The respiratory system is divided into upper and lower respiratory tracts: the upper airways consist of the nose, nasal conchae, sinus and pharynx; the lower respiratory tract includes the larynx, trachea, bronchi and lungs.² Larger airways are lined with stratified epithelial tissue, which have a relatively high cellular turnover rate; these cells protect and clear these large airways. There are also additional specialised features of this tissue including an extensive distribution of mucus/goblet cells and cilia, which facilitate the mucociliary clearance system and aid airway clearance.

Upper Respiratory Tract

The nasal cavities contain an extremely vascular and mucoid environment for warming and humidifying inhaled gases. To maximise exposure to this surface area, the nasal conchae create turbulent gas flow. Cilia at the top of the epithelial cells and mucus provide filtration and cleaning of the inhaled air. Mucus is moved by the cilia lining the conducting airways towards the pharynx at a rate of 1–2 cm per minute. One litre of mucus is produced every day with only a small part not reabsorbed by the body.^3,⁴

The pharynx is a muscular tube that transports food and air to the oesophagus and larynx, respectively. Inferior to the pharynx, the larynx consists mostly of cartilage attached to other cartilage and surrounding structures, and houses the vestibular (false) vocal folds and the true vocal cords (see Figure 13.2).⁵ An important pair of cartilages within the larynx is the pyramid-shaped arytenoids, which act as attachment points for the vocal cords. This area is easily damaged by pressure from endotracheal tubes; the most significant independent risk factor for injury to the arytenoids is the length of intubation time.⁶ The thyroid cartilage (‘Adam’s apple’) and the cricoid cartilage protect the glottis and the entrance to the trachea.⁴ Another cartilage in the larynx is the triangular-shaped elastic epiglottis which protects the lower airways from aspiration of food and fluids into the lungs. The epiglottis usually occludes the inlet to the larynx during swallowing. The primitive cough, swallow and gag reflexes further protect the airway.⁴

FIGURE 13.2 Larynx. (A) Cartilages and ligaments; (B) Neck muscles.⁵

Lower Respiratory Tract

The trachea is a hollow tube approximately 11 cm long and 2.5 cm in diameter, and marks the beginning of the lower respiratory tract. The trachea is supported by 16–20 C-shaped cartilages, and is another area at risk of pressure damage from artificial airways. The trachea divides at the carina into the left and right main bronchi. The bronchial tree has two main stem bronchi that are structurally different. The right bronchus is wider and angles slightly where it divides further into the three lobes of the right lung. The most common site of aspiration of foreign objects is the right bronchus because of its anatomical position. The acutely angled left main bronchus divides further into the two main lobes of the left lung.

The airways within each lung branch out further into secondary (or lobar) bronchi then tertiary (or segmental) bronchi. Further divisions within these conducting airways end with the terminal bronchioles, the smallest airways without alveoli. These conducting airways do not participate in gas exchange but form the anatomical dead space (approximately 150 mL).⁷

Larger airways have a greater proportion of supporting cartilage, ciliated epithelium, goblet and serous cells and hence a mucous layer. As the airways become smaller, cartilage becomes irregularly dispersed, the number of goblet cells and amount of mucus decreases until, at the alveolar level, there is only a single layer of squamous epithelial cells. Alveolar macrophages are present in these epithelial cells, and phagocytose any small particles that may enter the alveolar area. Smooth muscle surrounds and supports the bronchioles, enabling airway diameter change and subsequent changes in airway resistance to gas flow.⁸

Thorax/Lungs

The lungs and heart are protected within the thoracic cage. Expansion of the thorax enables the lungs to fill with air during inspiration when respiration is triggered, and to passively compress to expel air from the lungs during expiration. The diaphragm separates the thorax from the abdomen and actively participates in the ventilation process. The diaphragm is the most important inspiratory muscle, performing approximately 80% of the work of breathing. Inspiration is initiated from the medulla, sending impulses through the phrenic nerve to stimulate the diaphragm to contract and flatten. The phrenic nerve originates in the cervical plexus and involves the third to fifth cervical nerves. It splits into two parts, passing to the left and right side of the heart before it reaches the diaphragm. For this reason, patients can have ventilation difficulties if phrenic nerve damage is due to C3–C5 trauma.^8,⁹

The conducting airways move inspired air towards the respiratory unit, ending in the terminal bronchioles. The respiratory bronchioles, the alveolar ducts and alveolar sacs form the respiratory unit where the diffusion of gas molecules, or gas exchange, occurs. The respiratory unit makes up most of the lung with a volume of 2.5–3 L during rest ⁷ (see Figure 13.3).

FIGURE 13.3 Lower airway branches.⁵

Control of Ventilation

Normal breathing occurs automatically and is a complex function not fully understood. It is coordinated by the respiratory centre, regulated by controllers in the brain, effectors in the muscles and sensors including chemoreceptors and mechanoreceptors. There are also protective reflexes that respond to irritation of the respiratory tract such as coughing and sneezing.

Controller

In the brainstem, the medulla oblongata and the pons regulate automatic ventilation while the cerebral cortex regulates voluntary ventilation (see Figure 13.7). The respiratory rhythmic centre in the medulla can be divided into inspiratory and expiratory centres, with the following functions:⁸

• The inspiratory centre (or dorsal respiratory group) triggers inspiration.

• The expiratory centre (or ventral respiratory group) only functions during forced respiration and active expiration.

• The pneumotaxic and apneustic centre in the pons adjusts the rate and pattern of breathing.

• The cerebral cortex provides conscious voluntary control over the respiratory muscles. This voluntary control cannot be maintained when PCO₂ and hydrogen ion (H⁺) concentration become markedly elevated; an example is the inability to hold your breath for very long.⁸ Emotional and autonomic activities also often affect the pace and depth of breathing.

FIGURE 13.7 Respiratory centres and reflex controls.⁴

Effectors

The diaphragm is the major muscle of inspiration, although the external intercostal muscles are also involved. The accessory muscles of inspiration (scalenes, sternocleidomasteoid muscles and the pectoralis minor of the thorax) are active only during exercise or strenuous breathing. Expiration is a passive act and only the internal intercostal muscles are involved at rest. During exercise, the abdominal muscles also contribute to expiration.⁴ Inspiration is triggered by stimulus from the medulla, causing the diaphragm to contract downwards, and the external intercostal muscles to contract, lifting the thorax up and out. This action lowers pressure within the alveoli (intra-alveolar pressure) relative to atmospheric pressure. Air rushes into the lungs to equalise the pressure gradient. After contraction has ceased, the ribs and diaphragm relax, the pressure gradient reverses, and air is passively expelled from the lungs and return to their resting state due to elastic recoil.

Sensors

A chemoreceptor is a sensor that responds to a change in the chemical composition of the blood; there are two types: central and peripheral. Central chemoreceptors account for 70% of the feedback controlling ventilation, and respond quickly to changes in the pH of cerebral spinal fluid (CSF) (increase of PCO₂ in arterial blood).⁹ If the PCO₂ in arterial blood remains high for a prolonged period, as in chronic obstructive pulmonary disease (COPD), a compensatory change in HCO₃ occurs and the pH in CSF returns to its near normal value.⁷ Under these conditions a patient breathes due to hypoxic drive; that is, low levels of O₂ are detected by peripheral chemoreceptors and this triggers breathing. For this small percentage of the population with COPD, care is required when administering oxygen so that the stimulus to breathe is not compromised, as increases in PO₂ may reduce respiratory drive. Peripheral chemoreceptors respond to low partial pressure of oxygen in arterial blood (PaO₂) and contribute to maintaining ventilation, functioning optimally when oxygen levels fall below 70 mmHg.⁷

Central chemoreceptors located in the medulla respond to changes in hydrogen ion concentration in the CSF that surrounds these receptors. A change in the partial pressure of carbon dioxide in arterial blood (PaCO₂) causes movement of CO₂ across the blood–brain barrier into the CSF and alters the hydrogen ion concentration. This increase in hydrogen ions stimulates ventilation. Central chemoreceptors do not however respond to changes in PaO₂ levels. Opiates also have a negative influence on these chemoreceptors causing less sensitivity to changes in hydrogen ion concentration.⁷ Note also that hyperventilation may reduce the level of PaCO₂ to a level that could cause accidental unconsciousness if the breath is held after hyperventilation. This phenomenon is well known amongst divers and is due to increasing levels of CO₂ as the primary trigger of breathing. If the CO₂ level is too low due to hyperventilation, the breathing reflex is not triggered until the level of oxygen has dropped below what is necessary to maintain consciousness.

Peripheral chemoreceptors are located in the common carotid arteries and in the arch of the aorta. These receptors are sensitive to changes in PaO₂ and are the primary responders to hypoxaemia, stimulating the glossypharyngeal and vagus nerves and providing feedback to the medulla. Peripheral chemoreceptors also detect changes in PaCO₂ and hydrogen ion concentration/pH in arterial blood.⁹ Other receptors include stretch receptors located in the lungs that inhibit inspiration and protect the lungs from over-inflation (Hering–Breuer reflex), and in the muscles and joints (see Figure 13.7).

