3B: Internal Respiration & Gas Transport in Blood

Higher → Lower partial pressures

What the net movement of gas is dependent on.

100 mmHg

The PO₂ of oxygenated blood.

40 mmHg

The PO₂ in tissue.

Plasma → Tissues

The net movement of O₂ within plasma & tissues.

40 mmHg

The PCO₂ of oxygenated blood.

45 mmHg

The PCO₂ in tissue.

Tissues → Plasma

The net movement of CO₂ within plasma & tissues.

Gas Transport

The process of blood carrying O₂ & CO₂ in the blood.

Centrifugation

The process which forms the layers of the blood.

• Plasma

• WBCs & Platelets

• RBCs

The 3 main layers of centrifuged blood.

• Proteins

• Water

• Other solutions

The 3 components that make up plasma.

• Gas pressures found within the plasma

• The difference between the 2 media

2 things that gas exchange relies on.

PO₂/PCO₂ Gradient

The gradient that drives gas exchange across the membrane.

High PO₂ & Low PCO₂

The ratio of PO₂ & PCO₂ in alveolar space.

Low PO₂ & High PCO₂

The ratio of PO₂ & PCO₂ in venous blood.

Hemoglobin

The transport taxis in RBCs which carry O₂ after it enters the blood.

Bicarbonate (HCO₂^-)

The form in which most CO₂ is carried in in plasma.

4 O₂ molecules

The number of O₂ molecules 1 Hb molecule can bind.

Fe₂⁺ & porphyrin ring

The 2 components that make up each of the 4 haem groups or the 4 non-protein components of 1 Hb molecule.

2 alpha chains & 2 beta chains

The 4 protein components or 4 “globin” chains of 1 hb molecule.

O₂ is non polar & water is strongly polar

The reason why O₂ does not dissolve easily (long term) in plasma.

Plasma alone cannot carry enough O₂ for normal tissue demands

The problem which arises when there is not an O₂ carrier present in plasma.

Reversible & Loose

The nature of the binding of O₂ with Hb (Fe₂⁺).

1. Deoxyhemoglobin → pulmonary capillaries

2. Gas exchange happens (Fick’s Law) VIA O₂ partial pressure difference

3. O₂ in the capillaries first dissolves in plasma → post alveolar capillary PO₂ rises

   1. O₂ cannot stay in the plasma since it is non-polar

4. O₂ diffuses into RBCs & binds reversibly with Hb

5. Hb is transformed into oxyhemoglobin & PO₂ approaches alveolar PO₂

The 5 general steps of O₂ gas exchange to transport.

PO₂

The generic term for pressure exerted by gas.

PAO₂

The term for alveolar PO₂.

PcO₂

The term for pulmonary capillary PO₂.

PaO₂

The term for systemic arterial PO₂.

PvO₂

The term for venous PO₂.

PaO₂

The partial pressure of dissolved O₂ in the arteries. How much dissolved O₂ is exerting pressure in arterial blood.

60 - 100 mmHg

Normal PaO₂ levels.

Arterial Blood Gas (ABG)

What is directly used to clinically measure PaO₂. Indirectly measures SO₂.

SO₂

The term for hemoglobin O₂ saturation. The general term that indicates what percentage of Hb O₂-binding sites are occupied by O₂.

95 - 100%

Normal SO₂ levels in the arteries, also denoted by SaO₂.

All Hb in our body is normally bound with O₂ at rest

The implication of SaO₂ being normally 95 - 100%.

The higher the partial pressure the higher the saturation

The relationship of partial pressure PaO₂ & SaO₂.

Amount of O₂ bound to hemoglobin + Amount of O₂ dissolved in plasma

The formula for CaO₂.

Oxygen-Hemoglobin Dissociation Curve

How PO₂ controls hemoglobin saturation.

Relationship between PO₂ & hemoglobin O₂ saturation (SO₂)

What the O₂-Hb dissociation curve shows.

1. As PO₂ rises, more O₂ binds to Hb (external lung respiration)

2. As PO₂ falls, Hb releases O₂ (internal tissue respiration)

3. Sigmoidal not linear curve

3 key points of the O₂-Hb dissociation curve.

Cooperative Binding

What the sigmoidal shape of the O₂-Hb dissociation curve reflects.

O₂ binding to one hb subunit allosterically changes hb’s chape, shifting it towards a higher affinity shape to allow O₂ to bind easier.Loading hb state

How PO₂ reflects cooperative binding when it increases.

O₂ released from one hb subunit leads hb to shift to towards a lower-affinity shape, favoring O₂ release. Unloading hb state

How PO₂ reflects cooperative binding when it decreases.

Allows hb to load O₂ efficiently in the lungs while releasing it readily in tissues

How cooperative binding ultimately influence hb and O₂.

Protects O₂ loading in the lungs

The functional purpose of a non proportional fall of hb saturation in response to a moderate fall in arterial PO₂ at 60 - 100 mmHg.

Hb does not immediately let go of O₂ despite lessened PO₂, it will still load

The reason why asthma does not make a person’s tissues become immediately starved of O₂.

Allows hb to let go during internal respiration

The functional reason for a small fall in tissue PO₂ causing a large amount of O₂ to unload from hb.

1. PCO₂ level

2. Acidity (pH) of blood

3. 2,3-Biphosphoglycerate (BPG) level

4. Temperature

4 factors that influence hb’s affinity with O₂ besides PO₂.

Increased affinity for O₂ (Holds tight)

The interpretation of the O₂-hb dissociation curve shifting to the left.

