• Partial Pressures of O₂ and CO₂ in the body (normal, resting conditions):

• Alveoli
  • PO₂ = 100 mm Hg
  • PCO₂ = 40 mm Hg
• Alveolar capillaries
  • Entering the alveolar capillaries
    • PO₂ = 40 mm Hg (relatively low because this blood has just returned from the systemic circulation & has lost much of its oxygen)
    • PCO₂ = 45 mm Hg (relatively high because the blood returning from the systemic circulation has picked up carbon dioxide) 

• While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from the alveoli into the blood & carbon dioxide from the blood into the alveoli.

• Leaving the alveolar capillaries
  • PO₂ = 100 mm Hg
  • PCO₂ = 40 mm Hg
• Blood leaving the alveolar capillaries returns to the left atrium & is pumped by the left ventricle into the systemic circulation. This blood travels through arteries & arterioles and into the systemic, or body, capillaries. As blood travels through arteries & arterioles, no gas exchange occurs.
• • Entering the systemic capillaries
    • PO₂ = 100 mm Hg
    • PCO₂ = 40 mm Hg
  • Body cells (resting conditions)
    • PO₂ = 40 mm Hg
    • PCO₂ = 45 mm Hg
• Because of the differences in partial pressures of oxygen & carbon dioxide in the systemic capillaries & the body cells, oxygen diffuses from the blood & into the cells, while carbon dioxide diffuses from the cells into the blood.
• • Leaving the systemic capillaries
    • PO₂ = 40 mm Hg
    • PCO₂ = 45 mm Hg
• Blood leaving the systemic capillaries returns to the heart (right atrium) via venules & veins (and no gas exchange occurs while blood is in venules & veins). This blood is then pumped to the lungs (and the alveolar capillaries) by the right ventricle.

Characteristics of Facilitated Diffusion & Active Transport - both require the use of carriers that are specific to particular substances (that is, each type of carrier can 'carry' one type of substance) and both can exhibit saturation (movement across a membrane is limited by number of carriers & the speed with which they move materials

Hyperventilation

1. Treatments :Rebreath air, hold breath (Increase CO₂)
   Give oxygen for Hypoxemia

Basic Properties of Gases

A.    Dalton's Law of Partial Pressures

1.    partial pressure - the "part" of the total air pressure caused by one component of a gas 

     Gas            Percent            Partial Pressure (P)
    ALL AIR        100.0%                760 mm Hg
    Nitrogen       78.6%                   597 mm Hg    (0.79 X 760)
    Oxygen          20.9%                l59 mm Hg    (0.21 X 760)
    CO₂              0.04%                  0.3 mm Hg    (0.0004 X 760) 

2.    altitude - air pressure @ 10,000 ft = 563 mm Hg
3.    scuba diving - air pressure @ 100 ft = 3000 mm Hg

B.    Henry's Law of Gas Diffusion into Liquid

1.    Henry's Law - a certain gas will diffuse INTO or OUT OF a liquid down its concentration gradient in proportion to its partial pressure

2.    solubility - the ease with which a certain gas will "dissolve" into a liquid (like blood plasma)

HIGHest solubility in plasma            Carbon Dioxide
                                                      Oxygen
                                        
LOWest solubility in plasma             Nitrogen

C.    Hyperbaric (Above normal pressure) Conditions

1.    Creates HIGH gradient for gas entry into the body

2.    therapeutic - oxygen forced into blood during: carbon monoxide poisoning, circulatory shock, asphyxiation, gangrene, tetanus, etc.

3.    harmful - SCUBA divers may suffer the "bends" when they rise too quickly and Nitrogen gas "comes out of solution" and forms bubbles in the blood

The Body Regulates pH in Several Ways

• Buffers are weak acid mixtures (such as bicarbonate/CO₂) which minimize pH change
  • Buffer is always a mixture of 2 compounds
    • One compound takes up H ions if there are too many (H acceptor)
    • The second compound releases H ions if there are not enough (H donor)
  • The strength of a buffer is given by the buffer capacity
    • Buffer capacity is proportional to the buffer concentration and to a parameter known as the pK
  • Mouth bacteria produce acids which attack teeth, producing caries (cavities). People with low buffer capacities in their saliva have more caries than those with high buffer capacities.
• CO₂ gas (a potential acid) is eliminated by the lungs
• Other acids and bases are eliminated by the kidneys

Hemostasis - the  stopping of the blood. Triggered by a ruptured vessel wall it occurs in several steps:

1) vascular spasm - most vessels will constrict strongly when their walls are damaged. This accounts for individuals not bleeding to death even when limbs are crushed. It also can help to enhance blood clotting in less severe injuries.

2) platelet plug - platelets become sticky when they contact collagen, a protein in the basement membrane of the endothelium exposed when the vessel wall is ruptured. As they stick together they can form a plug which will stem the flow of blood in minor vessels.

3) Formation of the Blood Clot:

A) release of platelet factors - as platelets stick together and to the vascular wall some are ruptured releasing chemicals such as thromboxane, PF3, ADP and other substances. These become prothrombin activators. Thromboxane also makes the platelets even stickier, and increases the vascular constriction. These reactions are self perpetuating and become a cascade which represents a positive feedback mechanism.

B) prothrombin activators : prothrombin (already in the blood) is split into smaller products including thrombin, an active protease.

C) thrombin splits soluble fibrinogen, already present in the plasma, into monomers which then polymerize to produce insoluble fibrin threads. The fibrin threads weave the platelets and other cells together to form the actual clot. This occurs within four to six minutes when the injury is severe and up to 15 minutes when it is not. After 15 minutes the clot begins to retract as the fibrin threads contract, pulling the broken edges of the injury together and smoothing the surface of the clot causing the chemical processes to cease. Eventually the clot will dissolve due to enzymes such as plasmin also present in the blood.

The extrinsic pathway: when tissues are damaged the damaged cells release substances called tissue thromboplastin which also acts as a prothrombin activator. This enhances and speeds coagulation when tissue damage is involved.

Anti-thrombin III - this factor helps to prevent clotting when no trigger is present by removing any thrombin present. Its function is magnified many times when heparin is present. Therefore heparin is used clinically as a short-term anticoagulant.

Vitamin K - stimulates the production of clotting factors including prothrombin and fibrinogen in the liver. This vitamin is normally produced by bacteria in the colon. Coumarin (or coumadin) competes with Vitamin K in the liver and is used clinically for long-term suppression of clotting.

Several factors important to clotting are known to be absent in forms of hemophilia. These factors are produced by specific genes which are mutated in the deficient forms. The factors are  VIII, IX, and XI.

Calcium is necessary for blood clotting and its removal from the blood by complexing with citrate will prevent the blood from clotting during storage