Respiratory and Cardiovascular Systems Quiz

O2 and CO2 exchange occurs by diffusion, driven by partial pressure gradients for both gases. O2 has limited water solubility, while CO2 is 20 times more soluble than O2 in blood.

Atmospheric pressure decreases with altitude above sea level, leading to a decrease in PO2. This decrease in PO2 can cause hypoxia.

Diving increases the partial pressure of inspired gases, and O2 and N2 become potentially toxic as they dissolve into tissues at depth.

References include Boron & Boulpaep's 'Medical Physiology' (Chapter 30 and 61), Guyton & Hall's 'Textbook of Medical Physiology' (Chapter 40), Preston & Wilson's 'Lippincott’s Illustrated Reviews: Physiology' (Chapter 23), and Naish & Syndercombe Court's 'Medical Sciences' (Chapter 13).

The term 'partial pressure' refers to the pressure exerted by a single gas in a mixture of gases. It can be calculated using the equation $P_{gas} = P_{total} * X_{gas}$, where $P_{gas}$ is the partial pressure of the gas, $P_{total}$ is the total pressure of the gas mixture, and $X_{gas}$ is the mole fraction of the gas in the mixture.

Oxygen moves from alveolar air to the blood through the process of diffusion. In the alveoli, oxygen molecules move across the alveolar membrane into the capillaries, where they bind to hemoglobin in red blood cells and are transported to the tissues for cellular respiration.

At higher altitudes, the atmospheric pressure decreases, leading to a decrease in the partial pressure of oxygen ($P_{O2}$). This can result in hypoxemia, or low oxygen levels in the blood, which may cause symptoms such as shortness of breath, fatigue, and impaired cognitive function.

Physiological adaptations to altitude include increased erythropoietin release, hemoglobin concentration, angiogenesis, and cardiopulmonary system remodeling. These adaptations help to increase oxygen delivery to body tissues and compensate for the reduced oxygen levels at higher altitudes. The increased erythropoietin release stimulates the production of red blood cells, while the higher hemoglobin concentration enhances oxygen-carrying capacity. Angiogenesis promotes the growth of new blood vessels, improving oxygen delivery to tissues. Cardiopulmonary system remodeling involves changes in the structure and function of the heart and lungs to enhance overall oxygen uptake and utilization.

Diving at depth increases the partial pressure of gases, leading to gas toxicity effects such as nitrogen (N2) narcosis and oxygen (O2) poisoning. The increased partial pressure of gases can affect gas exchange in the lungs and lead to adverse physiological effects. N2 narcosis, also known as "rapture of the deep," can cause impaired judgment and cognitive function due to the narcotic effects of nitrogen at high pressures. O2 poisoning, on the other hand, can result in seizures, dizziness, and other central nervous system disturbances. The use of heliox, a breathing gas mixture of helium and oxygen, can help mitigate these gas toxicity effects by reducing the partial pressure of nitrogen and oxygen.

Gas exchange between alveolar and blood is influenced by factors such as surface area, solubility, and thickness of the membranes. The large surface area and thin membranes in the lungs facilitate rapid gas exchange, while the solubility of gases in the membranes also affects the efficiency of gas transfer. Changes in factors such as membrane thickness, surface area, and concentration gradients can impact gas exchange efficiency. Conditions like edema, emphysema, and pulmonary fibrosis can alter these factors, leading to reduced gas exchange efficiency. For example, thickening of the membranes or a decrease in surface area can hinder the diffusion of gases, resulting in impaired gas exchange.

The Henderson-Hasselbalch equation is pH = pKa + \log \left( \frac{[HCO3^-]},{[CO2]} \right)$, where bicarbonate is in mmol/L (mM) and [CO2] is calculated as PCO2 x solubility constant. It is used to calculate the plasma pH based on the concentrations of bicarbonate and CO2, taking into account the dissociation constant pKa.

