Respiratory system ppt 1.pptx- PHYSIOPATHOLOGY

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1. Dr SHILPA SHREE C

2. Organs of the Respiratory system Nose Pharynx Larynx Trachea Bronchi Lungs – alveoli

3. ▣ Gas exchange : Oxygen enters blood and carbon dioxide leaves ▣ Regulation of blood pH : Altered by changing blood carbon dioxide levels ▣ Voice production : Movement of air past vocal folds makes sound and speech ▣ Olfaction : Smell occurs when airborne molecules drawn into nasal cavity ▣ Protection : Against microorganisms by preventing entry and removing them

4. ▣ Upper tract Nose, pharynx and associated structures Larynx ▣ Lower tract T rachea, bronchi, lungs

5. ▣ Nose External nose Nasal cavity Functions 🢝 Passageway for air 🢝 Cleans the air 🢝 Humidifies, warms air 🢝 Smell 🢝 Along with paranasal sinuses are resonating chambers for speech ▣ Pharynx Common opening for digestive and respiratory systems Three regions Nasopharynx Oropharynx Laryngopharynx

6. ▣ Functions Maintain an open passageway for air movement Epiglottis and vestibular folds prevent swallowed material from moving into larynx Vocal folds are primary source of sound production

7. ▣ Windpipe ▣ Divides to form Primary bronchi Carina : Cough reflex

8. ▣ Conducting zone Trachea to terminal bronchioles which is ciliated for removal of debris Passageway for air movement Cartilage holds tube system open and smooth muscle controls tube diameter ▣ Respiratory zone Respiratory bronchioles to alveoli Site for gas exchange

9. Trachea (Windpipe) Slide 13.10 Connects larynx with bronchi Lined with ciliated mucosa Beat continuously in the opposite direction of incoming air Expel mucus loaded with dust and other debris away from lungs Walls are reinforced with C-shaped hyaline cartilage

10. Primary Bronchi Slide 13.11 Formed by division of the trachea Enters the lung at the hilus (medial depression) Right bronchus is wider, shorter, and straighter than left Bronchi subdivide into smaller and smaller branches

11. Lungs Slide 13.12a Occupy most of the thoracic cavity Apex is near the clavicle (superior portion) Base rests on the diaphragm (inferior portion) Each lung is divided into lobes by fissures Left lung – two lobes Right lung – three lobes

12. Lungs Slide 13.12b

13. Coverings of the Lungs Slide 13.13 Pulmonary (visceral) pleura covers the lung surface Parietal pleura lines the walls of the thoracic cavity Pleural fluid fills the area between layers of pleura to allow gliding

14. Respiratory Tree Divisions Slide 13.14 Primary bronchi Secondary bronchi Tertiary bronchi Bronchioli Terminal bronchioli

15. Bronchioles Slide 13.15a Smallest branches of the bronchi All but the smallest branches have reinforcing cartilage

16. Bronchioles Slide 13.15c Terminal bronchioles end in alveoli

17. Alveoli Slide 13.17 Structure of alveoli Alveolar duct Alveolar sac Alveolus Gas exchange occurs here.

18. Respiratory Membrane (Air- Blood Barrier) Slide 13.18a Thin squamous epithelial layer lining alveolar walls Pulmonary capillaries cover external surfaces of alveoli The blood–air barrier (alveolar– capillary barrier or membrane) exists in the gas exchanging region of the lungs. It exists to prevent air bubbles from forming in the blood, and from blood entering the alveoli.

19. Respiratory Membrane (Air-Blood Barrier) Slide 13.18b

20. Events of Respiration Slide 13.20a Pulmonary ventilation: O2 into lungs from inspired air; CO2 out of lungs from expired air. External respiration: Gas exchange between alveoli and the capillaries. Respiratory gas transport: Gasses are transported in blood (via vessels) to tissues. Internal respiration: Gas exchange between blood and tissue cells in systemic capillaries Cellular respiration.

21. Mechanics of Breathing (Pulmonary Ventilation) Slide 13.21b Two phases Inspiration – flow of air into lung Expiration – air leaving lung

22. ▣ Trachea lies in midline of neck ▣ Extends from vertebral level C6 in the lower neck to vertebral level T4 in the mediastium where it bifurcates into a right and left main bronchus.

23. ▣ Each lung is conical in shape ▣ It has:- ▣ APEX ▣ BASE ▣ THREE BORDERS ▣ TWO SURFACES

24. ▣ APEX- it lies above the level of first rib. It reaches 2- 5 cm above the medial one third of clavicle, just medial to supraclavicular fossa. ▣ BASE- rest on the diaphgram which seperates the right lung from the right lobe of the liver and the left lung from the left lobe of the liver, fundus of stomach and the spleen.

25. LEF T

26. ▣ BORDERS ▣ ANTERIOR BORDER- right lung continues running downwards till the 6 th costochondral junction. ▣ ANTERIOR BORDER- left lung continues running downwards till the 4 th costal cartilage then curves laterally ½ inch forming the cardiac notch then descends downwards till the 6 th costochondral junction.

