Tips for Anaesthesia Attachments

During your anaesthetic attachment, spend time in the post-anaesthesia care unit to:

• manage the airway of an unconscious patient;
  
• monitor vital signs:

oxygen saturation, ventilation;

blood pressure and pulse;

conscious level;

• recognize hypoxaemia and institute appropriate treatment;
  
• recognize impaired ventilation and institute appropriate treatment;
  
• assess patients’ pain;
  
• identify the need for, and give, analgesia;
  
• observe patients with regional anaesthesia for the management of postoperative pain;
  
• learn how to recognize and treat the side effects of epidural and spinal anaesthesia;
  
• plan postoperative fluid management regimes for different surgical procedures.

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The vast majority of patients recover from anaesthesia and surgery uneventfully but a small and unpredictable number suffer complications. It is now accepted that all patients should be nursed by trained staff, in an area with appropriate facilities to deal with any of the problems that may arise while recovering from anaesthesia. Such specialized areas are referred to as the post-anaesthesia care unit (PACU) or recovery unit. Most patients will be nursed on a trolley capable of being tipped head-down. Patients who have undergone prolonged surgery or where a prolonged stay in PACU is expected, may be nursed on their beds to minimize the number of transfers. Some patients, who have undergone specialist surgery – for example cardiac surgery patients – may be taken directly to a critical care area.

The Post-Anaesthesia Care Unit

The length of time any patient spends in PACU will depend upon a variety of factors, including duration and type of surgery, anaesthetic technique, and the occurrence of any complications. Most units have a policy determining the minimum length of stay (usually around 30 min), and agreed discharge criteria (Table 7.1).

Table 7.1 Minimum criteria for discharge from PACU

Postoperative Complications and their Management

This is the commonest cause of hypoxaemia after general anaesthesia. It is caused by a degree of respiratory depression leading to an insufficient flow of oxygen into the alveoli to replace that taken up by the blood. As a result alveolar PO₂ (PAO₂) and arterial PO₂ (PaO₂) fall. In most patients, increasing their inspired oxygen concentration will restore both. This is the rationale for giving all patients who have had a general anaesthetic oxygen therapy. Fig. 7.1 shows the variation of PaO₂ with ventilation (minute volume). Note the effect of giving 30% oxygen to a patient whose ventilation is 2 L/min (normally 5 L/min): The PaO₂ rises from being barely adequate to supranormal. This is because 30% oxygen contains nearly one-and-a-half times the amount of oxygen that is in air. If ventilation is further reduced, a point is eventually reached where there is only ventilation of the anatomical ‘dead space’ – that is, the volume of the airways that plays no part in gas exchange. If this occurs, irrespective of the inspired oxygen concentration, no oxygen reaches the alveoli and profound hypoxaemia will follow. Note that an increase in minute volume above normal only increases oxygenation minimally. This is because it does not alter the main determinant of alveolar oxygen tension, the inspired PO₂. Hypoventilation is always accompanied by hypercapnia, as there is an inverse relationship between alveolar ventilation and arterial carbon dioxide (PaCO₂) (Fig. 7.2).

Figure 7.1 Graph showing the relationship between PaO₂ and alveolar ventilation at two different inspired oxygen concentrations.

Figure 7.2 Graph showing the relationship between PaCO₂ and alveolar ventilation.

Common causes of hypoventilation include:

• Obstruction of the airway. Most often secondary to a reduced level of consciousness but also may be due to vomit, blood, or swelling (for example, post-thyroid surgery). Partial obstruction causes noisy breathing; in complete obstruction there is little noise despite vigorous efforts. There may be a characteristic ‘see-saw’ or paradoxical pattern of ventilation. A tracheal tug may be seen. The risk of obstruction can be reduced by recovering patients in the lateral position, particularly those recovering from surgery where there is a risk of bleeding into the airway (as in ear, nose and throat (ENT) surgery), or regurgitation (bowel obstruction or a history of reflux). If it is not possible to turn the patient (for instance, after a hip replacement), perform a chin lift or jaw thrust (see Chapter 4). An oropharyngeal or nasopharyngeal airway may be required to help maintain the airway (see Chapter 4). As the patient begins to obey commands they can be sat up at 30° if it is safe to do so.

• Central respiratory depression. This is usually due to drugs given during anaesthesia. Both anaesthetic drugs and opioid analgesics depress the normal increase in ventilation seen in response to hypoxia and hypercarbia, and the residual effects of these drugs are commonly present in the recovery period. If ventilation is inadequate it may need to be supported until the effects of the drugs have worn off, or, in the case of severe opioid-induced respiratory depression, the specific antagonist naloxone may be given (see Chapter 3).
  