The pKa for the bicarbonate/carbonic acid system is 6.1, while the normal plasma pH is 7.4. At a pH of 7.4, there is more HCO3^- than H2CO3. The pKa represents the pH at which 50% of the components are ionized and 50% are unionized. When the pH is higher than the pKa, there is more of the ionized form (HCO3^-), and when the pH is lower than the pKa, there is more of the unionized form (H2CO3).

Increased CO2 levels lead to more H2CO3 formation, shifting the bicarbonate/carbonic acid equilibrium to the right and resulting in more HCO3^- ions. Conversely, decreased CO2 levels lead to less H2CO3 formation, shifting the equilibrium to the left and resulting in more H2CO3. These changes in the bicarbonate/carbonic acid system can impact plasma pH.

The primary causes of acid-base disturbances are changes in CO2 levels for respiratory disorders and changes in bicarbonate levels for metabolic disorders. For example, conditions that can lead to respiratory acidosis include COPD, blocked airway, lung collapse, and drugs reducing respiratory drive. Conditions that can lead to metabolic alkalosis include vomiting, ingestion of alkali substances, and potassium depletion.

In acid-base disturbances, the respiratory system compensates by altering ventilation to change CO2 levels, while the renal system compensates by altering reabsorption and production of bicarbonate. Conditions that can lead to respiratory alkalosis include increased ventilation from hypoxic drive, and hyperventilation due to brainstem damage or infection driving fever. Conditions that can lead to metabolic acidosis include loss of HCO3- in diarrhea, exogenous acid overloading, endogenous acid production, and failure to secrete H+ in renal failure.

The Davenport diagram is a graphical tool that shows the relationship between pH, PCO2, and HCO3- levels. It illustrates how changes in PCO2 and non-volatile acid or base affect plasma pH. For example, an increase in PCO2 causes an increase in H+ concentration, leading to a decrease in pH. Renal compensation involves increased HCO3- reabsorption and production to raise pH towards normal.

The acid-base nomogram is used to analyze arterial blood gases by plotting PaCO2 and H+/pH values. If the plotted point lies outside the designated areas, it implies a mixed disturbance. This tool helps in identifying complex acid-base imbalances that involve multiple primary disorders.

PCO2 affects blood pH through the formation of carbonic acid, which dissociates into bicarbonate ions and hydrogen ions. An increase in PCO2 leads to an increase in hydrogen ion concentration, lowering blood pH, while a decrease in PCO2 leads to a decrease in hydrogen ion concentration, raising blood pH.

Blood pH can be calculated using the Henderson-Hasselbalch equation: pH = 6.1 + log([HCO3-] / 0.03 * PCO2), where [HCO3-] is the bicarbonate concentration and PCO2 is the partial pressure of carbon dioxide.

Primary causes of acid-base disturbances include respiratory and metabolic factors. Respiratory disturbances are caused by changes in PCO2, while metabolic disturbances are caused by changes in bicarbonate levels.

Oxygen is transported in the blood through a combination of dissolved oxygen and oxygen bound to hemoglobin. Each gram of Hb, when fully saturated, carries 1.35 ml of O2. The maximal oxygen bound to hemoglobin can be calculated using the equation: $max , \text{O}_2 , \text{bound} , \text{Hb} = \text{O}_2 , \text{capacity} \times [\text{Hb}]$.

Normal Hb (HbA) is a tetramer consisting of 2α and 2β chains, while fetal hemoglobin (HbF) has the β-chains replaced by γ-chains. This difference in structure affects the oxygen binding affinity and delivery, especially in the fetal circulation.

Deoxygenated Hb exists in a tensed state (T) compared with oxygenated Hb in a relaxed state (R). In the tensed state, strong ionic bonds form between the polypeptide chains, hindering oxygen binding. As oxygen binds, the bonds break and the Hb transitions to the relaxed state, allowing for efficient oxygen binding and the characteristic color change of blood from dark blue to bright red.

