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Respiratory Physiology and Acute Respiratory Failure PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Respiratory Physiology & Acute Respiratory Failure" by Dr. Priyanka Gupta.

This medical PowerPoint presentation talks about respiratory physiology, the study of how the respiratory system works to exchange gases (oxygen and carbon dioxide) between the body and the environment. The respiratory system includes the lungs, airways, and other organs and tissues that facilitate gas exchange.

Acute respiratory failure (ARF) is a condition in which the respiratory system fails to maintain adequate gas exchange, leading to a buildup of carbon dioxide and/or a decrease in oxygen levels in the blood. ARF can be caused by a variety of conditions, including lung diseases, heart failure, infections, trauma, and drug overdose. Symptoms of ARF include shortness of breath, rapid breathing, confusion, and cyanosis (bluish discoloration of the skin and mucous membranes).

Tags : Respiratory Physiology, Acute Respiratory Failure, respiratory system, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 1259 | Downloads : 6

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Slide 1-

Respiratory Physiology& Acute Respiratory FailureDr. Priyanka GuptaDept of Anaesthesia AIIMS, Rishikesh
Slide 2-

Respiratory physiology is central to the practice of Anaesthesia
Slide 3-

The most commonly used anaesthetics- the inhalational agents- depend on the lungs for uptake and elimination. The most important side effects of both inhalational and intravenously administered anaesthetics are primarily respiratory.
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Functions of the Respiratory System Gas Exchange O2, CO2 Acid-base balance CO2 +H2O←→ H2CO3 ←→ H+ + HCO3- Phonation Pulmonary defense Pulmonary metabolism and handling of bioactive materials 6
Slide 7-

Respiration The term respiration includes 3 separate functions: Ventilation: Breathing. Gas exchange: Between air and capillaries in the lungs. Between systemic capillaries and tissues of the body. 02 utilization: Cellular respiration. www.freelivedoctor.com
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Ventilation Mechanical process that moves air in and out of the lungs. [O2] of air is higher in the lungs than in the blood, O2 diffuses from air to the blood. C02 moves from the blood to the air by diffusing down its concentration gradient. Gas exchange occurs entirely by diffusion: Diffusion is rapid because of the large surface area and the small diffusion distance. www.freelivedoctor.com Insert 16.1
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Respiratory Zone Region of gas exchange between air and blood. Includes respiratory bronchioles and alveolar sacs. Must contain alveoli. www.freelivedoctor.com
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Alveoli Polyhedral in shape and clustered like units of honeycomb. ~ 300 million air sacs (alveoli). Large surface area (60–80 m2). Each alveolus is 1 cell layer thick. Total air barrier is 2 cells across (2 mm). 2 types of cells: Alveolar type I: Structural cells. Alveolar type II: Secrete surfactant. www.freelivedoctor.com
Slide 12-

Conducting Zone All the structures air passes through before reaching the respiratory zone. Warms and humidifies inspired air. Filters and cleans: Mucus secreted to trap particles in the inspired air. Mucus moved by cilia to be expectorated. www.freelivedoctor.com Insert fig. 16.5
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Tracheobronchial Tree: a) Trachea- conduit for ventilation Clearance of tracheal &bronchial secretions Begins at the lower border of the cricoid cartilage and extends to the level of the carina Average length of 10–13 cm The external diameters of the trachea is approximately 2.3 cm coronally and 1.8 cm sagitally in men and 2.0 cm & 1.4 cm, respectively, in women
Slide 14-

The trachea bifurcates at the carina into the right and left main stem bronchi Dichotomous division, starting with the trachea and ending in alveolar sacs, is estimated to involve 23 divisions. An estimated 300 million alveoli provide an enormous membrane (50–100 m2 ) for gas exchange in the average adult Gas exchange can occur only across the flat epithelium, which begins to appear on respiratory bronchioles
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Pulmonary Circulation & Lymphatics The lungs are supplied by two circulations, pulmonary and bronchial The bronchial circulation arises from lt heart Along their courses, the bronchial vessels anastomose with the pulmonary arterial circulation and continue as far as the alveolar duct. The pulmonary circulation normally receives the total output of the right heart via the pulmonary artery, which divides into rt and lt branches to supply each lung
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Deoxygenated blood passes through the pulmonary capillaries, where O2 is taken up and CO2 is eliminated The oxygenated blood is then returned to the lt heart by 4 main pulmonary veins (two from each lung)
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Innervation The diaphragm is innervated by the phrenic nerves, which arise from the C3–C5 nerve roots. U/L phrenic nerve palsy only modestly reduces most indices of pulmonary function (~ 25%). B/L phrenic nerve palsies produce more severe impairment The vagus nerves provide sensory innervation to the tracheobronchial tree
Slide 18-

