ANATOMY AND PHYSIOLOGY OF RESPIRATORY SYSTEM AND ACUTE

RESPIRATORY FAILURE

PRESENTED BY: DR. ABHISHEK SAINI

RESPIRATORY TRACT

• Nose

• Nasal cavity

• Sinuses

• Pharynx

The Lower Respiratory Tract

• Larynx

• Trachea

• Bronchial Tree

• Lungs

The Upper Respiratory Tract

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

• Lt. Main bronchus• Inf.

Lobar

bronchus(5)

• Middle

lobar

bronchus(2)

• Sup. Loba

r bronchus(5)

• Inf. Loba

r bronchus(4)• Apical

• Posterior • Anterior

• Lateral• Medial

• Superior • Medial

basal• Ant. Basal• Post basal• Lateral

basal

• Apical • Posterior• Anterior• Superior lingular • Inferior lingular

Superior lobar Bronchus(3)

•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 ANTOMYSTUCTURE 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

PHRENIC NERVE (C3-C5)

SUPERIOR AND INFERIOR PHRENIC VEIN

EXTERNAL &INTERCOSTAL MUSCLE

INTERCOSTAL ARTERIES

THORACIC NERVE (T1-T11)

INTERCOSTAL VEINS

BRONCHI TERMINAL BRONCHIOLS

BRONCHIAL ARTERY

PULMONARY PLEXUS(VAGUS AND SYMPTH)

BRONCHIAL VEIN

RESPIRATORY BRONCHIOLS ALVEOLI

PULMONARY ARTERY PULMONARY PLEXUS(VAGUS AND SYMPTH)

PULMONARY VEIN

CIRCULATION GANONG 23RD

PULMONARY CIRCULATION

BRONCHIAL CIRCULATION

• LOW-PRESSURE, HIGH-FLOW CIRCULATION

HIGH-PRESSURE, LOW-FLOW CIRCULATION

CONTAIN 100% CARDIAC OUTPUT

CONTAIN 1-3% CARDIAC OUTPUT

SUPPLIESRESPITARY 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 )

contdDURING 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 VOLUMESMEASUREMENT 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 waterFACTORS : 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 kg-m/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 ,berylliosis thickness increase.

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 TRANSPORTOXYGEN TRANSPORT GANONG 23RD

• FACTORSa)lung ventillatoinb)gas exchangec)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 CONTROL①VOLUNTARY 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 practised- Talking, 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 (pre-BÖTC) 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

CONTROLCAUSE(H+,CO₂,O

₂,OTHERS)

RECEPTOR(CENTRAL &

PERIPHERAL)

CENTERS=EFFECT(VOLUNTARY)

b)NON CHEMICAL RECEPTOR IN LUNG&AIRWAY GANONG 23RD

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 23RD

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 EFEICIENTRIBS-OBLIQUE,STERNUM-HARD,INTERCOSTAL MUSCLES-DEVELOPED

LESS EFEICIENT RIBS-HORIZANTAL,STERNUM-SOFT, 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 ADULT CHILDRENSMALL AIRWAYS(≤2mm diameter) 20% 50 %

AIRWAY RESISTANCE(A∞⅟r) LESS(13cm-water/l/sec) more(18cm-water/l/sec)

TENDENCY TO COLLAPSE(Laplace`law P=2T/r)

LESS MORE

APPLIED PHYSIOLOGY nelson 19th ,ganong 23rd • Neuromuscular disease such as Guillain-Barre syndrome Causes respiratory muscle weakness

• Pneumothorax 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

• Pulmonary fibrosis/lung edema Reduced lung compliance and therefore, have increased work of breathing, which is sensed as dyspnea

• Pulmonary emphysema Increased lung compliance Airway obstruction on expiration

• Atelectasis Deficiency of surfactant molecules alveolar collapse due to increased surface tension

• RDS of the newborn Deficiency of surfactant and is associated with prematurity and with infants of diabetic mothers

• Pleural effusion Increased fluid in pleural space resists lung expansion

• Thoracic musculoskeletal pain Patient avoids deep inspiration due to pain

• Rib fracture There is reflex spasm of intercostal muscles to produce rigid chest wall

• Morbid obesity Especially in supine position, weight of tissue on the chest wall and abdomen resists thoracic expansion

• Increased abdominal pressure(e.g. ascites, bowel obstruction)

Pressure from below resists descent of the diaphragm during inspiration

• Obstructive lung disease(asthma/emphysema/ chronic bronchitis)

Obstruction to air flow

• Restrictive lung disease 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 5TH MEDICAL EMERGENCIES)

RESPIRATORY DISTRESS+CYANOSIS WITH CNS* and/or CADIOVASCULAR* SIGNS OF HYPOXEMIACNS(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

SITE OF PATHOLOGY RESPIRATORY RATE RETRACTIONS AUDIBLE SOUNDS

EXTRATHORACIC AIRWAY ↑ ↑↑↑↑ STRIDOR

INTRATHORACIC EXTRA-PULMONARY ↑ ↑↑ WHEEZING

INTRATHORACIC INTRAPULMONARY ↑↑ ↑↑ WHEEZING

ALVEOLAR INTERSTITIAL ↑↑↑ ↑↑↑ GRUNTING

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

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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

TREATMENT

ETIOLOGY MANAGEMENT

• Any underlying diseases : upper airway obstruction, severe pneumothorax, massive pleural effusions

• Eliminate any factors that cause respiratory failure secondary to infection or shock

• Any factors leading to acute deterioration of chronic respiratory failure： infection, malnutrition, inappropriate medication usage

KEEP AIRWAYOPEN

• Bronchodilators(bronchospasm) β2-adrenoreceptor agonist,

anticholinergic, glucocorticoid

Mode of administration : parenteral first and then inhale

Airway humidify & nebulize• Establishing artificial airway

Endotracheal intubation Tracheostomy

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

66

Different kind of masks

67

TreatmentMechanical 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

APPROACH TO A CASE OF RESPIRATORY FAILURE MANAGEMENT

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