LUNG SURFACTANT

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Parenchyma of lungs is formed by respiratory unit that forms the terminal portion of respiratory tract. Respiratory unit is defined as the structural and functional unit of lung. Exchange of gases occurs only in this part of the respiratory tract..

Respiratory unit starts from the respiratory bronchioles . Each respiratory bronchiole divides into alveolar ducts. Each alveolar duct enters an enlarged structure called the alveolar sac. Space inside the alveolar sac is called antrum. Alveolar sac consists of a cluster of alveoli. Few alveoli are present in the wall of alveolar duct also. Thus, respiratory unit includes:.

Capillary beds Connective tissue Alveolar d Mucous gland Mucosal linin monary vein Pulmonary artery Alveoli Atrium.

Alveolar epithelium consists of alveolar cells or pneumocytes, which are of two types namely type I alveolar cells and type II alveolar cells..

Alveolar type II cell Lamellar body Tubular myelin Alveolar fluid Alveolar macrophage Alveolar type I cell Surfactant layer Air space.

Due to intermolecular force of attraction between the water molecules, Water molecules come closer..

It pulls water in the blood like the vacuum. Pulmonary Edema.

LAW OF LAPLACE. It applies to bubbles of unequal radius attached to a Y-tube. The pressure (P) in a bubble is equal to 4 times the surface tension (T) divided by the radius (r). As applied to the grape-like alveolus, where only the inner wall has a liquid surface exposed to gas, the formula is P = 2T/r. The pressure difference between the inside and the outside of an elastic sphere ("Laplace pressure") is inversely proportional to the radius and directly proportional to the surface tension. P= 2T/r where, P= Collapsing pressure T= Surface tension r = Radius.

Laplace's Law: 2y/r API = Air Hypo phase. LAPLACE'S LAW P = 50 Alveolus B Alveolus A 2T 2 x 50 2 r=2 P (Pressure) 2T 2 x 50 1 p 100 https://bodvtomv.com/lung-compliance-explained.

Consequences of LAPLACE LAW. Smaller partially deflated alveoli will have lower compliance and higher Laplace pressure at any given surface tension. Increased Laplace pressure upon small alveoli promotes their collapse, as they empty into neighbouring larger alveoli. Alveolar surface tension adds to the pulmonary capillary hydrostatic gradient (i.e. it promotes the ultrafiltration of oedema fluid). When the surface tension increases (or radius is small), the collapsing pressure increases and alveoli will collapse. When the surface tension decreases, the collapsing pressure decreases..

COLLAPSING TENDENCY OF LUNGS. Lungs are under constant threat to collapse even in resting conditions because of certain factors. Two factors are responsible for the collapsing tendency of lungs: 1. Elastic property of lung tissues: Elastic tissues of lungs show constant recoiling tendency and try to collapse the lungs 2. Surface tension: It is the tension exerted by the fluid secreted from alveolar epithelium on the surface of alveolar membrane. Fortunately, there are some factors, which save the lungs from collapsing..

In spite of elastic property of lungs and surface tension in the alveoli of lungs, the collapsing tendency of lungs is prevented by two factors:.

It is a surface acting material or agent that is responsible for lowering the surface tension of a fluid..

Atmospheric pressure Transpulmonary pressure: 760 mm Hg —756 mm Hg = 4 mm Hg Intrapleural pressure: 756 mm Hg (—4 mm Hg) Intra-alveolar pressure: 760 mm Hg (O mm Hg) Parietal pleura Visceral pleura Pleural cavity Thoracic wall Lung Diaphragm.

Surfactant is a lipoprotein complex formed by lipids especially phospholipids, proteins and ions.

Unsaturated PC Other 92% LIPIDS Chol Other 57. sp-A SP-D SP-B sp-c 8% PROTEINS.

