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Abhishek respiratory ANATOMY & PHYSIOLOGY , and ACUTE RESPIRATORY FAILURE
 

Abhishek respiratory ANATOMY & PHYSIOLOGY , and ACUTE RESPIRATORY FAILURE

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    Abhishek respiratory ANATOMY & PHYSIOLOGY , and ACUTE RESPIRATORY FAILURE Abhishek respiratory ANATOMY & PHYSIOLOGY , and ACUTE RESPIRATORY FAILURE Presentation Transcript

    • ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM AND ACUTE RESPIRATORY FAILURE PRESENTED BY: DR. ABHISHEK SAINI
    • RESPIRATORY TRACT The Upper Respiratory Tract • Nose • Nasal cavity • Sinuses • Pharynx The Lower Respiratory Tract • Larynx • Trachea • Bronchial Tree • Lungs
    • Tracheobronchial Tree MODEL • The most useful and widely MODEL accepted approach remains that of WEIBEL. He numbered successive generations of air passages from the trachea(generation 0) down to the alveolar sacs(generation 23)
    • Contd… TRACHEA Rt. Main bronchus Superior lobar Bronchus(3) • Apical • Posterior •Anterior Middle lobar bronchus(2) • Lateral • Medial Lt. Main bronchus Inf. Lobar Sup. Lobar bronchus(5) bronchus(5) • Superior •Medial basal • Ant. Basal • Post basal • Lateral basal • Apical •Posterior • Anterior •Superior lingular •Inferior lingular Inf. Lobar bronchus(4) •Apical •Ant basal •Lat basal •Post basal
    • CONTD
    • GRAYS ANATOMY
    • • There are about 300 million alveoli. • Between 75-300 micron in diameter. • Most gas exchange takes place at alveoli capillary membrane. • 85-90% alveoli are covered by capillary membrane. • The cross sectional area is approx. 70m square LINING EPITHELIUM Trachea Terminal bronchioles: ciliated psuedo stratified columnar epithelium Respiratory bronchioles alveolar ducts alveoli: non ciliated cuboidal epithelium
    • GRAYS ANTOMY STUCTURE ARTERIAL SUPPLY NERVE SUPPLY VENOUS DRAINAGE TRECHEA INFERIOR THYROID ARTERY(⅔ rd) MIDDLE CERVICAL PLEXUS(SYMPTH) INFERIOR THYROID VEIN DIAPHRAGM PHRENIC ARTERY,INTERNAL MAMARY ARTERY,INTRECOSTAL ARTERY EXTERNAL &INTERCOSTAL MUSCLE BRONCHI TERMINAL BRONCHIOLS RESPIRATORY BRONCHIOLS ALVEOLI INTERCOSTAL ARTERIES BRONCHIAL ARTERY PHRENIC NERVE (C3-C5) SUPERIOR AND INFERIOR PHRENIC VEIN THORACIC NERVE (T1-T11) INTERCOSTAL VEINS PULMONARY PLEXUS(VAGUS AND SYMPTH) BRONCHIAL VEIN PULMONARY ARTERY PULMONARY PLEXUS(VAGUS AND SYMPTH) PULMONARY VEIN
    • CIRCULATION GANONG 23 RD PULMONARY CIRCULATION BRONCHIAL CIRCULATION • LOW-PRESSURE, HIGH-FLOW CIRCULATION HIGH-PRESSURE, LOW-FLOW CIRCULATION CONTAIN 100% CARDIAC OUTPUT CONTAIN 1-3% CARDIAC OUTPUT SUPPLIES RESPITARY BRONCHIOLS TO ALVEOLI SUPPLIES BRONCHI TO TERMINAL BRONCHIOLS ARIES FROM HEART ARIES FROM AROTA EXCEPTION ARTERY CARRY DEOXYGENETED BLOOD SHUNT(COMMON)
    • RESPIRATORY PHYSIOLOGY GANONG23rd • A) PULMONARY FUNCTION • B) GAS TRANSPORT BETWEEN LUNG AND TISSUES • C) REGULATION OF RESPIRATION
    • For pulmonary ventilation to occur there should be a pressure gradient driving air in & out 1. The movement of air into & out of the lungs (ventilation) occurs as a result of pressure difference between the alveoli & environment. 2. The pressure differences in pulmonary system are induced by changes in lung volumes occurring as a result of coordinated movement of diaphragm & chest. 3. The lung volumes are affected by its physical properties; compliance, elasticity & surface tension.