Decreased affinity for O₂ (Lets go)

The interpretation of the O₂-hb dissociation curve shifting to the right.

Indirect

The relationship of

1. PCO₂ level

2. Acidity (pH) of blood

3. 2,3-Biphosphoglycerate (BPG) level

4. Temperature

with O₂ affinity

High PCO₂ makes Hb undergo a conformational change that favors O₂ unloading

The reason why higher PCO₂ levels cause a right shift & lower hb-O₂ affinity.

More H+ ions stabilizes the low affinity configuration of Hb, encouraging O₂ release into acidic/active tissues

The reason why lower pH in the blood cause a right shift & lower hb-O₂ affinity.

Biphosphoglycerate (BPG)

A molecule formed in the cells whenever they break down glucose in a process called glycolysis.

When there is low O₂ in the tissues

When higher 2,3-BPG synthesis is triggered.

Indicates increased tissue metabolism which destabilizes Hb-O₂ binding making O₂ easier to release to active tissues

The reason why higher temperature causes a right shift & lower hb-O₂ affinity.

Bohr Effect

The term which describes the joint effect of increased PCO₂ & increased H+ (acidic pH) lowering Hb-O₂ affinity.

Increased metabolism → Increased CO₂ + H⁺ → Right shift → Lower Hb affinity → Increased O_2, unloading

The process of increased O₂ unloading in active tissue due to the Bohr effect

It is polar

The reason why CO₂ dissolves easily in plasma.

Bicarbonate

The form in which CO₂ is converted to when it is transported in plasma.

Converted to bicarbonate which is dissolved in plasma, not bound to hb

The fate of most CO₂ in the circulatory system

1. Cells produce CO₂ through metabolism (Tissue PCO₂ > Capillary plasma PCO₂)

2. Co₂ diffuses from tissues into systemic capillary blood down its partial-pressure gradient

3. It first enters the dissolved CO₂ in plasma, then readily enters RBCs

4. Most CO₂ is converted to carbonic acid inside RBCs due to the carbonic anhydrase enzyme

5. Carbonic acid immediately dissociates into HCO₃^- & H+ ions

6. H+ & hb bind together inside the RBC & HCO₃^- diffuses out from the RBC to the plasma whilst Cl^- enters the RBC in exchange through the chloride shift

The 6 general steps of CO₂ gas exchange to transport.

Carbonic Anhydrase

The enzyme that converts CO₂ into carbonic acid inside the RBCs.

HCO₃^- & H+ ions

The 2 molecules that carbonic acid immediately dissociates into.

Chloride shift

The name for the process wherein HCO₃^- diffuses out from the RBC to the plasma whilst Cl^- in the process enters in exchange.

Maintenance of electrical neutrality during CO₂ transport

The relevance of a chloride shift occurring during CO₂ gas transport.

HCO₃^- re enters RBCs, regenerating CO₂ which diffuses out to plasma making the capillary PCO₂ > alveolar PCO₂ causing CO₂ to diffuse into alveoli and exhalation

What occurs when the bicarbonate in the plasma reaches the lungs during CO₂ gas transport.

Haldane Effect

The effect which describes how when O₂ binds hb in the lungs causing it to release H+ and drive bicarbonate back towards CO₂ so it can be exhaled.

Bound to Hb in RBCs

How O₂ is transported.

Bicarbonate in plasma

How CO₂ is transported.

Tissues needimg O₂

The main destination of O₂ transport.

Pulmonary Capillaries

The main destination of CO₂ transport.

• Increased heart rate

• Increased respiratory rate

• Conscious but confused

• Increased SpO₂

4 vital sign results that are aligned with carbon monoxide poisoning.

Pulse oximeter

A small device that clips onto a finger to measure the amount of O₂ saturation in the blood through infrared light through the finger.

May falsely identify Hb-CO as Hb-O₂

The main limitation of a pulse oximeter.

Co-oximetry

The gold standard means of investigating Carbon Monoxide poisoning that separately measures different forms of Hb. It detects more specifically what gas hb is attached to.

>20%

The co-oximetry reading range that is associated with carbon monoxide poisoning.

Instances where CO gas is chemically, spontaneously made and inhaled

The most common cause of CO poisoning.

CO binds very strongly to hemoglobin so it can no longer carry O₂ from the lungs to vital tissues leaving them starved

The pathophysiology of CO displacing O₂-Hb

1. Portable generator running in or near an enclosed or poorly ventilated house

2. Smoke inhalation during a house or building fire

3. Running motor vehicle in an enclosed or poorly ventilated garage

4. Charcoal burning in an enclosed room

5. Other fuel-burning engines or appliances used in enclosed spaces

5 causes of carbon monoxide poisoning.

Hypoxia

The condition wherein there is inadequate oxygen availability at the tissue level to meet cellular metabolic needs.

Hypoxemia

The condition wherein there is abnormally low oxygen tension, or PaO₂ in arterial blood.

Most Hb will hold Co but some can be bound with O₂, those Hb-O₂ will change behavior due to CO, specifically a left shift of the O₂ dissociation curve

The pathophysiology of CO making Hb hold O₂ too tightly.

Left shift

The effect of carbon monoxide poisoning on the O₂ dissociation curve.

Give 100% Oxygen

The management given to carbon monoxide poisoned patients after removal from exposure.

• Increases the inspired O₂

• Dramatically increases the PO₂ in plasma

• Forcibly displaces Co from hemoglobin

• Accelerates CO elimination

What giving 100% oxygen does to patients with carbon monoxide poisoning.