Anatomy and Physiology Exercise 36 Review Sheet Anatomy of the Respriatory Ststem
Indian J Anaesth. 2015 Sep; 59(9): 533–541.
Anatomy and physiology of respiratory system relevant to anaesthesia
Apeksh Patwa
aneKailash Cancer Infirmary and Research Centre, Muni Seva Ashram, Goraj, Vadodara, Gujarat, Republic of india
twoDepartment of Anaesthesia, Vadodara Establish of Neurological Sciences, Vadodara, Gujarat, India
Amit Shah
1Kailash Cancer Hospital and Research Heart, Muni Seva Ashram, Goraj, Vadodara, Gujarat, India
2Department of Anaesthesia, Vadodara Institute of Neurological Sciences, Vadodara, Gujarat, India
Abstract
Clinical application of anatomical and physiological knowledge of respiratory system improves patient'due south safety during anaesthesia. Information technology also optimises patient's ventilatory condition and airway patency. Such knowledge has influence on airway management, lung isolation during anaesthesia, management of cases with respiratory disorders, respiratory endoluminal procedures and optimising ventilator strategies in the perioperative flow. Agreement of ventilation, perfusion and their relation with each other is important for understanding respiratory physiology. Ventilation to perfusion ratio alters with anaesthesia, torso position and with one-lung amazement. Hypoxic pulmonary vasoconstriction, an of import safe machinery, is inhibited by majority of the anaesthetic drugs. Ventilation perfusion mismatch leads to reduced arterial oxygen concentration mainly because of early closure of airway, thus leading to decreased ventilation and atelectasis during amazement. Diverse anaesthetic drugs change neuronal control of the animate and bronchomotor tone.
Keywords: Anatomy, bronchomotor tone, functional residual chapters, physiology, respiratory system, tracheobronchial tree, ventilation-perfusion
INTRODUCTION
Accurate knowledge of anatomy and physiology of the respiratory tract is important not only in the field of pulmonology but as well in anaesthesiology and critical care. Nearly seventy–80% of the morbidity and mortality occurring in the perioperative period is associated with some course of respiratory dysfunction.[1] General anaesthesia and paralysis are associated with alterations in the respiratory function.[2,3] Dynamic anatomical changes and physiological amending happening during anaesthesia arrive imperative for an anaesthesiologist to have sound knowledge of the respiratory system and apply it for safe and polish conduct of anaesthesia. Such knowledge has influence on clinical practice of airway direction, lung isolation during anaesthesia, management of cases with respiratory disorders, respiratory endoluminal procedures and surgeries, optimising ventilator strategies in perioperative period and designing airway devices.
Anatomy OF RESPIRATORY SYSTEM
The respiratory arrangement, functionally, can be separated in 2 zones; conducting zones (nose to bronchioles) form a path for conduction of the inhaled gases and respiratory zone (alveolar duct to alveoli) where the gas exchange takes place. Anatomically, respiratory tract is divided into upper (organ outside thorax - olfactory organ, pharynx and larynx) and lower respiratory tract (organ within thorax - trachea, bronchi, bronchioles, alveolar duct and alveoli).
The discussion is mainly full-bodied on the lower respiratory tract and the related physiology.
Nose and nasal cavity are divided into two halves by the nasal septum. The lateral wall of the nose consists of three turbinates or conchae (superior, middle and inferior). The passage junior to junior turbinate is preferred passage for nasotracheal intubation.[4] The pharynx is a tube-like passage that connects the posterior nasal and oral cavities to the larynx and oesophagus. It is divided into nasopharynx, oropharynx and laryngopharynx. Increase in soft tissue within bony enclosure of pharynx or decrease in bony enclosure size would result in anatomical imbalance and cause limitation of space available for airway [Figure i].[5]
Excessive soft tissue (obesity) in prepare bony enclosure leads to compromised pharyngeal passage
There are three narrowest portions of pharynx; passage posterior to the soft palate (retro palatal space), passage posterior to the natural language (retroglossal space) and passage posterior to epiglottis (retroepiglotic space). There is pregnant reduction of these spaces with sedation and anaesthesia[6] which would lead to upper airway obstruction.
