Physiology of Gasses of the Cardiovascular System
High-Yield Summary
- Gas/solute exchange happens at the capillaries, driven by blood pressure and concentration gradients (diffusion).
- Each hemoglobin molecule carries up to 4 O₂ (one per heme group), with cooperative binding — each successive O₂ binds more easily.
- Bohr effect: increased CO₂/H⁺ (lower pH), increased temperature, increased 2,3-DPG all shift the dissociation curve right — hemoglobin releases O₂ more readily.
- Fetal hemoglobin has a higher O₂ affinity than adult hemoglobin, helping it pull oxygen from maternal blood.
- CO₂ travels 3 ways: dissolved in plasma, bound to hemoglobin, and (mostly) converted to bicarbonate.
- Starling forces: hydrostatic pressure pushes fluid out (strongest at arteriole end); oncotic pressure pulls fluid in (dominant at venule end). Imbalance → edema, resolved by the lymphatic system.
- Coagulation: platelet aggregation at exposed collagen → clotting cascade → thrombin converts fibrinogen to fibrin → clot forms → plasmin (from plasminogen) dissolves it once healed.
Oxygen-Hemoglobin Dissociation Curve Shifts
| Right Shift (O₂ released more easily) | Left Shift (O₂ held more tightly) |
|---|---|
| Increased pCO₂ | Decreased pCO₂ |
| Increased [H⁺] (lower pH) | Decreased [H⁺] (higher pH) |
| Increased temperature | Decreased temperature |
| Increased 2,3-DPG | Decreased 2,3-DPG |
Three Forms of CO₂ Transport
- 1Dissolved directly in plasma (small amount).
- 2Bound to hemoglobin (not at the O₂-binding site).
- 3Converted to bicarbonate — CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (the majority, fully reversible; central to blood pH).
Starling Forces
| Hydrostatic Pressure | Oncotic Pressure |
|---|---|
| Force blood pushes against capillary walls | Created by plasma proteins (mainly albumin) |
| Pushes fluid OUT into tissue | Pulls fluid back IN to the capillary |
| Strongest at the arteriole end (~36 mmHg) | Dominant at the venule end (~25 vs. 15 mmHg) |
Coagulation
- 1Vessel injury exposes collagen; platelets adhere and activate — platelet aggregation recruits more platelets, forming a temporary plug.
- 2Clotting cascade triggered in parallel; ends with thrombin converting fibrinogen (soluble) into fibrin (insoluble mesh).
- 3Fibrin mesh stabilizes the platelet plug, sealing the breach.
- 4After healing, plasmin (activated from plasminogen embedded in the clot) digests fibrin and dissolves the clot.
Common MCAT Trap
- Fetal hemoglobin has a HIGHER O₂ affinity than adult hemoglobin — the opposite of what the Bohr effect's "more CO₂/H⁺ → less affinity" pattern might suggest applies universally.
- Edema results from a Starling-forces imbalance (too much fluid staying in tissue) — the lymphatic system, not the venous system, is what returns the extra fluid.
- Plasminogen is built into the clot early, then activated later as plasmin — it's not recruited fresh at resolution time.
Quick Recall
What four factors shift the oxygen-hemoglobin dissociation curve right?
What is the most significant form of CO₂ transport in blood?
What enzyme converts fibrinogen to fibrin, and what triggers it?
Which Starling force dominates at the venule end of a capillary?