• Impaired mechanics of ventilation. Pain, particularly after upper abdominal or thoracic surgery, prevents coughing, leading to sputum retention and atelectasis. The solution to this is provision of adequate analgesia (consider central neural block). Residual neuromuscular blockade causes weakness and impaired ventilation. The patient will usually show signs of unsustained, jerky movements with rapid, shallow breathing, hypertension and tachycardia. The diagnosis may be confirmed by using a peripheral nerve stimulator, which may show evidence of fade with a tetanic stimulus (see Chapter 2). The patient should be given oxygen, reassured, sat upright to improve the efficiency of ventilation, and a (further) dose of neostigmine and an anticholinergic given. If rocuronium has been given, sugammadex may be used.
  
• Diaphragmatic splinting. Abdominal distension and obesity cause the diaphragm to be pushed into the thorax and increase the work of breathing. Sitting these patients up helps them greatly.
  
• Cerebral haemorrhage or ischaemia. May cause direct damage to the respiratory centre or, more commonly, a deeply unconscious patient unable to maintain a patent airway.
  
• Pneumothorax or haemothorax. Both will prevent ventilation of the underlying lung and will require the insertion of a chest drain.
  
• Hypothermia. Reduces ventilation but, in the absence of any contributing factors, it is usually adequate for the body’s needs.

Ventilation and Perfusion Mismatch within the Lungs

Normally, alveolar ventilation (V) and perfusion with blood (Q) are well matched (V/Q = 1) and the haemoglobin in blood leaving the lungs is almost fully saturated with oxygen (97–98%). This is disturbed (ventilation/perfusion (V/Q) mismatch) during anaesthesia and the recovery period, with development of areas where:

• Perfusion exceeds ventilation (V/Q < 1). This results in blood with reduced oxygen content.
  
• Ventilation exceeds perfusion (V/Q > 1). This can be considered wasted ventilation. Only a small additional volume of oxygen is taken up as the haemoglobin is already almost fully saturated.

In the most extreme situation, there is perfusion of areas of the lung but no ventilation (V/Q = 0). Blood leaving these areas remains ‘venous’ and is often referred to as ‘shunted blood’ (that is, it is effectively shunted directly from the venous to arterial system). This is then mixed with oxygenated blood leaving ventilated areas of the lungs. The net result is:

• Blood perfusing alveoli ventilated with air has an oxygen content of approximately 20 mL/100 mL of blood.
  
• Blood perfusing unventilated alveoli remains venous, with an oxygen content of 15 mL/100 mL of blood.
  
• The final oxygen content of blood leaving the lungs will be dependent on the relative proportions of shunted blood and non-shunted blood.

The aetiology of V/Q mismatch is multifactorial but the following are recognized as being of importance:

• Mechanical ventilation reduces cardiac output. This reduces perfusion of non-dependent areas of the lungs, whilst maintaining ventilation. This is worst in the lateral position, when the upper lung is better ventilated and the lower lung better perfused.
  
• A reduced functional residual capacity (FRC). In supine, anaesthetised patients, particularly those over 50 years of age, the FRC falls below their closing capacity – the lung volume below which some airways close and distal alveoli are no longer ventilated. Eventually, areas of atelectasis develop, mainly in dependent areas of the lung, as a result of perfusion but no ventilation.
  
• Pain restricts breathing and coughing, leading to poor ventilation of the lung bases, sputum retention, basal atelectasis and, ultimately, infection. The highest incidence of this is seen in the following circumstances:

smokers;

obesity;

pre-existing lung disease;

elderly;

after upper gastrointestinal or thoracic surgery;

three days after surgery.

The effects of small areas of V/Q mismatch can be compensated for by increasing the inspired oxygen concentration. However, because of the disproportionate effect of areas where V/Q < 1, once more than 30% of the pulmonary blood flow is passing through such areas, even breathing 100% oxygen will not eliminate hypoxaemia. The oxygen content of the blood leaving alveoli ventilated with 100% oxygen will only have increased by 1 mL/100 mL of blood over what was achieved when being ventilated with air (Table 7.2). This is insufficient to offset the lack from the areas of low V/Q. Oxygen therapy is relatively ineffective when the cause of hypoxaemia is V/Q mismatch compared to when hypoventilation exists. Treatment should be aimed at optimizing ventilation of non aerated alveoli. The simplest manoeuvre is to sit the patient upright in bed, which relieves upward pressure on the diaphragm, easing the work of breathing and so improving aeration of the lung bases. The next manoeuvre is to apply continuous positive airways pressure (CPAP) via a closely fitting face mask and a suitable circuit. This recruits alveoli but may be poorly tolerated by patients for periods of more than a few hours.