FORMATION OF SURFACTANT. Type II alveolar epithelial cells and Clara cells have a special type of membrane bound organelles called lamellar bodies, which form the intracellular source of surfactant. Laminar bodies contain surfactant phospholipids and surfactant proteins. These materials are synthesized in endoplasmic reticulum and stored in laminar bodies. By means of exocytosis , lipids and proteins of lamellar bodies are released into surface fluid lining the alveoli. Here, in the presence of surfactant proteins and calcium, the phospholipids are arranged into a lattice (meshwork) structure called tubular myelin. Tubular myelin is in turn converted into surfactant in the form of a film that spreads over the entire surface of alveoli. Most of the surfactant is absorbed into the type II alveolar cells, catabolized and the products are loaded into lamellar bodies for recycling.

Factors necessary for the formation and spreading of surfactant.

Relation between surface tension and surfactant. It lowers the surface tension of fluid lining the lining the alveoli. Surface tension is inversely proportional to surfactant concentration. During inspiration surfactant molecules move apart as lungs are expanded and during expiration surfactant molecules become concentrated as lungs shorten. When there is no surfactant, surface tension is 50 dynes/cm. When surfactant is present it is 5-30 dynes/cm depending upon the concentration ..

FUNCTIONS OF SURFACTANT. Surfactant reduces the surface tension in the alveoli of lungs and prevents collapsing tendency of lungs. Surfactant acts by the following mechanism: Phospholipid molecule in the surfactant has two portions. One portion of the molecule is hydrophilic. This portion dissolves in water and lines the alveoli. Other portion is hydrophobic and it is directed towards the alveolar air. This surface of the phospholipid along with other portion spreads over the alveoli and reduces the surface tension. SP­B and SP­C play active role in this process..

Surfactant is responsible for stabilization of the alveoli, which is necessary to withstand the collapsing tendency. It plays an important role in the inflation of lungs after birth. In fetus, the secretion of surfactant begins after the 3rd month. Until birth, the lungs are solid and not expanded. Soon after birth, the first breath starts because of the stimulation of respiratory centers by hypoxia and hypercapnea . Although the respiratory movements are attempted by the infant, the lungs tend to collapse repeatedly. And, the presence of surfactant in the alveoli prevents the lungs from collapsing. Another important function of surfactant is its role in defense within the lungs against infection and inflammation. Hydrophilic proteins SP­A and SP­D destroy the bacteria and viruses by means of opsoni za tion . These two proteins also control the formation of inflammatory mediators ..

EFFECT OF DEFICIENCY OF SURFACTANT. Absence of surfactant in infants, causes collapse of lungs and the condition is called respiratory distress syndrome or hyaline membrane disease . Deficiency of surfactant occurs in adults also and it is called adult respiratory distress syndrome (ARDS). In addition, the deficiency of surfactant increases the susceptibility for bacterial and viral infections.

HYALINE MEMBRANE DISEASE. Hyaline membrane disease (HMD), also called respiratory distress syndrome (RDS), is a condition that causes babies to need extra oxygen and help breathing. HMD is one of the most common problems seen in premature babies . The more premature the baby, the higher the risk and the more severe the HMD. HMD typically worsens over the first 48 to 72 hours and then improves with treatment. More than 90 percent of babies with HMD survive..

DIAGNOSIS. HMD is usually diagnosed by a combination of assessments, including: appearance, color, and breathing efforts (these signs indicate your baby's need for oxygen) x-rays of lungs : x-rays are electromagnetic energy used to produce images of bones and internal organs onto film. In HMD, they often show a unique “ground glass” appearance called a reticulogranular pattern. blood gasses (tests for oxygen, carbon dioxide, and acid in arterial blood): often show lowered amounts of oxygen and increased carbon dioxide. echocardiography (EKG) : may be used to rule out heart problems that could cause symptoms similar to HMD. An electrocardiogram is a test that records the electrical activity of the heart, shows arrhythmias (abnormal rhythms), and detects damage to the heart muscle..

HMD occurs when there is not enough of a substance in the lungs called surfactant. Surfactant is made by the cells in the airways and consists of phospholipids and protein. It begins to be produced in the fetus at about 24 to 28 weeks of pregnancy , and is found in amniotic fluid between 28 and 32 weeks. By about 35 weeks gestation, most babies have developed adequate amounts of surfactant..

