Basics of Respiratory Anatomy, Physiology and Respiratory failure

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1 Basics of Respiratory Anatomy, Physiology and Respiratory failure Dr Gopal Raval CONSULTANT PULMONOLOGIST & CRITICAL CARE SPECIALIST

2 Basics of the Respiratory System Exchange of gases Directionality depends on gradients! Atmosphere to blood Blood to tissues Regulation of ph Dependent on rate of CO 2 release Protection Vocalization

3 What structural aspects must be considered in the process of respiration? The conduction portion The exchange portion The structures involved with ventilation Skeletal & musculature Pleural membranes Neural pathways All divided into Upper respiratory tract Entrance to larynx Lower respiratory tract Larynx to alveoli (trachea to lungs)

4 Divisions of the Respiratory System Upper respiratory tract (outside thorax) Nose Nasal Cavity Sinuses Pharynx Larynx

5 Nasal mucosa Respiratory mucosa lined with pseudostratified columnar epithelium Has rich blood supply esp. over inferior turbinate

6 Paranasal sinuses Air containing spaces that open into nasal cavity 4 pairs Frontal Maxillary Ethmoid Sphenoid

7 Functions of Nose Air passageway Warms, moistens, filters air Sinuses act to provide resonance for voice

8 Functions of larynx Air passageway Filters, warms, humidifies air Protects airway against entrance of solid or liquids Voice production

9 What is the function of the upper respiratory tract? Warm Humidify Filter Vocalize Raises incoming air to 37 Celsius Raises incoming air to 100% humidity Forms mucociliary escalator

10 Divisions of the Respiratory System Lower respiratory tract (within thorax) Trachea Bronchial Tree Lungs

11 Bones, Muscles & Membranes

Function of these Bones, Muscles & Membranes Create and transmit a pressure gradient Relying on the attachments of the muscles to the ribs (and overlying tissues) The attachment of the diaphragm to

12 Function of these Bones, Muscles & Membranes Create and transmit a pressure gradient Relying on the attachments of the muscles to the ribs (and overlying tissues) The attachment of the diaphragm to the base of the lungs and associated pleural membranes The cohesion of the parietal pleural membrane to the visceral pleural membrane Expansion & recoil of the lung and therefore alveoli with the movement of the overlying structures -Pleural Membrane Detail Cohesion between parietal and visceral layers is due to serous fluid in the pleural cavity Fluid (30 ml of fluid) creates an attraction between the two sheets of membrane As the parietal membrane expands due to expansion of the thoracic cavity it pulls the visceral membrane with it - And then pulls the underlying structures which expand as well Disruption of the integrity of the pleural membrane will result in a rapid equalization of pressure and loss of ventilation function = collapsed lung or pneumothorax

13 The Respiratory Tree connecting the external environment to the exchange portion of the lungs similar to the vascular component larger airway = higher flow & velocity small cross-sectional area smaller airway = lower flow & velocity large cross-sectional area

14 The Respiratory Tree Upper respiratory tract is for all intensive purposes a single large conductive tube The lower respiratory tract starts after the larynx and divides again and again and again to eventually get to the smallest regions which form the exchange membranes Trachea Primary bronchi Secondary bronchi conductive portion Tertiary bronchi Bronchioles Terminal bronchioles Respiratory bronchioles with start of alveoli outpouches exchange portion Alveolar ducts with outpouchings of alveoli

15 Conducting zone: Includes all the structures that air passes through before reaching the respiratory zone. Warms and humidifies until inspired air becomes: 37 degrees Saturated with water vapor Filters and cleans: Mucus secreted to trap particles Mucus/particles moved by cilia to be expectorated. Respiratory zone Region of gas exchange between air and blood - Respiratory bronchioles - Alveolar ducts, Alveolar Sacs and - Alveoli

19 What is the function of the lower respiratory tract? Exchange of gases. Due to Huge surface area = 1x10 5 m 2 of type I alveolar cells (simple squamous epithelium) Associated network of pulmonary capillaries 80-90% of the space between alveoli is filled with blood in pulmonary capillary networks Exchange distance is approx 1 um from alveoli to blood! Protection Free alveolar macrophages (dust cells) Surfactant produced by type II alveolar cells (septal cells)

20 Characteristics of exchange membrane High volume of blood through huge capillary network results in Fast circulation through lungs Pulmonary circulation = 5L/min through lungs. Systemic circulation = 5L/min through entire body! Blood pressure is low Means» Filtration is not a main theme here, we do not want a net loss of fluid into the lungs as rapidly as the systemic tissues» Any excess fluid is still returned via lymphatic system