Table 7.2 Effect of alveolar oxygen concentration on oxygen content of blood

Diffusion Hypoxia

Nitrous oxide absorbed during anaesthesia has to be excreted during recovery. It is very insoluble in blood, and so rapidly diffuses down a concentration gradient into the alveoli, where it reduces the partial pressure of oxygen making the patient hypoxaemic. This can be treated by giving oxygen via a facemask to increase the inspired oxygen concentration (see below).

Pulmonary Diffusion Defects

Any chronic condition causing thickening of the alveolar membrane, such as fibrosing alveolitis, impairs transfer of oxygen into the blood. In the recovery period it may also occur secondary to the development of pulmonary oedema following fluid overload or impaired left ventricular function. It should be treated by first administering oxygen to increase the partial pressure of oxygen in the alveoli and then by management of any underlying cause.

A Reduced Inspired Oxygen Concentration

As the inspired oxygen concentration is a prime determinant of the amount of oxygen in the alveoli, reducing this will lead to hypoxaemia. There are no circumstances where it is appropriate to administer less than 21% oxygen.

Management of Hypoxaemia

All patients should be given oxygen in the immediate postoperative period to:

• counter the effects of diffusion hypoxia when nitrous oxide has been used;
  
• compensate for any hypoventilation;
  
• compensate for V/Q mismatch;
  
• meet the increased oxygen demand when shivering.

Patients who continue to hypoventilate, have persistent V/Q mismatch, are obese, anaemic or have ischaemic heart disease, will require additional oxygen for an extended period of time. The need for, and effectiveness of oxygen therapy is best determined either by arterial blood gas analysis or by using a pulse oximeter. Oxygen therapy should aim to maintain the SpO₂ between 94–98%, unless the patient is known to have severe COPD when a value of 88–92% is acceptable.

Devices Used for Delivery of Oxygen

Variable-Performance Devices: Masks or Nasal Cannulae

These are adequate for the majority of patients recovering from anaesthesia and surgery. The precise concentration of oxygen inspired by the patient is unknown as it is dependent upon the patient’s respiratory pattern and the flow of oxygen used (usually 2–12 L/min). The inspired gas consists of a mixture of:

• oxygen flowing into the mask;
  
• oxygen that has accumulated under the mask during the expiratory pause;
  
• alveolar gas from the previous breath which has collected under the mask;
  
• air entrained during peak inspiratory flow from the holes in the side of the mask and from leaks between the mask and face.

The most commonly used device is the Hudson mask (Fig. 7.3a). As a guide, it will increase the inspired oxygen concentration to 25–60% with oxygen flows of 2–12 L/min.

Figure 7.3 (a) Hudson mask. (b) Nasal catheters in position.

Patients unable to tolerate a facemask who can nose breathe may find either a single foam-tipped catheter or double catheters, placed just inside the vestibule of the nose, more comfortable (see Fig. 7.3b). Lower flows, 2–4 L/min, of oxygen are used, which increases the inspired oxygen concentration to 25–40%.

If higher inspired oxygen concentrations are needed in a spontaneously breathing patient, a Hudson mask with a reservoir bag can be used (see Fig. 7.4a). A one-way valve diverts the oxygen flow into the reservoir during expiration. The contents of the reservoir, along with the high flow of oxygen (12–15 L/min) can almost meet the demand of peak inspiration gas flow, resulting in minimal entrainment of air, raising the inspired concentration to approximately 85%. An inspired oxygen concentration of 100% can only be achieved by using either an anaesthetic system with a close-fitting facemask or a self-inflating bag with reservoir and non-rebreathing valve and an oxygen flow of 12–15 L/min.

Figure 7.4 (a) Hudson mask with reservoir. (b) High airflow oxygen enrichment (HAFOE; Venturi) mask.

Fixed-Performance Devices

These are used when it is important to deliver a precise concentration of oxygen, unaffected by the patient’s ventilatory pattern, for example patients with COPD and carbon dioxide retention. These masks work on the principle of high airflow oxygen enrichment (HAFOE). Oxygen is fed into a Venturi that entrains a much greater but constant flow of air. The total flow into the mask should be as high as 45 L/min. The high gas flow has two effects: it meets the patient’s peak inspiratory flow, stopping air being drawn in around the mask, and flushes expiratory gas, reducing rebreathing. Masks either deliver a fixed concentration or have interchangeable Venturis to vary the oxygen concentration (Fig. 7.4b).

The above systems all deliver dry gas to the patient that may cause crusting or thickening of secretions and difficulty with clearance. For prolonged use, a HAFOE system should be used with a humidifier.

