Respiratory failure Medical Assignment Help

Types and causes

The respiratory system consists of a gas exchanging organ(the lungs) and a ventilatory pump (respiratory  muscleslthorax) either or both of which can fail and precipitate respiratory failure.
Respiratory failure occurs when pulmonary gas exchange is sufficiently impaired to cause hypoxaemia with or without hypercarbia. In practical terms respiratory failure is present when the Pa02 is <8 kPa (60 mmHg) or the Pac02 is >7 kPa (55 mmHg).
It can be divided into:
• Type I respiratory failure, in which the Pa02 is low and the Pac02 is normal or low
• Type II respiratory failure, in which the Pa02 is low and the Pac02 is high
TYPE I or ‘acute hypoxaemic’ respiratory failure ·occurs with diseases that damage lung tissue, with hypoxaemia due to right-to-left shunts or \rlo. mismatch. Common causes include pulmonary oedema, pneumonia, ARDS and, in the chronic situation, pulmonary fibrosing alveolitis.
TYPE II or ‘ventilatory failure’ occurs when alveolar ventilation is insufficient to excrete the volume of carbon dioxide being produced by tissue metabolism. Inadequate  alveolar ventilation is due to reduced ventilatory effort, inability to overcome an increased resistance to ventilation, failure to compensate for an increase in dead space and/or carbon dioxide production, or a combination of these factors. The most common cause is chronic bronchitis and emphysema. Other causes include chest-wall deformities, respiratory muscle weakness (e.g. Guillain- Barre syndrome) and depression of the respiratory centre. Deterioration in the mechanical properties of the lungs and/or chest wall increases the work of breathing and the oxygen consumption/carbon dioxide production of the respiratory muscles. The concept that respiratory muscle fatigue (either acute or chronic) is an important factor in the pathogenesis of respiratory failure is controversial.

MONITORING

A clinical assessment of respiratory distress should be made on the following criteria:
• The use of accessory muscles of respiration
• Tachypnoea
• Tachycardia
• Sweating
• Pulsus paradoxus
• Inability to speak
• Signs of carbon dioxide retention
• Asynchronous respiration (a discrepancy in the rate of movement of the abdominal and thoracic compartments)
• Paradoxical respiration (abdominal and thoracic compartments move in opposite directions)
• Respiratory alternans (breath-to-breath alteration in the relative contribution of intercostal/accessory muscles and the diaphragm)
This can be supplemented by measuring tidal volume and vital capacity. Blood gas analysis should be performed to guide oxygen therapy and to provide an objective assessment of respiratory function.
The most sensitive clinical indicator of increasing respiratory difficulty is a rising respiratory rate. Tidal volume is a less sensitive indicator. Minute ventilation rises initially in acute respiratory failure and falls precipitously only at a late stage when the patient is exhausted. Vital capacity is often a better guide to deterioration and is particularly useful in patients with respiratory inadequacy due to neuromuscular problems, e.g. the Guillain-Barre syndrome, in which the vital capacity decreases as weakness increases.

Pulse oximetry

Lightweight oximeters which measure the changing amount of light transmitted through pulsating arterial blood and provide a continuous, non-invasive assessment of 5a02 can be applied to an ear lobe or finger. These devices are reliable, easy to use and do not require calibration, although it is important to appreciate that pulse oximetry is not a very sensitive guide to changes in oxygenation.

Blood gas analysis

Automation of measurements can give a false impression of reliability and accuracy and may lead to an uncritical acceptance of the results. Errors can result. from m~nction of the analyser or incorrect sampling techniques. Care must be taken over the following.
1 The sample should be analysed immediately or the srringe should be immersed in iced water (the end having first been sealed with a plastic cap) to prevent the continuing metabolism of white cells causing a reduction in P02 and a rise in Pco;
2 The sample must be adequately anticoagulated to prevent clot formation within the analyser. However, excessive dilution of the blood with heparin, which is acidic, will significantly reduce its pH. Heparin (1000 i.u. ml-‘) should just fill the dead space of the syringe, i.e. approximately 0.1 ml. This will adequately anti oagulate a 2 ml sample.
3 Airalmost inevitably enters the sample. The gas tensions within these air bubbles will equilibrate with  hose in the blood, thereby lowering the Pco2, and, usually, raising the P02 of the sample. However, provided the bubbles are ejected immediately by inverting the syringe and expelling the air that rises to the top of the sample, their effect is insignificant. Normal values of blood gas analysis are shown. The interpretation of the results of blood gas analysis can be considered in two separate parts:
• Disturbances of acid-base balance
• Alterations in oxygenation
Interpretation of results requires a knowledge of the history, the age of the patient, the inspired oxygen conc~ntration and any other relevant treatment (e.g. the adrninistration of sodium bicarbonate, and the ventilator settings for those on mechanical ventilation).
Disturbances of acid-base balance The physiology of acid-base control is discu~sed ~n p. 514. Acid-base disturbances can be descnbed in relation to the diagram illustrated, which shows Paco2 plotted against arterial [H+).
Both acidosis and alkalosis can occur, each of which may be either metabolic (primarily affecting the. bicarbonate component of the system) or respiratory (primarily affecting Pco2). Compensatory changes may also be apparent. In clinical practice, arterial [H+) values outside the range 18-126 nmol litre-I (pH 6.9-7.7) are very rarely encountered.