21 Respiratory Physiology Basic Atmospheric conditions Pressure is typically measured in mm Hg Atmospheric pressure is 760 mm Hg Atmospheric components Nitrogen = 78% of our atmosphere Oxygen = 21% of our atmosphere Carbon Dioxide =.033% of our atmosphere Water vapor, krypton, argon,. Make up the rest A few laws to remember Dalton s law Fick s Laws of Diffusion Boyle s Law Ideal Gas Law

22 Dalton s Law Law of Partial Pressures each gas in a mixture of gases will exert a pressure independent of other gases present Or The total pressure of a mixture of gases is equal to the sum of the individual gas pressures. What does this mean in practical application? If we know the total atmospheric pressure (760 mm Hg) and the relative abundances of gases (% of gases) We can calculate individual gas effects! P atm x % of gas in atmosphere = Partial pressure of any atmospheric gas» P O 2 = 760mmHg x 21% (.21) = 160 mm Hg Now that we know the partial pressures we know the gradients that will drive diffusion!

23 Fick s Laws of Diffusion Things that affect rates of diffusion Distance to diffuse Gradient sizes Diffusing molecule sizes Temperature What is constant & therefore out of our realm of concern? So it all comes down to partial pressure gradients of gases determined by Dalton s Law!

24 Boyle s Law Describes the relationship between pressure and volume the pressure and volume of a gas in a system are inversely related P 1 V 1 = P 2 V 2

25 How does Boyle s Law work in us? As the thoracic cavity (container) expands the volume must up and pressure goes down If it goes below 760 mm Hg what happens? As the thoracic cavity shrinks the volume must go down and pressure goes up If it goes above 760 mm Hg what happens

26 Ideal Gas law The pressure and volume of a container of gas is directly related to the temperature of the gas and the number of molecules in the container PV = nrt n = moles of gas T = absolute temp R = universal gas J/K mol Do we care?

27 Can t forget about poor Charles and his law or Henry and his law Aptly named Charles s Law & Henry s Law As the temp goes up in a volume of gas the volume rises proportionately V T At a constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid. OR the solubility of a gas in a liquid at a particular temperature is proportional to the pressure of that gas above the liquid. *also has a constant which is different for each gas

28 Respiratory Physiology Pulmonary Ventilation = breathing Mechanism Movement of gases through a pressure gradient - hi to low. When atmospheric pressure (760 mmhg) is greater than lung pressure ---- air flows in = inspiration. When lung pressure is greater than atmospheric pressure ---- air flows out = expiration. External respiration Exchange of gases between lungs and blood Internal respiration Exchange of gases between blood and body cells

29 Ventilation What is the relationship between alveolar pressure and intrapleural pressure and the volume of air moved?

Ventilation Inspiration Occurs as alveolar pressure drops below atmospheric pressure For convenience atmospheric pressure = 0 mm Hg A (-) value then indicates pressure below atmospheric P A (+) value

30 Ventilation Inspiration Occurs as alveolar pressure drops below atmospheric pressure For convenience atmospheric pressure = 0 mm Hg A (-) value then indicates pressure below atmospheric P A (+) value indicates pressure above atmospheric P At the start of inspiration (time = 0), atmospheric pressure = alveolar pressure» No net movement of gases! At time 0 to 2 seconds Expansion of thoracic cage and corresponding pleural membranes and lung tissue causes alveolar pressure to drop to -1 mm Hg Air enters the lungs down the partial pressure gradient

Ventilation Expiration Occurs as alveolar pressure elevates above atmospheric pressure due to a shrinking thoracic cage At time 2-4 seconds Inspiratory muscles relax, elastic tissue of corresponding

31 Ventilation Expiration Occurs as alveolar pressure elevates above atmospheric pressure due to a shrinking thoracic cage At time 2-4 seconds Inspiratory muscles relax, elastic tissue of corresponding structures initiates a recoil back to resting state This decreases volume and correspondingly increases alveolar pressure to 1 mm Hg» This is above atmospheric pressure, causing? At time 4 seconds Atmospheric pressure once again equals alveolar pressure and there is no net movement

32 Circulation Overview

33 Ventilation Both inspiration and expiration can be modified Forced or active inspiration Forced or active expiration The larger and quicker the expansion of the thoracic cavity, the larger the gradient and The faster air moves down its pressure gradient

34 Ventilation Things to consider surfactant effect airway diameter Minute volume respiration (ventilation rate times tidal volume) & anatomical dead space Leading to a more accurate idea of alveolar ventilation rates Changes in ventilation patterns

35 Ventilation Surfactant is produced by the septal cells Disrupts the surface tension & cohesion of water molecules Impact prevents alveoli from sticking together during expiration

36 Ventilation Airway diameter & other factors that affect airway resistance?

37 Ventilation The relationship between minute volume (total pulmonary ventilation) and alveolar ventilation & the subsequent mixing of air

38 Pleural pressure Pressure of fluid in the narrow space b/w visceral pleura & parietal pleura. At beginning of inspiration is about -5cm of H2o. Required to hold lungs open to their resting level. During normal inspiration,the expansion of chest cage pulls on lungs with still greater force. Creates still more negative pressure to an average of about -7.5 cm of H2o. During expiration events are reversed.