27. ▣ INFERIOR BORDER- Is sharp and seperates the base from costal surface. ▣ POSTERIOR BORDER- Is rounded, thick and lies beside the vertebral column.

28. SURFACES ▣ COASTAL SURFACE- lies immediately adjacent to the ribs and intercostal spaces of the thoracic wall ▣ MEDIAL SURFACE- It is divided into two parts: Anterior(mediastinal part): Contains a HILUM in the middle(depression in which bronchi,vessels and nerves forming the root of lungs. Posterior(vertebral part): It is related to: - bodies of thoracic vertebrae, IV discs, posterior intercostal vessels. ▣ DIAPHRAGMATIC SURFACE

29. RIGHT LEFT

30. ▣ LOBES ▣ The right lung have 3 lobes- Upper, Middle and lower lobes ▣ The left lung have 2 lobes- Upper and Lower lobes

31. ▣ FISSURES ▣ OBLIQUE FISSURE: (right and left lung) It starts at the 3 rd thoracic spine while the arms are elevated, decends downwards, laterally and anteriorly along the medial border of the scapula touching the inferior angle of scapula cutting the midaxillary line in the 5 th rib and ending the 6 th costal cartilage 3 inches from the midline.

32. ▣ HORIZONTAL FISSURES( right lung) It follows the 4 th intercostal space from the sternum until it meets the oblique fissure as it crosses the 5 th rib.

33. Mechanics of Breathing (Pulmonary Ventilation) Completely mechanical process Depends on volume changes in the thoracic cavity Volume changes lead to pressure changes, which lead to the flow of gases to equalize pressure

34. Mechanics of Breathing (Pulmonary Ventilation) Two phases Inspiration – flow of air into lung Expiration – air leaving lung

35. Inspiration Diaphragm and intercostals muscles contract The size of the thoracic cavity increases External air is pulled into the lungs due to an increase in intrapulmonary volume

36. Inspiration Figure 13.7a

37. 1. Sternocleidomast oid muscles, which lift upward on the sternum Anterior serrati, which lift many of the ribs Scaleni, which lift the first two ribs.

38. Exhalation Largely a passive process which depends on natural lung elasticity As muscles relax, air is pushed out of the lungs Forced expiration can occur mostly by abdominal recti, which have the powerful effect of pulling downward on the lower ribs and internal intercostal muscles depress the rib cage

39. Exhalation Figure 13.7b

40. Lung recoil It is due to Elastic recoil and surface tension. Elastic recoil: Elastic forces of the lung tissue it is determined mainly by elastin and collagen fibers. Surface tension: It is the elastic tendency of a fluid surface which makes it acquire the least surface area possible. As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli are highly elastic, they do not resist surface tension on their own, which allows the force of that deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity .

41. . Surfactant: Reduces tendency of lungs to collapse It is secreted by special surfactant- secreting epithelial cells called type II alveolar epithelial cells

42. Pleural fluid produced by pleural membranes Acts as lubricant Helps hold parietal and visceral pleural membranes together

43. The difference between the alveolar pressure and the pleural pressure, this is called the transpulmonary pressure. ▣ TPP can be measured by performing oesophageal manometry # Pneumothorax : In this an abnormal collection of air in the pleural space between the lung and the chest wall. https://www.hamilton- medical.com/en_IN/Solutions/Transpulmona ry-pressure- measurement.html https:// www.hamilton-medical.com/en_IN/Solutions/Transpulmonary- pressure-measurement.html

44. Measure of the ease with which lungs and thorax expand A lower-than-normal compliance means the lungs and thorax are harder to expand

45. ▣ Tidal volume : Volume of air inspired or expired during a normal inspiration or expiration , Usually 500 millilitres in the adult male ▣ Inspiratory reserve volume: Amount of air inspired forcefully after inspiration of normal tidal volume , It is usually equal to about 3000 millilitres Expiratory reserve volume: Amount of air forcefully expired after expiration of normal tidal volume It is usually 1100 milliliters Residual volume: Volume of air remaining in respiratory passages and lungs after the most forceful expiration. It is usually 1200 milliliters.

46. All pulmonary to 25 percent less in women than in men, and they are greater in large and athletic people than in small and asthenic people.

47. ▣ Inspiratory capacity: Tidal volume plus inspiratory reserve volume (about 3500 milliliters) ▣ Functional residual capacity: Expiratory reserve volume plus the residual volume (about 2300 milliliters) ▣ Vital capacity: Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume (about 4600 milliliters) ▣ Total lung capacity: Sum of all volume (about 5800 milliliters)

48. ▣ Minute ventilation : Total amount of air moved into and out of respiratory system per minute ▣ Respiratory rate or frequency : Number of breaths taken per minute. It is about 12 breaths per minute. ▣ Anatomic dead space : It is the total volume of the conducting airways from the nose or mouth down to the level of the terminal bronchioles, and is about 150 ml on the average in humans. ▣ Alveolar ventilation : How much air per minute enters the parts of the respiratory system in which gas exchange takes place

49. One of the most important problems in all the respiratory passageways is to keep them open and allow easy passage of air to and from the alveoli . multiple cartilage rings less extensive curved cartilage plates The bronchioles are not prevented from collapsing by the rigidity of their walls. Instead, they are kept expanded mainly by the same transpulmonary pressures that expand the alveoli

50. In addition to keeping the surfaces moist, the mucus traps small particles out of the inspired air and keeps most of these from ever reaching the alveoli. These particles are either swallowed or coughed to the exterior. 200 cilia on each epithelial cell Cilia beat continually at a rate of 10 to 20 times per cilia in the lu n s g e c s o b n e d a t upward, whereas those in the nose beat downward .