Normal values for measurements

Normal values for measurements

RESPIRATORY ACIDOSIS. This is caused by retention of carbon dioxide. The Paco2 and [H+) rise. A chronically raised PaC02is compensated by renal retention of bicarbonate and the [H+) returns towards normal. A constant arterial bicarbonate concentration is then usually established within 5 days. This represents a primary respiratory acidosis with a compensatory metabolic alkalosis. Common causes of respiratory acidosis include ventilatory failure and chronic bronchitis and emphysema (type II respiratory failure where there is a high Pac02 and a low P.o2).
RESPIRATORY ALKALOSIS. In this case the reverse occurs and there is a fall in Pac02 and [H+), often with a small reduction in bicarbonate concentration. If hypocarbia persists, some degree of renal compensati?n may occur, producing a metabolic acidosis, although in practice this is unusual. A respiratory alkalosis is often produced, intentionally or unintentionally, when patients are artificially ventilated; it may also be seen with hypoxaemic (type I) respiratory failure , sp~ntaneous hyperventilation and in those living at high altitudes.
METABOLIC ACIDOSIS. This may be due to excessive acid production, most commonly lactic acid during a.n episode of shock or following cardiac arrest. A metabolic acidosis may also develop in chronic renal failure and following the loss of large amounts of alkali, e.g. from the gut or from the kidney in renal tubular. acidosis.

Respiratory compensation for a metabolic ~cldosls. IS usually slightly delayed because the blood-brain .barner initially prevents the respiratory centre from sensmg the increased blood [H+). Following this short delay, however, the patient hyperventilates and ‘blows off carbon dioxide to produce a compensatory respiratory alkalosis. There is a limit to this respiratory compensation, since values for Pac02 less than about 1.4 kPa (11 mmHg) are, in practice, never achieved. It should also be noted that respiratory compensation cannot occur if the patient:s ventilation is controlled or if their respiratory centre IS depressed, for example by drugs or head injury.
METABOLIC ALKALOSIS. This can be caused by loss of acid, e.g. from the stomach with nasogastric suction or in high intestinal obstruction, or excessive admi~ist~ation of absorbable alkali. Overzealous treatment With intravenous sodium bicarbonate is frequently implicated. Respiratory compensation for a metabolic alkalosis is often slight and it is rare to encounter a Paco2 >6.5 kPa (50 mmHg , even with severe alkalosis.

Alterations in oxygenation

When interpreting the Pa02 it is important to remember that it is the oxygen content of the arterial blood that matters and that this is determined by the percentage saturation of haemoglobin with oxygen. The relationship between the latter and the P02 is determined by the oxyhaemoglobin dissociation curve. In general, if the saturation is greater than 90%, oxygenation can be considered to be adequate. It must be remembered, however, that on the steep portion of the oxygen dissociation curve small falls in Pa02 will cause significant reductions in oxygen content. Pa02 is also influenced by factors other than pulmonary function, including alterations in Pv02 caused by changes in the metabolic rate and/or cardiac output.

MANAGEMENT

Conventional management of patients with respiratory failure includes the administration of supplemental oxygen, the control of secretions, the treatment of pulmonary infection, the control of airways obstruction and measures to limit pulmonary oedema. Correction of abnormalities which may lead to respiratory muscle weakness, such as hypophosphataemia and malnutrition, is also important.