Pulmonary Volumes and Capacities

In healthy individuals, the lungs are readily distensible or compliant; when exposed to high expanding pressures or in disease states, compliance is increased or decreased. A range of lung volumes and capacities are illustrated in Figure 13.8. Tidal volume (TV) is the volume of air entering the lungs during a single inspiration and is normally equal to the volume leaving the lungs on expiration (around 500 mL). During inspiration, the TV of inspired air is added to the 2400 mL of air already in the lungs. This volume of air that remains in the lungs after a normal expiration is the functional residual capacity (FRC),⁴ which:

• has an important role in keeping small alveoli open and avoiding atelectasis

• can be reduced during anaesthesia or neuromuscular blockade, most likely due to loss of muscle tone ¹²

• if reduced, results in the smallest alveoli closing at the end of the expiration (the ‘closing volume’).

FIGURE 13.8 For lung volume measurements, all values are approximately 25% less in women. ERV, expiratory reserve volume; IC, inspiratory capacity; IRV, inspiratory reserve volume; FRC, functional residual capacity; TLC, total lung capacity; RV, residual volume; VC, vital capacity; VT, tidal volume.¹⁰

The closing volume plus the residual volume is called the ‘closing capacity’. The closure of the smallest airways may occur because dependent areas of the lungs are compressed, although this is not the only mechanism as these airways also close in the weightlessness of space. The closing volume is dependent on patient age; in a young healthy person it is 10% of vital capacity, while for an individual aged 65 years it increases to 40%, approximating total FRC.¹¹

Alveolar Ventilation

Minute volume (MV), often referred to during mechanical ventilation, is TV multiplied by respiratory frequency (e.g. 500 mL × 12 breaths per minute = 6000 mL MV). Importantly, only the first 350 mL of inhaled air in each breath reaches the alveolar exchange surface, with 150 mL remaining in the conducting airways (called the ‘anatomic dead space’). Alveolar ventilation is the amount of inhaled air that reaches the alveoli each minute (e.g. 350 mL × 12 = 4200 mL of alveolar ventilation).⁸

Work of Breathing

In a resting state, energy requirements to breathe is minimal (less than 5% of total O₂ consumption).⁷ However, changes in airway resistance and lung compliance affect the work of breathing (WOB), resulting in increased oxygen consumption (VO₂).¹³ As noted earlier, the lungs are very distensible and expand during inspiration. This expansion is called the elastic or compliance work and refers to the ease by which lungs expand under pressure. Lung compliance is often monitored when patients are mechanically ventilated, and is calculated by dividing the change in lung volume by the change in trans-pulmonary pressure.³ For the lung to expand, it must overcome lung viscosity and chest wall tissue (called ‘tissue resistance work’). Finally, there is airway resistance work – movement of air into the lungs via the airways. The work associated with resistance and compliance is easily overcome in healthy individuals but in pulmonary disease, both resistance and compliance work is increased.^3,¹⁴ During exertion, when increased muscle function heightens metabolic rate, oxygen demand rises to match consumption and avoid anaerobic metabolism, and work of breathing is increased. The term ‘work of breathing’ is often used in those who are critically ill, when basic respiratory processes are challenged and breathing consumes a far greater proportion of total energy.

Principles of Gas Transport and Exchange in Alveoli and Tissues

Oxygen and carbon dioxide is transported in the bloodstream between the alveoli and the tissue cells by the cardiac output. Delivery of oxygen to tissues and transfer of carbon dioxide from the tissues to the capillary occurs by diffusion and is therefore dependent on the pressure gradient between the capillary and the cell. Diffusion involves molecules moving from areas of high concentration to low concentration. Other determinants of the rate of diffusion include the thickness of the alveolar membrane, the amount of surface area of the membrane available for gas transfer and the inherent solubility of the gas. Carbon dioxide diffuses about 20 times more rapidly than oxygen because of the much higher solubility of carbon dioxide in blood.⁷ At the most distal ends of the conducting airways lies an extensive network of approximately 300 million alveoli. The surface area of the lungs if spread out flat is about 90 m² – about 40 times greater than the surface of the skin.⁴ Gas exchange occurs through the exceptionally thin alveolar membranes. Oxygen uptake takes place from the external environment via the lungs through to the blood in the adjacent alveolar capillary networks. Similarly, carbon dioxide diffuses from capillaries to the alveoli and is then expired.

Oxygen Transport

In oxygenated blood transported by the pulmonary capillaries, there is 20 mL of oxygen in each 100 mL of blood. Oxygen is transported in two ways; dissolved in plasma (about 0.3 mL; 1.5%) with the remainder bound to haemoglobin.⁸ The 1.5% of oxygen dissolved in the blood is what constitutes PaO₂ and measured by arterial blood gases.⁴ One gram of haemoglobin carries 1.34 mL oxygen, and the level of saturation within the total circulating haemoglobin can be measured clinically, commonly by pulse oximetry. The amount of oxygen actually bound to haemoglobin compared with the amount of oxygen the haemoglobin can carry is commonly reported as SaO₂. Oxygen is attached to the haemoglobin molecule at four haem sites. As the majority of oxygen transport is via haemoglobin, if all four sites are occupied with oxygen molecules the blood is determined to be ‘fully saturated’ (SaO₂ = 100%).¹⁴

A large reserve of oxygen is available if required, without the need for any increase in respiratory or cardiac workload. Oxygen extraction is the percentage of oxygen extracted and utilised by the tissues. At rest, just 25% of the total oxygen delivered to the tissue is extracted, although this amount does vary throughout the body, with some tissue beds extracting more and others taking less. Normally, the oxygen saturation of venous blood is 60–75%; values below this indicate that more oxygen than normal is being extracted by tissues. This can be due to a reduction in oxygen delivery to the tissues, or to an increase in the tissue consumption of oxygen.^8,⁹

Oxygen delivery (DO₂) and oxygen consumption (VO₂) are important aspects to consider in the management of a critically ill patient. Normal oxygen delivery in a healthy person at rest is approximately 1000 mL/min. Normal oxygen consumption is 200–250 mL/min,⁹ but this can increase significantly during episodes of sepsis, fever, hypercatabolism and shivering.¹⁴ The difference between normal delivery and normal consumption highlights the large degree of oxygen reserve available to the body.

Oxygen–Haemoglobin Dissociation Curve

As blood is transported to the tissues and end-organs, the affinity of haemoglobin and oxygen to combine decreases, relative to the surrounding arterial oxygen tension. This relationship is illustrated by the oxyhaemoglobin dissociation curve (see Figure 13.9). As oxygen is offloaded at the tissue level, carbon dioxide binds more readily with haemoglobin, to be transported back to the lungs for removal.⁴

FIGURE 13.9 Shift of the oxyhaemoglobin dissociation curve (A) to the right and (B) to the left.⁸⁵

In the upper part of the curve (within the lungs), relatively large changes in the PaO₂ cause only small changes in haemoglobin saturation. Therefore, if the PaO₂ drops from 100 to 60 mmHg (14–8 kPa), the saturation of haemoglobin changes only 7% (from a normal 97% to 90%). The lower portion (steep component) of the oxygen–haemoglobin dissociation curve, when PaO₂ is between 60 and 40 mmHg (8–5 kPa) reflects however that as haemoglobin is further de-saturated, larger amounts of oxygen are released for tissue use, ensuring an adequate oxygen supply to peripheral tissues is maintained even when oxygen delivery is reduced.⁴ Oxygen saturation still remains at 70–75%, leaving a significant amount of oxygen in reserve. The relationship between the two axes of this curve assumes normal values for haemoglobin, pH, temperature, PaCO₂ and 2,3-DPG. Changes to any of these values will shift the curve to the right or left and therefore reflect different values for PaO₂ and SaO₂.⁸

Carbon Dioxide Transport

Carbon dioxide is transported by blood in three forms: combined with water as carbonic acid (80–90%), dissolved (5%), or attached to plasma proteins (5–10%), including haemoglobin. The dissolved carbon dioxide constitutes PaCO₂ and is measured by arterial blood gases. The greater solubility of CO₂ when compared with oxygen results in rapid diffusion across the capillary membranes, and therefore the gas can be easily removed for elimination.⁴ Carbon dioxide, a byproduct of cellular respiration, is produced at a rate of 200 mL/min, with only minor differences in normal concentrations in arterial (480 mL/L) and venous (520 mL/L) blood.⁹

Relationship Between Ventilation and Perfusion

Gas exchange is the key function of the lungs, and the unique anatomy of capillaries and alveoli facilitates this process. However, a number of physiological factors mean that the ventilation (V) to perfusion (Q) ratio is not matched in a 1 : 1 relationship. As normal alveolar ventilation is about 4 L/min and pulmonary capillary perfusion is about 5 L/min, the normal ventilation to perfusion ratio (V/Q) is 0.8.⁷ In addition, pressure in the pulmonary circulation is low relative to systemic pressure, and is influenced much more by gravity/hydrostatic pressure. In the upright position, lung apices receive less perfusion compared with the bases.⁷ In the supine position, apical and basal perfusion is almost equal, but the posterior (dependent) portion of the lungs receives greater perfusion than the anterior lung area. Ventilation is also uneven throughout the lung, with the bases receiving more ventilation per unit volume than the apices.⁷

Pressure within the surrounding alveoli also influences blood flow through the pulmonary capillary network. The pressure gradients between the arterial and venous ends of a capillary network normally determine blood flow. However, alveolar pressure can be greater than venous and/or arterial pressure, and therefore influences blood flow and gas exchange.