51. ▣ The bronchi and trachea are so sensitive to light touch that very slight amounts of foreign matter or other causes of irritation initiate the cough reflex Sneeze Reflex The sneeze reflex is like the cough reflex, except that it applies to the nasal passageways instead of the lower respiratory passages. The initiating stimulus of the sneeze reflex is irritation in the nasal passageways.

52. ▣ In respiratory physiology, one deals with mixtures of gases, mainly of oxygen, nitrogen, and carbon dioxide. ▣ The rate of diffusion of each of these gases is directly proportional to the pressure caused by that gas alone, which is called the partial pressure of that gas.

53. ▣ Diffusion of gases through the respiratory membrane Depends on membrane’s thickness, the diffusion coefficient of gas, surface areas of membrane, partial pressure of gases in alveoli and blood ▣ Relationship between ventilation and pulmonary capillary flow Increased ventilation or increased pulmonary capillary blood flow increases gas exchange Physiologic shunt is deoxygenated blood returning from lungs

54. Oxygen is transported by hemoglobin (98.5%) and is dissolved in plasma (1.5%) Oxygen- hemoglobin dissociation curve shows that hemoglobin is almost completely saturated when P0 2 is 80 mm Hg or above. At lower partial pressures, the hemoglobin releases oxygen. A shift of the curve to the left because of an increase in pH, a decrease in carbon dioxide, or a decrease in temperature results in an increase in the ability of hemoglobin to hold oxygen

55. The substance 2.3- bisphosphoglycerate increases the ability of hemoglobin to

56. In lung capillaries, bicarbonate ions and hydrogen ions move into RBCs and chloride ions move out. Bicarbonate ions combine with hydrogen ions to form carbonic acid. The carbonic acid is converted to carbon dioxide and water. The carbon dioxide diffuses out of the RBCs. Increased plasma carbon dioxide lowers blood pH. The respiratory system regulates blood pH by regulating plasma carbon dioxide levels

57. ▣ Normal rate of respiration in adults is 12- 16/min ,with tidal volume of 500ml.This rate and depth of respiration i.e total pulmonary ventilation can be adjusted to the requirements of the body. ▣ The size of thorax is altered by the action of the respiratory muscles ,which contract as a result of nerve impulses transmitted to them from centers in the brain and relax in absence of nerve impulses. ▣ These nerve impulses are sent from clusters of neurons located bilaterally in the medulla oblongata and pons of the brain stem .This widely dispersed group of neurons collectively called the respiratory center .

58. This rhythmic discharge from the brain that produces spontaneous respiration is regulated by 2 mechanisms:- NERVOUS REGULATORY MECHANISM CHEMICAL REGULATORY MECHANISM

59. ▣ TWO SYSTEM:- ▣ AUTOMATIC CONTROL :Medullary rhythmicity area in the medulla oblongata. ▣ Pneumotaxic area in pons. ▣ Apneustic area in pons . ▣ VOLUNTARY CONTROL : via cerebral cortex .

60. ▣ Composed of neurons in medullary rhythmic area(MRA)in medulla oblongata, pneumatoxic & apneustic area in pons. ▣ MRA (Medullary rhythmic area) located in ventrolateral medulla overlying olivary nucleus .There are two types of respiratory neuron I and E neuron.

61. Function of MRA to control basic rhythm of respiration . Inspiratory & expiratory area within MRA During quiet breathing inhalation lasts for about 2sec and exhalation for about 3 sec . Nerve impluse generated in inspiratory area Establish basic rhythm of breathing Active insp. area generate nerve impluse for about 2 sec . Impluse propogated to ext IC muscles via IC nerve and diagram via phrenic nerve

62. ▣ When nerve impluse reach diaphragm and ext IC muscles muscle contract and inhalation occur . ▣ At the end of 2sec insp. area become inactive nerve impulse ceases with no impulse arriving daiphragm and ext.IC muscles relax for about 3 sec ,allowing passive elastic recoil of lung ,thoracic wall and the cycle repeats .

63. ▣ Neurons in exp. Area remain inactive during quiet breathing .However during forceful breathing nerve impulse from insp.area activate the exp.area. ▣ Impulses from the exp. area cause contarction of int.IC muscle and abdominal muscle which decrease size of thoracic cavity and causes forceful exhalation .

64. ▣ Help to coordinate transition between inhalaton and exhalation ( in upper pons ) .Transmit inhibitory impulses to inspiratory area.These impulses shorten the duration of inhalation .When the pneumotaxic area is more active ,breathing rate is more rapid. APNEUSTIC AREA ▣ This is in lower pons. This sends stimulatory impulses to the inspiratory area that activate and prolong inhalation .The result is long deep inhalation. ▣ When pneumotaxic area is active ,it overrides signal from the apneustic area.