39 Trans pulmonary pressure Pressure difference b/w alveolar pressure & pleural pressure. Pressure difference b/w that in alveoli & that on outer surface of lungs. Measure of elastic forces in lungs that tend to collapse at each instant respiration.

40 Compliance of lungs Extent to which lungs expand for each unit increase in trans pulmonary pressure. Total compliance of both lungs together in normal human being average about 200ml of air /1 cm of H2o. Two compliance. a) dynamic b) static

41 Pulmonary Function Spirometry Breathe into a closed system, with air, water, moveable bell Insert fig

42 Lung Volumes

43 Pulmonary Circulation Left ventricle pumps to entire body, Right ventricle only to lungs. Both ventricles pump 5.5 L/min! Pulmonary circulation: various adaptations. - Low pressure, low resistance. - Prevents pulmonary edema. - Pulmonary arteries dilate if P0 2 is low (opposite of systemic)

44 Gas Transport O2 transport in blood Hemoglobin O2 binds to the heme group on hemoglobin, with 4 oxygens/hb PO2 PO2 is the most important factor determining whether O2 and Hb combine or dissociate O2-Hb Dissociation curve

46 Controls of Respiration Medullary Rhythmicity Area Medullary Inspiratory Neurons are main control of breathing Pons neurons influence inspiration, with Pneumotaxic area limiting inspiration and Apneustic area prolonging inspiration. Lung stretch receptors limit inspiration from being too deep o Medullary Expiratory Neurons Only active with exercise and forced expiration

48 Respiratory Failure The inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

Respiratory failure is a syndrome in which the

exchange functions: oxygenation and carbon dioxide

In practice, respiratory failure is defined as a

49 Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO 2 value of less than 60 mm Hg while breathing air or a PaCO 2 of more than 50 mm Hg. normal reference values : PaO 2 < 60mmHg(8kPa) with or without PaCO 2 > 50mmHg(6.67kPa) RFI = PaO 2 /FiO 2 300

50 hypoxemic (Group Ⅰ) respiratory failure a PaO 2 of less than 60 mm Hg with a normal or low PaCO 2 or without widening of aveolar-arterial oxygen gradient. with hypercapnic (Group Ⅱ ) respiratory failure a PaO 2 low 60 mm Hg and PaCO 2 of more than 50 mm Hg. assessment of the PH with HCO3 to decide acute, acute on chronic or chronic failure. a aveolar-arterial oxygen gradient should be assessed.

51 Respiratory system includes: CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature

53 Hypoxemic Respiratory Failure- (Affects the po2) V/Q Mismatch Shunt Diffusion Limitation Alveolar Hypoventilation- Low inspired pressure of oxygen- high altitude

54 ventilation/perfusion relationship The dysfunction of gas exchange can arise secondary to ventilation /perfusion mismatching. V A Q V A / Q Top 1.2L/min 0.4L/min 3.0 Middle 1.8L/min 2.0L/min 0.9 Bottom 2.1L/min 3.4L/min 0.6

55 Range of V/Q Relationships Fig. 68-4

56 V/Q mismatch: Dead space ventilation Alveoli that are normally ventilated but poorly perfused Anatomic dead space Gas in the large conducting airways that does not come in contact with the capillaries. Physiologic dead space Alveolar gas that does not equilibrate fully with capillary blood

57 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

58 Shunt V/Q ratio below 1.0 occurs when pulmonary capillary blood flow is excessive relative to ventilation. It does not participate in pulmonary gas exchange. True shunt ; total absence of gas exchange b/w capillary blood and alveolar gas & is equivalent to an anatomic shunt b/w rt & lt sides of the heart. Venous admixture ; represent the capillary flow that does not equilibrate completely with alveolar gas (0 <V/Q <1). As the venous admixture increase,the V/Q ratio decrease until it becomes a true shunt.( V/Q= 0). The fraction of cardiac output that represents intrapulmonary shunt is known as the shunt fraction.