For a patient in an upright position, in:

• Zone 1 (upper area of the lungs): alveolar pressure is generally greater than both arterial and venous capillary pressure [P_A>P_a>P_v], and blood flow is reduced, leading to alveolar dead space (alveoli ventilated but not adequately perfused).

• Zone 2 (middle portion of the lungs): perfusion and gas exchange is influenced more by pressure differences between arterial and alveolar pressures than by the usual difference between arterial and venous pressures [P_a>P_A>P_v], with a normal V/Q ratio.

• Zone 3 (lung bases): alveolar pressure is lower than both arterial and venous pressures [P_a>P_v>P_A], and ventilation is reduced leading to intrapulmonary shunting (alveoli perfused but not adequately ventilated)⁷ (see Figure 13.10).

FIGURE 13.10 The effects of gravity and alveolar pressure on pulmonary blood flow. Notice the three lung zones.⁸⁶

These physiological relationships are more complex in a critically ill patient when ventilation and/or lung perfusion is further compromised by disease processes and positive pressure ventilation, and the patient is in a supine or semi-recumbent position.⁷

Acid–Base Control: Respiratory Mechanisms

The respiratory system plays a vital role in acid–base balance. Changes in respiratory rate and depth can produce changes in body pH by altering the amount of carbonic acid (H₂CO₃) in the blood. When dissolved, CO₂ forms bicarbonate ion (HCO₃⁻), carbonic acid (H₂CO₃) and carbonate ion (CO₃²⁻); these concentrations affect the acid–base balance. In common with other acids, carbonic acid partially dissociates when in solution, to form CO₂ and water or bicarbonate and hydrogen ion:

The strength of the dissociation is defined by the Henderson–Hasselbach equation that describes the relationship between bicarbonate, CO₂ and pH, and explains why an increase in dissolved CO₂ causes an increase in the acidity of the plasma, while an increase in HCO₃⁻ causes the pH to rise (i.e. acidity falls):

(6.1 = the dissociation constant in plasma).¹¹

Respiratory acidosis is caused by CO₂ retention and increases the denominator in the Henderson–Hasselbach equation resulting in a decreased pH level. This condition occurs when a patient takes small breaths at a low respiratory rate (hypoventilation). In the acute state the body cannot compensate. If the patient develops chronic CO₂ retention over a long period, there will be a renal response to the increase in CO₂. The renal system retains bicarbonate to return the pH to normal (i.e. respiratory acidosis is compensated).

Respiratory alkalosis occurs when a patient hyperventilates with large, frequent breaths; CO₂ decreases in arterial blood and pH rises. If this condition is maintained (e.g. walking at high altitude), the kidney excretes bicarbonate and pH returns to normal (i.e. the respiratory alkalosis is compensated).¹¹

Pathophysiology

Three common pathophysiological concepts that influence respiratory function in critically ill patients are hypoxaemia, inflammation and oedema. The principles for these phenomena are discussed below. Related presenting disease states including respiratory failure, pneumonia, acute lung injury, asthma and chronic obstructive pulmonary disease are described in Chapter 14.

Hypoxaemia

Hypoxaemia describes a decrease in the partial pressure of oxygen in arterial blood (PaO₂) of less than 60 mmHg.⁴ This state leads to less efficient anaerobic metabolism at the tissue and end-organ level, and resulting compromised cellular function. Hypoxia is abnormally low PO₂ in the tissues, and can be due to:

• ‘hypoxic’ hypoxia: low PaO₂ in arterial blood due to pulmonary disease

• ‘circulatory’ hypoxia: reduction of tissue blood flow due to shock or local obstruction

• ‘anaemic’ hypoxia: reduced ability of the blood to carry oxygen due to anaemia or carbon monoxide poisoning

• ‘histotoxic’ hypoxia: a cellular environment that does not support oxygen utilisation due to tissue poisoning (e.g. cyanide poisoning).⁷

A hypoxic patient can show symptoms of fatigue and shortness of breath if the hypoxia has developed gradually. If the patient has severe hypoxia with rapid onset, they will have ashen skin and blue discolouration (cyanosis) of the oral mucosa, lips, and nail beds. Confusion, disorientation and anxiety are other symptoms. In later stages, unconsciousness, coma and death occur.¹⁵

Acute respiratory failure is a common patient presentation in ICU that is characterised by decreased gas exchange with resultant hypoxaemia.¹⁶ Two different mechanisms cause acute respiratory failure: Type I presents with low PO₂ and normal PCO₂; Type II presents with low PO₂ and high PCO₂¹ (see Chapter 14 for further discussion).

In general, impaired gas exchange results from alveolar hypoventilation, ventilation/perfusion mismatching and intrapulmonary shunting, each resulting in hypoxaemia. Hypercapnia may also be present depending on the underlying pathophysiology.¹⁷

Alveolar hypoventilation occurs when the metabolic needs of the body are not met by the amount of oxygen in the alveoli. Hypoxaemia due to alveolar hypoventilation is usually extrapulmonary (e.g. altered metabolism, interruption to neuromuscular control of breathing/ventilation) and associated with hypercapnia.¹⁷

Ventilation/perfusion (V/Q) mismatch results when areas of lung that are perfused are not ventilated (no participation in gas exchange) because alveoli are collapsed or infiltrated with fluid from inflammation or infection (e.g. pulmonary oedema, pneumonia). This results in an overall reduction in blood oxygen levels, which can usually be countered by compensatory mechanisms.¹

Intrapulmonary shunting is an extreme case of V/Q mismatch. Shunting occurs when blood passes alveoli that are not ventilated. There can be significant intrapulmonary shunting, and therefore overwhelming reductions in PaO₂.¹⁸ Carbon dioxide levels may still be normal but depending on the onset and progression of the respiratory pathophysiology, compensatory mechanisms may not be able to maintain homeostasis^1,¹¹ (see Figure 13.11).

FIGURE 13.11 Ventilation perfusion mismatch.¹⁸

Tissue Hypoxia

There are few physiological changes with mild hypoxaemia (when O₂ saturation remains at 90% despite a PaO₂ of 60 mmHg [8 kPa]), with only a slight impairment in mental state. If hypoxaemia deteriorates and the PaO₂ drops to 40–50 mmHg (5.3–6.7 kPa), severe hypoxia of the tissues ensues. Hypoxia at the central nervous system level manifests with headaches and somnolence. Compensatory mechanisms include catecholamine release, and a decrease in renal function results in sodium retention and proteinuria.¹⁹

Different tissues vary in their vulnerability to hypoxia, with the central nervous system and myocardium at most risk. Hypoxia in the cerebral cortex results in a loss of function within 4–6 seconds, loss of conscious in 10–20 seconds and irreversible damage in 3–5 minutes.¹¹ In an environment that lacks oxygen, cells function by anaerobic metabolism and produce much less energy (adenosine triphosphate [ATP]) than with aerobic metabolism (2 versus 38 ATP molecules per glucose molecule), and lactic acid increases. With less available energy, the efficiency of cellular functions such as the Na+/K+ pump, nerve conduction, enzyme activity and transmembrane receptor function diminishes.¹⁹ The overall effect of interruption to these vital cellular activities is a reduction in organ or tissue function, which in turn compromises system and body functions.

Changes to the oxyhaemoglobin dissociation curve also occur in states related to hypoxia. The curve shifts to the right when there is acidosis and/or raised levels of PCO₂ as commonly seen in respiratory failure. Although this change may alter patient oxygen saturation readings, the increased release of oxygen from haemoglobin to the tissues has obvious benefits for tissue oxygenation and cellular metabolism.⁷

Compensatory Mechanisms to Optimise Oxygenation

When PO₂ in the alveolus is reduced, hypoxic pulmonary vasoconstriction occurs, with contraction of smooth muscles in the small arterioles in the hypoxic region, directing blood flow away from the hypoxic area of the lung.⁷ Peripheral chemoreceptors also detect hypoxaemia and initiate compensatory mechanisms to optimise cellular oxygen delivery. Initial responses are increased respiratory rate and depth of breathing, resulting in increased minute ventilation, and raised heart rate with possible vasoconstriction as the body attempts to maintain oxygen delivery and uptake. This overall up-regulation cannot be sustained indefinitely, particularly in a person who is critically ill, and compensatory mechanisms begin to fail with worsening hypoxaemia and cellular and organ dysfunction. Unless the hypoxaemia is reversed and/or respiratory and cardiovascular support is provided, irreversible hypoxia and death will ensue.

Inflammation

Inflammatory processes can occur at a local level (e.g. as a result of inhalation injuries, aspiration or respiratory infections) or are secondary to systemic events (e.g. sepsis, trauma). Damage to the pulmonary endothelium and type I alveolar cells appear to play a key role in the inflammatory processes associated with ALI.²⁰ Once triggered, inflammation results in platelet aggregation and complement release. Platelet aggregation attracts neutrophils, which release inflammatory mediators (e.g. proteolytic enzymes, oxygen free radicals, leukotrienes, prostaglandins, platelet-activating factor [PAF]). Neutrophils also appear to play a key role in the perpetuation of ALI/ARDS.¹ As well as altering pulmonary capillary permeability, resulting in haemorrhage and fluid leak into the pulmonary interstitium and alveoli, mediators released by neutrophils and some macrophages precipitate pulmonary vasoconstriction. Resulting pulmonary hypertension leads to diminished perfusion to some lung areas, with dramatic alterations to both perfusion and ventilation leading to significant V/Q mismatches, and the subsequent signs and symptoms typically seen in patients with pulmonary inflammation/oedema.