65. ▣ Cerebral cortex has connections with respiratory center, we can voluntarily alter our pattern of breathing .We can refuse to breathe for short period of time. ▣ Voluntary control is protective as it enables us to prevent water or irritating gases entering from lungs.This ability to not to breathe is limited by the build up of CO ₂ and H ⁺ in the body. ▣ When Pco₂ and H⁺ conc. Increase to a certain level ,the inspiratory area is strongly stimulated , nerve impluses are sent along phrenic and IC nerves to respiratory muscles ,and breathing resumes.

66. ▣ Some chemical stimuli modulate how quickly and deeply we breathe.The respiratory system functions to maintain proper levels of CO ₂ and O ₂ and is very responsive to changes in the levels of these gases in body fluids . ▣ There are some sensory neurons that are responsive to chemicals called chemoreceptors .Chemoreceptors in 2 locations monitor levels of CO₂,H⁺,O₂ and provide input to respiratory center .

67. ▣ 2 types of chemoreceptors :- ▣ CENTRAL CHEMORECEPTORS :- Are located near medulla oblongata in CNS.They respond to changes in H ⁺ conc. Or pCO ₂ or both in CSF . ▣ PERIPHERAL CHEMORECEPTORS :- Are located in the aortic bodies( clusters of chemoreceptors located in the wall of the arch of aorta ) and cartoid bodies (oval nodules in the wall of the left and right common carotid arteries .These are part of PNS and are sensitive to changes in Po₂,H⁺,Pco₂ in blood . ▣ Axons of sensory neurons from the aortic bodies are part of the vagus nerve and those of carotid bodies are part of right and left glosdopharyngeal nerves.

68. ▣ Normally ,Pco ₂ in arterial blood is 40 mmHg .Slight increase in it cause condition called hypercarbia or hypercapina. Central chemoreceptors are stimulated by both high Pco₂ and the rise in H ⁺. ▣ When Po₂ in arterial blood falls from normal level of 100mmHg but is still above 50mmHg ,peripheral chemoreceptors are stimulated .Deficiency of O₂ depresses activity of central chemoreceptors and inspiratory area which then don’t respond to any input and send fewer impulses to muscles of inhalation .As a result breathing rate decreases.

69. ▣ Chemoreceptors participate in a negative feedback that regulates level of CO ₂ ,O ₂ and H ⁺in blood ,as a result of increased H⁺ ,Pco₂ input from the central and peripheral chemoreceptor causes inspiratory area to become highly active .Rate and depth of breathing increases called hyperventilation, allows the inhalation of more O₂ and exhalation of more CO₂ until level of Pco₂ and H⁺ are lowered to normal. ▣ If arterial Pco ₂ is lower than 40mmHg – hypocapnia and hypocarbia, both the chemoreceptor are not stimulated therefore impulses are not sent to inspiratory area.As a result the area sets to it own pace until CO₂ accumulates and rises above 40 mmHg .The inspiratory area is stimulated more strongly when Pco₂ level rises above normal and Po₂ fall below normal.

70. ▣ EXERCISE rate and depth of breathing ,even before changes in Po ₂ ,Pco ₂,H⁺level occur. ▣ Main stimulus for these changes is input from propiroceptors which mointor movement of joint and musles nerve impulse from propiroceptors stimulate inspiratory area of the medulla oblongata. ▣ At same time axon collateral of UMN that originate in primary motor cortex also feed exctitatory response to inspiratory area.

71. ▣ Recent advances have clarified how the brain detects CO ₂to regulate breathing (central respiratory chemoreception ).These mechanism are reviewed and their significance is presented in the general context of CO₂/pH homeostasis via breathing . ▣ At rest resp. chemoreflexes initiated at peripheral and central sites mediate rapid stabilization of arterial PCO₂and PH . neurons ( retrotrapezoid ) are activated by PCO₂ and ▣ Specific brainstem nucleus,serotonergic stimulate breathing .

72. ▣ RTN neurons detect CO ₂via intrinsic proton receptors ,synaptic input from peripheral chemoreceptors and signals from astrocytes . chemoreflexes are arousal state ▣ Respiratory dependent whereas chemoreceptor stimulation produces arousal . ▣ When abnormal these interactions lead to sleep disorderd breathing .During exercise ,” central command “ and reflexes from exercising muscles produce the breathing stimulation required to maintain arterial PCO₂ and ph despite elevated metabolic activity .

73. ▣ New advances in the neural control of breathing. ▣ This issue contain 3 review articles based on talks given as part of a symposium entitled “New Advances in the neural control of breathing “ took place during the 1 st pan American congress of Physiological sciences on 3 aug 2014 by Brazilian society of physiology and sponsored by “The Journal of Physiology “.