Oxygen therapy

Methods of oxygen administration

Oxygen is initially given via a face mask. In the majority of patients (except patients with chronic bronchitis and chronically elevated Paco2) the concentration of oxygen given is not important and oxygen can therefore be given by a simple face mask or nasal cannula. With these devices the inspired oxygen concentration varies from about 35 to 55%, with oxygen flow rates of between 6 and lO litres min -I. Nasal cannulae are often preferred because they are less claustrophobic and do not interfere with feeding or speaking, but they can cause ulceration of the nasal or pharyngeal mucosa. should be compared with the fixed performance mask shown, with which the oxygen concentration can be controlled. It is vital to use this latter type of mask in patients with chronic bronchitis and emphysema with chronic type II failure.
Oxygen toxicity Experimentally, mammalian lungs have been shown to be damaged by continuous exposure to high concentrations of oxygen; oxygen toxicity in humans is less well proven. Nevertheless, it is reasonable to assume that high concentrations of oxygen might damage the lungs and so the lowest inspired oxygen concentration compatible with adequate arterial oxygenation should be used. Long-term administration of 50% oxygen or less, or of lOO%oxygen
for less than 24 hours, is probably safe. Dangerous hypoxia should never be tolerated through a fear of oxygen toxicity.

Methods of administering supplemental oxygen

Methods of administering supplemental oxygen

Respiratory support

If, despite the above measures, the patient continues to deteriorate or fails to improve, the institution of some form of respiratory support should be considered. Some of the techniques of respiratory support currently available are shown. Negative-pressure ventilation is now seldom used, but is occasionally employed for long-term ventilation of patients with chronic respiratory failure due to neuromuscular disease or skeletal deformity. The patient’s body is enclosed in an airtight ‘tank’ within which a negative pressure is created intermittently by a separate pump. Cuirass ventilators encase only the thorax.

Techniques for respiratory support.

Techniques for respiratory support.

INTERMITTENT POSITIVE-PRESSURE VENTILATION (IPPV)

IPPV has a number of important advantages over negative- pressure ventilation. In particular, the airway is secured and protected and secretions can be aspirated more easily. In addition, IPPV can be used more successfully in those with diseases involving the lung parenchyma. Furthermore, access to and movement of the patient is relatively unrestricted. A number of refinements and modifications of IPPV have been developed, including IPPV with positive endexpiratory pressure (PEEP), intermittent mandatory ventilation (IMV), and low volume pressure limited inverseratio ventilation. Other techniques include highfrequency jet ventilation (HFJV) and extracorporeal respiratory assistance. These will be discussed later.
The rational use of IPPV depends on a clear understanding of its potential beneficial effects, as well as its dangers.

Beneficial effects

These include:
IMPROVED CARBON DIOXIDE ELIMINATION. By adjusting the volume of ventilation, the PaC02can be returned to within normal limits.
RELIEF FROM EXHAUSTION. Artificial ventilation removes the work of breathing and relieves the extreme exhaustion that may be present in patients with respiratory failure. In some cases, if ventilation is not instituted, this exhaustion may culminate in respiratory arrest.
EFFECTS ON OXYGENATION. In those with severe pulmonary parenchymal disease, the lungs may be very stiff and the work of breathing is therefore greatly increased. Under these circumstances the institution of IPPV may significantly reduce total body oxygen consumption; consequently Pv02′ and thus Pao2, may improve. Because ventilated patients are connected to a leak-free circuit it is possible to administer high concentrations of oxygen (up to 100%) accurately and to apply a positive end-expiratory pressure. In selected cases the latter may reduce shunting and increase Pao2 .

Indications

ACUTE RESPIRATORY FAILURE with signs of severe respiratory distress (e.g. respiratory rate >40 min -1, inability to speak, patient exhausted) persisting despite maximal therapy. Confusion, restlessness, agitation, a decreased conscious level, a rising PaC02 and extreme hypoxaemia are further indications. Care should be taken before ventilating patients with chronic lung disease as patients previously severely incapacitated will be difficult to wean off the ventilator and also relapse early. The most important criteria are the patient’s previous exercise tolerance and ability to lead an independent existence.
ACUTE VENTILATORY FAILURE due, for example, to myasthenia gravis or Guillain-Barre syndrome. Artificial ventilation should be instituted when the vital capacity has fallen to 10–15 ml kg-I. This will avoid complications such as atelectasis and infection as well as preventing respiratory arrest. The tidal volume and respiratory rate are relatively insensitive in the above conditions and change late in the course of the disease. A high Pac02 (particularly if rising) is an indication for urgent artificial ventilation.
OTHER INDICATIONS include:
• Prophylactic postoperative ventilation in poor risk patients
• Head injury-to avoid hypoxia and hypercarbia which increase cerebral blood flow and intracranial pressure, hyperventilation to reduce intracranial pressure
• Trauma-chest injury and lung contusion
• Severe left ventricular failure with pulmonary oedema
• Coma with breathing difficulties, e.g. following drug overdose