Oedema

Pulmonary oedema also alters gas exchange, and results from abnormal accumulation of extravascular fluid in the lung. The two main reasons for this are: ‘increased pressure’ oedema, where there is an increase in hydrostatic or osmotic forces (e.g. left heart ventricular dysfunction or volume overload); and ‘increased permeability’ oedema, that results from increased membrane permeability of the epithelium or endothelium in the lung, allowing accumulation of fluid (also called ‘non-cardiogenic’). Resulting clinical syndromes are acute lung injury (ALI) or acute respiratory distress (ARDS) (see Chapter 14 for further discussion).

Changes to Respiratory Function

During the early exudative phase of ALI/ARDS, tachypnoea, signs of hypoxaemia (apprehension, restlessness) and an increase in the use of accessory muscles are usually evident as a result of infiltration of fluids into the alveoli. With impaired production of surfactant during the proliferative phase, respiratory function deteriorates, and dyspnoea, agitation, fatigue and the emergence of fine crackles on auscultation are common.^1,¹¹ Airway resistance is increased when oedema affects larger airways. Lung compliance is reduced as interstitial oedema interferes with the elastic properties of the lungs, and patients may be quite a challenge to adequately ventilate. Infiltration of type II alveolar cells into the epithelium may lead to interstitial fibrosis on healing,²¹causing chronic lung dysfunction.

Respiratory Dysfunction: Changes to Work of Breathing

If respiratory compromise is not reversed, there will be significant increases to the work of breathing. Clinical manifestations include tachypnoea, tachycardia, dyspnoea, low tidal volumes and diaphoresis. Hypercapnia will ensue, which further compromises respiratory muscle function and precipitates diaphragmatic fatigue. Oxygen consumption during breathing can be so great that reserve capacity is reduced. If patients with preexisting COPD (who may breathe close to the fatigue work level) experience an acute exacerbation, this can easily tip them into a fatigued state. Early identification and management of respiratory compromise before these stages improves patient outcomes.¹⁹

Assessment

Respiratory insufficiency is a common reason for admission to a critical care unit, for either a potential or an actual problem, so comprehensive and frequent respiratory assessments are an essential practice role. This section outlines history, physical examination, bedside monitoring and diagnostic testing focused on a critically ill patient with respiratory dysfunction.

Assessment is a systematic process comprising history taking of a patient’s present and previous illnesses, and physical examination of their thorax, lungs and related systems. History taking and physical examination can be done simultaneously if the patient is very ill. Related diagnostic findings inform an accurate and comprehensive assessment. A thorough assessment, followed by accurate ongoing monitoring, enables early detection of condition changes and assessment of the impact of treatment. Depending on a patient’s situation, assessment can be either brief or detailed.

Patient History

History-taking determines a patient’s baseline respiratory status on admission to ICU. If the patient is in distress only a few questions may be asked but, if the patient is able, a more comprehensive interview can be performed, focusing on four areas: the current problem, previous problems, symptoms and personal and family history. Question a family member or close friend if a patient is not able to provide their own history.

When introducing yourself, ask the patient’s name, seek eye contact and create a rapport with the patient and the family. Ensure that the patient is in a comfortable position, ideally sitting up in the bed. Provide privacy so that the interview is confidential and the physical examination can be done while maintaining the patient’s dignity and modesty. To minimise distress for a patient who is acutely breathless, the use of short closed questions is preferable.

Practice tip

History-taking is a nursing interview and an interactive experience, especially the initial interview where both the patient and the nurse learn a lot about each other. This knowledge has a considerable influence on building rapport between the patient and the nurse.

Current Respiratory Problems

Begin by asking why the patient is seeking care. If possible, let the patient describe the respiratory problem in his or her own words. Be focused and listen actively. Ask for location, onset and duration of the respiratory symptoms.

Previous Respiratory Problems

Many respiratory disorders can be chronic and pulmonary diseases may recur (e.g. tuberculosis), and new diseases can complicate old ones.²² Ask about problems with breathing and their chest, number of hospitalisations, treatments, and childhood respiratory diseases.

Symptoms

Assess any presenting symptoms in relation to: onset and duration, pattern, severity, and episodic or continuous. Also ask about the patient’s perception of their respiratory problem, their opinion about its cause and if the symptoms cause fatigue, anxiety or stress. Ask the patient specifically about: dyspnoea, cough, sputum production, haemoptysis, wheezing, chest pain or other pain, sleep disturbances and snoring.

Dyspnoea (shortness of breath) is subjective and therefore difficult to grade. The mechanism that underlies the sensation of dyspnoea is poorly understood but it is extremely uncomfortable and frightening.²² Assess the severity of dyspnoea by asking about breathing in relation to activities (e.g. breathlessness when dressing or walking across a room). Ask the patient how many pillows they need to sleep as this may indicate the severity of any orthopnoea. If the patient becomes short of breath when lying flat (orthopnoea) it can be a symptom of increased blood in the pulmonary circulation due to left ventricular failure, pulmonary oedema, bronchitis, asthma or obstructive sleep apnoea.

A cough can be dry or wet, episodic or continuous and, if exacerbated when the patient is lying flat, can imply heart failure. A cough can also be related to viral infections and allergies or it can indicate intra-thoracic disease. Ask the patient if they wake during the night due to the cough, how long the cough has been present and if it is getting better or worse.

Sputum production should be considered for amount, colour or the presence of blood. Yellow or green sputum is typical in bacterial infection. Haemoptysis or sputum mixed with blood is a significant finding and can indicate tuberculosis or lung cancer. Wheezing can indicate vocal cord disorder or asthma.²²

Chest pain can result from multiple causes, therefore appropriate assessment is essential. Chest pain that occurs during inspiration can be due to irritation or inflammation of the pleural surface. Pleural pain is experienced mostly on one side of the chest, is knifelike in character and occurs in pneumonia and spontaneous pneumothorax. The most significant chest pain occurs as a result of myocardial ischaemia, due to too little oxygen to the coronary blood vessels. This pain is termed angina pectoris and can arise from chronic stable angina or acute myocardial infarction ²² (see Chapter 10 for further discussion). Chest pain also occurs with fractured ribs.

Sleep disturbance and snoring may be related to obstructive sleep apnoea (OSA). If the patient complains about drowsiness in the daytime, ask how many hours of continuous sleep they have at night, and whether they take a nap during the day.

Personal and Family History

Patient family history and environment can influence pulmonary presentations. The focus of this questioning is on: tobacco use, allergies, recent travel, type of occupation, home situation and family history. Use of tobacco, current or past, is important in evaluating pulmonary symptoms. Ask the patient to quantify the amount of cigarette packs per week and how many years they have smoked. The majority of smokers have reduced lung function. Tobacco smoking is responsible for 80–90% of the risk of developing chronic obstructive pulmonary disease but only 10–15% of these patients will develop clinically significant symptoms.²³ Exposure to secondhand smoke may also be of interest. There is evidence that exposure to secondhand smoke for an extended period is a major cause in developing chronic bronchitis.²⁴ A history of recent travel increases the possibility of exposure to infectious diseases affecting the respiratory system.²⁵ Recent long flights are also responsible for the possibility of deep venous thrombosis which can lead to pulmonary embolism.²⁶ An occupation with exposure to allergens and toxins in the work place is important information to collect because this can be associated with a decline in lung function.²⁷ Ask about the patient’s home situation and whether they live with someone with an infection or disease such as influenza or tuberculosis. Ask about children who are close to the patient, as innocuous viral infections in small children may account for severe disease in adults.²² Check also whether there is a family history of cancer, heart or respiratory diseases.

Physical Examination

The four activities of physical examination are inspection, palpation, percussion and auscultation. Percussion is rarely used by critical care nurses, so only the other three techniques are discussed here. Prior to commencing the examination, prepare the patient as best as is possible by providing privacy, warmth, good light and quiet surroundings (this can be difficult to achieve in the critical care environment). Explain to the patient that the examination is a standard procedure and that you will use your eyes, hands and a stethoscope. Help the patient into a comfortable sitting position in the bed if possible and have all the necessary equipment easily accessible.

Inspection

Inspection involves carefully observing the patient for signs of respiratory problems. Focus on: patient position, chest wall inspection, respiratory rate and rhythm, respiratory effort, central or peripheral cyanosis and clubbing. Note what position appears preferable for the patient, whether they look comfortable in bed, having trouble breathing, or appear anxious. Observe from head to toe. Observe the patient’s chest wall symmetry during the respiratory cycle, anatomical structures, and the presence of scars. The most important sign of respiratory distress is respiratory rate and rhythm. Count the rate for a one-minute period. Normal respiratory rate for adults is 12–15 per minute.⁴ Abnormal breathing patterns are noted in Table 13.1. Observe respiratory effort, in particular the use of accessory muscles, abdominal muscles, nasal flaring, body position and mouth-breathing.