74. discuss cellular and molecular by which the brain control ▣ AIM : To mechanism breathing . ▣ TOPIC: Includes:- ▣ Network basis of respiratory rhythmogenesis by pre botzinger complex. ▣ Role of purinergic signalling in central and peripheral chemoreception . ▣ Role of serotonergic raphe neurons in control of breathing .

75. The next caudal segment of the VRC, the B¨otzinger complex, contains GABAergic expiratory neurons which modulate respiratory rhythm . The next most rostral region is the pre- B¨otC; neurons in this region form the core respiratory rhythm-generating circuit and relay this inspiratory drive to more rostral premotor populations that control breathing. Finally, the rostral and caudal segments of the VRG contain premotor neurons dedicated to the control of inspiratory and expiratory activities, respectively. The authors propose that respiratory rhythm generation by the pre- B¨otC is not dependent on intrinsic pacemaker .Specifically, they suggest that pre-inspiratory ‘burstlets’ produced by the convergent activity of a few neurons can produce a subthreshold rhythm that is translated into an inspiratory burst by a recurrently connected network of excitatory preB¨otC neurons. These exciting new insights will enhance our understanding of mechanisms underlying respiratory rhythmogenesis, and in a broader context, may provide useful insight into the complex underpinnings of other rhythmic microcircuits.

76. ▣ The review by Moreira and colleagues entitled ‘Independent purinergic mechanisms of central and peripheral chemoreception in the rostral ventrolateral medulla.’ describes the role of purinergic signalling at the level of the ventrolateral medulla in coordinating cardiorespiratory responses to hypoxia and hypercapnia by activating RTN chemoreceptors and presympathetic neurons. In the context of central chemoreception, evidence suggests that RTN astrocytes respond to high CO ₂ by releasing ATP via 26 hemichannels . This purinergic signal up- regulates the activity of local RTN chemoreceptors and contributes to the ventilatory response to CO ₂ . The authors also describe the contribution of purinergic signalling to peripheral chemoreceptor modulation of breathing and blood pressure by a P2Y1- receptor- dependent mechanism.

77. The review by Mulk and colleagues entitled ‘Molecular underpinnings of ventral surface chemoreceptor function: focus on KCNQ channels’ describes key regulators of intrinsic excitability of RTN chemoreceptors .They summarize evidence suggesting that KCNQ channels regulate the activity of RTN chemoreceptors. They also put forth a model where KCNQ and TASK- 2 channels work together to limit activity under control conditions and during activation by high CO2/H+. Considering that respiratory failure is thought to be an underlying cause of sudden unexplained death in epilepsy (SUDEP), and since KCNQ channels regulate the activity of neurons that control breathing and loss of function mutations in certain KCNQ channels can cause certain types of epilepsy, the authors propose that KCNQ channels represent a common substrate for epilepsy and respiratory problems.

78. Pulmonary function tests are a group of tests that measure how well the lung works i.e., how well your lungs take in and release air and how well they move oxygen into the blood.

79. ▣ Compare your lung function with known standards that show how well your lungs should be working. ▣ Measure the effect of chronic diseases like asthma, chronic obstructive pulmonary disease (COPD), or cystic fibrosis on lung function. ▣ Identify early changes in lung function that might show a need for a change in treatment. ▣ Detect narrowing in the airways. ▣ Decide if a medicine (such as a bronchodilator) could be helpful to use. ▣ Show whether exposure to substances in your home or workplace have harmed your lungs. ▣ Determine your ability to tolerate surgery and medical procedures.

80. ▣ Pediatric neuromuscular disorder such as Duchenne muscular Dystrophy. ▣ Musculoskeletal deformities such as kyphoscoliosis (contribute to restrictive lung disease) ▣ Chronic dyspnoea ▣ Asthma ▣ Chronic obstructive pulmonary disease (COPD) ▣ Restrictive lung disease ▣ Preoperative testing

81. ▣ Recent eye surgery ▣ Thoracic , abdominal and cerebral aneurysms ▣ Active hemoptysis ▣ Pneumothorax ▣ Unstable angina/ recent MI within 1 month

82. Standard PFTs include: Spirometry Lung volumes Diffusion capacity

83. ▣ Spirometry (meaning the measuring of breath ) is the most common of the pulmonary function tests (PFTs), measuring lung function, specifically the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled. ▣ The most common parameters measured in spirometry are Vital capacity (VC), Forced vital capacity (FVC), Forced expiratory volume (FEV) at timed intervals of 0.5, 1.0 (FEV1), 2.0, and 3.0 seconds, Forced expiratory flow 25–75% (FEF 25–75) and Maximal voluntary ventilation (MVV)

84. In a spirometry test, you breathe into a mouthpiece that is connected to an instrument called a spirometer. The spirometer records the amount and the rate of air that you breathe in and out over a period of time. The primary signal measured in spirometry may be volume or flow. The test effort can be presented as a ‘flow- volume loop’ or as a ‘volume- time curve’. Normal values vary and depend on: height – directly proportional age – inversely proportional gender ethnicity

