GROUP 27 physiology.ppt
- 1. Group 27 presentation • Discuss the control of respiratory rate and depth by the brainstem. • How do the respiratory muscles coordinate during forced breathing? • Explain the process of ventilation-perfusion matching in the lungs. • What happens during a bronchoconstriction and its effects on airflow? • Discuss the impact of altitude on respiratory physiology. 1. MUSIIMENTA GRACE VU-BPC-2301-0403-DAY 2. MUTONYI SHARON AMORA VU-BPC-2301-0071-DAY 3. MUTYABA MARTIN VU-BPC-2301-1562-DAY 4. MUYAMA GETRUDE VU-BPC-2301-1196-DAY
- 2. CONTROL OF RESPIRATORY RATE AND DEPTH BY THE BRAINSTEM The brainstem, particularly the medulla oblongata and pons, plays a central role in regulating these respiratory parameters. The respiratory center receives input from a variety of sources, including: The peripheral chemoreceptors, which are located in the carotid bodies and aortic bodies. These receptors sense the levels of carbon dioxide (CO2) and oxygen (O2) in the blood. The central chemoreceptors, which are located in the medulla oblongata. These receptors sense the pH of the cerebrospinal fluid. The stretch receptors in the lungs. These receptors sense the amount of air in the lungs. The cerebral cortex. The cerebral cortex can voluntarily control breathing, but this is usually overridden by the automatic control of the respiratory center.
- 3. Nervous control: respiratory neuronal center Composed of several groups of neurons. Located in the entire length of the medulla and pons. Can be divided into four major groups of neurons:- 1-Dorsal respiratory group. 2-Ventral respiratory group. 3-The apneustic center. 4-The pneumotaxic center. Several mechanisms are involved which can be grouped into two main categories which are closely integrated:- 1- Nervous control mechanism. 2- Chemical control mechanism CONTROL OF VENTILATION
- 4. Medullary Respiratory centers 1. Inspiratory area (Dorsal Respiratory Group)-DRG: -Determines basic rhythm of breathing (rhythmicity center). -Causes contraction of diaphragm and external intercostals. -The rhythmicity center received impulses from: 1-Higher brain centers. 2-Centers in the brain stem (medulla and pons). 3-Special receptors (respiratory reflexes). -The rhythmicity center sends excitatory impulses via the intercostal and phrenic nerves to the external intercostal muscles and diaphragm. -The medullary respiratory center stimulates basic inspiration for about 2 seconds and then basic expiration for about 3 seconds (5sec/ breath = 12breaths/min).
- 5. 2. Expiratory area (Ventral Respiratory Group)-VRG: -Although it contains both inspiratory and expiratory neurons, It is inactive during normal quiet breathing. -Activated by inspiratory area during forceful breathing. -Causes contraction of the internal intercostals and abdominal muscles ( mainly expiratory). Pontine Respiratory centers pons 1. Apneustic area: Stimulates inspiratory area of medulla to prolong inhalation. Therefore, slow respiration and prolonged respiratory cycles will result if it is stimulated. It receives inhibitory impulses from the sensory vagal fibers and inhibitory impulses from the pneumotaxic center. 2. Pneumotaxic area: It transmits inhibitory impulses to the apneustic center and to the inspiratory area to switch off inspiration. Therefore, breathing is more rapid when pneumotaxic area is active.
- 6. Hering-Breuer inflation reflex • When the lung becomes overstretched (tidal volume is about 1.5 L), stretch receptors located in the wall of bronchi and bronchioles transmit signals through vagus nerve to DRG producing effect similar to pneumotaxic center stimulation. • Switches off inspiratory signals and thus stops further inspiration . • This reflex also increases the rate of respiration as does the pneumotaxic center. • This reflex appears to be mainly a protective mechanism for preventing excess lung inflation
- 7. CHEMICAL CONTROL OF VENTILATION The rhythmicity center is affected by chemical changes in the blood via two types of chemoreceptors:- 1-Peripheral chemoreceptors. 2-Central chemoreceptors.
- 8. PERIPHERAL CHEMORECEPTORS: • Located mainly in the carotid and aortic bodies, but may be found anywhere in the circulatory system. • When stimulated, send excitatory impulses to the rhythmicity center (via glossopharyngeal and vagus nerves). • Highly sensitive to changes in arterial PO2 and to a lesser extent to PCO2 and pH. • Fall of PO2, rise in PCO2 and fall of pH, stimulate the chemoreceptors to increase ventilation. • Most probably located on the ventrolateral surface of medulla oblongata (which is bathed with cerebrospinal fluid) • Highly sensitive to the hydrogen ion concentration of the CSF(cereprospinal fluid). • evoked by arterial PCO2 (CO2 can freely cross the blood-brain barrier(BBB) into CSF, while BBB is relatively impermeable to H+ and HCO- 3 ions)
- 9. Effect of CO2 on central chemoreceptors Although carbon dioxide has little direct effect in stimulating the neurons in the chemosensitive area, it does have a potent indirect effect. It does this by reacting with the water of the tissues to form carbonic acid, which dissociates into hydrogen and bicarbonate ions; the hydrogen ions then have a potent direct stimulatory effect on respiration.