TABLE 13.1 Description of different respiration patterns ¹⁴

Inspect the lips, tongue and sublingual area for central cyanosis (a late sign of hypoxia that is almost impossible to detect in a patient with anaemia).¹ Observe the extremities for oedema (can be a sign of heart failure), fingers and toes for peripheral cyanosis and clubbing of the nailbeds. Peripheral cyanosis can appear with low blood flow to peripheral areas. Clubbing of finger or toe nailbeds can be idiopathic in nature or more commonly due to respiratory and circulatory diseases (e.g. chronic hypoxia in congenital heart disease).^14,²²

Note also if the patient requires oxygen and observe the dose. If the patient is intubated and mechanically ventilated (monitoring is explained later in this chapter), ensure the airway is adequately secured. If the patient is orally intubated, observe the mouth for the presence of lesions or pressure on the oral mucosa and lips; and observe the size of the tube, the length at the lips or teeth margin, and how it is secured. If the patient has a tracheostomy, observe the stoma for signs of infection or pressure areas; and observe the type and size of tracheostomy tube, the length at the hub if it is a tracheostomy with an adjustable flange, and the way in which it is secured.

Palpation

Palpate the patient’s chest with warm hands, focusing on: areas of tenderness, tracheal position, presence of subcutaneous emphysema and tactile fremitus. Assess for symmetry (left compared to right) and anterior and posterior surfaces (see Figure 13.12). Check the thorax for areas of tenderness or bony deformities, and note symmetry of chest movement during breathing. Use the palm of your hand to assess skin temperature of the skin, noting for clammy, hot or cold skin. To test for chest wall symmetry on inspiration, place both hands with thumbs together on the patient’s posterior thorax and ask the patient to take a deep breath. Your thumbs should separate equally 3–5 cm during normal deep inspiration¹ (see Figure 13.13). Asymmetry can occur in pneumothorax, pneumonia or other lung disorders where inspiration is affected.

FIGURE 13.12 Sequence of systematic movements for auscultation and palpation of the anterior (A) and posterior (B) chest. Comparison of the right and left sides of the chest should be performed by moving from side to side, beginning proximally and moving distally down the chest wall. Palpation and auscultation of the thorax is performed in a sequential fashion.⁸⁴

FIGURE 13.13 Assessment of thoracic expansion. (A) Exhalation; (B) Inhalation.¹

Palpation of tracheal position is useful to detect a mediastinal shift; deviation of the trachea from midline may indicate a pulmonary problem. With a large pneumothorax or after pneumonectomy, the trachea may shift away from the affected side.²⁸ The presence of subcutaneous emphysema indicates air in the subcutaneous tissue and most commonly occurs in the face, neck and chest after blunt or penetrating trauma to the chest (e.g. stabbing, gun shot, fractured ribs); facial fractures; tracheostomy; upper respiratory tract surgery; and patients who are mechanically ventilated. Subcutaneous emphysema feels like crackling under your fingers due to air pockets in the tissue.²⁹

Palpation is also used to assess for the presence of tactile (vocal) fremitus, a normal palpable vibration. Place your hands on the patient’s chest and ask the patient to vocalise repeatedly the term ‘ninety nine’. Fremitus is decreased (that is, impaired transmission of sounds) in pleural effusion and pneumothorax. Fremitus is increased over those regions of the lungs were transmission is increased (e.g. pneumonia, consolidation).²² In mechanically ventilated patients, fremitus can be detected over the lungs when there are secretions in the airways.

Practice tip

Prior to performing palpation and auscultation of a patient’s chest, warm your hands and stethoscope diaphragm before placing them on their skin.

Practice tip

Prior to use, remember to use an alcohol wipe to clean the earpieces on the stethoscope to protect you from infection.

Auscultation

Careful interpretation of breath sounds and integration of this assessment data with other findings can provide important information about lung disorders. Use the diaphragm of the stethoscope and ensure full contact with the skin for optimal listening. For a spontaneously breathing patient, ask them to breathe through their mouth (nose breathing may alter the pitch of the breath sounds). Auscultation is performed in a systematic way so as to compare the symmetry of breath sounds (see Figure 13.12). Normal breath sounds reflect air movement through the bronchi, and sounds change as air moves from larger to smaller airways. Sounds also change when air passes though fluid or narrowed airways. Breath sounds therefore differ depending on the area auscultated; the three general types of normal breath sounds are bronchial, bronchiovesicular and vesicular breath sounds (see Table 13.2).

TABLE 13.2 Normal breath sounds ¹

Sound	Characteristics
Vesicular	Heard over most of lung field; low pitch; soft and short exhalation, and long inhalation.
Bronchovesicular	Heard over main bronchus area and over upper right posterior lung field; medium pitch; exhalation equals inhalation.
Bronchial	Heard only over trachea; high pitch; loud and long exhalation.

Practice tip

When performing chest inspection and auscultation, check for symmetry between one side of the body with the other.

Identify and become familiar with normal breath sounds before beginning to listen and identify abnormal breath sounds. Abnormal breath sounds are either continuous or discontinuous. Continuous sounds include wheezes and rhonchi, while discontinuous sounds include crackles (see Table 13.3). Stridor is an abnormal loud high-pitched breath sound caused by obstruction in the upper airways as a result of a foreign body, tissue swelling or vocal cord; this emergent condition requires immediate attention.³⁰ Absent or diminished breath sounds indicate no airflow through that area of the lung and also requires immediate treatment.^22,³¹

TABLE 13.3 Description of abnormal breath sounds ¹

Abnormal Sound	Description	Condition
Absent breath sounds	No airflow to particular portion of lung	Pneumothorax Pneumonectomy Emphysematous blebs Pleural effusion Lung mass Massive atelectasis Complete airway obstruction
Diminished breath sounds	Little airflow to particular portion of lung	Emphysema Pleural effusion Pleurisy Atelectasis Pulmonary fibrosis
Displaced bronchial sounds	Bronchial sounds heard in peripheral lung fields	Atelectasis with secretions Lung mass with exudates Pneumonia Pleural effusion Pulmonary oedema
Crackles (rales)	Short, discrete popping or crackling sounds	Pulmonary oedema Pneumonia Pulmonary fibrosis Atelectasis Bronchiectasis
Rhonchi	Coarse, rumbling, low-pitched sounds	Pneumonia Asthma Bronchitis Bronchospasm
Wheezes	High-pitched, squeaking, whistling sounds	Asthma Bronchospasm
Pleural friction rub	Creaking, leathery, loud, dry, coarse sounds	Pleural effusion Pleurisy

Practice tip

Respiratory rate is an early warning sign for respiratory distress. If a patient has a high respiratory rate it can be a sign of hypoxia as they attempt to compensate for a low PO₂.

Documentation and Charting

Document the findings of your respiratory assessment in the patient’s chart; if this is the first respiratory assessment, describe the patient’s respiratory history carefully. Any abnormal findings including abnormal sounds and their characteristics should be described to enable subsequent re-assessment.³⁰

Respiratory Monitoring

A thorough and comprehensive assessment, with accurate ongoing monitoring, enables early detection of condition changes and assessment of responses to treatment for a critically ill patient. This section describes the main aspects of bedside respiratory monitoring and the instruments used to assess the efficiency of a patient’s gas transfer mechanisms, including pulse oximetry, capnography, airway pressures and ventilator waveforms and loops.

Pulse Oximetry

A pulse oximeter is a non-invasive device that measures the arterial oxygen saturation of haemoglobin in a patient’s blood flow. The technology is commonly standard in critical care units and other acute care areas. It is important to note that the device does not provide information on the patient’s ventilatory state, but it can determine their oxygen saturation and detect hypoxaemia.³² This prompt non-invasive detection of hypoxaemia enables identification of clinical deterioration and more rapid treatment to avoid associated complications.³³

Pulse oximetry works by emitting two wavelengths of light: red and infrared, from a diode (positioned on one side of the probe) to a photodetector (positioned on the opposite side) through a pulsatile flow of blood. The signal emitted is measured over five pulses, causing a slight delay when monitoring. Oxygenated blood absorbs light differently from deoxygenated blood; the oximeter measures the amount of light absorbed by the vascular bed and calculates the saturation of oxygen in those capillaries.

Measurement of indirect arterial oxygen saturation of the peripheral circulation via pulse oximetry is referred to as SpO₂ (the letter ‘p’ denotes peripheral) and is displayed digitally on the monitor as a percentage, along with heart rate and a plethysmographic waveform. Interpreting this waveform is essential in distinguishing a true oximetry signal from one displaying dampening or artefact (see Figure 13.14). The probe is commonly sited on a finger, but can also be placed on the toe, earlobe or forehead. Change the probe position frequently to maintain adequate perfusion of the site and skin integrity.³²

FIGURE 13.14 Common pulse oximetry waveforms.

Practice tip

In cool environments, wrap the patient’s hand or foot that has the sensor probe attached; this may improve saturation readings.

It is important to understand that pulse oximetry (SpO₂) measures peripheral arterial oxygen saturation (SaO₂) and that this differs from arterial oxygen tension (arterial partial pressure of oxygen; PaO₂). Note that SaO₂ and PaO₂ are physiologically related; this is illustrated by the two axes of the oxyhaemoglobin dissociation curve (see Figure 13.9, and the previous Physiology section for more discussion). A fit healthy adult (with a normal haemoglobin level) breathing room air has a SpO₂ of 97–99%.³⁴

Practice tip

Place the pulse oximeter probe on the finger of the opposite arm to where blood pressure is being taken, particularly if there is no arterial line and frequent non-invasive BP measurement is occurring.

Limitations of Pulse Oximetry

The limitations of pulse oximetry can be seen as follows:

• Pulse oximetry in isolation does not provide all the necessary information on ventilation status and acid–base balance. Arterial blood gas testing is therefore also needed to assess other parameters.³⁵

• Pulse oximeters are relatively reliable when the SaO₂ is 90% or above, however accuracy deteriorates when the SaO₂ falls to 80% or less.³³ When SpO₂ appear abnormal, assess the ABGs.