Thoracic Cavity Diaphragm: Sheets of striated muscle divides anterior body cavity into 2 parts. Above diaphragm: thoracic cavity: Contains heart, large blood vessels, trachea, esophagus, thymus, and lungs. Below diaphragm: abdominopelvic cavity: Contains liver, pancreas, GI tract, spleen, and genitourinary tract. Intrapleural space: Space between visceral and parietal pleurae. www.freelivedoctor.com
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Intrapulmonary and Intrapleural Pressures Visceral and parietal pleurae are flush against each other. The intrapleural space contains only a film of fluid secreted by the membranes. Lungs normally remain in contact with the chest walls. Lungs expand and contract along with the thoracic cavity. Intrapulmonary pressure: Intra-alveolar pressure (pressure in the alveoli). Intrapleural pressure: Pressure in the intrapleural space. Pressure is negative, due to lack of air in the intrapleural space. www.freelivedoctor.com
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Transpulmonary Pressure Pressure difference across the wall of the lung. Intrapulmonary pressure – intrapleural pressure. Keeps the lungs against the chest wall. www.freelivedoctor.com
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Intrapulmonary and Intrapleural Pressures (continued) During inspiration: Atmospheric pressure is > intrapulmonary pressure (-3 mm Hg). During expiration: Intrapulmonary pressure (+3 mm Hg) is > atmospheric pressure. www.freelivedoctor.com
Slide 22-

Boyle’s Law Changes in intrapulmonary pressure occur as a result of changes in lung volume. Pressure of gas is inversely proportional to its volume. Increase in lung volume decreases intrapulmonary pressure. Air goes in. Decrease in lung volume, raises intrapulmonary pressure above atmosphere. Air goes out. www.freelivedoctor.com
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Physical Properties of the Lungs Ventilation occurs as a result of pressure differences induced by changes in lung volume. Physical properties that affect lung function: Compliance. Elasticity. Surface tension. www.freelivedoctor.com
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Compliance Distensibility (stretchability): Ease with which the lungs can expand. Change in lung volume per change in transpulmonary pressure. DV/DP 100 x more distensible than a balloon. Compliance is reduced by factors that produce resistance to distension. www.freelivedoctor.com
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Elasticity Tendency to return to initial size after distension. High content of elastin proteins. Very elastic and resist distension. Recoil ability. Elastic tension increases during inspiration and is reduced by recoil during expiration. www.freelivedoctor.com
Slide 26-

Surface Tension Force exerted by fluid in alveoli to resist distension. Lungs secrete and absorb fluid, leaving a very thin film of fluid. This film of fluid causes surface tension. Fluid absorption is driven (osmosis) by Na+ active transport. Fluid secretion is driven by the active transport of Cl- out of the alveolar epithelial cells. H20 molecules at the surface are attracted to other H20 molecules by attractive forces. Force is directed inward, raising pressure in alveoli. www.freelivedoctor.com
Slide 27-

