Blood PCO2 & Breathing
PCO2 importance:
Crucial for maintaining blood pH balance.
Low PCO2, called hypocapnia, arises from hyperventilation, potentially leading to respiratory alkalosis.
High PCO2, termed hypercapnia, occurs during hypoventilation, increasing blood acidity and possibly causing respiratory acidosis.
Oxygen Partial Pressure (PO2):
Must decrease to approximately half of normal levels before it begins to significantly affect ventilation rates.
Breathing Regulation
Automatic Breathing:
Primarily controlled by a rhythmicity center located in the medulla oblongata.
This rhythmic breathing pattern is influenced by the pons and sensory feedback from the body’s chemoreceptors.
Conscious Breathing:
Governed by voluntary control from the cerebral cortex, enabling purposeful alterations in breathing rate and depth.
Automatic Breathing Influences
Chemoreceptor Types:
These receptors monitor both blood and cerebrospinal fluid (CSF) for pH levels, PCO2, and PO2.
Central Chemoreceptors:
Located in the medulla oblongata.
Highly sensitive to H+ concentration changes due to rising CO2 levels in CSF.
Peripheral Chemoreceptors:
Situated in the aortic and carotid bodies.
Directly respond to H+ changes in blood caused by elevated CO2 levels.
Central Chemoreceptors
PCO2 Increase Response:
An increase in arterial PCO2 causes an initial rise in CSF PCO2, resulting in a decreased pH.
This triggers increased ventilation to expel excess CO2.
The response time is typically within minutes and accounts for 70-80% of the increase in ventilation with rising CO2 levels.
Note that H+ ions cannot cross the blood-brain barrier.
Peripheral Chemoreceptors
Location:
Found in the aortic arch and carotid arteries.
Rapid Response to Blood pH Changes:
Respond quickly to decreased pH levels caused by elevated CO2, facilitating immediate adjustments in ventilation rates.
Blood Oxygen Content
Oxygen and Hemoglobin:
A significant majority of oxygen (O2) binds to hemoglobin (Hb), which critically increases the blood’s overall O2 carrying capacity.
Oxygen Saturation:
Determined by PO2 levels: Higher PO2 corresponds to a higher percentage of hemoglobin saturation with O2.
Total Blood O2 Content:
Total oxygen content is calculated by adding plasma O2 with Hb-bound O2.
Oxyhemoglobin Saturation
Definition:
Refers to the percentage of hemoglobin in the form of oxyhemoglobin compared to the total hemoglobin available.
Measurement of Lung Function:
Typical saturation levels are around 97% in arterial blood and approximately 75% in venous blood.
Oxygen Loading & Unloading
Loading:
Occurs in the lungs where oxygen is absorbed into the bloodstream.
Unloading:
Takes place in tissues where oxygen is released from hemoglobin for cellular use.
Factors Affecting Affinity:
High PO2 in the lungs favors increased loading of oxygen onto hemoglobin.
Low PO2 and higher CO2 concentrations in the tissues favor increased unloading of oxygen.
The bond strength between Hb and O2 is significant, with carbon monoxide interfering with this binding process.
Bohr Effect
Concept:
Describes the physiological phenomenon where O2 delivery to muscles is enhanced during periods of physical activity.
Rightward Shift in Curve:
Indicates decreased Hb-O2 affinity, promoting O2 unloading during conditions of lower pH, increased PCO2, and raised temperature.
Leftward Shift in Curve:
Reflects increased Hb-O2 affinity, hindering O2 unloading seen in higher pH, lower PCO2, and reduced temperature.
2,3-DPG and Oxygen Transport
Role of 2,3-Diphosphoglycerate (2,3-DPG):
Produced by red blood cells during glycolysis, especially in states of low oxygen availability.
Shifts the Hb-O2 dissociation curve to the right, consequently decreasing the affinity of hemoglobin for oxygen.
Clinical Importance:
Increased levels of 2,3-DPG are commonly associated with conditions such as high altitude adaptations and anemia.
CO2 Transport
Forms of CO2 in Blood:
Dissolved CO2 accounts for 5-9% of total CO2 in blood.
Approximately 20% is bound to hemoglobin, while 70% is converted to bicarbonate ions (HCO3-).
Carbonic Anhydrase Function:
Catalyzes the conversion of carbon dioxide and water into carbonic acid (H2CO3) within red blood cells.
Chloride and Reverse Chloride Shifts
Chloride Shift in Tissues:
Elevated CO2 levels initiate the formation of H+ and HCO3-, with H+ ions contributing to the Bohr effect.
The bicarbonate ion (HCO3-) then diffuses out of red blood cells while chloride (Cl-) ions enter.
Reverse Chloride Shift in Lungs:
As CO2 exits the blood, H+ and HCO3- recombine to form CO2 for expulsion.
This causes chloride ions to diffuse out of red blood cells back into the plasma.
Clinical Conditions
Emphysema:
Characterized by the destruction of alveoli leading to decreased gas exchange surface area.
Often linked to smoking, which exacerbates inflammation and alveolar destruction.
Chronic Obstructive Pulmonary Disease (COPD):
Encompasses chronic inflammation and the gradual narrowing of airways, resulting in alveolar damage.
Frequently initiated by smoking, which promotes excess mucus production and provokes inflammation by immune cells.