Oxygen is transported in the blood in two ways: physically dissolved in plasma and combined with haemoglobin. Approximately 2% of oxygen is physically dissolved in plasma, and about 98% is combined with haemoglobin. The amount of oxygen dissolved in plasma depends on its solubility and partial pressure in the blood, according to Henry’s Law, which states that at equilibrium for a given temperature $[O2]_{Dis} = solubility\ of\ O2 \times PO2$. The solubility of oxygen in plasma is poor at 37°C, leading to only a small amount of oxygen being physically dissolved in the plasma.

The oxygen-haemoglobin dissociation curve illustrates the relationship between the partial pressure of oxygen (PO2) and the saturation of haemoglobin with oxygen. It is sigmoidal in shape, allowing for efficient loading and unloading of oxygen. The curve shifts to the right in response to factors such as increased temperature, increased levels of 2,3-diphosphoglycerate (2,3-DPG), and decreased pH, promoting the release of oxygen to the tissues. Conversely, the curve shifts to the left in response to decreased temperature, decreased levels of 2,3-DPG, and increased pH, enhancing the affinity of haemoglobin for oxygen.

Carbon dioxide is carried in the blood in three forms: physically dissolved in plasma (7-10%), converted to bicarbonate (70%), and bound to haemoglobin as carbaminohemoglobin (20%). Red blood cells play a crucial role in carbon dioxide carriage by facilitating the conversion of carbon dioxide to bicarbonate through the enzyme carbonic anhydrase, allowing for efficient transport of carbon dioxide from the tissues to the lungs for expiration.

The Bohr effect refers to the phenomenon where changes in pH and carbon dioxide levels affect the affinity of hemoglobin for oxygen. In systemic capillaries, where there are increases in CO2, temperature, and decrease in pH, the hemoglobin shifts to a low affinity state, leading to the release of more oxygen (right shift). In pulmonary capillaries, where the temperature is lower, Pco2 is lower, and pH is higher, the hemoglobin shifts to a higher affinity state, resulting in more oxygen being taken up by hemoglobin (left shift). This effect is depicted by the Bohr shift on the oxygen-hemoglobin dissociation curve.

Myoglobin (MyHb) and fetal hemoglobin (HbF) shift the oxygen-hemoglobin dissociation curve to the left. HbF consists of 2 α-chains and 2 γ-chains and has higher oxygen affinity than HbA due to the special properties of the γ-chains. This left shift in the curve allows for increased oxygen uptake at lower partial pressures of oxygen, which is beneficial in the fetal circulation and in tissues with lower oxygen levels.

2,3-diphosphoglycerate (DPG) interacts with β chains of hemoglobin, destabilizing the interaction of oxygen with hemoglobin. In red blood cells, the by-product of glycolysis stimulates glycolysis, resulting in increased levels of 2,3-DPG. This interaction leads to a right shift in the oxygen-hemoglobin dissociation curve, decreasing the affinity of hemoglobin for oxygen and facilitating the release of oxygen to the tissues.

Carbon monoxide (CO) has a 200-fold greater affinity for hemoglobin than oxygen, leading to the formation of carboxyhemoglobin. This reduces the maximal oxygen capacity and impairs oxygen delivery to tissues. Additionally, CO increases the oxygen affinity of hemoglobin, shifting the oxygen-hemoglobin dissociation curve to the left. As a result, hemoglobin does not release oxygen efficiently when it reaches the tissues, leading to tissue hypoxia.

The VRG (ventral respiratory group) is responsible for generating the basic rhythm of respiration through its control over the motor neurons that innervate the diaphragm and external intercostal muscles. It consists of inspiratory and expiratory neurons and is located in the medulla oblongata.

The basic pattern of neural activity in the control of respiration can be altered at different levels, including the respiratory control center (source of central pattern generator), central and peripheral chemoreceptors, and pulmonary mechanoreceptors. These alterations allow for adjustments in alveolar ventilation rate to maintain stable levels of PO2 and PCO2 in the arterial blood.