85. No coughing: especially during first second of FVC Good start of test: <5% of FVC exhaled prior to a max expiratory effort. (<5% extrapolation) No early termination of expiration: exhalation time of six seconds or a plateau of 2 seconds No variable flows: flow rate should be consistent and as fast as possible throughout exhaled VC Good reproducibility or consistency of efforts: 2 best FVC's and 2 best FEV1's should agree within 5% or 100 ml (whichever is greatest)

86. ▣ Place the nose clip. ▣ Have patient seated comfortably ▣ Have patient take a deep breath (inspiration) as fast as possible. ▣ Place the spirometer on mouth (should be sealed within the lips),blow out as hard as they can until you tell them to stop.(expiration)

87. ▣ Flow volume loops provide a graphical illustration of a patient's spirometric efforts. Flow is plotted against volume to display a continuous loop from inspiration to expiration. The overall shape of the flow volume loop is important in interpreting spirometric results

88. (A) Normal. Inspiratory limb of loop is symmetric and convex. Expiratory limb is linear. Flow rates at the midpoint of the inspiratory and expiratory capacity are often measured. Maximal inspiratory flow at 50% of forced vital capacity (MIF 50%FVC) is greater than maximal expiratory flow at 50% FVC (MEF 50%FVC) because dynamic compression of the airways occurs during exhalation.

89. (B) Obstructive disease (e.g, emphysema, asthma ). Although all flow rates are diminished, expiratory prolongation predominates, and MEF < MIF. Peak expiratory flow is sometimes used to estimate degree of airway obstruction but is dependent on patient effort.

90. (C) Restrictive disease (eg, interstitial lung disease, kyphoscoliosis) . The loop is narrowed because of diminished lung volumes, but the shape is generally the same as in normal volume. Flow rates are greater than normal at comparable lung volumes because the increased elastic recoil of lungs holds the airways open.

91. (D) Fixed obstruction of the upper airway (eg, tracheal stenosis). The top and bottom of the loops are flattened so that the configuration approaches that of a rectangle. Fixed obstruction limits flow equally during inspiration and expiration, and MEF = MIF.

92. (E) Variable extrathoracic obstruction (eg, unilateral vocal cord paralysis, vocal cord dysfunction). When a single vocal cord is paralyzed, it moves passively with pressure gradients across the glottis. During forced inspiration, it is drawn inward, resulting in a plateau of decreased inspiratory flow. During forced expiration, it is passively blown aside, and expiratory flow is unimpaired. Therefore, MIF 50%FVC < MEF 50%FVC. Expiratory flow unimpair d

93. ▣ Asthma and COPD have many similarities and can occur together in the same patient. ▣ The major difference between asthma and COPD is that airflow obstruction is largely reversible in asthma, but in COPD it is largely irreversible. ▣ When spirometry shows an obstructive pattern, it is important to establish whether the obstruction is reversible. ▣ In order to establish the diagnosis, reversibility should be tested with both short- acting bronchodilators and corticosteroids (when FEV1 is less than 60% of the predicted value).

94. The reversibility test is as follows : Spirometry test ( with at least two reproducible flow- volume loops) Intake of a fast acting bronchodilator (often salbutamol) thorough inhalation. 15 minutes pause. A second spirometry test (with at least two reproducible flow- volume loops) A positive response is demonstrated by: FVC increase >10% FEV 1 increase of 200ml or 15% over baseline

95. FEV1 FVC FEV1/ FVC NORMAL > 80% of predicted > 80% of predicted >70% of predicted OBSTRUCTUVE Decreased: Close to 80 Borderline 65- 79 Mild 50- 64 Moderate < 50 severe Normal Decreased (<70%) RESTRICTIVE Normal or decreased Decreased: Close to 80 Borderline 65- 79 Mild 50- 64 Moderate < 50 severe Normal or increased

96. ▣ The diffusing capacity of the lungs (DL) estimates the transfer of oxygen from alveolar gas to red blood cells.

97. The amount of oxygen transferred is largely determined by three factors: ▣ One factor is the area (A) of the alveolar–capillary membrane, which consists of the alveolar and capillary walls. The greater the area, the greater the rate of transfer and the higher the DL. Area is influenced by the number of blood-containing capillaries in the alveolar wall. ▣ The second factor is the thickness (T) of the membrane. The thicker the membrane, the lower the DL. ▣ The third factor is the driving pressure, that is, the difference in oxygen tension between the alveolar gas and the venous blood (∆PO2). Alveolar oxygen tension is higher than that in the deoxygenated venous blood of the pulmonary artery. The greater this difference (∆PO2), the more oxygen transferred.

98. ▣ Measuring the diffusing capacity of carbon monoxide (DLCO) provides a valid reflection of the diffusion of oxygen. ▣ The subject exhales to residual volume and then inhales a gas mixture containing a very low concentration of carbon monoxide (CO) plus an inert gas, usually helium. After a maximal inhalation, the patient holds his or her breath for 10 seconds and then exhales completely. During the breath hold, CO is absorbed while helium is equilibrating with alveolar gas. A sample of exhaled alveolar gas is collected and analyzed.