Surfactant Phospholipid produced by alveolar type II cells. Lowers surface tension. Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules. Surface tension in alveoli is reduced. As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Disorders: RDS. ARDS. www.freelivedoctor.com Insert fig. 16.12
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Quiet Inspiration Active process: Contraction of diaphragm, increases thoracic volume vertically. Parasternal and external intercostals contract, raising the ribs; increasing thoracic volume laterally. Pressure changes: Alveolar changes from 0 to –3 mm Hg. Intrapleural changes from –4 to –6 mm Hg. Transpulmonary pressure = +3 mm Hg. www.freelivedoctor.com
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Expiration Quiet expiration is a passive process. After being stretched by contractions of the diaphragm and thoracic muscles; the diaphragm, thoracic muscles, thorax, and lungs recoil. Decrease in lung volume raises the pressure within alveoli above atmosphere, and pushes air out. Pressure changes: Intrapulmonary pressure changes from –3 to +3 mm Hg. Intrapleural pressure changes from –6 to –3 mm Hg. Transpulmonary pressure = +6 mm Hg. www.freelivedoctor.com
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Insert fig. 16.15 Pulmonary Ventilation www.freelivedoctor.com
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Lung volumes and capacities 4 lung volumes: tidal (~500 ml) inspiratory reserve (~3100 ml) expiratory reserve (~1200 ml) residual (~1200 ml) 4 lung capacities inspiratory (~3600 ml) functional residual (~2400 ml) vital (~4800 ml) total lung (~6000 ml)
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Terms Used to Describe Lung Volumes and Capacities www.freelivedoctor.com
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Anatomical Dead Space Not all of the inspired air reached the alveoli. As fresh air is inhaled it is mixed with air in anatomical dead space. Conducting zone and alveoli where [02] is lower than normal and [C02] is higher than normal. Alveolar ventilation = F x (TV- DS). F = frequency (breaths/min.). TV = tidal volume. DS = dead space. www.freelivedoctor.com
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Restrictive and Obstructive Disorders Restrictive disorder: Vital capacity is reduced. FVC is normal. Obstructive disorder: Diagnosed by tests that measure the rate of expiration. VC is normal. FEV1 is < 80%. www.freelivedoctor.com Insert fig. 16.17
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Gas Exchange in the Lungs Dalton’s Law: Total pressure of a gas mixture is = to the sum of the pressures that each gas in the mixture would exert independently. Partial pressure: The pressure that an particular gas exerts independently. PATM = PN2 + P02 + PC02 + PH20= 760 mm Hg. 02 is humidified = 105 mm Hg. H20 contributes to partial pressure (47 mm Hg). P02 (sea level) = 150 mm Hg. PC02 = 40 mm Hg. www.freelivedoctor.com
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Partial Pressures of Gases in Inspired Air and Alveolar Air www.freelivedoctor.com Insert fig. 16.20
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Partial Pressures of Gases in Blood When a liquid or gas (blood and alveolar air) are at equilibrium: The amount of gas dissolved in fluid reaches a maximum value (Henry’s Law). Depends upon: Solubility of gas in the fluid. Temperature of the fluid. Partial pressure of the gas. [Gas] dissolved in a fluid depends directly on its partial pressure in the gas mixture. www.freelivedoctor.com
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Significance of Blood P02 and PC02 Measurements At normal P02 arterial blood is about 100 mm Hg. P02 level in the systemic veins is about 40 mm Hg. www.freelivedoctor.com PC02 is 46 mm Hg in the systemic veins. Provides a good index of lung function.
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Pulmonary Circulation Rate of blood flow through the pulmonary circulation is = flow rate through the systemic circulation. Driving pressure is about 10 mm Hg. Pulmonary vascular resistance is low. Low pressure pathway produces less net filtration than produced in the systemic capillaries. Avoids pulmonary edema. Autoregulation: Pulmonary arterioles constrict when alveolar P02 decreases. Matches ventilation/perfusion ratio. www.freelivedoctor.com
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Pulmonary Circulation (continued) In a fetus: Pulmonary circulation has a higher vascular resistance, because the lungs are partially collapsed. After birth, vascular resistance decreases: Opening the vessels as a result of subatmospheric intrapulmonary pressure. Physical stretching of the lungs. Dilation of pulmonary arterioles in response to increased alveolar P02. www.freelivedoctor.com
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Lung Ventilation/Perfusion Ratios Functionally: Alveoli at apex are underperfused (overventilated). Alveoli at the base are underventilated (overperfused). www.freelivedoctor.com Insert fig. 16.24
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Brain Stem Respiratory Centers Neurons in the reticular formation of the medulla oblongata form the rhythmicity center: Controls automatic breathing. Consists of interacting neurons that fire either during inspiration (I neurons) or expiration (E neurons). www.freelivedoctor.com Insert fig. 16.25
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Brain Stem Respiratory Centers (continued) I neurons project to, and stimulate spinal motor neurons that innervate respiratory muscles. Expiration is a passive process that occurs when the I neurons are inhibited. Activity varies in a reciprocal way. www.freelivedoctor.com
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Rhythmicity Center I neurons located primarily in dorsal respiratory group (DRG): Regulate activity of phrenic nerve. Project to and stimulate spinal interneurons that innervate respiratory muscles. E neurons located in ventral respiratory group (VRG): Passive process. Controls motor neurons to the internal intercostal muscles. Activity of E neurons inhibit I neurons. Rhythmicity of I and E neurons may be due to pacemaker neurons. www.freelivedoctor.com
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Pons Respiratory Centers Activities of medullary rhythmicity center is influenced by pons. Apneustic center: Promotes inspiration by stimulating the I neurons in the medulla. Pneumotaxic center: Antagonizes the apneustic center. Inhibits inspiration. www.freelivedoctor.com
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Chemoreceptors 2 groups of chemo-receptors that monitor changes in blood PC02, P02, and pH. Central: Medulla. Peripheral: Carotid and aortic bodies. Control breathing indirectly via sensory nerve fibers to the medulla (X, IX). www.freelivedoctor.com Insert fig. 16.27
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Effects of Blood PC02 and pH on Ventilation Chemoreceptor input modifies the rate and depth of breathing. Oxygen content of blood decreases more slowly because of the large “reservoir” of oxygen attached to hemoglobin. Chemoreceptors are more sensitive to changes in PC02. H20 + C02 H2C03 H+ + HC03- Rate and depth of ventilation adjusted to maintain arterial PC02 of 40 mm Hg. www.freelivedoctor.com
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Chemoreceptor Control Central chemoreceptors: More sensitive to changes in arterial PC02. H20 + CO2 H2C03 H+ H+ cannot cross the blood brain barrier. C02 can cross the blood brain barrier and will form H2C03. Lowers pH of CSF. Directly stimulates central chemoreceptors. www.freelivedoctor.com
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Chemoreceptor Control of Breathing www.freelivedoctor.com
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Effects of Blood P02 on Ventilation Blood PO2 affected by breathing indirectly. Influences chemoreceptor sensitivity to changes in PC02. Hypoxic drive: Emphysema blunts the chemoreceptor response to PC02. Choroid plexus secrete more HC03- into CSF, buffering the fall in CSF pH. Abnormally high PC02 enhances sensitivity of carotid bodies to fall in P02. www.freelivedoctor.com
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Effects of Pulmonary Receptors on Ventilation Lungs contain receptors that influence the brain stem respiratory control centers via sensory fibers in vagus. Unmyelinated C fibers can be stimulated by: Capsaicin: Produces apnea followed by rapid, shallow breathing. Histamine and bradykinin: Released in response to noxious agents. Irritant receptors are rapidly adaptive receptors. Hering-Breuer reflex: Pulmonary stretch receptors activated during inspiration. Inhibits respiratory centers to prevent undue tension on lungs. www.freelivedoctor.com
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Hemoglobin and 02 Transport 280 million hemoglobin/RBC. Each hemoglobin has 4 polypeptide chains and 4 hemes. In the center of each heme group is 1 atom of iron that can combine with 1 molecule 02. www.freelivedoctor.com Insert fig. 16.32
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Hemoglobin Oxyhemoglobin: Normal heme contains iron in the reduced form (Fe2+). Fe2+ shares electrons and bonds with oxygen. Deoxyhemoglobin: When oxyhemoglobin dissociates to release oxygen, the heme iron is still in the reduced form. Hemoglobin does not lose an electron when it combines with 02. www.freelivedoctor.com
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Hemoglobin (continued) Methemoglobin: Has iron in the oxidized form (Fe3+). Lacks electrons and cannot bind with 02. Blood normally contains a small amount. Carboxyhemoglobin: The reduced heme is combined with carbon monoxide. The bond with carbon monoxide is 210 times stronger than the bond with oxygen. Transport of 02 to tissues is impaired. www.freelivedoctor.com
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Hemoglobin (continued) Oxygen-carrying capacity of blood determined by its [hemoglobin]. Anemia: [Hemoglobin] below normal. Polycythemia: [Hemoglobin] above normal. Hemoglobin production controlled by erythropoietin. Production stimulated by PC02 delivery to kidneys. Loading/unloading depends: P02 of environment. Affinity between hemoglobin and 02. www.freelivedoctor.com
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Oxyhemoglobin Dissociation Curve www.freelivedoctor.com Insert fig.16.34
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Effects of pH and Temperature The loading and unloading of O2 influenced by the affinity of hemoglobin for 02. Affinity is decreased when pH is decreased. Increased temperature and 2,3-DPG: Shift the curve to the right. www.freelivedoctor.com Insert fig. 16.35
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Effect of 2,3 DPG on 02 Transport Anemia: RBCs total blood [hemoglobin] falls, each RBC produces greater amount of 2,3 DPG. Since RBCs lack both nuclei and mitochondria, produce ATP through anaerobic metabolism. Fetal hemoglobin (hemoglobin f): Has 2 g-chains in place of the b-chains. Hemoglobin f cannot bind to 2,3 DPG. Has a higher affinity for 02. www.freelivedoctor.com
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C02 Transport C02 transported in the blood: HC03- (70%). Dissolved C02 (10%). Carbaminohemoglobin (20%). www.freelivedoctor.com H20 + C02 H2C03 ca High PC02
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Chloride Shift at Systemic Capillaries H20 + C02 H2C03 H+ + HC03- At the tissues, C02 diffuses into the RBC; shifts the reaction to the right. Increased [HC03-] produced in RBC: HC03- diffuses into the blood. RBC becomes more +. Cl- attracted in (Cl- shift). H+ released buffered by combining with deoxyhemoglobin. HbC02 formed. Unloading of 02. www.freelivedoctor.com
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Carbon Dioxide Transport and Chloride Shift www.freelivedoctor.com Insert fig. 16.38
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At Pulmonary Capillaries H20 + C02 H2C03 H+ + HC03- At the alveoli, C02 diffuses into the alveoli; reaction shifts to the left. Decreased [HC03-] in RBC, HC03- diffuses into the RBC. RBC becomes more -. Cl- diffuses out (reverse Cl- shift). Deoxyhemoglobin converted to oxyhemoglobin. Has weak affinity for H+. Gives off HbC02. www.freelivedoctor.com
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Reverse Chloride Shift in Lungs www.freelivedoctor.com Insert fig. 16.39
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Respiratory Acidosis Hypoventilation. Accumulation of CO2 in the tissues. PCO2 increases. pH decreases. Plasma HCO3- increases. www.freelivedoctor.com
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Respiratory Alkalosis Hyperventilation. Excessive loss of CO2. PCO2 decreases. pH increases. Plasma HCO3- decreases. www.freelivedoctor.com
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Ventilation During Exercise During exercise, breathing becomes deeper and more rapid. Produce > total minute volume. Neurogenic mechanism: Sensory nerve activity from exercising muscles stimulates the respiratory muscles. Cerebral cortex input may stimulate brain stem centers. Humoral mechanism: PC02 and pH may be different at chemoreceptors. Cyclic variations in the values that cannot be detected by blood samples. www.freelivedoctor.com Insert fig. 16.41
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Acute Respiratory Failure Results from inadequate gas exchange Insufficient O2 transferred to the blood Hypoxemia Inadequate CO2 removal Hypercapnia
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Classification of RF Type 1 Hypoxemic RF PaO2 < 60 mmHg with normal or ↓ PaCO2 Associated with acute diseases of the lung Pulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse Type 2 Hypercapnic RF PaCO2 > 50 mmHg Hypoxemia is common Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthma
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Pathophysiologic causes of Acute RF ●Hypoventilation ●V/P mismatch ●Shunt ●Diffusion abnormality
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Classification of Respiratory Failure Fig. 68-2
Slide 71-