• As satisfactory arterial perfusion of the monitoring area is required, low cardiac output states, vasoconstriction, peripheral vascular disease and hypothermia can cause inaccurate pulse signals and falsely low oxygen saturation readings. In these cases, confirm oxygen saturation with intermittent arterial blood gas testing.

• As cardiac arrhythmias can impair perfusion and flow, signal quality may be compromised (see Figure 13.14). In these cases, use a more central probe (earlobe or forehead) to improve signal quality.

• Motion artefact (see Figure 13.14) caused by patient movement or shivering, is a significant cause of erroneously low readings and false alarms.³⁶ Keep the patient warm (if not contraindicated) and encourage them to minimise movement as this may be a problem. Using an ear probe may also reduce motion artefact.

• There is conflicting evidence as to whether nail varnish or acrylic nails interfere with SpO₂ readings.³⁶ Blue, green and black nail varnishes may affect accuracy of readings. To ensure accuracy, it is recommended that nail varnish and acrylic nails be removed if possible.

• Dark skin pigmentation can lead to falsely elevated SpO₂ values especially at low saturation levels.³⁷ A target SpO₂ level for patients with dark skin should be 95% to account for any over-estimation caused by pigmentation.³³

• External light, especially fluorescent light and heat lamps, can lead to an over- or under-estimation of SpO₂.³⁵ Covering the probe with an opaque barrier, such as a washcloth, can prevent this problem.

• Dyshaemoglobins, particularly carboxyhaemoglobin and methaemoglobin render SpO₂ monitoring unreliable.³³ The pulse oximetry sensor cannot differentiate between oxyhaemoglobin, carboxyhaemoglobin and methaemoglobin, and therefore provides a falsely elevated oxygen saturation reading.³⁵

• Injection of intravenous dyes may lead to a false underestimation of SpO₂ for up to 20 minutes after their administration (methylene blue, indocyanine green, indigo carmine).³³

FIGURE 13.15 Normal capnogram. A: end inspiration; B: expiratory upstroke; C: expiratory plateau; D: end-tidal carbon dioxide tension (PetCO₂).³⁹

Practice tip

Correlate the heart rate reading displayed in the pulse oximetry section of the monitor to the heart rate calculated by the ECG. If they do not correlate, this may indicate that not all pulsations are being detected and the pulse oximetry reading may not be accurate.

Capnography

Capnography monitors expired CO₂ during the respiratory cycle (also termed end-tidal CO₂ [PetCO₂] monitoring) by infrared spectrometry. The percentage of CO₂ exhaled at end expiration is displayed on the monitor in addition to the waveform, called a capnogram ¹ (see Figure 13.15 and Chapter 15 for waveform analysis and further discussion of PetCO₂ monitoring). Continuous capnography detects subtle changes in a patient’s lung dynamics (i.e. changes to physiological shunting or alveolar recruitment) and can be measured in both intubated and non-intubated patients. It can be used to estimate PaCO₂ levels in patients with a normal ventilation-perfusion ratio (usually 1–5 mmHg less than PaCO₂). However, levels are affected by conditions common in the critically ill (e.g. low cardiac output states, elevated alveolar pressures, sepsis, hypo/hyperthermia, pulmonary embolism), so use PetCO₂ to estimate PaCO₂ levels in these patients with caution.³⁸ Investigate any sudden changes in PetCO₂ levels with arterial blood gas analysis.

Despite this limitation, PetCO₂ monitoring has many uses in the care of a critically ill patient:

• it is the best method of confirming correct ETT placement and maintaining correct positioning of the ETT, ensuring tube patency and detecting leaks or disconnection of the circuit

• monitoring ventilation status during weaning from mechanical ventilation and after extubation

• assessing the effectiveness of cardiopulmonary resuscitation compressions and detecting return of spontaneous circulation

• monitoring ventilation continuously during sedation and anaesthesia

• assessing ventilation/perfusion status.⁴⁰

Practice tip

The capnography monitoring line can fill with condensation, particularly if the patient has a humidified ventilator circuit. Regularly check for this and drain or replace the line as necessary, as condensation can interfere with accuracy of readings.

Capnography is recommended as a standard component of respiratory monitoring in intubated and mechanically ventilated patients in the ICU,⁴¹ during transport of a critically ill patient⁴² and during anaesthesia.⁴³

Ventilation Monitoring

Mechanical ventilation is a common intervention in ICU for patients with respiratory failure or who require respiratory support. Advances in ventilation technology have led to an increased ability to monitor many ventilator parameters. A detailed understanding of mechanical ventilation principles and functions enables patient data to be interpreted accurately and managed appropriately. Chapter 15 provides a detailed discussion of mechanical ventilation, including ventilation monitoring, airway pressures (peak airway pressure, plateau pressure and positive end-expiratory pressure) and waveforms and loop displays.

Bedside and Laboratory Investigations

Bedside and laboratory investigations add to the information available regarding a patient’s respiratory status and assist in the diagnosis and treatment. This section focuses on the common investigations used to assess a patient’s respiratory status and their response to treatment: arterial blood gas analysis; blood testing; and sputum and tracheal aspirates.

Arterial Blood Gases

Arterial blood gases (ABGs) are one of the most commonly performed laboratory tests in critical care, and accurate interpretation of ABG analysis is therefore an important clinical skill. ABG measurements enable rapid assessment of oxygenation and ventilation and all ICUs are recommended to have a blood gas analyser as a minimum standard.⁴¹

Blood for ABG analysis is sampled by arterial puncture, or more commonly in critically ill patients, from an arterial catheter usually sited in the radial or femoral artery. Both techniques are invasive but only allow for intermittent analysis. The advantage of the arterial catheter is that it facilitates ABG sampling without repeated arterial punctures. Continuous blood gas monitoring is possible using fibreoptic sensor in-line with the intra-arterial line but this practice is yet to have wide application in Australasia due to cost and accuracy concerns.^44,⁴⁵

Sampling Technique

A correct sampling technique is essential for accurate results. Approximately 1 mL of arterial blood is collected anaerobically and aseptically using a premixed syringe containing dry heparin. If drawing the sample from an intra-arterial line, a portion of blood is discarded to prevent dilution and contamination of the sample by saline present in the flush line. The discard amount is twice the dead space volume to ensure clinically accurate ABG and electrolyte measurement and to prevent unnecessary blood loss ⁴⁶ (dead space is defined as the priming volume from sampling port to catheter tip; this differs depending on the arterial line set up that is used). Arterial blood exerts its own pressure, which is sufficient to fill the syringe to the required level; active negative pressure is to be avoided, as this causes frothing. Any excess air will also cause inaccurate readings and is expelled before the syringe is capped with a hub, which prevents further contamination with air. The sample is analysed within 10 minutes if not packed in ice, or within 60 minutes if iced; delays cause degradation of the sample. Degradation also occurs if the sample is shaken; therefore gently roll the syringe/collection tube between your fingers to mix the sample with the heparin and prevent clotting.⁴⁷

Arterial Blood Gas Analysis

ABG analysis includes the measurement of the partial pressure of oxygen in arterial blood (PaO₂), the partial pressure of carbon dioxide in arterial blood (PaCO₂), the hydrogen ion concentration of the blood (pH), and the chemical buffer, bicarbonate (HCO₃⁻). Normal values for ABG parameters are listed in Table 13.4. Use a systematic approach when interpreting the results of ABG analysis (see Table 13.5).

TABLE 13.4 Arterial blood gas normal values

Blood gas measurements	Description	Normal value
Temperature (T)	Patient’s body temperature. Analyser defaults to 37°C if not entered.	37°C
Haemoglobin (Hb)	Samples should be fully mixed so should be constantly agitated until analysed.	Females: 115–165 g/L Males: 130–180 g/L
Acid–Base status (pH)	Overall acidity or alkalinity of blood.	7.36–7.44 (36–44 mmol/L)
Carbon dioxide (CO₂)	Partial pressure of arterial CO₂. A potential acid.	35–45 mmHg (4.7–6 kPa)
Oxygen (O₂)	Partial pressure of O₂. Varies with age.	80–100 mmHg (10.7–13.3 kPa)
Bicarbonate (HCO₃⁻)	Standardised HCO₃⁻ (actual HCO₃⁻ minus the HCO₃⁻ produced by respiratory dysfunction) estimates true metabolic function. An alkali or base.	22–32 mmol/L
Base Excess (BE)	Measures acid–base balance. The number of molecules of acid or base required to return 1 litre of blood to the normal pH (7.4).	−3 to +3 mmol/L
Oxygen saturation (SaO₂)	Haemoglobin saturation by oxygen in arterial blood	94.5–98.2%

TABLE 13.5 Steps for arterial blood gas interpretation

Step	Interpretation
1	Assess oxygenation. PaO₂ < 60 mmHg indicates hypoxaemia.
2	Assess the pH level. <7.36 indicates acidosis, >7.44 indicates alkalosis.
3	Assess PaCO₂ level. <35 mmHg indicates respiratory acidosis; >45 mmHg indicates respiratory alkalosis.
4	Assess HCO₃⁻ level. <22 indicates metabolic acidosis; >32 indicates metabolic alkalosis.
5	Assess pH, CO₂ and HCO₃⁻. Is there an acid–base disturbance and is it fully compensated, partially compensated or uncompensated?
6	Assess other ABG results. Are they within normal limits for the patient?