99. LOW DLCO (<80% predicted) Causes: EMPHYSEMA , INTERSTITIAL LUNG DISEASE , PULMONARY HYPERTENSION , PULMONARY EMBOLISM , PULMONARY EDEMA , RIGHT TO LEFT SHUNT TOF, ANAEMIA . HIGH DLCO( >120- 140% predicted) Causes: ASTHMA, POLYCYTHEMIA , LEFT TO RIGHT SHUNT: Ventricular septal defect (VSD) Patent ductus arteriosus (PDA) Atrial septal defect (ASD), OBESITY, PULMONARY HEMORRHAGE .

100. ▣ Lung volumes can be measured by: Helium dilution method Nitrogen washout method Body plethysmography

101. ▣ Nitrogen washout (or Fowler’s method) is a test to measure the anatomic dead space in the lung during a respiratory cycle, as well as some other parameters related to closure of airways. ▣ A nitrogen washout can be performed with a single nitrogen breath, or multiple ones. Both tests can estimated the functional residual capacity (FRC)

102. ▣ The subject breathes 100% oxygen, and all the nitrogen in the lungs is washed out. ▣ The exhaled volume and the nitrogen concentration in that volume are measured by analyzer. ▣ The difference in nitrogen volume at the initial concentration and at the final exhaled concentration allows a calculation of intrathoracic volume, usually FRC. ▣ Most people with normal distribution of airway resistances will reduce their expired end- tidal nitrogen concentrations to less than 2.5% within seven minutes.

103. The helium dilution technique is a way to measure the functional residual capacity (FRC) of the lungs. This technique is a closed circuit system where a spirometer is filled with a mixture of helium and oxygen. The amount of helium in the spirometer is known at the beginning of the test. (concentration x volume = amount) The subject is asked to breathe (normal breaths) in the mixture starting from FRC, which is the gas volume in the lung after a normal breath out.

104. ▣ The spirometer measures the helium concentration. ▣ Because there is no leak of substances in the system, the amount of helium remains constant during the test, and the FRC is calculated using the following equation: C1 x V1 = C2 x V2 C1 x V1 = C2 x (V1+FRC) FRC= ((C1 x V1)/C2) – V1 Where, V2= total gas volume (FRC+ volume of spirometer) V1= volume of gas in spirometer C1= initial (unknown) concentration of helium C2= final concentration of helium (measured by spirometer).

105. ▣ Body plethysmography is a test to find out how much air is in your lungs after you take in a deep breath, and how much air is left in your lungs after breathing out as much as you can. ▣ Based on principle of BOYLE’S LAW(P*V=k) ▣ Principle advantage over other two method is it quantifies non ‐ communicating gas volumes.

106. ▣ The subject is placed inside a sealed chamber with a single mouthpiece. ▣ At the end of normal expiration, the mouthpiece is closed. The subject is then asked to make an inspiratory effort. ▣ As the subject tries to inhale, the lungs expand, decreasing pressure within the lungs and increasing lung volume. ▣ This, in turn, increases the pressure within the box since it is a closed system and the volume of the box compartment has decreased to accommodate the new volume. ▣ Boyles law is used to calculate the unknown volume within the lungs.

107. It is a diagnostic procedure in which a blood is obtained from an artery directly by an arterial puncture or accessed by a way of indwelling arterial catheter.

108. ▣ ABG analysis is one of the first tests ordered to assess respiratory status because it helps evaluate gas exchange in the lungs. ▣ An ABG test can measure how well the person's lungs and kidneys are working and how well the body is using energy. ▣ It measures the acidity ( pH ) and the levels of oxygen and carbon dioxide in the blood from an artery . This test is used to check how well your lungs are able to move oxygen into the blood and remove carbon dioxide from the blood.

109. ▣ Respiratory failure - in acute and chronic states. ▣ Any severe illness which may lead to a metabolic acidosis - for example: Cardiac failure. Liver failure. Renal failure. Hyperglycaemic states associated with diabetes mellitus. Multiorgan failure. Sepsis. Burns. Poisons/toxins. ▣ Ventilated patients. ▣ Sleep studies.

110. ▣ An arterial blood gas (ABG) test is done to: ▣ Check for severe breathing problems and lung diseases , such as asthma , cystic fibrosis , or chronic obstructive pulmonary disease (COPD) . ▣ See how well treatment for lung diseases is working. ▣ Find out if you need extra oxygen or help with breathing (mechanical ventilation). ▣ Find out if you are receiving the right amount of oxygen when you are using oxygen in the hospital. ▣ Measure the acid- base level in the blood of people who have heart failure , kidney failure , uncontrolled diabetes , sleep disorders , severe infections, or after a drug overdose.

111. ▣ Overlying infection or burn at insertion site. ▣ Absence of collateral circulation. ▣ Synthetic graft. SITES ▣ Preferred site- Radial and femoral artery. ▣ Less common- Dorsalis pedis and post tibial artery. ▣ Avoid – artery without collateral supply.

