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RESPIRATORY SYSTEM
Respiration is a process of uptake of oxygen and removal of carbon dioxide from tissues of the body. Exchange of gases between the aünosphere and lungs is called external respiration. Exchange of gases between blood and tissues is called internal respiration. Respiration involves two processes Inspiration During this phase air is taken into the lungs from aünosphere. Expiration It is a phase during which air is expelled out of the lungs. Normal respiratory rate is 12 to 18 cycles/min.
FUNCTIONAL ANATOMY
Respiratory tract includes nasal cavities, paranasal sinuses, pharynx, larynx, trachea, bronchi, bronchioles, respiratory bronchioles and alveoli.
Upper respiratory tract
The part of respiratory passage from nostrils upto the vocal cords is called upper respiratory tract.
Lower respiratory tract
The respiratory passage below the vocal cords is lower respiratory tract. Lower respiratory tract begins with the trachea, divides into two bronchi, which subdivides repeatedly to end in alveoli. Respiratory tract divides 23 times. First 16 generations form the conducting zone. 17 th to 19 th generations form the transition zone. 20th^ to 23rd^ generations form the exchange zone. Exchange of gases can take place from 17 th to 23 rd generation.
HISTOLOGY The respiratory tract is made up of three layers
- Outer fibrous layer
- Middle muscular layer
- Inner epithelial layer.
Outer fibrous layer
It has C shaped cartilaginous rings in the trachea. As the respiratory tract divides, cartilage decreases and there is no cartilage in the terminal bronchiole and alveoli. Middle muscular layer It is made up of smooth muscles. When these muscles contract, there is narrowing of bronchial lumen producing bronchoconstriction. Relaxation of the muscles result in broncho dilatation.
Inner epithelial layer
It is formed by mucus membrane. It is made up of ciliated columnar cells in the upper respiratory tract. Cilia help to clear dust particles. Epithelium in the respiratory bronchiole is cuboidal and has no cilia. Alveoli are lined by Type I & Type Il cells. Other cells present are alveolar macrophages, mast cells, plasma cells & APUD cells.
NERVE SUPPLY
Respiratory tract is supplied by autonomic nervous system. Sympathetic stimulation causes dilatation of bronchioles by relaxation of smooth muscles. Parasympathetic
FUNCTIONS OF NASAL CAVITY
- Filtration of dust particles.
- Humidification.
- Olfaction.
- Modification of temperature of inspired air. RESPIRATORY FUNCTIONS
- Uptake of 02 from the atmosphere. Oxygen is taken from the inspired air. It is transported through blood to the tissues where it is utilized.
- Expulsion of C02 from the body. Carbon di oxide in the tissues is taken up by the blood and delivered to the lungs from where it is expelled. NON RESPIRATORY FUNCTIONS
- Defensive action.
- It produces secretory antibody IgA. Alveolar macrophages are phagocytic. i.e they engulfforeign particles.
- Cilia trap microbes.
- Synthesis of surfactant, collagen and elastic fibres.
- Fibrinolysis and removal of clots.
- Conversion of angiotensin Il by ACE (Angiotensin converting en zyme).
- Temperature regulation.
- Heat is lost from the body along with water during expiration.
- Acid base balance.
- Lungs regulate C02 content of blood and thereby help in acid base balance. Excretory function — removal ofvolatile substances.
- Voice production - it helps in speech.
PULMONARY VOLUMES & CAPACITIES
VOLUMES
TIDAL VOLUME (TV)
This is the volume of air inspired or expired during normal respiration at rest. Normal value — 500 ml.
INSPIRATORY RESERVE VOLUME
(IRV)
It is the volume of air inspired with maximum effort over and above the normal tidal volume. Normal value — 3, ml. EXPIRATORY RESERVE VOLUME (ERV) It is the volume of air expired forcefully after a normal expiration. Normal value— 1, 100 ml.
RESIDUAL VOLUME (RV)
This is the volume of air remaining in the lungs after a forceful expiration. Normal value— 1 ,200 ml. CAPACITIES
INSPIRATORY CAPACITY (IC)
This is the volume of air a person can inspire forcefully after a normal expiration.
IC = Tv + IRV
Normal value — 3,500 ml.