When assessing PaO₂, hypoxaemia (<60 mmHg) will be the most common abnormality, and supplemental oxygen will be required to maintain adequate tissue oxygenation. Hyperoxia rarely occurs unless a patient is receiving supplemental oxygen therapy. Oxygen can be toxic to cells if delivered at high concentrations for a prolonged period.⁴⁸ The pH level is assessed to determine if it falls on the acidic or alkaline side of 7.4.

On the pH scale of 1–14 (1 = the strongest acid, 14 = the strongest alkali), a pH of 7.4 is the middle of the normal range. pH measures the acid–base balance of the blood sample, where Hydrogen (H⁺) ions are the acid and HCO₃⁻ is the base or buffer. The body’s acid–base balance is affected by both the respiratory and metabolic systems.⁴⁸ Acidaemia is present with a pH of <7.36; alkalaemia is present with a pH of >7.44.

PaCO₂ is an indicator of the effectiveness of ventilation in removing CO₂. CO₂ is a potential acid as it combines with H₂O in the blood to form carbonic acid (H₂CO₃). Retention of CO₂ (through hypoventilation) leads to increased H⁺ resulting in a lower pH, and similarly a loss of CO₂ (through hyperventilation) results in a higher pH.⁴⁹ A PaCO₂ of >45 mmHg (6 kPa) indicates alveolar hypoventilation, due to chronic obstructive pulmonary disease, asthma, pulmonary oedema, airway obstruction, over sedation, narcosis, drug overdose, pain, neurological deficit or permissive hypercapnia in mechanically ventilated patients.⁵⁰ Conversely, a PaCO₂ of <35 mmHg (4.7 kPa) reflects alveolar hyperventilation, and can be due to hypoxia, pain, anxiety, pregnancy, permissive hypocapnia in mechanically ventilated patients or as a compensatory mechanism for metabolic acidosis.⁵⁰

Bicarbonate (HCO₃⁻) is regulated by the renal system and indicates metabolic functioning. A HCO₃⁻ of < 22 mmol/L can be caused by renal failure, ketoacidosis, lactic acidosis, diarrhoea, or cardiac arrest. A HCO₃⁻ of >32 can be caused by severe vomiting, continuous nasogastric suction, diuretics, corticosteroids, or excessive citrate administration from stored blood or renal replacement therapy.⁵⁰ Base excess is an additional parameter measured as part of the ABG report and it reflects the excess (or deficit) of base to acid in the blood. A positive figure indicates a base excess (more base than acid; i.e. alkalosis if >+3); a negative figure indicates a base deficit (more acid than base i.e. acidosis if >−3). If the base excess is +2 mmol/L, then removal of 2 mmol of base per litre of blood is required to return the pH to 7.4. If the base excess is −2 mmol/L (i.e. a base deficit), then 2 mmol of base per litre of blood needs to be added to have a pH of 7.4. Understanding this concept is useful as it can determine how much treatment is necessary to restore a patient’s pH to normal.^49,⁵¹

The final step of interpretation is to examine the pH, CO₂ and HCO₃⁻ levels collectively to determine if the patient has fully compensated or partially compensated the primary dysfunction, or is in an uncompensated state. With the respiratory system regulating the acid (CO₂) and the metabolic system regulating the base (HCO₃⁻), restoration of normal acid–base balance and homeostasis is possible.⁴⁹ The ability of the body to achieve this determines whether the imbalance is fully compensated (pH returned to normal), partially compensated (pH outside of normal limits) or uncompensated. To assess compensation, pH, CO₂ and HCO₃⁻ are examined in the context of a patient’s clinical presentation:

• in a fully compensated state, the pH is returned to within normal limits, but the other two parameters will be outside normal limits as the body has successfully manipulated CO₂ and HCO₃⁻ levels to restore pH

• in a partially compensated state, the pH is not within normal limits, and the other parameters will also be outside of normal limits but not enough to bring pH back to within normal limits

• in a non-compensated state, the pH will be outside normal limits, and the primary disruption (either CO₂ or HCO₃⁻) will also be outside normal limits while the remaining parameter has not compensated for this derangement and has stayed within normal limits.

It can be difficult to differentiate the patient’s primary problem from their compensatory response. As a quick guide, if the CO₂ is moving in the opposite direction to pH, then the primary disruption is respiratory; if the HCO₃⁻ is moving in the same direction as pH, the disruption is metabolic.⁵² Table 13.6 provides a guide to ABG findings for each acid–base disorder. Other parameters measured on the ABG sample, such as lactate, electrolytes, haemoglobin and glucose, are also considered in determining patient status.

TABLE 13.6 Arterial blood gas findings for acid–base disturbances

Oxygen Tension Derived Indices

The alveolar-arterial gradient is a marker of intrapulmonary shunting (i.e. blood flowing past collapsed areas of alveoli not involved in gas exchange). The index is calculated as PAO₂ − PaO₂ (PAO₂ is the partial pressure of oxygen in the alveoli). PAO₂ is determined by a complex equation, the alveolar gas equation. PAO₂ and PaO₂ are equal when perfusion and ventilation are perfectly matched. The gradient increases with age but a value of 5–15 is normal up until approximately middle age. Despite questions about its clinical usefulness, particularly in the critically ill,⁵³ it is used in clinical practice as a trending tool to track intrapulmonary shunting. Simply put, the larger the gradient between PAO₂ and PaO₂, the larger the degree of intrapulmonary shunting.⁵⁴

The PaO₂/FiO₂ ratio was introduced as a simpler way of estimating pulmonary shunting, even though it does not formally measure alveolar partial pressure. It remains widely used to define ALI or ARDS. A PaO₂/FiO₂ ratio of <300 indicates ALI and a ratio of <200 indicates ARDS. For example, for a patient receiving an FiO₂ of 0.65 with a PaO₂ of 90 mmHg (12 kPa), their PaO₂/FiO₂ ratio is 138.5, indicating an ARDS state.⁵⁵

Blood Tests

Investigation of haematology and biochemistry values for a patient with respiratory dysfunction can aid their overall treatment. Full blood count (FBC), including a leukocyte differential count, can track a patient’s white cell count (WCC) if they have a confirmed or suspected infective process. When infections are severe, the FBC will show a dramatic rise in the number of immature neutrophils. Blood cultures can also be drawn to assist in diagnosis of bacterial or yeast infections and isolation of the causative organism. Viral studies may be conducted to aid diagnosis for respiratory infections of unknown origin. If the patient is suspected of having a pulmonary embolism, a D-dimer test can determine the presence of a thrombus. Urea and electrolytes will also be routinely measured to monitor a patient’s renal function and acid–base status.⁵⁶

Practice tip

Monitoring lactate levels is important as this reflects the effectiveness and efficiency of resuscitative therapies. A persistently elevated lactate level is associated with higher morbidity and poorer patient outcomes.

Sputum, Tracheal Aspirates and Nasopharyngeal Aspirates

Colour, consistency and volume of sputum provides useful information in determining changes in a patient’s respiratory status and progress. Regular cultures of tracheal sputum facilitates tracking of colonisation by opportunistic organisms, or the identification of the cause of an acute chest infection or sepsis. Many ICUs have routine surveillance monitoring (weekly or twice-weekly) of tracheal aspirates in long-term mechanically-ventilated patients. In spontaneously breathing patients, sputum specimens can be provided into a sterile specimen receptacle. These specimens are best collected early in the morning and assisting the patient to clean their teeth prior to sample collection prevents secondary contamination. In an intubated patient, a sputum sample is collected by suctioning the artificial airway using a sputum trap between the suction catheter and suction tubing. Maintain a sterile technique so that the specimen is not contaminated.⁵⁷

If obtaining an adequate sputum specimen in non-intubated patients is difficult, there is evidence that administration of nebulised saline (isotonic or hypertonic) can assist in producing a sample.⁵⁸ There is no evidence to support this for mechanically ventilated patients, but anecdotally nebulised normal saline may assist in moistening the airways and thinning secretions to facilitate sputum production. Physiotherapy is often useful in producing a sputum sample,^59,⁶⁰ as manual hyperinflation and head downtilt during the physiotherapy session has increased sputum production.^61,⁶²

Instilling normal saline in an endotracheal tube (ETT) to facilitate clearance of tenacious sputum and obtain a tracheal aspirate remains a controversial issue. There is no evidence that instillation facilitates secretion clearance, while there is some evidence that it is more uncomfortable for a patient and increases the risk of contamination of the lower airway with bacteria. The practice is therefore not recommended.⁶³

Nasopharyngeal aspirates (NPA) or nasopharyngeal swabs (NPS) may be necessary to diagnose viral respiratory infections. The NPA is collected by inserting a fine sterile suction catheter (8 or 10 F), attached to a sputum trap and suction, through the nare and back to the nasopharynx. Suction is applied while withdrawing the catheter slowly using a rotating motion. Flush the catheter through to the sputum trap with sterile normal saline or transport medium if available. A NPS is collected by inserting a specially designed swab to the back of the nasopharynx and rotating for 5–10 seconds, withdrawing slowly then placing the swab into the plastic vial containing transport medium.⁶⁴

Diagnostic Procedures

Assessment and monitoring of the respiratory status of a critically ill patient commonly relies on diagnostic tests, including various medical imaging tests and bronchoscopy. Data generated through diagnostic procedures are used to determine the cause of illness, the severity of the illness episode, relevant comorbidities and the patient’s response to treatment.