59 Perfusion without ventilation Intra-cardiac (Shunting) Any cause of right to left shunt eg Fallot s, Eisenmenger Intra-pulmonary Pneumonia, Pulmonary oedema (Alveoli are filled with fluid ) Asthma (Small airways occluded ) Pulmonary embolism ( capillary flow is excessive to non embolised regions in the lung) Atelectasis (Alveolar collapse ) Collapse Pulmonary haemorrhage or contusion

60 AS Intrapulmonary shunt increase from 10% to 50%, an increase in FIO2 produces less of an increment in the arterial PO2. Patients with shunts are more hypoxemic than those with VQ mismatch and they may require mechanical ventilators

Diffusion abnormality: Less common Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area Reduction of diffusion membrane

61 Diffusion abnormality: Less common Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area Reduction of diffusion membrane area Abnormalities of diffusion may not cause arterial hypoxia in persons at rest unless they are extremely severe. (total: 80 mm 2; at rest: 30~40 mm 2 ) Causes include: Acute Respiratory Distress Syndrome Fibrotic lung disease

62 Diffusion Limitation Fig. 68-5

63 Alveolar Hypoventilation Mainly due to hypercapnic respiratory failure but can cause hypoxemia Increased pco2 with decreased PO2 Obstructive & Restrictive lung disease CNS diseases Neuromuscular diseases

64 Hypercapnic Respiratory Failure PaCO 2 >50 mmhg (Type II) Hypoxemia is always present ph depends on level of HCO 3 HCO 3 depends on duration of hypercapnia Renal response occurs over days to weeks

65 Acute Hypercapnic Respiratory Failure (Type II) Acute Arterial ph is low Causes - sedative drug over dose - acute muscle weakness such as myasthenia gravis - severe lung disease: alveolar ventilation can not be maintained (i.e. Asthma or pneumonia) Acute on chronic: This occurs in patients with chronic CO 2 retention who worsen and have rising CO 2 and low ph. Mechanism: respiratory muscle fatigue

66 Hypercapnic Respiratory Failure Ventilatory Failure- affects CO2 1. Abnormalities of the airways and alveoli- air flow obstruction and air trapping Asthma, COPD, Brochiectasis and cystic fibrosis 2. Abnormalities of the CNS- suppresses drive to breathe drug OD, narcotics, head injury, spinal cord injury, cv stroke,hypothyroidism,tumor, respi centre dysfunction,sleep apnea,ohs

67 Hypercapnic Respiratory Failure 3. Abnormalities of the chest wall Flail chest, morbid obesity, kyphoscoliosis, pneumothorax 4. Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis multiple sclerosis,polymyositis,poliomyelitis,poly neuropathies,cervical cord lesion. Metabolic.

68 Tissue Oxygen needs Tissue O2 delivery is determined by: Amount of O2 in hemoglobin Cardiac output *Respiratory failure places patient at more risk if cardiac problems or anemia

69 Signs and Symptoms of Respiratory hypoxemia po2<60 Failure- ABG s May be hypercapnia pco2>50 only one cause- hypoventilation *In patients with COPD watch for acute drop in po2 and O2 sats along with inc. C02 and KNOW BASELINE!!!

70 Hypoxemia Compensatory Mechanisms- early Tachycardia- more O2 to tissues Hypertension- Tachypnea take in more O2 Restlessness and apprehension Dyspnea Cyanosis Confusion and impaired judgment **Later dysrhythmias and metabolic acidosis, dec. B/P and Dec. CO.

71 Hypercapnia Dyspnea to respiratory depression- if too high CO2 narcosis Headache-vasodilation- Increases ICP Papilledema Tachycardia and inc. B/P Drowsiness and coma Respiratory acidosis **Administering O2 may eliminate drive to breathe especially with COPD patients- WHY??

72 Specific Clinical Manifestations Respirations- depth and rate Patient position- Pursed lip breathing Orthopnea Inspiratory to expiratory ratio (normal 1:2) Retractions and use of accessory muscles Breath sounds

73 Diagnosis History & Physical Assessment Pulse oximetry (90% is PaO2 of 60) ABG CXR CBC Electrolytes EKG,2 D Echo Sputum and blood cultures, CT chest with Pulmonary angio or V/Q scan Pulmonary function tests (PFT s) Electromyography (EMG) Nerve conduction study

74 Treatment Goals O2 therapy Mobilization of secretions Positive pressure ventilation(ppv) Drug Therapy Medical Supportive Treatment Nutrition

75 Drug Therapy Relief of bronchospasm- bronchodilators Reduction of airway inflammation-corticosteroids by inhalation or IV or oral Reduction of pulmonary congestion-diuretics and nitroglycerine with heart failure. Treatment of pulmonary infections- IV antibiotics, Reduction of anxiety, pain and agitation. May need sedation or neuromuscular blocking agent if on ventilator.

76 Medical Supportive Treatment Treat underlying cause Maintain adequate cardiac output- monitor B/P and MAP. Maintain adequate Hemoglobin concentration- need 9g/dl or greater **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs

77 Nutrition During acute phase- enteral or parenteral nutrition In a hypermetabolic state- need more calories If retain CO2- avoid high carb diet

78 THANK YOU Sterling hospital & SPARSH (The Healing Touch) Chest Diseases Centre Ahemedabad

Respiratory System. Part 2

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