112. Arterial blood can be obtained by direct arterial puncture most usually at the wrist (radial artery) as it is easy to palpate and has a good collateral presentation. Alternatives to the radial artery include the femoral and brachial artery. It is important to ensure good collateral circulation as there is a theoretical risk of thrombus occlusion. ▣ If the radial artery is to be used, perform Allen's test to confirm collateral blood flow to the hand. ▣ Allen's test ▣ Elevate the hand and make a fist for approximately 30 seconds. ▣ Apply pressure over the ulnar and the radial arteries occluding both (keep the hand elevated). ▣ Open the hand which will be blanched. ▣ Release pressure on the ulnar artery and look for perfusion of the hand (this takes under eight seconds). ▣ If there is any delay then it may not be safe to perform radial artery puncture.

113. ▣ The patient's arm is placed palm- up on a flat surface, with the wrist dorsiflexed at 45°. A towel may be placed under the wrist for support. The puncture site should be cleaned with alcohol or iodine, and a local anaesthetic should be infiltrated. ▣ Local anaesthetic makes arterial puncture less painful for the patient. The radial artery should be palpated for a pulse, and a pre- heparinised syringe with a 23 or 25 gauge needle should be inserted at an angle just distal to the palpated pulse.A small quantity of blood is sufficient. If repeated arterial blood gas analysis is required, it is advisable to use a different site (such as the other radial artery) or insert an arterial line.

114. ▣ Bleeding at the puncture site. ▣ Blood flow problems at puncture site (rare). ▣ Bruising at the puncture site. ▣ Delayed bleeding at the puncture site. ▣ Fainting or feeling light- headed. ▣ Hematoma (blood accumulating under the skin). ▣ Infection (a slight risk any time the skin is broken).

115. ▣ PH: measures hydrogen ion concentration in the blood, it shows blood’ acidity or alkalinity ▣ PCO2 : It is the partial pressure of CO2 that is carried by the blood for excretion by the lungs, known as respiratory parameter ▣ PO2: It is the partial pressure of O2 that is dissolved in the blood , it reflects the body ability to pick up oxygen from the lungs ▣ HCO3 : known as the metabolic parameter, it reflects the kidney’s ability to retain and excrete bicarbonate

116. 7.35 – 7.45 ▣ PH = ▣ PCO2 = ▣ PO2 = ▣ HCO3 = 35 – 45 mmhg 80 – 100 mmhg 22 – 26 meq/L

117. ▣ The following indices should be looked at in the following order : ▣ Blood pH - high indicates alkalosis, low indicates acidosis and normal indicates either normal, mixed defect or a compensated defect. ▣ PaCO 2 level - is it a respiratory problem? If not, look at the bicarbonate level. High PaCO 2 with an acidosis indicates a respiratory problem. If the PaCO 2 is normal or low it indicates compensation. ▣ Bicarbonate - if the bicarbonate fits with the pH it suggests a primary metabolic problem. If not, it indicates compensatory changes. ▣ Look for any compensation - eg, low PaCO 2 in severe metabolic acidosis. ▣ Anion gap in metabolic acidosis ▣ O 2 level - is hypoxaemia present?

118. ▣ It is possible to have a mixed respiratory and metabolic disorder that makes interpretation of an arterial blood gas result difficult. As a general rule, when a normal pH is accompanied by an abnormal PaCO2 or HCO3ˉ then a mixed metabolic- respiratory disorder exists. (Table) provides some common clinical examples of mixed respiratory and metabolic disturbances.

119. Disorder Characteristics Selected situations Respiratory acidosis with ↓in pH Cardiac arrest metabolic acidosis ↓ in HCO 3 Intoxications ↑ in PaCO 2 Multi-organ failure Respiratory alkalosis with ↑in pH Cirrhosis with diuretics metabolic alkalosis ↑ in HCO 3 - Pregnancy with vomiting ↓ in PaCO 2 Over ventilation of COPD Respiratory acidosis with pH in normal range COPD with diuretics, vomiting, NG suction metabolic alkalosis ↑ in PaCO 2 , Severe hypokalemia ↑ in HCO 3 - Respiratory alkalosis with pH in normal range Sepsis metabolic acidosis ↓ in PaCO 2 Salicylate toxicity ↓ in HCO 3 Renal failure with CHF or pneumonia Advanced liver disease Metabolic acidosis with pH in normal range Uremia or ketoacidosis with vomiting, NG metabolic alkalosis HCO 3 - normal suction, diuretics, etc.

120. ▣ Alveolar- arterial oxygen gradient - (A-a)pO 2 ; difference in oxygen partial pressures between the alveolar and arterial side.It provides a measure of oxygen diffusion across the alveoli into the blood. Thus, will be impaired in lung disease such as COPD. Raised (A- a)pO 2 may also represent the presence of an intrapulmonary shunt, ie a lung that is perfused but not ventilated - for example, pneumonia.

121. ▣ The anion gap is the difference in the measured cations (positively charged ions) and the measured anions (negatively charged ions) in serum , plasma , or urine . ▣ Anion gap can be classified as either high, normal or, in rare cases, low. ▣ A high anion gap indicates acidosis . ▣ A low anion gap is frequently caused by hypoalbuminemia . ▣ Usually done when primary metabolic acidosis is suspected. Anion gap helps determine the etiology of the metabolic acidosis. ▣ Normal=10- 18mmol/L