Mechanisms of hypoxemia Alveolar hypoventilation V/Q mismatch Shunt Diffusion limitation
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Alveolar Hypoventilation Restrictive lung disease CNS disease Chest wall dysfunction Neuromuscular disease
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Perfusion without ventilation (shunting) Intra-pulmonary Small airways occluded ( e.g asthma, chronic bronchitis) Alveoli are filled with fluid ( e.g pulm edema, pneumonia) Alveolar collapse ( e.g atelectasis)
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Dead space ventilation DSV increase: Alveolar-capillary interface destroyed e.g emphysema Blood flow is reduced e.g CHF, PE Overdistended alveoli e.g positive- pressure ventilation
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Diffusion limitation Severe emphysema Recurrent pulmonary emboli Pulmonary fibrosis Hypoxemia present during exercise
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Diffusion Limitation Fig. 68-5
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Hypercarbia Hypercarbia is always a reflection of inadequate ventilation PaCO2 is directly related to CO2 production Inversely related to alveolar ventilation PaCO2 = k x VCO2 VA
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Hypercarbia When CO2 production increases, ventilation increases rapidly to maintain normal PaCO2 Alveolar ventilation is only a fraction of total ventilation VA = VE – VD Increased deadspace or low V/Q areas may adversely effect CO2 removal Normal response is to increase total ventilation to maintain appropriate alveolar ventilation
Slide 79-