FUNCTIONAL RESIDUAL CAPACITY
HELIUM DILUTION METHOD
Spirometer is filled with air mixed with helium of known concentration. The subject inhales air from the spirometer commencing from the end of normal expiration. FRC can be determined by the degree of dilution of helium. NITROGEN WASHOUT METHOD Subject is asked to breathe normally. At the end of normal expiration, subject inspires pure oxygen and later exhales into a Douglas bag. This procedure is repeated for 7 minutes till the nitrogen in the lungs is displaced by oxygen. FRC can be calculated by knowing the volume of air in the Douglas bag, N2 concentration in the atmosphere & the air sample in Douglas bag. Once FRC is determined, RV & TLC can be calculated by
RV = FRC - ERV
TLC = FRC + IC.
FEV —volume of air expired forcefully in three seconds. Normal value = 97 % - 100 0 /0. FEV values are decreased significantly in obstructive airway diseases like asthma & emphysema. In restrictive airway diseases, vital capacity is reduced but FEV can be normal. FEV values help to distinguish between obstructive and restrictive lung disorders.
5. PEAK EXPIRATORY FLOW RATE
(PEFR)
The maximum rate at which air can be exhaled forcefully after a deep inspiration is known as PEFR.
Normal value = 300 — 400 L/min.
PEFR is measured by using an instrument called Wright's peak flow meter. This is useful in assessing airway diseases like asthma, cystic fibrosis and emphysema. PULMONARY VENTILATION It is the process by which air enters the lungs or the air moves out ofthe lungs. ALVEOLAR VENTILATION It is the volume ofair entering the alveoli in one minute. This is used for exchange of gases. Alveolar ventilation = (Tidal volume — dead space) x 12 = (500-150) x 12 = 350 x 12 = 4, ml/min. BREATHING RESERVE This is the volume of air breathed in and out with maximum respiratory effort over and above the normal respiration. It is the difference between maximum voluntary ventilation and respiratory minute volume. Breathing Reserve = MVV - RMV
DYSPNEIC INDEX (D.I)
This is an index to evaluate if a person has dyspnea. D.I= MVV-RMV x 100
MVV
Value less than 70 % indicates that the person is dyspneic. VENTILATION PERFUSION RATIO It is the ratio between alveolar ventilation and the volume ofblood perfusing the alveoli. It is expressed as Alveolar ventilation= VA Perfusion Q Normal value — 0. It is more at the apex ( upto 3) than at the base (0.6) of lungs. Ventilation perfusion ratio is altered in respiratory diseases like emphysema & pulmonary embolism. DEAD SPACE The part of respiratory passage where exchange of gases does not take place is called dead space. It corresponds to the conducting zone of respiratory passage. Dead space is of two types.
- Anatomical dead space.
- Physiological dead space. ANATOMICAL DEAD SPACE (ADS) It is that part of the respiratory passage, which is not involved in exchange of gases. This includes air in the nose, pharynx, larynx, trachea and bronchi upto terminal bronchioles. Gas exchange does not occur in these areas because the walls of respiratory passages are too thick for gas exchange. Normal value — 150 ml. Measurement — Single breath nitrogen analyzer method. PHYSIOLOGICAL DEAD SPACE (PDS) This includes anatomical dead space and the part of lungs where exchange of gases does not take place. Physiological dead space = anatomical dead space + alveolar dead space In healthy individuals ADS = PDS. Physiological dead space is more significant than anatomical dead space. It is increased in case of arteriovenous shunts and pulmonary embolism.
Contraction of external intercostals increase transverse diameter by bucket handle movement. The antero-posterior diameter is increased by pump handle movement. This occurs by elevation of anterior portion of the ribs. The 2 nd to 5 th ribs assume horizontal position due to contraction of external intercostal muscles. Sternum moves forwards & upwards. Expansion ofthe thoracic cage creates negative pressure within the lungs. Air enters the lungs from atmosphere to equalize the pressure. During forced expiration neck muscles like sternocleidomastoid and scaleni are used. Exercise induced increase in respiratory effort involves all the accessory muscles of respiration. EXPIRATION In quiet breathing, expiration is a passive process. It is produced by relaxation of inspiratory muscles assisted by elastic recoil of the thoracic cage. Expiratory muscles are active during forced expiration.