- 10. Effect of CO2 and H Ion Concentration on Chemoreceptor Activity. An increase in either carbon dioxide concentration or hydrogen ion concentration also excites the peripheral chemoreceptors and, in this way, indirectly increases respiratory activity. There is one difference between the peripheral and central effects of carbon dioxide: the stimulation of the peripheral chemoreceptors occurs as much as five times as rapidly as central stimulation, so that the peripheral chemoreceptors might be especially important in increasing the rapidity of response to carbon dioxide at the onset of exercise.
- 11. Other Factors Influencing Respiration
- 12. FORCED BREATHING Forced breathing, also known as active or deep breathing, occurs when we need to increase the volume of air exchanged in our lungs. It is typically required during physical exertion, such as exercise, or in situations where we need to inhale more oxygen or exhale more carbon dioxide than during normal, quiet breathing During forced breathing, the respiratory muscles coordinate to expand the chest cavity more than during normal breathing. This expansion allows for a larger volume of air to be inhaled or exhaled. The key respiratory muscles involved in forced breathing are the diaphragm, intercostal muscles, and accessory muscles. The coordination of these respiratory muscles is controlled by the respiratory centers in the brainstem. These centers receive input from various sensors in the body that monitor factors like oxygen and carbondioxide levels in the blood. Based on this input, the respiratory centers adjust the rate and depth of breathing, activating the appropriate muscles for forced breathing when needed.
- 13. Active Inspiration Active inspiration involves the contraction of the accessory muscles of breathing (in addition to those of quiet inspiration, the diaphragm and external intercostals). All of these muscles act to increase the volume of the thoracic cavity: • Diaphragm, a dome-shaped muscle located just below the lungs, contracts and flattens during inhalation. This contraction increases the vertical dimension of the thoracic cavity, allowing the lungs to expand more fully. The diaphragm is primarily responsible for the majority of the volume increase during forced breathing Scalenes – elevates the upper ribs. Sternocleidomastoid – elevates the sternum. Pectoralis major and minor – pulls ribs outwards. Serratus anterior – elevates the ribs (when the scapulae are fixed). Latissimus dorsi – elevates the lower ribs.
- 14. Active Expiration • Active expiration utilises the contraction of several thoracic and abdominal muscles. These muscles act to decrease the volume of the thoracic cavity: Anterolateral abdominal wall – increases the intra- abdominal pressure, pushing the diaphragm further upwards into the thoracic cavity. Internal intercostal – depresses the ribs. Innermost intercostal – depresses the ribs.
- 16. Ventilation perfusion matching • Ventilation is the amount of air used for gaseous exchange in the alveolar while perfusion is the blood flow in the pulmonary capillaries for gaseous exchange. • Ventilation perfusion matching is a relationship between airflow in the alveolar and blood flow in the pulmonary capillaries that maintains the concentration gradient of the gases aiding diffusion of gases across the respiratory membrane. • Ventilation perfusion ratio is the ratio of airflow to blood flow. Written as V/Q and has a range of 0.8-1.2. V/Q ratio is affected by; Gravity affects perfusion and Lung conditions that obstruct the airway and those that alter perfusion like pulmonary edema, asthma, COPD, pulmonary embolism. These conditions lead to a disruption in the V/Q ratio causing a mismatch.
- 17. Process To match local blood flow and airflow at the respiratory membrane, pulmonary capillaries can be adjusted by vasoconstriction or vasodilation and the airways by bronchoconstriction or bronchodilation. If perfusion is greater than airflow, gases do not have enough time to exchange properly. V/Q ratio is low, therefore: • CO2 is high triggering bronchodilation to increase airflow • O2 is low triggering vasoconstriction to decrease blood flow. If blood flow is slower than airflow, excess gaseous takes place. V/Q ratio is high, therefore: • CO2 is low triggering bronchoconstriction to decrease airflow. • O2 is high triggering vasodilation to increase blood flow.
- 18. V/Q Ratio Normal ventilation is 4-6 L/min and pulmonary blood flow has a similar range. V/Q must be estimated on an alveolar-capillary level, since different units have different ratios and not for the lungs because it only gives an approximate of the situation in all alveolar-capillary units. If V/Q ratio is not matched then there is a mismatch or an inequality (airflow and blood flow ratio are not properly corresponding).