Institution

IPPV requires endotracheal intubation. If the patient is conscious the procedure must be fully explained before anaesthesia is induced. Intubating patients in severe respiratory failure is an extremely hazardous undertaking and should only be performed by experienced staff. In extreme emergencies it may be preferable to ventilate the patient by hand using an oropharyngeal airway, a face mask and a self-inflating bag until experienced help arrives. The patient is usually hypoxic and hypercarbic, with increased sympathetic activity, and the stimulus of laryngoscopy and intubation can precipitate dangerous arrhythmias and even cardiac arrest. If possible, therefore, the ECG and oxygen saturation should be monitored, and the patient preoxygenated with 100% oxygen before intubation. In some deeply comatose patients, no sedation will be required, but in the majority of patients a shortacting intravenous anaesthetic agent followed by muscle relaxation will be necessary.
The complications of endotracheal intubation are given.
Endotracheal tubes can now safely be left in place forseveral weeks and tracheostomy is therefore less often performed. Tracheostomy may be required for the longterm control of excessive bronchial secretions, particularlyin those with a reduced conscious level, and/or to  maintain an airway and protect the lungs in those with impaired pharyngeal and laryngeal reflexes. A life-threatening obstruction of the upper respiratory tract that cannot be bypassed with an endotracheal tube should have a cricothyroidotomy, which is safer, quicker and easier to perform. Tracheostomy performed under these circumstances can be extremely hazardous. Other indications are head and neck injuries, including burns to the face and upper airway. Tracheostomy has a mortality rate of up to 3%. Complications of tracheostomy are shown.
Minitracheostomy involves inserting a small diameter tube percutaneously into the trachea via the cricothyroid membrane using a guide wire. It can be performed under local anaesthesia. This technique facilitates the clearance of copious secretions in those who are unable to cough effectively but can protect their airway.

Complications of endotracheal intubation.

Complications of endotracheal intubation.

Complications of tracheostomy.

Complications of tracheostomy.

Dangers of IPPY

General dangers include:
COMPLICATIONS of endotracheal intubation or tracheostomy.
DISCONNECTION OR MECHANICAL FAILURE. These are unusual but dangerous. A method of manual ventilation, e.g. a self-inflating bag, and oxygen must always be available by the bedside.
BAROTRAUMA. Overdistension of the lungs during IPPV can rupture alveoli and cause air to dissect centrally along the perivascular sheaths. This pulmonary interstitial air can sometimes be seen on chest X-ray as linear or circular perivascular collections or subpleural blebs. Other complications are pneumothorax, pneumomedi astinum, pneumoperitoneum and subcutaneous emphysema. Intra-abdominal air originating from the alveoli is probably always associated with pneumomediastinum.
The incidence of barotrauma is greatest in those patients who require high inflation pressures, with or without a positive end-expiratory pressure, and the risk of pneumothorax is increased in those with destructive lung disease (e.g. staphylococcal pneumonia,
emphysema), asthma or fractured ribs. A tension pneumothorax can be rapiclly fatal in ventilated patients with respiratory failure. Suggestive signs include the development or worsening of hypoxia,
fighting the ventilator, an unexplained increase in inflation pressure, as well as hypotension and tachycardia, sometimes accompanied by a rising CVP. Examination may reveal unequal chest expansion, mediastinal shift (deviated trachea, displaced apex beat) and a hyperresonant hemithorax. Although, traditionally, breath sounds are diminished over the pneumothorax,
this sign can be extremely misleading in ventilated patients. If there is time, the diagnosis can be confirmed by chest X-ray.
Other dangers of IPPV include:
RESPIRATORY COMPLICATIONS. IPPV is frequently complicated by a deterioration in gas exchange due to VIO mismatch and collapse of peripheral alveoli. The latter can largely be prevented by using large tidal volumes (l0-15 rnl kg-I) and reducing the respiratory  rate (usually to 10-12 min-I) to avoid hypocarbia or by the application of PEEP (see below). Secondary pulmonary infection is a common complication of IPPV and high inflation pressure may contribute to ‘ventilation induced’ lung injury.
~ARDIOVASCULARCOMPLICATIONS. The intermittent application of positive pressure to the lungs and thoracic wall impedes venous return and distends alveoli, thereby ‘stretching’ the pulmonary capillaries and causing a rise in pulmonary vascular resistance. Both these mechanisms can produce a fall in cardiac output. In normal subjects, the fall in cardiac output is prevented by constriction of capacitance vessels, which restores venous return. Hypovolaemia, pre-existing pulmonary hypertension, right ventricular failure and autonomic dysfunction (as may be present in those with Guillain-Barre syndrome, acute spinal cord injury or diabetes) will exacerbate the haemodynamic disturbance. Expansion of the circulating volume, on the other hand, can often restore cardiac output. In patients with heart failure, cardiac output and blood pressure are usually unaffected, or even increased by positive pressure ventilation. Therefore, IPPV should be used without hesitation in patients with cardiogenic pulmonary oedema who have severe respiratory distress and exhaustion.
GASTROINTESTINAL COMPLICATIONS. Initially, many artificially ventilated patients will develop abdominal distension associated with an ileus. The cause is unknown, although the use of non-depolarizing neuromuscular blocking agents and opiates may in part be responsible.
SALT AND WATER RETENTION. IPPV, particularly with PEEP, causes increased ADH secretion and possibly a reduction in circulating levels of atrial natriuretic peptide. Combined with a fall in cardiac output and a reduction in renal cortical blood flow, these can cause salt and water retention. This fluid retention is often particularly noticeable in the lungs.