ANATOMICAL FACTORS WHICH COMPROMISES PHARYNGEAL PATENCY
Inefficient contraction of pharyngeal dilator muscles [Figure 2]
Upper airway showing pharyngeal dilator muscles and pharyngeal airway space
(ane) The tensor palatine retracts the soft palate abroad from the posterior pharyngeal wall, thereby maintaining retro palatal patency. (2) The genioglossus moves the tongue anteriorly to open the retroglossal infinite. (3) Hyoid muscles (geniohyoid, sternohyoid and thyrohyoid) make the hyoid move anteriorly and stabilise the retroepiglotic laryngopharynx. Excessive fatty deposition around these muscles would upshot in inefficient wrinkle of pharyngeal dilator muscles. This would atomic number 82 to pharyngeal airway obstruction during sedation and amazement.[7]
Anatomical imbalance of oropharyngeal soft tissue
Enlarged tongue (in the case of acromegaly or obesity) in normal bony enclosure of oropharynx or a smaller bony enclosure (receding mandible) of oropharynx would be unable to conform the natural language into oropharynx and thus shift the tongue into hypopharynx (laryngopharynx). Hypo pharyngeal natural language decreases laryngopharyngeal airway patency. This is one reason for obstructive sleep apnoea and difficult mask ventilation during anaesthesia.[8]
Tracheal tug
There is constant traction on trachea, pharynx and larynx during inspiration considering of negative intrathoracic pressure which elongates pharyngeal airway during inspiration that would result in decreased pharyngeal luminal space in obese patients. This is also 1 of the reasons for difficult mask ventilation and obstructive slumber apnoea.[9]
Larynx
It serves as a sphincter, transmitting air from oropharynx and nasopharynx to trachea.
TRACHEOBRONCHIAL TREE
It is a complex system that transports gases from the trachea down to the acini, the gas exchange units of the lung. It is partitioned into 23 generations of dichotomous branching, extending from trachea (generation 0) to the last order of final bronchioles (generation 23). At each generation, each airway is being divided into two smaller girl airways[10] [Effigy three].
Tracheobronchial tree showing 23 generations
From the trachea to the terminal bronchioles (generation fifteen–sixteen), the airways are purely conducting pipes. Since no gas exchanges accept place in this region, the book in these pipes is called as the expressionless space volume (average 150 ml). The final bronchioles (generation 16) divide into respiratory bronchioles or transitional bronchioles (generations 17–19) every bit they have occasional alveoli at the walls. These respiratory bronchioles farther divide into alveolar ducts (generations 20–22) which are completely lined with alveoli. This region is known as acinus (generations 16–23). The acinus is comprised of respiratory airways and forms functional tissues (gas exchange units) of lung. The alveolar ducts are small tubes supported past a rich matrix of rubberband and collagen fibres. The distal ends of alveolar ducts open into the alveolar sac which is fabricated up past alveoli.
TRACHEA AND RIGHT/LEFT MAIN BRONCHUS
The trachea is a hollow conduit for gases and bronchial secretions. It extends from the level of C6 (cricoid cartilage) to the carina, approximately located at the level of T4–T5.[eleven] In adults, its length is approximately 11–xiii cm, with ii–4 cm being extra-thoracic.[12] The trachea has 16 to 22 horseshoe bands (c-shaped) of cartilages. The posterior tracheal wall lacks cartilage and is supported past the trachealis muscle. Depending on the level of inspiration, the posterior wall of the trachea becomes flat, convex or slightly concave.[thirteen,14] The posterior wall of the trachea either flattens or bows slightly frontwards during expiration. In normal subjects, in that location is up to 35% reduction in antero-posteior tracheal lumen in forced expiration, whereas the transverse bore decreases but by 13%.[fifteen] The trachea is generally midline in position, oftentimes displaced slightly to the correct and posteriorly as it approaches carina. The bending of the tracheal bifurcation is called as the carinal/subcarinal bending, which is measured unremarkably as 73° (35–90°).[16,17,18] The carinal angle is wider in individuals with an enlarged left atrium, in females and obese patients.
The trachea divides at carina into the right and left main bronchus. The distance of the carina from the teeth varies markedly with change in cervix position from flexion to extension (tracheal length variation is ± 2 cm), torso position and position of diaphragm.[19] This explains the change in position of endotracheal tube during alter in position of patient or flexion – extension of cervix. The right main stem bronchus has a more than direct down course, is shorter than the left and begins to ramify earlier than the left main bronchus.[xi] This leads to higher chances of right endobronchial intubation. The right main stalk bronchus divides into (secondary bronchi) right upper lobe bronchus and bronchus intermedius which further divides into right heart and lower lobe bronchus. The left bronchus passes inferolaterally at a greater angle from the vertical axis than the right bronchus. The left primary stem bronchus divides into (secondary bronchi) the left upper and lower lobe bronchi.