Hypotension

This can be due to a variety of factors, alone or in combination:

• a reduction in circulating volume (preload);
  
• a reduced cardiac output (reduced myocardial contractility, valvular dysfunction, arrhythmias);
  
• vasodilatation (afterload).

These should be assessed and treated using a step-wise approach.

Step 1: Assess the Circulating Volume (preload)

Hypovolaemia is the commonest cause of hypotension after anaesthesia and surgery. Although intraoperative blood loss is usually obvious, continued bleeding, especially in the absence of surgical drains, may not be. Fluid loss may also occur as a result of tissue damage leading to oedema, or from evaporation during prolonged surgery on body cavities, for example the abdomen or thorax (see below). The diagnosis can be confirmed by finding:

• Cold clammy skin, delayed capillary refill (>2 s) in the absence of fear, pain and hypothermia.
  
• Tachycardia, with a pulse of poor volume.
  
• Hypotension; initially, systolic blood pressure may be reduced minimally but the diastolic elevated as a result of compensatory vasoconstriction (narrow pulse pressure). The blood pressure must always be interpreted in conjunction with the other assessments.
  
• Inadequate urine output (<0.5 mL/kg/h), best measured hourly via a catheter and urometer. Consider also the following as causes of reduced urine output:

a blocked catheter (blood clot or lubricant);

hypotension;

hypoxia;

renal damage intraoperatively (e.g. during aortic aneurysm surgery).

The extent to which these changes occur will depend primarily upon the degree of hypovolaemia. A tachycardia may not be seen in the patient taking beta blockers, and a fit, young patient may lose up to 15% of their blood volume without detectable signs.

Treatment

This is covered in detail in Chapter 8.

Step 2: Assess Cardiac Output

The commonest causes of a reduction in cardiac output are; left ventricular dysfunction due to ischaemic heart disease (or more rarely valvular heart disease) or an arrhythmia.

Left ventricular dysfunction

It is not uncommon to mistake this condition for hypovolaemia based on the presence of poor peripheral circulation, tachycardia and tachypnoeic. However, further examination may reveal:

• distended neck veins, raised JVP;
  
• basal crepitations on auscultation of the lungs;
  
• wheeze with a productive cough;
  
• a triple rhythm on auscultation of the heart.

A chest X-ray may be diagnostic. Echocardiography will demonstrate reduced contractility (hypokinesis) despite adequate ventricular filling suggesting myocardial ischaemia.

Treatment

• Sit the patient upright.
  
• Give 100% oxygen.
  
• Monitor the ECG, blood pressure and peripheral oxygen saturation.

Further details are given in Chapter 8.

Arrhythmias

Disturbances of cardiac rhythm are a common cause of hypotension and occur more frequently in the presence of:

• hypoxaemia;
  
• hypovolaemia;
  
• hypercarbia;
  
• hypothermia;
  
• sepsis;
  
• pre-existing ischaemic heart disease;
  
• electrolyte abnormalities;
  
• acid–base disturbances;
  
• inotropes, antiarrhythmics, bronchodilators.

Correction of the underlying problem will result in spontaneous resolution of many arrhythmias. Specific intervention is required if there is a significant reduction in cardiac output and hypotension. The management outlined below is based upon the guidelines issued by the Resuscitation Council (UK).

Tachycardias

Cardiac filling occurs during diastole, which is progressively shortened as the heart rate increases. The result is insufficient time for ventricular filling, leading to a reduced cardiac output and eventually a fall in blood pressure. If the contribution from atrial contraction is also lost (for example, in atrial fibrillation) there is further compromise. As coronary artery flow is dependent on diastolic time (and diastolic blood pressure) myocardial ischaemia is more likely particularly in combination with hypotension.

• Sinus tachycardia (>100 beats/min). The commonest arrhythmia after anaesthesia and surgery, usually as a result of:

pain;

hypovolaemia;

if there is associated pyrexia, it may be an early indication of sepsis;

rarely, it may be the first sign of malignant hyperpyrexia.

Treatment consists of oxygen, analgesia and adequate fluid replacement. If the tachycardia persists, a small dose of a beta blocker may be given intravenously whilst monitoring the ECG, providing there are no contraindications.

Treatment of a supraventricular tachycardia (most commonly atrial fibrillation) is covered in Chapter 8.

Bradycardias

Related posts:

Anaesthetic Assessment and Preparation for Surgery Local and Regional Anaesthesia Drugs and Fluids Used During Anaesthesia The Practice of General Anaesthesia Special Circumstances Anaesthetic Equipment and Monitoring