Hypercapnic Respiratory Failure Imbalance between ventilatory supply and demand
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Etiology and Pathophysiology Airways and alveoli Asthma Emphysema Chronic bronchitis Cystic fibrosisS
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Etiology and Pathophysiology Central nervous system Drug overdose Brainstem infarction Spinal chord injuries
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Etiology and Pathophysiology Chest wall Flail chest Fractures Mechanical restriction Muscle spasm
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Etiology and Pathophysiology Neuromuscular conditions Muscular dystrophy Multiple sclerosis
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Diagnosis of RF1 – Clinical (symptoms, signs) Hypoxemia Dyspnea, Cyanosis Confusion, somnolence, fits Tachycardia, arrhythmia Tachypnea (good sign) Use of accessory ms Nasal flaring Recession of intercostal ms Polycythemia Pulmonary HTN, Corpulmonale, Rt. HF Hypercapnia ↑Cerebral blood flow, and CSF Pressure Headache Asterixis Papilloedema Warm extremities, collapsing pulse Acidosis (respiratory, and metabolic) ↓pH, ↑ lactic acid
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Respiratory FailureSymptoms CNS: Headache Visual Disturbances Anxiety Confusion Memory Loss Weakness Decreased Functional Performance
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Respiratory FailureSymptoms Cardiac: Orthopnea Peripheral edema Chest pain Other: Fever, Abdominal pain, Anemia, Bleeding
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Clinical Respiratory compensation Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation
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Clinical Respiratory compensation Tachypnoea RR > 35 Breath /min Accessory muscles Recesssion Nasal flaring Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation
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Clinical Respiratory compensation Sympathetic stimulation HR BP Sweating Tissue hypoxia Altered mental state HR and BP (late) Haemoglobin desaturation cyanosis
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Respiratory FailureLaboratory Testing Arterial blood gas PaO2 PaCO2 PH Chest imaging Chest x-ray CT sacn Ultrasound Ventilation–perfusion scan
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Management of ARF ICU admission 1 -Airway management Endotracheal intubation: Indications Severe Hypoxemia Altered mental status Importance precise O2 delivery to the lungs remove secretion ensures adequate ventilation
Slide 92-