BRONCHO-PULMONARY SEGMENT
Broncho-pulmonary segment may be defined as an surface area of distribution of any bronchus [Figure 4]. Each lobar bronchi divides into segmental bronchi (tertiary bronchi), which supply the broncho-pulmonary segment of each lobe. Technically, there are 10 broncho-pulmonary segments in each lung, only in left lung, some of these segments fuse and there are every bit few as viii broncho-pulmonary segments. The bronchi go along to divide into smaller and smaller bronchi up to 23 generations of divisions from main bronchus. As bronchi go smaller, their structure changes:
Tracheobronchial tree with broncho-pulmonary segments
-
Cartilaginous ring becomes irregular and so disappear. When bronchi lose all cartilaginous support, the airway is then referred equally bronchioles
-
The epithelium changes from pseudostratified columnar to columnar to cuboidal in the last bronchioles
-
There are no cilia and mucous producing cells in bronchioles
-
The amount of smooth muscle in the tube wall increases as the airway becomes smaller.
DIMENSIONS OF TRACHEOBRONCHIAL TREE [Table i]
Table 1
Dimensions and features of tracheobronchial tree
Ascertaining the parameters of tracheobronchial tree such as length, diameters and angulations helps optimizing procedures such as intubation, lung isolation techniques and jet ventilation during interventional endoscopic surgeries of trachea or bronchi.[xx]
Tracheobronchial anatomical variations
Tracheobronchial tree exhibits a wide range of variations and its prevalence is 4%.[28] The most common main bronchus anomalies are the tracheal bronchus and the accessory cardiac bronchus. Knowledge of tracheobronchial variants is important for clinical aspect in pre-operative evaluation in view of intubation, lung isolation techniques and other endo-bronchial procedures.
Tracheal bronchus
This is a bronchus usually originating from the right side of the trachea above the carina and within two–6 cm from it.[29] Right tracheal bronchus has a prevalence of 0.1–2% and left bronchus has a prevalence of 0.3–1%.[xxx,31,32,33,34] The tracheal bronchus may cause complications such as atelectasis or pneumothorax in the cases of obstruction to its archway or tube entering into it during intubation.[35,36,37]
Accessory cardiac bronchus
It is a congenital, short and thin bronchus towards pericardium originating either from right bronchus or intermediate bronchus. Its prevalence is 0.08%.[31] It is associated with recurrent infections in few cases.[38]
PHYSIOLOGY OF RESPIRATORY Organization
Motion of inspired gas into and exhaled gas out of lung is called as ventilation. Understanding of lung volumes, lung compliance, ventilation-perfusion and bronchomotor tone are essential for clinical application of respiratory physiology in anaesthesia and critical care.
Lung volumes [Figure 5]
Normal requirements of the body can be easily met by normal tidal ventilation which is approximately four–8 ml/kg. Trunk has kept mechanism to provide actress ventilation in the class of inspiratory reserve volume and expiratory reserve volume whenever required (eastward.one thousand., do). When an individual, subsequently tidal expiration, takes total inspiratory breath followed by expiration to reserve book, it is called every bit vital chapters breath and is 4–five 50 in an average seventy kg private. In that location is always some corporeality of air remaining in the alveoli which prevents it from collapsing. The volume remaining in the lungs after vital capacity breath is chosen as residual volume.
Remainder book with expiratory reserve book is called as functional remainder capacity (FRC). FRC is basically the amount of air in the lungs after a normal expiration. Gases remaining in the lungs at the finish of expiration not only foreclose alveolar collapse but also it continues to oxygenate the pulmonary blood flowing though the capillaries during this time period.[39] Reported FRC values vary with various reports but on average it is between 2.8 and 3.1 L[40] in continuing position. FRC varies with change of position, amazement and trunk weight. FRC is the reserve which prolongs non-hypoxic apnoea time.
The portion of the minute ventilation which reaches alveoli and takes role in the gas commutation is called as alveolar ventilation. Normal value of alveolar ventilation is approximately v L/min which is similar to the volume of blood flowing through the lung (cardiac output 5 L/min). This makes alveolar ventilation to perfusion ratio approximately ane.[39]
RESPIRATORY MECHANICS
Lungs are like inflatable balloon which distend actively by positive pressure inside and/or negative pressure created in pleural space. In normal respiration, negative pleural pressure (Ppl) is sufficient to distend the lungs during inspiratory phase. Understanding of distending pressure is very important to empathize the respiratory mechanics. Distending pressure can be known as transpulmonary pressure (Ptp), which is expressed by the post-obit equation:
Ptp = Manus−Ppl, (Ptp = transpulmonary pressure level, Paw = alveolar pressure level, Ppl = Pleural pressure).