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TREATMENT. Treatment for HMD may include : placing an endotracheal tube (breathing tube, also called an ET) into baby's windpipe mechanical breathing machine (to do the work of breathing for baby ) supplemental oxygen (extra amounts of oxygen) continuous positive airway pressure (CPAP): a mechanical breathing machine that pushes a continuous flow of air or oxygen to the airways to help keep tiny air passages in the lungs open. surfactant replacement with artificial surfactant : this treatment has been shown to reduce the severity of HMD, and is most effective if started in the first six hours of birth. It may be given as preventive treatment for babies at very high risk for HMD, or used as a “rescue” method. The drug comes as a powder that is mixed with sterile water and given through the ET tube. This treatment is usually administered in several doses. medications (to help sedate and ease baby's pain during treatment).

ACUTE RESPIRATORY DISTRESS SYNDROME. Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function. ARDS typically occurs in people who are already critically ill or who have significant injuries. Severe shortness of breath — the main symptom of ARDS — usually develops within a few hours to a few days after the precipitating injury or infection. Many people who develop ARDS don't survive. The risk of death increases with age and severity of illness. Of the people who do survive ARDS, some recover completely while others experience lasting damage to their lungs..

SYMPTOMS. The signs and symptoms of ARDS can vary in intensity, depending on its cause and severity, as well as the presence of underlying heart or lung disease. They include : Severe shortness of breath or breathlessness. Rapid and labored breathing. Extreme tiredness and muscle fatigue. Confusion . Rapid heart rate. Bluish color of fingernails and lips due to low oxygen level in the blood. Cough and chest pain. If ARDS is caused by severe infection (sepsis), symptoms of sepsis may also be present ( fever , low blood pressure)..

CAUSES. The mechanical cause of ARDS is fluid leaked from the smallest blood vessels in the lungs into the tiny air sacs where blood is oxygenated. Normally, a protective membrane keeps this fluid in the vessels. Severe illness or injury, however, can cause damage to the membrane, leading to the fluid leakage of ARDS . Underlying causes of ARDS include: Sepsis. The most common cause of ARDS is sepsis, a serious and widespread infection of the bloodstream. Inhalation of harmful substances. Breathing high concentrations of smoke or chemical fumes can result in ARDS, as can inhaling (aspirating) vomit or near-drowning episodes. Severe pneumonia. Severe cases of pneumonia usually affect all five lobes of the lungs. Head, chest or other major injury. Accidents, such as falls or car crashes, can directly damage the lungs or the portion of the brain that controls breathing. Coronavirus disease 2019 (COVID-19). People who have severe COVID-19 may develop ARDS. Others. Pancreatitis (inflammation of the pancreas), massive blood transfusions and burns..

Treated I Normal lung lung surfactant produced by type II alveolar cells destruction of I type II alveolar cells activation of tissue macrophages Cytokine 1 secretion COVID-19 associated ARDS massive macropage infiltration Alveolar macrophage ctivation Cyto ine „storm" (IL-6, TNFc) destruction of type II alveolar cells vere loss of anti- inflammatory lung protective surfactant lung surfactant.

DIAGNOSIS. When symptoms of ARDS occur, a combinations of tests may be done: Chest X-ray to measure fluids in the lungs. A blood test to determine oxygen level in the blood to help determine the severity of ARDS. Echocardiogram (ultrasound of the heart) to evaluate heart function.

TREATMENT. ARDS is usually treated in the intensive care unit (ICU) along with treatment of the underlying cause. Mechanical ventilation (a ventilator) is often used in caring for patients with ARDS. For milder cases of ARDS, oxygen may be given through a fitted face mask or a cannula fitted over the nose. Steps to minimize complications from ARDS are commonly used. These include: Sedation to manage pain. Breathing tests to determine when it’s safe to remove the tube and ventilator. Blood thinners to prevent clots. Minimizing fluid buildup in the lungs. Minimizing stress ulcers in the stomach. Active mobility and physical therapy to prevent muscle weakness. No direct drug therapy has been shown to improve survival in ARDS, but researchers continue to work on finding treatment..

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