- 21. Summary • The magnitude of V and Q as well as their distribution isimportant in determining pulmonary gas exchange. • Distribution of V and Q is predominately gravity and intrinsic lung structure. • V/Q ratiosare nonuniformin different regions of the lungs. • V/Q mismatch is the most important cause of gaseous exchange abnormalities inlung diseases
- 22. Bronchoconstriction is defined as the abnormal contraction of the smooth muscles of the bronchi and bronchioles resulting into narrowing of the airways in the lungs and difficult breathing. Air flow in air passages can get restricted in three ways: spasmodic state of the smooth muscles in airway, inflammations of the bronchi and bronchioles and excessive production of mucus. Bronchoconstriction can cause symptoms such as wheezing, coughing, chest tightness, and a feeling of breathlessness. These symptoms are common in conditions like asthma and chronic obstructive pulmonary disease (COPD). Bronchoconstriction
- 23. MECHANISM OF BRONCHIAL SPASM 1.Parasympathetic Nervous System Activation: When the parasympathetic nervous system is activated, it leads to the release of acetylcholine. 2.Release of Acetylcholine: Postganglionic parasympathetic fibers release acetylcholine, which acts as a neurotransmitter. 3.Muscarinic M3 Receptors: Smooth muscle cells surrounding the bronchi have muscarinic M3 receptors on their cell membranes. These receptors are activated by acetylcholine. 4.G Protein Activation: When acetylcholine binds to the M3 receptors, it activates an intracellular G protein associated with these receptors. 5.Phospholipase C Pathway Activation: The activated G protein, in turn, activates the phospholipase C pathway. Phospholipase C is an enzyme that cleaves a membrane phospholipid to produce inositol trisphosphate (IP3) and diacylglycerol (DAG). 6.Intracellular Calcium Increase: IP3 acts on intracellular calcium stores (like the endoplasmic reticulum), causing the release of calcium ions into the cytoplasm of the smooth muscle cell. This results in an increase in intracellular calcium concentrations. 7.Smooth Muscle Contraction: Elevated intracellular calcium concentrations trigger the contraction of the smooth muscle cells surrounding the bronchi. 8.Bronchial Constriction: As the smooth muscle contracts, it narrows the diameter of the bronchus. This narrowing leads to increased resistance to airflow through the bronchus.
- 24. The effects of bronchoconstriction on airflow are: • Increased resistance to airflow: The increased resistance to airflow makes it more difficult for air to move in and out of the lungs. This can cause shortness of breath and wheezing • Decreased airflow rate: The decreased airflow rate means that less air is able to reach the lungs with each breath. This can lead to hypoxemia, which is a low level of oxygen in the blood • Increased work of breathing: The increased work of breathing is the effort that the respiratory muscles must make to breathe. This can lead to fatigue and respiratory failure • Decreased lung compliance: The decreased lung compliance means that the lungs are less able to expand and contract. This can make it difficult to breathe deeply.
- 25. IMPACT OF ALTITUDE ON RESPIRATORY PHYSIOLOGY As altitude increases, atmospheric pressure decreases. At sealevel, atmosphericpressure is approximately 760mmHg(compared to approximately 253mmHgatthe peakofMountEverest). These atmosphericpressurescanbe usedto calculatethe partial pressureofoxygen(pO2) in air. This shows that thepO2is approximately159mmHgat sea level and 43mmHgatthe summitofMountEverest.
- 26. Acclimatisation • Acclimatisation describes the normal physiological changes through which the body adapts to decreasing levels of oxygen. It explains why in parts of the world such as Tibet, many generations of people have lived at high altitude whereas climbers have to take considerable care when moving to high altitudes.
- 28. Changes in blood Increased red blood cell production Increased hemoglobin concentration to about 20g/dL due to increased erythropoietin secretion Increased hematocrit Increased plasma volume Increased production of 2,3-diphosphoglycerate (DPG) Changes in respiratory system Increased pulmonary ventilation and blood flow Increased diffusion capacity by the lungs due to stimulation of chemoreceptors Changes in cardio vascular system Increased heart rate, cardiac output and BP Increased blood flow to the vital organs like, brain, heart and muscles Changes in tissue Increased quantities of oxidative enzymes involved in metabolism present in cells Increased mitochondria in cells Increased myoglobin content
- 29. Acute mountain sickness (AMS) is a group of symptoms that can occur when the body is not able to adapt to the decreased oxygen levels at high altitude. Symptoms of AMS can include headache, nausea, vomiting, dizziness, and fatigue. In severe cases, AMS can be fatal. AMS is most common at altitudes above 8,000 feet (2,400 m). The risk of AMS increases with the altitude and with the rate of ascent. severe cases of acute mountain sickness this can lead to a number of serious complications, including: • High altitude pulmonary edema (HAPE) • High altitude cerebral edema (HACE) Treatment options include • Rest: This allows the body to rest and to recover from the stresses of ascent. • Acetazolamide: This medication helps to reduce the symptoms of AMS. • Descent: If symptoms are severe, it is important to descend to a lower altitude.
- 30. High-Altitude Pulmonary Edema (HAPE) • Life threatening form of non cardiogenic edema due to leaky capillaries • Starts at first 1-2 days at high altitude Symptoms include shortness of breath, cough, rapid breathing, and cyanosis • Treatment: immediate descent, oxygen, and medications. • HAPE is a medical emergency; timely action is critical.