Co2 dissociation curve with graph explain

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CO₂ Dissociation Curve

What It Is

The CO₂ dissociation curve plots the total CO₂ content of blood (in all forms) on the Y-axis against the partial pressure of CO₂ (PCO₂) on the X-axis. It describes how blood picks up CO₂ at the tissues and releases it at the lungs.

Graph 1 - The Basic CO₂ Dissociation Curve

From Guyton and Hall Textbook of Medical Physiology:

CO₂ dissociation curve showing CO₂ in blood (volumes %) vs gas pressure of CO₂ (mm Hg) with the normal operating range highlighted between 40-45 mm Hg

Key features of this curve:

The curve rises steeply at low PCO₂ values and flattens at high values (it is not sigmoidal like the O₂ curve, but more hyperbolic/linear in the physiologic range)
Normal arterial PCO₂ = 40 mm Hg → ~48 vol% CO₂ in blood
Normal venous PCO₂ = 45 mm Hg → ~52 vol% CO₂ in blood
Only 4 vol% of CO₂ is exchanged during one pass (tissues → lungs), even though total blood CO₂ is ~50 vol%

Compared to the O₂ dissociation curve, the CO₂ curve is much steeper and more linear in the physiologic working range, meaning small changes in PCO₂ produce relatively large changes in CO₂ content. - Murray & Nadel's Textbook of Respiratory Medicine

Graph 2 - CO₂ Dissociation Curve Showing All Three Forms

From Morgan & Mikhail's Clinical Anesthesiology (based on Nunn's Applied Respiratory Physiology):

CO₂ dissociation curve for whole blood showing bicarbonate (large orange area), carbamino CO₂ (green band), and dissolved CO₂ (thin red line) with normal arterial and venous points marked

This graph shows the three forms of CO₂ transport that make up the total CO₂ content:

Form	Contribution	Mechanism
Bicarbonate (HCO₃⁻)	~70%	CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (catalyzed by carbonic anhydrase in RBCs); HCO₃⁻ exits RBC via chloride shift
Carbaminohemoglobin	~20-30%	CO₂ binds directly to amine groups on Hb (and plasma proteins); loose bond, easily released at lungs
Dissolved CO₂	~5-10%	Physically dissolved in plasma; directly proportional to PCO₂

The large orange area = bicarbonate (dominant form)
The green/purple band at the top = carbamino CO₂ (venous vs. arterial difference)
The thin red line at the bottom = dissolved CO₂
Normal arterial point = PCO₂ 40 mm Hg, ~22 mmol/L
Normal mixed venous point = PCO₂ 45 mm Hg, ~24 mmol/L

Graph 3 - Effect of Oxygen Saturation (Haldane Effect)

From Murray & Nadel's Textbook of Respiratory Medicine:

Three CO₂ dissociation curves at different hemoglobin oxygen saturations (0%, 75%, 97.5% HbO₂) showing that deoxygenated blood carries more CO₂ at any given PCO₂; inset shows physiologic curve between arterial point (a) and mixed venous point (v)

This graph shows that the CO₂ dissociation curve shifts upward when hemoglobin is less saturated with O₂ - this is the Haldane Effect.

Graph 4 - The Haldane Effect Explained

From Guyton and Hall:

Graph showing two CO₂ dissociation curves at PO₂ = 40 mm Hg (dashed, tissues) and PO₂ = 100 mm Hg (solid, lungs), with point A in the tissues and point B in the lungs, demonstrating the Haldane shift doubles CO₂ release

The Haldane Effect

Point A (tissues): PCO₂ = 45 mm Hg, PO₂ = 40 mm Hg → 52 vol% CO₂ in blood
Point B (lungs): PCO₂ = 40 mm Hg, PO₂ = 100 mm Hg → 48 vol% CO₂ in blood
When O₂ binds Hb in the lungs, Hb becomes a stronger acid → this:
1. Reduces Hb's affinity for CO₂ as carbamate → displaces carbamino CO₂
2. Releases H⁺ → H⁺ + HCO₃⁻ → H₂CO₃ → CO₂ + H₂O → CO₂ driven out
Without the Haldane effect, only ~2 vol% CO₂ would be released in lungs; with it, ~4 vol% is released - the effect doubles CO₂ transport

Key Differences: CO₂ vs. O₂ Dissociation Curve

Feature	CO₂ Curve	O₂ Curve
Shape	Hyperbolic / nearly linear in physiol. range	Sigmoidal (S-shaped)
Steepness	Much steeper	Less steep
Arterial-venous difference (content)	Small (~4 vol%) despite small ΔP	Large despite similar ΔP
Arterial-venous ΔP	Small (40 → 45 mm Hg)	Large (100 → 40 mm Hg)
Effect of O₂ on curve	Haldane effect (O₂ shifts curve down)	Bohr effect (CO₂ shifts curve right)
Primary transport form	Bicarbonate (~70%)	Oxyhemoglobin (~97%)

Clinical Relevance

The steepness of the CO₂ curve in the physiologic range means that small changes in ventilation (PCO₂) produce large changes in CO₂ content - this is why hypercapnia develops quickly in hypoventilation
Acetazolamide (carbonic anhydrase inhibitor) impairs CO₂ transport, causing tissue PCO₂ to rise to ~80 mm Hg; used in altitude sickness to stimulate breathing
Arterial pH changes minimally (7.41 arterial → 7.37 venous) despite CO₂ loading at tissues, because bicarbonate acts as a buffer
CO₂ stores in the body are large (~120 L in adults), so a new CO₂ equilibrium after ventilation changes takes 20-30 minutes (vs. <5 min for O₂)

Sources: Guyton and Hall Textbook of Medical Physiology, p. 529-530 | Morgan & Mikhail's Clinical Anesthesiology, 7e, p. 970 | Murray & Nadel's Textbook of Respiratory Medicine, p. 305-306 | Fishman's Pulmonary Diseases and Disorders, p. 258

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