    • PRESSURES WITHIN THE THORACIC CAVITY Boyle’sLaw (P∞1/V)
    • Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing. (TP = ALp - IPp) Ventilation cycle. Lung volume changes due to airflow into or out of the lung. Gas flow depends on a gradient of pressure from the mouth to the alveolus; alveolar pressure change occurs in response to altered intrapleural pressure.
    • MUSCLES OF RESPIRATION
    • Muscles of inspiration Primary muscles 1. Diaphragm • Increase AP-VERTICAL diameter,phrenic nerve(C3-C5 2.External intercostal muscles(inspiratory muscles) • Run obliquely downward and forward from rib to rib. • Innervated by segmental spinal nerves. • Their contraction has 2 result. • Bucket-handle effect-( increase in transverse diameter ). • Water-pump-handle effect-( increase in AP diameter )
    • contd DURING FORCED INSPIRATION • The accessory (or secondary) muscles of inspiration also come into play. • 1.Scalene.( lift the first two ribs) • 2.Sternocleidomastoids (lift the sternum outward) • 3.Neck and back muscles.(increasing the transverse area) MUSCLES OF EXPIRATION • No primary muscles of expiration, passive process. FORCED EXPIRATION Expiratory(internal intercostals),abdominal muscles.
    • Lung volumes(adult) Ganong 23rd
    • CHILDREN VOLUMES MEASUREMENT VALUE(ML/KG) TIDAL VOLUME 8-10 RESIDUAL VOLUME 18-20 FUNCTIONAL RESIDUAL CAPACITY 25-30 VITAL CAPACITY 35-40 TOTAL LUNG CAPACITY 55-70 ADULT RESPIRATORY MINUTE VENTILLATION(RMV) 6L/MIN ALVEOLAR VENTILLATION(AV) 4.2L /MIN IN CHILDREN RMV & AV VARY WITH AGE
    • LungCompliance(CL) (CL) is change in lung volume per unit change in airway pressure, it reflects stretchability of lung and chest wall. CL = ΔV / ΔP compliance of both lungs = .2liter/ per centimeter of water FACTORS : Elastic recoil elasticity of the pulmonary cells the extracellular matrix(e.g. elastin and collagen) surface tension High CL EMPHYSEMA Low CL Interstitial pulmonaryfibrosis,hydropneumothorax, asthama ,pneumonia.
    • Pressure-volume (compliance) curve for a maximal breath. TLC, total lung capacity; FRC, functional residual capacity; RV, residual volume.
    • SURFACE TENSION .
    • Surfactant
    • The pulmonary surfactant present at the alveolar air-water interface has three major effects: 1. Because surfactant reduces surface tension, it increases compliance, making it far easier to inflate the lungs. 2. By reducing surface tension, surfactant minimizes fluid accumulation in the alveolus.(20 mm hg) 3. Surfactant helps keep alveolar size relatively uniform during the respiratory cycle. Ganong 23rd
    • WORK OF BREATHING in quiet respiration is.3-.7 kgm/min.it can be calculated by pressure volume curve. ELASTIC WORK(65%) STRETCHING THE ELASTIC TISSUES OF THE CHEST WALL &LUNGS NONELASTIC WORK a) VISCOUS RESISTANCE(7%) MOVING IN ELASTIC TISSUE b) AIRWAY RESISTANCE(28%) MOVING AIR THROUGH RESPIRATORY PASSAGES
    • GAS EXCHANGE IN LUNG • Diffusion of gases oocur according to pressure gradient. • Equilibrium reach in .75 sec • Diffusion Capacity of Lung: The diffusing capacity is defined as the volume of gas that diffuses through the alveolar membranes per second for a pressure difference of 1 kPa. • The diffusing capacity of the lung for a given gas is directly proportionate to the surface area of the alveolocapillary membrane and inversely proportionate to its thickness. • Sarcoidosis increase. ,berylliosis thickness