Management of ARF Correction of hypoxemia O2 administration via nasal prongs, face mask, intubation and Mechanical ventilation Goal: Adequate O2 delivery to tissues PaO2 = > 60 mmHg Arterial O2 saturation >90%
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Indications for intubation and mechanical ventilation Innability to protect the airway Respiratory acidosis (pH<7.2) Refractory hypoxemia Fatigue/increased metabolic demands impending respiratory arrest Pulmonary toilet
Slide 94-

Management of ARF Mechanical ventilation Increase PaO2 Lower PaCO2 Rest respiratory ms (respiratory ms fatigue) Ventilator Assists or controls the patient breathing The lowest FIO2 that produces SaO2 >90% and PO2 >60 mmHg should be given to avoid O2 toxicity
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Management of ARF PEEP (positive End-Expiratory pressure Used with mechanical ventilation Increase intrathoracic pressure Keeps the alveoli open Decrease shunting Improve gas exchange Hypoxemic RF (type 1) ARDS Pneumonias
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Management of ARF Noninvasive Ventilatory support (IPPV) Mild to moderate RF Patient should have Intact airway, Alert, normal airway protective reflexes Nasal or full face mask Improve oxygenation, Reduce work of breathing Increase cardiac output AECOPD, asthma, CHF
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Management of ARF Treatment of the underlying causes After correction of hypoxemia, hemodynamic stability Antibiotics Pneumonia Infection Bronchodilators (COPD, BA) Salbutamol reduce bronchospasm airway resistance
Slide 98-

Management of ARF Treatment of the underlying causes Physiotherapy Chest percussion to loosen secretion Suction of airways Help to drain secretion Maintain alveolar inflation Prevent atelectasis, help lung expansion
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Management of ARF Weaning from mechanical ventilation Stable underlying respiratory status Adequate oxygenation Intact respiratory drive Stable cardiovascular status Patient is a wake, has good nutrition, able to cough and breath deeply
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Thank you