RESPIRATORY PRESSURE CHANGES Lungs are present within the thoracic cavity, Visceral pleura covers the outer surface of lungs. Parietal pleura lines the inner surface of thoracic cavity. Space between the parietal and visceral pleura forms the pleural cavity. 4— 8 ml of fluid (pleural fluid) is present in this cavity. It lubricates movement of the lungs. INTRA PLEURAL PRESSURE Pressure within the pleural cavity is termed intra pleural pressure. Intra pleural pressure is normally negative. However during forced expiration it can be positive. The normal intra pleural pressure varies between — 5 to — 8 cm of H2O (2.5 to — 6 mm of Hg). At the beginning of inspiration it is— 5 cm of H O and at the peak of inspiration it is— 8 cm of H O. At the end of expiration it comes back to — 5 cm of H2O. Intra pulmonary pressure Intra pleural pressure INTRA PULMONARY PRESSURE Pressure within the lung is termed intra pulmonary pressure. During inspiration this bcomes negative (— 1.5 mm of Hg). During expiration it becomes positive (+1mm of Hg). At the end of inspiration and expiration intra pulmonary pressure will be zero.
Respiratory effort by baby at birth expands the alveoli. Surfactant prevents the collapse of alveoli. In premature babies production of surfactant is reduced. Small diameter of alveoli along with reduced surfactant increases tendency for the alveoli to collapse. This is called as Infant respiratory distress syndrome or Hyaline membrane disease. This condition can be fatal if proper treatment is not given.
Treatment
- Continuous positive pressure breathing.
- Administration of bovine surfactant. COMPLIANCE Compliance is stretchability of the lungs. It is the extent to which lungs expand for each unit increase in trans pulmonary pressure. Normal compliance is 200ml/cm of H2O. This means, every time the trans pulmonary pressure increases by 1 cm ofH20, lungs expand by 200ml. Compliance is due to elasticity of the lungs and thoracic cage.
Change in volume V
Compliance = Change in pressure P
COMPLIANCE CURVE Pleural pressure is plotted along X axis and lung volumes are plotted on Y axis. Trans pulmonary pressure is changed in small steps. Record of lung volumes show two separate curves — one inspiratory and another expiratory curve. This is called "compliance curve". Inspiratory and expiratory curves do not overlap. The curve obtained is due to elastic forces of the lungs. REGULATION OF RESPIRATION
Respiration involves the process of
inspiration and expiration. It is controlled
by
1. Neural regulation
2. Chemical regulation
Neural regulation is by the involvement of
- Respiratory centres
- Peripheral receptors
- Higher centres RESPIRATORY CENTRES
Respiratory centres are a group of neurons present in the brainstem. They are
paired. These centres are
Dorsal respiratory group
Ventral respiratory group
Apneustic centre
Pneumotaxic centre
Dorsal respiratory group (DRG)
This is situated in the dorsal portion of the medulla around the nucleus of tractus solitarius. The basic rhythm of respiration is generated & maintained by this group of neurons. This group is responsible for the generation of inspiratory ramp. Inspiratory signals begin weakly and increase in a ramp manner. Later they stop abruptly resulting in expiration. Ramp signals steadily increase the volume of lungs during inspiration. DRG is autorhythmic (can generate its own signals). It can maintain respiration even when all the external signals are cut off.
Ventral Respiratory Group
It is present in the ventral aspect ofmedulla. The neurons ofthis group remain inactive during normal respiration. When the respiratory drive becomes greater than normal, they participate in respiration. Apneustic Centre This is present in lower pons. It gets feedback through vagus from other respiratory centres. It acts with pneumotaxic centre to control the depth ofinspiration. Stimulation ofapneustic centre produces deep inspiration. Pneumotaxic Centre This centre is located in upper part ofpons in the nucleus parabrachialis medialis. It controls the duration of inspiration by regulating the switch offpoint of inspiratory ramp. Strong stimulation ofpneumotaxic centre decreases the duration ofinspiration and hence increases the rate ofrespiration. Damage to pneumotaxic centre causes slower respiration and an in tidal volume.
BASICS OF MEDICAL PHYSIOLOGY Neuron s ofdorsa l respirat ory group generat e rhythm ic inspirat ory signals. Signals are weak in the beginni ng, but rise rapidly to reach a peak in a 'ramp' fashion and stop abruptl y. After a brief period, the inspirat ory neuron
RESPIRATORY SYSTEM s start dischar ging the impuls es again. This cycle gets repeate d. A negativ e feedba ck loop in the medull a regulat es the cyclica l dischar ges from theinsp iratory neuron s. Pneum otaxic also plays an import ant role in regulati ng the