Medical Imaging

A range of imaging techniques may be available for supporting care of a critically ill patient with a respiratory dysfunction, depending on the level of broader health service resources available. This sub-section describes X-ray, ultrasound, computerised tomography, magnetic resonance imaging and ventilation/perfusion scan techniques.

Chest X-ray

Chest X-ray (CXR) is a common diagnostic tool used for respiratory examination of critically ill patients. Chest radiography allows basic information regarding abnormalities in the chest to be obtained relatively quickly. The image provides information about lung fields and other thoracic structures as well as the placement of various invasive lines and tubes.^65,⁶⁶ In the critically ill ventilated patient, serial chest X-rays also enable sequential assessment of lung status in relation to therapy.⁶⁶

In-unit X-rays of patients using portable equipment are inferior to those taken using a fixed camera in the radiology department. Patient preparation is therefore important to optimise the quality of the film. Patients should ideally be positioned sitting or semi-erect for this procedure; images using a supine position are less effective at revealing gravity-related abnormalities such as haemothorax. Lateral view chest X-rays can also be taken to view lesions in the thorax. Film plate location in relation to the patient’s thorax determine the view; posterior-anterior (PA) has the plate against the patient’s anterior thorax (see Figure 13.16) while the anterior-posterior (AP) view has the plate against the patient’s back surface. For mobile X-rays, the AP view is used. Images from the AP view magnify thoracic structures and can be less distinct or even distorted, so interpret findings with caution, particularly if comparing them with previous PA images.⁶⁷

FIGURE 13.16 Chest X-ray, PA view.

Courtesy the University of Auckland Faculty of Medical and Health Sciences.

Practice tip

When preparing your patient for a chest X-ray, minimise the amount of monitoring leads and unnecessary equipment in the CXR field to optimise the image.

Interpretation of the CXR follows a systematic process designed to identify common pathophysiological processes and location of lines and other items. Table 13.7 provides a comprehensive guideline for viewing and interpreting a CXR.

TABLE 13.7 Guide to normal CXR interpretation ⁶⁵

Item	Recommendation
Technical issues	• Check X-ray belongs to correct patient; note date and time of film. • Ensure you are viewing the X-ray correctly (i.e. right and left markings correspond to thoracic structures). • Determine whether X-ray was taken supine or erect, and whether PA or AP. • Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs and anterior aspects of 5th/6th ribs should be visible above diaphragm). • Note the penetration of the film: dark films are overpenetrated and may require a strong light to view; white films are underpenetrated; good penetration will allow visualisation of the vertebrae behind the heart.

Item

Recommendation

Technical issues

• Check X-ray belongs to correct patient; note date and time of film.

• Ensure you are viewing the X-ray correctly (i.e. right and left markings correspond to thoracic structures).

• Determine whether X-ray was taken supine or erect, and whether PA or AP.

• Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs and anterior aspects of 5th/6th ribs should be visible above diaphragm).

• Note the penetration of the film: dark films are overpenetrated and may require a strong light to view; white films are underpenetrated; good penetration will allow visualisation of the vertebrae behind the heart.

Bones

• Check along each rib from vertebral origin, looking for fractures.

• Ensure clavicles and scapulas are intact.

Mediastinum

• Check for presence of trachea and identify carina (approximately level of 5th–6th vertebrae).

• Check width of mediastinum: should not be more than 8 cm.

Apex

• Ensure blood vessels are visible in both apices, particularly looking to rule out pneumothoraces that present as clear black shading on the X-ray. Erect X-rays are essential to facilitate visibility of pneumothoraces.

Hilum

• Check for prominence of vessels in this region: it generally indicates vascular abnormalities such as pulmonary oedema or pulmonary hypertension, or congestive heart failure.

Heart

• Cardiac silhouette should be not more than 50% of the diameter of the thorax, with of heart shadow to the right of the vertebrae and of shadow to the left of the vertebrae; this positioning helps to rule out a tension pneumothorax. It should be noted that, post-cardiac surgery, if the mediastinum is left open the heart may appear wider than this; also in AP films this may be the case due to the plate being further away from the heart.

Lung

• Identify the lobes of the lungs and determine if infiltrate or collapse is present in one or more of them. Lobes are approximately located as follows:

• left upper lobe occupies upper half of lung;

• left lower lobe occupies lower half of lung;

• right lower lobe occupies costophrenic portion of lung;

• right middle lobe occupies cardiophrenic portion of lung;

• right upper lobe occupies upper portion of lung.

Diaphragm

• Check levels of diaphragm: right diaphragm will normally be 1–2 cm above the left diaphragm to accommodate the liver.

Gastric

• Check for pneumoperitoneum and dilated loops of bowel.

Catheters and lines

• Identify distal end of endotracheal tube and ensure above the carina (i.e. not in the right main bronchus).

• Trace nasogastric tube along length and ensure tip is in stomach, or below stomach if nasoenteric tube.

• Check position of intra-aortic balloon pump and ensure it is in the descending thoracic aorta.

• Trace all central catheters and ensure distal tip in correct location.

• Identify other lines (e.g. intercostal catheters, pacing wires) and note location.

PA = posterior-anterior; AP = anterior-posterior.

Common abnormalities that can be detected by CXR include:

• Lobar collapse or atelectasis: The image reveals all or some of the following features: loss of lung volume, displacement of fissures and vascular markings, and diaphragmatic elevation on the affected side.

• Pneumothorax: Check for lack of pulmonary vascular markings on the affected side so the lung field appears black; there will be mediastinal and possibly tracheal shift away from the affected side in a tension pneumothorax.

• Pleural effusion: Visualised in the dependent areas of the pleural spaces; costophrenic angles are blunted by fluid and there may be a shift of the mediastinum away from a large effusion; best visualised with the patient upright, and will only be evident on an AP image with 200–400 mL of fluid in the pleural space.

• Pulmonary oedema: Lung fields, particularly central and perihilar areas, appear white; Kerley B lines (small horizontal lines no more than 2 cm long) may be present in the lung periphery near the costophrenic angles.

• Pulmonary embolism: Although not the optimal diagnostic tool, areas of infarction may be visualised although these can be mistaken for collapse or consolidation.

• Pneumoperitonium: Free air under the diaphragm elevates the diaphragm.^66,⁶⁸

Ultrasound

Ultrasound imaging (sonography) is a useful bedside diagnostic tool for a select group of critically ill patients ⁶⁹ and can add to the diagnostic information provided by chest X-rays and computerised tomography (CT) scanning. The technique uses high-frequency sound waves which when probed on the body, reflect and scatter. The advantages are no need for transport of a critically ill patient outside the ICU, and it is radiation-free. Ultrasound is most useful for patients with fluid in the pleural space (i.e. pleural effusion, haemothorax or empyema), as it provides more detailed diagnostic information than chest X-rays alone;⁷⁰ it estimates the volume of fluid present, the exact location of the fluid, and provides a guide for aspirating a fluid-filled area or the placement of chest tubes.⁷¹

Computed Tomography

Computed tomography (CT) is a diagnostic investigation that provides greater specificity in chest anatomy and pathophysiology than a plain CXR, as it uses multiple beams in a circle around the body. These beams are directed to a specific area of the body and provide detailed, consecutive cross-sectional slices of the scanned regions. CT scans can be performed with or without intravenous contrast.⁷² Contrast improves diagnostic precision but is used with caution in patients with renal impairment; renal failure may preclude a patient from receiving contrast. CT scanning is useful in the detection and diagnosis of pulmonary, pleural and mediastinal disorders (e.g pleural effusion, empyema, haemothorax, atelectasis, pneumonia, ARDS).⁷³ CT pulmonary angiography (CTPA) produces a detailed view of blood vessels and is therefore the most definitive method for diagnosing pulmonary embolism.⁷⁴

A significant limitation of CT scanning is that the patient is transported away from the ICU. Transport usually requires at least two appropriately trained staff to accompany the patient and involves added risk to the critically ill patient. Detailed planning by the health care team (including imaging staff) includes ventilator support, monitoring requirements and maintenance of infusions during the scanning period. See Chapter 6 for discussion of in-hospital transfers, and Chapter 22 for inter-hospital transport. Portable CT scanners are available in some centres, but the image quality is inferior to fixed CT scanners.⁷⁵

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) uses radiofrequency waves and a strong magnetic field rather than X-rays to provide clear and detailed pictures of internal organs and soft tissues.⁷⁶ These high-contrast images of soft tissue are clearer than those generated by X-ray or CT scans. The strong magnetic field around the scanner means that ferromagnetic objects (metallic objects containing material that can be attracted by magnets, such as iron or steel) can become potentially fatal projectiles. MRI scans may therefore be unsuitable for patients with implanted pacemakers, defibrillators or neurostimulation devices; some types of intracranial aneurysm clips; and loose dental fillings. The magnetic force can either attract these items and dislodge them from the body or interfere with their functioning.⁷⁶ The strong magnetic fields also have the potential to interfere with ventilators, infusion pumps and monitoring equipment. Similar to CT scans, an MRI requires transport of the critically ill patient. The benefits of the diagnostic data obtained from the MRI is balanced against any potential risk to the patient.⁷⁷