Positive end-expiratory pressure (PEEP)

A positive airway pressure can be maintained at a chosen level throughout expiration by attaching a threshold resistor valve to the expiratory limb of the circuit. PEEP should be considered if it proves impossible to achieve adequate oxygenation of arterial blood (more than 90% saturation) using conventional positive-pressure ventilation without raising the inspired oxygen concentration to potentially dangerous levels (conventionally 50%). PEEP is not, however, a panacea for all patients who are hypoxic and, indeed, it may often be detrimental, not least because the use of levels of PEEP in excess of 5 cmH20 is associated with an increased risk of barotrauma. Most recommend that pressures in excess of 15- 20 cmH20 should not be exceeded. The primary effect of PEEP is to re-expand underventilated lung units thereby reducing shunt and increasing the Pa02.
Unfortunately, the inevitable rise in mean intrathoracic pressure that follows the application of PEEP may further impede venous return, increase pulmonary vascular resistance and thus reduce cardiac output. This effect is probably least when the lungs are stiff. The fall in cardiac output can be ameliorated by expanding the circulating  volume, although in some cases inotropic support may be required. Thus, although arterial oxygenation is often improved by the application of PEEP, a simultaneous fallin cardiac output can lead to a reduction in total oxygen  delivery.

OTHER TECHNIQUES FOR RESPIRATORY SUPPORT

Continuous positive airway pressure (CPAP)

The application of CPAP achieves for the spontaneously breathing patient what PEEP does for the ventilated patient. Oxygen and air are delivered under pressure via an endotracheal tube or via a tightly fitted face mask. Not only can it improve oxygenation but the lungs become less stiff, breathing becomes easier and vital capacity
improves.

Intermittent mandatory ventilation

This technique allows the patient to breathe spontaneously between the ‘mandatory’ tidal volumes delivered by the ventilator. It is important that these mandatorybreaths are timed to coincide with the patient’s own inspiratory effort (synchronized IMV:SIMV). SIMV can  be used with or without PEEP or CPAP. It was originally introduced as a technique for weaning patients from artificial ventilation but is now used extensively as an alternative to conventional IPPV. Spontaneous respiration may be assisted during SIMV by applying a constant preset airway pressure at the start of inspiration (‘pressure support’). The level of pressure support can be reduced as the patient improves.

High-frequency jet ventilation

Adequate oxygenation -and CO2 elimination can be achieved by injecting gas into the trachea at rates of up to several thousand breaths per minute. In clinical practice rates of between 60 and 300 breaths per minute are usually employed.
Potential advantages of HFJV are largely related to the low peak airway pressures; for example the risk of barotrauma is reduced. Moreover, HFJV can be used to ventilate patients with large air leaks due, for example, to a bronchopleural fistula or lung lacerations. The place of HFJV in the management of patients with acute respiratory failure is less clear.
Low volume, pressure limited inverse-ratio mechanical ventilation. A constant preset inspiratory pressure is delivered for a prescribed time, generating low tidal volumes and reducing peak inspiratory pressure. Respiratory rate is increased in order to achieve adequate carbon dioxide removal. When combined with a prolonged inspiratory  time and low level PEEP this technique may provide optimal oxygenation whilst minimising the high peak airway pressures which are thought to exacerbate pulmonary damage. Hypercarbia is inevitable but should be accepted (‘permissive hypercarbia’).

Extracorporeal respiratory assistance

Recently there has been renewed interest in the use of extracorporeal gas exchange to reduce ventilation requirements and ‘rest’ the lungs. Carbon dioxide is removed using low flow veno-venous bypass through a membrane lung. The combination of normal pulmonary perfusion and minimum ventilation may reduce barotrauma and provide optimal conditions for lung healing. The indications for the use of this demanding technique are at present unclear.

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