Compliance and ventilation of lung
Compliance is expressed every bit the distension of lung for a given level of Ptp. It is usually 0.ii–0.3 L/cm H2O.[41] Compliance (power of lung to distend) depends upon the volume of the lung. Compliance is lowest at extremes of FRC. It implies that expanded lung and completely deflated lung has lower capacity to distend to a given pressure [Effigy 6]. In the upright lung, intra-Ppl varies from the meridian to the base of the lungs. Intra-Ppl becomes 0.2 cm H2O positive for every centimetre altitude from apex to base of lung. Average height of lung is virtually 35 cm. In quite animate, the intra-Ppl at apex is about − 8 cm of H2O while at base of operations information technology is − 1.5 cm of H2O. This means that the alveoli at the noon are exposed to a greater distending pressure (PA−Ppl = 0 − (−8) =8 cm H2O) compared to those at the base (PA−Ppl = 0 − (−ane.5) =1.five cm H2O). As already distended, upmost region becomes less compliant than other area of lung. This explains the preferential distribution of ventilation to the alveoli at the base of operations of the lungs in upright posture. Distribution of ventilation changes with the position of individual considering of the change of Ppl with the gravity.
Airway closure during expiration is normal miracle, with reopening of airways during the succeeding inspiration.[42] The book remaining above the residual book where expiration beneath FRC closes some airways is termed as closing volume and this volume added to the residuum book is termed as the closing capacity. In upright position, closing capacity approaches near FRC in older private (65–seventy years) which would effect in airway closure even at normal tidal expiration. Change in body position from upright to supine, lateral or decumbent reduces FRC. Reduction in FRC promotes airway closure in dependent lung regions. Early airway closure thus decreases ventilation in the dependent regions. Since lung blood flow passes preferentially to dependent regions, matching between ventilation and perfusion is impeded.[43]
Perfusion of lung
Pulmonary circulation differs from systemic circulation. The pulmonary vessels are thin-walled and take less musculature to help fast diffusion of gases. They are subjected to less pressure compared to systemic circulation. Because of less pressure and structural differences of pulmonary vasculature to assist diffusion, they are subjected to Paw inside the thorax and gravity.[44]
On the ground of the influence of gravity, perfusion of lung is divided into three zones.[45] The distribution of blood flow in these zones depends upon three factors: Alveolar pressure level (PA), pulmonary arterial force per unit area (Pa) and pulmonary venous force per unit area (Pv).
Apical region where PA tin can be higher than Pa and Pv is considered as zone I. Since PA > Pa > Pv in zone I, no arterial claret flow occurs and this zone is considered as physiological expressionless space. Though such zone I practise non be in healthy bailiwick under normal perfusion pressure, in condition of haemorrhage or positive pressure, ventilation zone I may go reality and adds to expressionless space ventilation.
In center zone or zone Two, difference of Pa to PA decides the perfusion (Pa > PA > Pv) while in lower zone or zone Iii, divergence of Pa to Pv (Pa > Pv > PA) decides the perfusion. Few studies as well include 4th zone of less blood supply because of the compression of vessels due to the weight of lungs.[46]
The zones described before are purely physiological and not anatomical. The borders between zones changes with many physiological and pathophysiological alterations or weather condition. Paw changes are minimal during the course of a quiet breath but they are much greater during speech, exercise and other conditions. The patients on positive pressure level ventilation with positive end expiratory force per unit area (PEEP) may have substantial zone I due to high PAs. Pa alters with severe haemorrhage or during full general anaesthesia resulting in zone I conditions. Pulmonary artery pressure level is high during exercise, eliminating any existing zone I into zone II and moving the boundary between zones 3 and II upward
Ventilation to perfusion matching
The alveolar partial pressure of oxygen and carbon dioxide are determined past the ratio of ventilation (V) to perfusion (Q). Equally discussed before, ventilation and perfusion both increase from top to bottom in lungs, but perfusion increases more than in comparing to ventilation.
Proportionately, ratio of ventilation to perfusion is more in upper lung and less towards the base of lungs [Figure 7]. This gradient occurs in vertical axis of the lung fields irrespective of body positions. (i.e., if patient is in upright posture, apex has more ventilation while base of operations has more perfusion. If patient is in lateral posture, nondependent lung gets more ventilation while dependent lung gets more perfusion).
