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Issue 12 (2000) Article 11: Page 1 of 3   Go to page: 1 2 3

Respiratory Physiology
Dr Fred Roberts,
Royal Devon & Exeter Hospitals, Exeter, UK


* Introduction * Respiratory Process
* Anatomy * Oxygen Transport
* Mechanism of Breathing * Non-Respiratory Lung Functions
 

Introduction

The main function of the lungs is to provide continuous gas exchange between inspired air and the blood in the pulmonary circulation, supplying oxygen and removing carbon dioxide, which is then cleared from the lungs by subsequent expiration. Survival is dependent upon this process being reliable, sustained and efficient, even when challenged by disease or an unfavourable environment. Evolutionary development has produced many complex mechanisms to achieve this, several of which are compromised by anaesthesia. A good understanding of respiratory physiology is therefore essential to ensure patient safety during anaesthesia. [Top]

Anatomy

The respiratory tract extends from the mouth and nose to the alveoli. The upper airway serves to filter airborne particles, humidify and warm the inspired gases. The patency of the airway in the nose and oral cavity is largely maintained by the bony skeleton, but in the pharynx is dependent upon the tone in the muscles of the tongue, soft palate and pharyngeal walls.

Larynx

The larynx lies at the level of upper cervical vertebrae, C4-6, and its main structural components are the thyroid and cricoid cartilages, along with the smaller arytenoid cartilages and the epiglottis, which sit over the laryngeal inlet. A series of ligaments and muscles link these structures, which, by a co-ordinated sequence of actions, protect the larynx from solid or liquid material during swallowing as well as regulating vocal cord tension for phonation (speaking). The technique of cricoid pressure is based on the fact that the cricoid cartilage is a complete ring, which is used to compress the oesophagus behind it against the vertebral bodies of C5-6 to prevent regurgitation of gastric contents into the pharynx. The thyroid and cricoid cartilages are linked anteriorly by the cricothyroid membrane, through which access to the airway can be gained in an emergency.

Trachea and bronchi

The trachea extends from below the cricoid cartilage to the carina, the point where the trachea divides into the left and right main bronchus, with a length of 12-15cm in an adult and an internal diameter of 1.5-2.0cm. The carina lies at the level of T5 (5th thoracic vertebra) at expiration and T6 in inspiration. Most of its circumference is made up of a series of C-shaped cartilages, but the trachealis muscle, which runs vertically, forms the posterior aspect.

When the trachea bifurcates, the right main bronchus is less sharply angled from the trachea than the left, making aspirated material more likely to enter the right lung. In addition, the right upper lobe bronchus arises only about 2.5cm from the carina and must be accommodated when designing right-sided endobronchial tubes.

Lungs and pleura

The right lung is divided into 3 lobes (upper, middle and lower) whereas the left has only 2 (upper and lower), with further division into the broncho-pulmonary segments (10 right, 9 left). In total there are up to 23 airway divisions between trachea and alveoli. The bronchial walls contain smooth muscle and elastic tissue as well as cartilage in the larger airways. Gas movement occurs by tidal flow in the large airways. In the small airways, by contrast, (division 17 and smaller) it results from diffusion only.

The pleura is a double layer surrounding the lungs, the visceral pleura enveloping the lung itself and the parietal pleura lining the thoracic cavity. Under normal circumstances the interpleural space between these layers contains only a tiny amount of lubricating fluid. The pleura and lungs extend from just above the clavicle down to the 8th rib anteriorly, the 10th rib laterally and the level of T12 posteriorly.

Blood supply

The lungs have a double blood supply, the pulmonary circulation for gas exchange with the alveoli and the bronchial circulation to supply the parenchyma (tissue) of the lung itself. Most of the blood from the bronchial circulation drains into the left side of the heart via the pulmonary veins and this deoxygenated blood makes up part of the normal physiological shunt present in the body. The other component of physiological shunt is from the thebesian veins, which drain some coronary blood directly into the chambers of the heart.

The pulmonary circulation is a low-pressure (25/10mmHg), low-resistance system with a capacity to accommodate a substantial increase in blood flowing through it without a major increase in pressure. Vascular distension and recruitment of unperfused capillaries achieve this. The main stimulus which produces a marked increase in pulmonary vascular resistance is hypoxia. [Top]

Mechanism of Breathing

A pressure gradient is required to generate flow. In spontaneous respiration inspiratory flow is achieved by creating a sub-atmospheric pressure in the alveoli (of the order of -5cmH2O during quiet breathing) by increasing the volume of the thoracic cavity under the action of the inspiratory muscles. During expiration the intra-alveolar pressure becomes slightly higher than atmospheric pressure and gas flow to the mouth results.

Motor pathways

The main muscle generating the negative intrathoracic pressure that produces inspiration is the diaphragm, a sheet separating the thorax from the abdomen. Its muscular part is peripheral, attached to the ribs and lumbar vertebrae, with a central tendon. Innervation is from the phrenic nerves (C3-5) with contraction moving the diaphragm downwards forcing the abdominal contents down and out. Additional inspiratory efforts are produced by the external intercostal muscles (innervated by their intercostal nerves T1-12) and the accessory muscles of respiration (sternomastoids and scalenes), although the latter only become important during exercise or respiratory distress.

During quiet breathing expiration is a passive process, relying on the elastic recoil of the lung and chest wall. When ventilation is increased, such as during exercise, expiration becomes active with contraction of the muscles of the abdominal wall and the internal intercostals. The same muscles are also used when producing a Valsalva manoeuvre (*BACK* Cardiovascular Physiology - Part 1, Update in Anaesthesia 1999;10:2).

Central control

The mechanism by which respiration is controlled is complex. There is a group of respiratory centres located in the brainstem producing automatic breathing activity. This is then regulated mainly by input from chemoreceptors (see below). This control can be overridden by voluntary control from the cortex. Breath-holding, panting or sighing at will are examples of this voluntary control. The main respiratory centre is in the floor of the 4th ventricle, with inspiratory (dorsal) and expiratory (ventral) neurone groups. The inspiratory neurones fire automatically, but the expiratory ones are used only during forced expiration. The 2 other main centres are the apneustic centre, which enhances inspiration, and the pneumotaxic centre, which terminates inspiration by inhibition of the dorsal neurone group above.

The chemoreceptors that regulate respiration are located both centrally and peripherally. Normally control is exercised by the central receptors located in the medulla, which respond to the CSF hydrogen ion concentration, in turn determined by CO2, which diffuses freely across the blood-brain barrier from the arterial blood. The response is both quick and sensitive to small changes in arterial CO2 (PaCO2 ). In addition, there are peripheral chemoreceptors located in the carotid and aortic bodies most of which respond to a fall in O2, but some also to a rise in arterial CO2. The degree of hypoxia required to produce significant activation of the O2 receptors is such that they are not influential under normal circumstances, but will do so if profound hypoxia (<8kPa or 60mmHg) occurs, for example at high altitude when breathing air (see later - Special circumstances). It also happens when the response to CO2 is impaired, which can occur if the PaCO2 is chronically elevated, leading to a blunting of the central receptor sensitivity. In this event the plasma bicarbonate (HCO3- ) concentration will also be elevated. [Top]

(Continued ...)


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