    • Alveocapillary membrane
    • VENTILLATION/PERFUSION RATIO at rest .8(4.2L/min ventillation divided by 5.5L/min blood flow)
    • Functions of the lung
    • B)GAS TRANSPORT OXYGEN TRANSPORT GANONG 23 RD • FACTORS a)lung ventillatoin b)gas exchange c)blood flow(cardiac output) d)capacity-blood-carry 0₂ amount of hemoglobin affinity of hemoglobin • Affinity of hemoglobin Ph(H˖) Temp CO₂ 2,3BPG(biphosphoglycerete) HbO₂+2,3BPG↔Hb-2,3BPG+O₂
    • O2 Dissociation Curve
    • CO2 TRANSPORT
    • EFFECTS • BOHR EFFECT deoxygenated hemoglobin (deoxyhemoglobin) binds H+ more actively than does oxygenated hemoglobin (oxyhemoglobin). • HALDANE EFFECT binding of O2 to hemoglobin reduces its affinity for CO2. • FLOW DOWNHILL
    • C)REGULATION OF RESPIRATION GANONG 23RD A) NEURAL CONTROL ①VOLUNTARY CONTROL ② AUTONOMIC CONTROL ①VOLUNTARY CONTROL Mediated by a pathway originating from cerebral cortex, bypass the medullary respiratory centres to project directly on the spinal respiratory neurons. EXAMPLES : Voluntary breathing practisedTalking, Singing, Swimming Breath holding spell(50-60 sec) Voluntary hyperventillation .
    • ②AUTONOMIC (RECIPROCAL INNERVATION) Medulla MOTOR NEURON THORACIC CORD(T1-T11) EXTERNAL INTERCOSTAL INTERNAL INTERCOSTAL MOTOR NEURON CERVICAL CORD(C3-C5) DIAPHRAGM (PHRENIC)
    • MEDULLARY CENTER GANONG 23RD • DRG : “INSPIRATORY RAMP” NORMAL BREATHING • VRG : BOTH “INSPIRATORY & EXPIRATORY” FORCED • APNEUSTIC CENTER(PONS) PREVENT SWITCH OFF INSPIRATORY RAMP INHIBIT BY VAGUS&PNEUMOTAXIC CENTER • PNEUMOTAXIC CENTER(PONS) SWITCHING IN BETWEEN INSPIRATION & EXPIRATION • VAGUS NERVE INHIBIT RESPIRATION
    • • Pre-Bötzinger complex (preBÖTC) PACEMAKER • Between nucleus ambiguus and the lateral reticular nucleus( dorsal medulla) • TRANSECTIONS & SPIROMETER TRACINGS
    • B)NON NEURAL CONTROL • a) CHEMICAL CONTROL PERIPHERAL RECEPTOR AROTIC & CAROTID BODIES CENTRAL MEDULLARY RECEPTOR • b) NON-CHEMICAL CONTROL DIFFERENT MECHANISMS
    • PERIPHERAL RECEPTOR
    • CONTROL CAUSE(H+,CO₂, O₂,OTHERS) RECEPTOR(CEN TRAL & PERIPHERAL) CENTERS=EFFEC T(VOLUNTARY)
    • b)NON CHEMICAL RECEPTOR IN LUNG&AIRWAY GANONG 23 RD
    • CONTD • MYELINATED (slowely adapting) Hering–Breuer inflation reflex Hering Breuer deflation reflex • MYELINATED (rapidly adapting /irritant) Stimulated by histamine,prostaglandins causes coughing, bronchoconstriction, and mucus secretion • UNMYELINATED/C FIBERS/J RECEPTOR(PATHOLOGICAL) Pulmonary congestion , embolization, pneumonia Exogenous and endogenous substances (eg, capsaicin, bradykinin, serotonin) Response that is produced is apnea followed by rapid breathing, bradycardia, and hypotension (pulmonary chemoreflex)