Ventilation perfusion ratio from apex to the base of lung
HYPOXIC PULMONARY VASOCONSTRICTION
Hypoxic pulmonary vasoconstriction (HPV) is compensatory blood menses away from hypoxic lung regions to better oxygenated regions. HPV occurs in response to low alveolar oxygen tension. This machinery improves the V/Q mismatch. All inhalation agents except newer agents, sevoflurane and desflurane, inhibit the HPV.[39]
PHYSIOLOGICAL VARIATION WITH POSITION AND Amazement
Supine position
General anaesthesia promotes basal atelectasis irrespective of the modes of ventilation (spontaneous or controlled) or drugs (intravenous or inhalation) used. Nearly, xv–20% of the lung is atelectatic during general amazement. Atelectasis decreases towards the apex, which ordinarily remains aerated.[42] The area of atelectasis becomes the area of shunt where no gas exchange occurs in spite of perfusion. Early on airway closure in tidal breathing with supine position, promotes ventilation perfusion mismatch (V/Q < i) and impairment of gas commutation. The combination of atelectasis and airway closure explains nearly 75% of the overall damage in oxygenation in anaesthetised subject.[47]
Lateral position and i-lung ventilation
Anaesthesia in lateral position causes ventilation perfusion mismatch where upper or nondependent lung receives more ventilation and lower or dependent lung receives college (60–65%) perfusion. Dependent lung as well exhibits signs of early airway closure and formation of atelectasis. With addition of PEEP, most lxxx% of blood flow is directed to lower dependent lung.[47] During ane-lung ventilation, HPV can divert blood flow away from the non-ventilated lung. One should avert drugs causing inhibition of HPV.
Prone position
Prone position decreases ventilation perfusion mismatch and improves the oxygenation. Various reasons (east.g., compatible vertical distribution of perfusion, amend ventilation distribution because of smaller vertical pleural gradient, increased FRC, more compatible gas distribution and less lung compression by heart) have been proposed by different authors for comeback in ventilation with prone position. There are no reports of atelectasis in decumbent position, probably considering weight of heart transferred on the sternum instead of lungs equally opposed to supine position.[42]
NEUROLOGICAL CONTROL OF BREATHING
The respiratory centres are located in pons and medulla. They contain different types of inspiratory and expiratory neurons that fire during the three phases of the respiratory cycle, namely inspiratory phase of sudden discharge of signals to inspiratory muscles and the dilator muscles of the pharynx, followed by gradual reject of signals in post-inspiratory phase. Inspiration is followed by no signals in expiratory phase except in forced expiration or high minute ventilation.[48] Inhalational agents influence rate, rhythm and intensity of discharge from the respiratory centres which receive inputs from the chemoreceptors, cortex, hypothalamus, pharyngeal mechanoreceptors, vagus nerve and other afferents. Peripheral chemoreceptors answer quickly to hypoxia, hypercapnia and hydrogen ion concentration. The central chemoreceptors are slow responders relative to peripheral chemoreceptors.
BRONCHOMOTOR TONE
Bronchomotor tone is the state of wrinkle or relaxation of the smooth musculus in the bronchial walls that regulates the calibre of the airways. Number of factors influences the alter of bronchomotor tone, eastward.g. depth of amazement, drugs and diverse procedures on airway, respiratory diseases (bronchial asthma) and inhalational agents. Using computed tomography, Brown et al. had showed that halothane causes greater broncho-dilatation than isoflurane at low concentrations.[49] Sevoflurane (one minimum alveolar concentration) reduced respiratory arrangement resistance (adamant using an isovolume technique) by 15% in patients undergoing constituent surgery. In contrast, desflurane did not significantly alter resistance.[50]
SUMMARY
Clinical application of the anatomical knowledge of respiratory organisation definitely improves prophylactic of conduct of anaesthesia and also optimises patient ventilatory condition and airway patency. Such knowledge has influence on the clinical do of airway management, lung isolation during amazement, direction of cases with respiratory disorders, respiratory endoluminal procedures and surgeries, optimising ventilator strategies in perioperative period, applying jet ventilation during emergency and endoluminal surgeries and designing airway devices.
An anaesthesiologist should understand that FRC is the well-nigh of import parameter. Its relation with closing capacity is an important determinant of ventilation of patient. Ventilation and perfusion both are afflicted by the gravity. Overall ventilation to perfusion ratio is 1 but it alters with anaesthesia, torso positions and with 1-lung anaesthesia. HPV, an important safety mechanism, is inhibited by majority of anaesthetic drugs. Ventilation perfusion mismatch leading to reduced arterial oxygen concentration is mainly because of early closure of airway leading to decreased ventilation and atelectasis occurring with the anaesthesia. Various anaesthetic drugs alter neuronal control of the breathing and bronchomotor tone.
Financial back up and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Articles from Indian Journal of Anaesthesia are provided here courtesy of Wolters Kluwer -- Medknow Publications
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613399/
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