Respiratory Physiology Overview Quiz

The pressure exerted by a single gas in a mixture of gases. It's a measure of the concentration of that gas. For example, the partial pressure of oxygen (PO2) in the air we breathe is 159.6 mm Hg.

The total pressure of a gas mixture is equal to the sum of the partial pressures of each individual gas in the mixture.

Partial pressure of oxygen in the alveoli (tiny air sacs in the lungs). It's approximately 100 mm Hg, reflecting the pressure of oxygen that is available for diffusion into the blood.

The movement of oxygen across the respiratory membrane from the alveoli into the blood, driven by the difference in partial pressure (PO2 gradient).

Factors influencing the rate of oxygen diffusion into the blood: 1. PO2 gradient, 2. Functional surface area of the respiratory membrane, 3. Respiratory minute volume, 4. Alveolar ventilation.

The primary form in which carbon dioxide (CO2) is transported in the blood. It is formed when CO2 reacts with water inside red blood cells (RBCs), catalyzed by carbonic anhydrase. This reaction produces carbonic acid (H2CO3) which then dissociates into HCO3- and protons (H+).

The exchange of bicarbonate ions (HCO3-) leaving the RBC for chloride ions (Cl-) entering the RBC. This maintains electrical neutrality within the RBC as bicarbonate diffuses out to the blood plasma.

An enzyme present in red blood cells that catalyzes the reaction of CO2 with water to create carbonic acid (H2CO3). This reaction is reversible, meaning it can proceed in both directions depending on the concentrations of reactants and products.

The production of bicarbonate ions (HCO3-) and carbaminohemoglobin (HbCO2) results in the generation of protons (H+). This increase in H+ concentration lowers blood pH (increased acidity), indicating higher levels of CO2 in the blood.

The direction of the reaction between CO2 and water to form bicarbonate is determined by the partial pressure of CO2 (PCO2). When PCO2 is high, the reaction favors the production of bicarbonate. Conversely, when PCO2 is low, the reaction favors the breakdown of bicarbonate back to CO2 and water.

During metabolism, cells produce carbon dioxide (CO2), increasing its partial pressure (PCO2) in the tissues. This higher PCO2 then diffuses into the capillaries.

Elevated PCO2 in the blood triggers the formation of carbaminohemoglobin (CO2 bound to hemoglobin) and bicarbonate (HCO3-) ions. This helps buffer the blood's acidity.

At the lungs, the processes that formed carbaminohemoglobin and bicarbonate in the tissues reverse. CO2 is released from the blood and exhaled.

The primary regulator of blood gas balance is the adjustment of ventilation, or how much air we breathe in and out.

The nervous control of breathing is primarily found in the brainstem, specifically in the medulla, which houses both inspiratory and expiratory control centers.

The pons contains additional respiratory control centers that act as 'pattern generators' and 'controllers'. They help regulate the rhythm and depth of breathing.

Chemoreceptors are specialized cells that detect changes in blood chemistry, particularly levels of oxygen, carbon dioxide, and pH.

When chemoreceptors sense low oxygen (hypoxia), high carbon dioxide (hypercapnia), or increased acidity (lower pH), they send signals to the brain to increase breathing rate and depth.

Central chemoreceptors, responsible for regulating breathing, are located in the medulla oblongata of the brainstem. They are bathed in cerebrospinal fluid (CSF), not blood.

Central chemoreceptors are indirectly stimulated by CO2. CO2 diffuses from the blood into the CSF, where it reacts with water to form carbonic acid (H2CO3). This acid dissociates, releasing hydrogen ions (H+), which directly stimulate the chemoreceptors.

The blood-brain barrier, a protective membrane, is highly permeable to CO2, allowing it to readily diffuse into the CSF. However, it is less permeable to hydrogen ions (H+) and bicarbonate ions (HCO3-), limiting their passage.

In chronic conditions like COPD, where PCO2 is consistently elevated, blood buffers can diffuse into the CSF over time, reducing the change in pH. This leads to desensitization of the chemoreceptors, making them less responsive to CO2.

Central chemoreceptors are not directly responsive to changes in oxygen (O2) levels. Even with a significant drop in PaO2, the oxygen saturation (SaO2) may still be within a normal range.

Peripheral chemoreceptors, also involved in breathing regulation, are located in the carotid bodies (near the carotid arteries) and the aortic bodies (near the aorta).

Peripheral chemoreceptors are stimulated by decreased PaO2 (low oxygen levels), increased PCO2 (high carbon dioxide levels), and decreased arterial pH (acidity). This stimulation causes an increase in their firing rate.

While both central and peripheral chemoreceptors respond to changes in blood pH, their response to CO2 is different. Peripheral chemoreceptors respond directly to changes in blood pH due to increased CO2, whereas central chemoreceptors respond indirectly due to the buildup of H+ in the CSF.

The stimulation of breathing due to low oxygen levels in the blood. This is a backup system when the normal carbon dioxide (CO2) sensing system is compromised.

The responsiveness of the hypoxic drive to low oxygen levels. It increases when levels of carbon dioxide (CO2) in the blood are higher than normal (above 40 mmHg).

In chronic obstructive pulmonary disease (COPD), the hypoxic drive becomes especially important. Patients with COPD often rely on the hypoxic drive to breathe because their primary CO2-sensing system is weakened.

Giving oxygen to COPD patients can potentially worsen their condition by suppressing the hypoxic drive, leading to higher CO2 levels in the blood.

Conditions that reduce the total amount of oxygen in the blood (like carbon monoxide poisoning or anemia) but don't affect the amount of dissolved oxygen won't stimulate the hypoxic drive.

When neurons in the respiratory centers experience extreme oxygen deprivation, their function is impaired. This can lead to reduced or absent ventilation signals, ultimately decreasing or completely stopping breathing.

When alveolar oxygen levels are low, blood vessels supplying those alveoli constrict. This redirects blood flow to alveoli with higher oxygen levels, ensuring efficient gas exchange.

Acidity in the blood (low pH) enhances hypoxic pulmonary vasoconstriction. This further aids in optimizing ventilation-perfusion matching.

Sudden increases in arterial pressure trigger a decrease in ventilation rate. Conversely, a sudden drop in arterial pressure leads to an increase in the rate and depth of breathing.

Stretch receptors in the lungs are stimulated during lung expansion. This signal triggers inhibition of the inspiratory center, which helps regulate breathing depth.

The cerebral cortex can override normal breathing rhythms to modify breathing patterns. This is known as 'voluntary' control.

Sudden and involuntary cessation of breathing caused by stimuli like pain, cold exposure, or throat irritation.

The portion of the respiratory system where gas exchange does not occur. It's essentially 'wasted' space within the lungs.