    • NON CHEMICAL CONTD GANONG 23 RD RECEPTOR LOCATION EFFECT PROPIORECEPTOR JOINT,MUSCLE & TENDON EXCERCISE(↑ RATE & DEPTH OF RESPIRATION) HIGHER CENTERS LIMBIC SYSTEM & HYPOTHALAMUS( PAIN & EMOTIONAL STIMULI) ↑ RATE & DEPTH OF RESPIRATION BARORECEPTOR CAROTID SINUSES, AORTIC ARCH, ATRIA, AND VENTRICLES ↓RATE & DEPTH OF RESPIRATION(LITTLE EFFECT) CHEST WALL STRETCH RECEPTORS MUSCLE SPINDLES (INTERCOSTALS MUSCLES) COORDINATE BREATHING DURING CHANGE IN POSTURE OR DURING SPEECH. THERMORECEPTOR SKIN,HYPOTHALAMUS ↑ RATE & DEPTH OF RESPIRATION
    • ADULT v/s CHILDREN MEHARBAN SINGH 5TH MEDICAL EMERGENCIES CHARECTER ADULT CHILDREN BUCKET HANDLE EFFECT MORE EFEICIENT RIBS-OBLIQUE,STERNUMHARD,INTERCOSTAL MUSCLES-DEVELOPED LESS EFEICIENT RIBSHORIZANTAL,STERNUMSOFT, INTERCOSTAL MUSCLES-LESS DEVELOPED DIAPHRAGM CURVATURE MORE( LESSWORK ) LESS(MORE WORK) CORDINATION MOVEMENTS (RIBCAGE-ABDOMINAL WALL) CORDINATED POORLY CORDINATD LUNG VOLUMES MORE (50 ml/500ml=10%) LESS (50 ml/100ml=50%) 10 kg
    • ADULT v/s CHILDREN CONTD CHARECTER SMALL AIRWAYS(≤2mm diameter) AIRWAY RESISTANCE(A∞⅟r) TENDENCY TO COLLAPSE (Laplace`law P=2T/r) ADULT CHILDREN 20% 50 % LESS(13cm-water/l/sec) LESS more(18cm-water/l/sec) MORE
    • APPLIED PHYSIOLOGY nelson 19th ,ganong 23rd • Neuromuscular disease such as Guillain-Barre syndrome Causes respiratory muscle weakness • Pneumothorax • Pulmonary fibrosis/lung edema • Pulmonary emphysema • Atelectasis • RDS of the newborn • Pleural effusion Deficiency of surfactant molecules alveolar collapse due to increased surface tension Deficiency of surfactant and is associated with prematurity and with infants of diabetic mothers Increased fluid in pleural space resists lung expansion • Thoracic musculoskeletal pain Patient avoids deep inspiration due to pain • Rib fracture • Morbid obesity There is reflex spasm of intercostal muscles to produce rigid chest wall Especially in supine position, weight of tissue on the chest wall and abdomen resists thoracic expansion • Increased abdominal pressure(e.g. ascites, bowel obstruction) Obstructive lung disease(asthma/emphysema/ chronic bronchitis) Restrictive lung disease • • If the chest wall is punctured, air will flow into the pleural space until PIP equals atmospheric pressure; the lung will then collapse and the chest wall will spring outward Reduced lung compliance and therefore, have increased work of breathing, which is sensed as dyspnea Increased lung compliance Airway obstruction on expiration Pressure from below resists descent of the diaphragm during inspiration Obstruction to air flow Reduces lung volume
    • DEFINITION NELSON19TH RESPIRATORY FAILURE • Respiratory failure is defined as inability of the lungs to provide sufficient oxygen (hypoxic respiratory failure) or remove carbon dioxide (ventilatory failure) to meet metabolic demands. RESPIRATORY FAILURE MEHARBAN SINGH 5 TH MEDICAL EMERGENCIES) RESPIRATORY DISTRESS+CYANOSIS WITH CNS* and/or CADIOVASCULAR* SIGNS OF HYPOXEMIA CNS(RESTLESNESS,ALTERED SENSORIUM,SEIZURE,COMA) CVS(TACHYCARDIA,BRADYCARDIA,HYPOTENSION,CARDIAC ARREST) ABG (PCO₂>50mmHg and/or PO₂<60mmHg,40% O₂)
    • CLASSIFICATION • GAS EXCHANGE ORGAN LUNG ATMOSPHERE ALVEOLAR VENTILATION PULMONARY CAPILLARY PERFUSION ALVEOLAR CAPILLARY MEMBRANE • PUMP : CHEST WALL, RESPIRATORY MUSCLES, BRAIN, TRACTS AND NERVES • TYPES • TYPE I/HYPOXIC/ (V/Q)MISMATCH FAILURE • TYPE II/VENTILLATORY/ PUMP/HYPERCAPNIC