Experimental evidence suggests that the respiratory neurons are located in the medulla oblongata and pons. Sectioning above the level of the pons allows the basic rhythm to continue, while sectioning below the medulla results in the cessation of all breathing. This indicates the critical role of these regions in the control of respiration.

The pneumotaxic centre, located dorsally in the upper pons, controls the switch-off point of the inspiratory ramp, thus regulating the filling phase of the lung cycle. It modulates the duration of inspiration, influencing the respiratory pattern without being essential for normal respiratory output.

The dorsal respiratory group, located mainly within the nucleus tractus solitarius, receives sensory input from the organs of the thorax and abdomen and emits repetitive bursts of inspiratory neuronal action potentials. These bursts contribute to the generation of the basic rhythm of respiration.

The exact location of central chemoreceptors is controversial, with identified candidate regions near the ventrolateral medulla and chemosensitive neurons beneath the ventral surface of the medulla and in the medullary raphe.

The carotid body can sense decreased arterial PO2, increases in arterial PCO2, and decreases in arterial pH, leading to modulation of respiratory output.

The cough reflex involves three phases: preparatory inspiration, compressive phase with closed glottis, and expulsive phase with the sudden opening of glottis.

Slowly adapting pulmonary stretch receptors, responsible for the Hering-Breuer reflex, help prevent over-inflation of the lungs. Rapidly adapting pulmonary stretch (Irritant) receptors and C-fibre receptors (J Receptors) are responsible for coughing, sneezing, and responding to chemical and mechanical stimuli.

Voluntary activities such as hyperventilation, breath-holding, speaking, and singing involve higher brain center activity that influences respiratory control.

Buffers play a crucial role in maintaining the pH of the body by minimizing changes in hydrogen ion concentration. Important buffering systems in the human body include proteins, hemoglobin, and the bicarbonate/carbonic acid system.

Arterial blood gas (ABG) is obtained by drawing blood from an artery and measuring the levels of oxygen, carbon dioxide, and pH. ABG results are significant in assessing acid-base balance as they provide information about the patient's oxygenation, ventilation, and acid-base status.

Respiratory acid-base disturbances can be caused by problems with ventilation, such as hypoventilation or hyperventilation. The body compensates for these disturbances through mechanisms including renal retention or excretion of bicarbonate and changes in respiratory rate and depth.

The alveolar-arterial oxygen gradient represents the difference in oxygen tension between the alveoli and the arterial blood. It is clinically significant in assessing oxygenation as it helps identify the efficiency of gas exchange in the lungs and can indicate the presence of ventilation-perfusion abnormalities.

A stepwise approach to interpreting ABG results involves first assessing the patient's oxygenation by looking at the partial pressure of oxygen (pO2) and then evaluating ventilation by examining the partial pressure of carbon dioxide (pCO2). This approach helps in identifying hypoxemia, hypercapnia, and potential respiratory acidosis or alkalosis.

The equation for the bicarbonate buffer system in the blood is $CO2 + H2O ightleftharpoons H2CO3 ightleftharpoons H^+ + HCO3^-$. This system helps regulate blood pH by balancing the levels of carbon dioxide and bicarbonate ions.

The recommended target oxygen saturation levels for patients with hypoxia are 94-96% under normal conditions, and 88-92% for type 2 respiratory failure.

In respiratory acidosis, the body compensates by increasing renal retention of bicarbonate. An example of this is acute respiratory acidaemia. In respiratory alkalosis, compensation occurs through renal excretion of bicarbonate, with an example being chronic respiratory alkalosis.

The arterial blood gas results for a patient with acute severe asthma show pH 7.55, pO2 17.0kPa, pCO2 3.3kPa, and HCO3- 22mmol/l. This indicates respiratory alkalosis and hypoxemia induced hyperventilation.

The arterial blood gas results for a patient with Type 1 Diabetes Mellitus show pH 7.28, pO2 12.7kPa, pCO2 3.0kPa, and HCO3- 16mmol/l. This indicates a state of metabolic acidosis, which may lead to compensatory respiratory alkalosis.