (nhlbi.nih.gov) | Rang & Dale's Pharmacology, 9th ed.
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