    • NELSON 19TH
    • LUNG PUMP
    • CONTD IAP
    • NON PULMONARY CAUSES NELSON 23RD
    • asssesment • • • • • • • • • • STABILIZE A B C HISTORY & PHYSICAL EXAMINATION GENERAL CONDITION COLOUR CHEST DEFORMITY/FACIAL DEFORMITY/AIRWAY PROBLEMS TACHYPNEA,BRADYPNEA OR APNEA AUDIBLE WHEEZE/STIDOR BREATH SOUNDS ACESSORY MUSCLE COUGH
    • LOCALIZING SIGN NELSON 19TH RESPIRATORY RATE SITE OF PATHOLOGY RETRACTIONS AUDIBLE SOUNDS EXTRATHORACIC AIRWAY ↑ ↑↑↑↑ STRIDOR INTRATHORACIC EXTRA↑ PULMONARY ↑↑ WHEEZING INTRATHORACIC INTRAPULMONARY ↑↑ WHEEZING ↑↑↑ GRUNTING ↑↑ ALVEOLAR INTERSTITIAL ↑↑↑ CENTRAL CAUSES ↑↑↑ ↔ NONE
    • NELSON 19TH
    • BASIC INVESTIGATIONS • • • • • • • Pulse oxymeter Complete blood count & blood culture Renal profile Arterial blood gas(ABG) analysis X RAY ECG SPECIAL(Bronchoscopy,CT SCAN)
    • DIAGNOSTIC APROACH RESPIRATORY DISTRESS IAP TEXT BOOK OF PAEDIATRICS 2013.
    • Treatment • • • • (outline of principle) IAP 2013 Etiology Management Keep airway open Oxygen therapy Ensure adequate alveolar ventilation, correct CO2 retenti  Mechanical Ventilation • General supportive care      Transfer to ICU for critical care and treatment Infection control Management of electrolyte and acid-base disturbance Management of multi-organ dysfunction syndrome(MODS). Nutrition support 63
    • TREATMENT ETIOLOGY MANAGEMENT KEEP AIRWAYOPEN • Any underlying diseases : • Bronchodilators(bronchosp upper airway obstruction, asm) severe pneumothorax,  β2-adrenoreceptor agonist, massive pleural effusions anticholinergic, • Eliminate any factors that glucocorticoid cause respiratory failure  Mode of administration : secondary to infection or parenteral first and then shock inhale • Any factors leading to acute  Airway humidify & nebulize deterioration of chronic respiratory failure: • Establishing artificial airway infection, malnutrition,  Endotracheal intubation inappropriate medication  Tracheostomy usage
    • TREATMENT Indications of oxygen therapy : • Pump failure: improve ventilation • Pneumonia, Pulmonary embolism, acute attack of asthma • Severe pulmonary edema, ARDS • Acute deterioration or worsening of COPD • INon-invasive positive pressure ventilation, NIPPV • INDICATION  Conscious and cooperative  Stable circulation  Be able to protect airway  No facial trauma, injury and deformity  Be endurable to mask
    • Different kind of masks 66
    • Treatment Mechanical ventilation Goals of Mechanical Ventilation:  improve alveolar ventilation, decrease PaCO2;  improve pulmonary gas exchange;  Decrease work of breathing, reverse respiratory muscle fatigue.  Indications for mechanical ventilation :     Deteriorating respiratory status despite oxygen and nebulization therapy. Apnea severe hypoxemia(Pao2<55 mm hg),hypercapnia(PaCO2>60mmhg) progressive patient fatigue,anxious,sweaty child with deteriorating mental status despite appropriate treatment.  Adjust modes and settings for mechanical ventilation according to blood gas analysis and clinical judgment 67
    • APPROACH TO A CASE OF RESPIRATORY FAILURE MANAGEMENT IAP TEXT BOOK OF PAEDIATRICS 2013.
    • 69