21 Resuscitation

In any severe failure of the cardiorespiratory system, the order of priority should be to secure the airway, maintain respiration (manual ventilation if necessary), restore the circulation (with external cardiac massage if necessary), and consider mechanical ventilation. Initial assessment should include airway patency, palpation of pulses, measurement of blood pressure, presumptive diagnosis, and consideration of treatment of the cause.

The airway should be opened by tilting the head back with one hand on the forehead and lifting the chin with the fingers of the other hand. If there is a neck injury or an inadequate airway with the head tilt and chin lift, a jaw thrust should be performed. The fingers should be placed behind the angle of the mandible on both sides, and the mandible lifted forward and upward until the lower teeth (or gum) are in front of the upper teeth (or gum). The mouth and pharynx should be cleared by suction and loose fitting dentures removed. If necessary, an oropharyngeal (Guedel) airway may be inserted.

Once the airway is protected the patient who is not breathing requires manual ventilation with a self‐inflating bag and mask (Ambu bag). Oxygen should be delivered in high concentration (FIO₂ 1.0 for manual ventilation, FIO₂ 0.6–1.0 for spontaneously breathing patients) to achieve adequate arterial oxygen saturation. Hyperoxia should not be allowed to persist as this can be detrimental. If the patient breathes inadequately (poor arterial saturation, hypercapnia, rapid shallow breathing), ventilatory support should continue.

If pulses are impalpable or weak, or if the patient has a severe bradycardia, external cardiac massage is required and treatment should continue as for a cardiac arrest. Hypotension should be treated initially with a fluid challenge although life‐threatening hypotension may require blind treatment with epinephrine 0.05–0.2mg IV increments at 1–2min intervals until a satisfactory blood pressure is restored. Such treatment should not be prolonged without circulatory monitoring to ensure the adequacy of cardiac output as well as correction of hypotension.

Venous access must be secured early during basic resuscitation. Large‐bore cannulae are necessary, e.g. 14G. In cases of haemorrhage, two cannulae are required. Small peripheral veins should be avoided; forearm flexure veins are appropriate if nowhere else is available. In very difficult patients, a Seldinger approach to the femoral vein or a central vein may be appropriate. The latter has the advantage of providing central venous monitoring.

Oxygen therapy, p38; Airway maintenance, p40; Endotracheal intubation, p42; Ventilatory support—indications, p44; Electrical cardioversion, p94; Central venous catheter—insertion, p168; Colloids, p246; Inotropes, p264; Vasopressors, p268; Cardiac arrest, p340; Fluid challenge, p342.

As with basic resuscitation, the order of priority is airway, breathing, circulation, and drug treatment. If cardiac arrest is witnessed, a precordial thump may revert ventricular tachycardia or fibrillation. Initial management of airway and breathing is as described for basic resuscitation. Only attempt intubation after adequate pre‐oxygenation. If intubation is difficult, maintain manual ventilation with an Ambu bag, mask, and 100% O₂.

Therapeutic hypothermia is useful to improve cerebral outcome, post‐cardiac arrest (particularly out‐of‐hospital VF or pulseless VT).

External massage provides minimal circulatory support during cardiac arrest. A rate of 100/min with a compression depth of 5cm is recommended. Once an artificial airway is established, give manual breaths at a rate of 8–10/min. Compressions should not be paused for ventilation.

Cardioversion is performed urgently if VT or VF cannot be excluded. Restart cardiac massage immediately without waiting to review the ECG. Cerebral damage continues while there is no blood flow.

Few drugs are necessary for first‐line cardiac arrest management. Drugs should be given via a large vein since vasoconstriction and poor flow delay peripheral injections reaching the central circulation. If early venous access cannot be secured, the intraosseous route may be used, or double or triple doses of epinephrine may be given via the endotracheal tube.

The A constrictor effects predominate during cardiac arrest, helping to maintain diastolic blood pressure, and coronary and cerebral perfusion. Irrespective of rhythm give 1mg (10mL of 1:10000 solution) every 3–5min.

A recent trial comparing vasopressin and epinephrine showed improved outcomes with vasopressin in asystole. The vasopressin dose is 40IU, and may be repeated after 3min if the first dose is ineffective.

A dose of 8mmol can be given in refractory VF, torsades de pointes, hypomagnesaemia, or if digoxin toxicity is suspected.

A single 3mg dose is given early in asystole or pulseless bradycardia.

If VF/VT persists after three shocks, give amiodarone 300mg IV bolus.

Used in pulseless electrical activity if there is hyperkalaemia, hypocalcaemia, or calcium antagonist use. Give 10mL 10% solution.

Only used if cardiac arrest is due to hyperkalaemia or tricyclic poisoning. A dose of 50mL of 8.4% solution is given.

Electrical cardioversion, p94; Therapeutic hypothermia, p100; ECG monitoring, p162; Sodium bicarbonate, p244; Inotropes, p264; Vasopressors, p268; Basic resuscitation, p338.

Treat hypovolaemia urgently to avoid the serious complication of multi‐organ failure. Ensure an adequate circulating volume before considering other methods of circulatory support. Clinical signs of hypovolaemia (reduced skin turgor, low CVP, oliguria, tachycardia, and hypotension) are late indicators. Lifting the legs of a supine patient and watching for an improvement in the circulation is a useful indicator of hypovolaemia. A high index of suspicion must be maintained; normal heart rate, BP, and CVP do not exclude hypovolaemia The CVP is particularly unreliable in pulmonary vascular disease, right ventricular disease, isolated left ventricular failure, and valvular heart disease. The absolute CVP or PAWP are also difficult to interpret since peripheral venoconstriction may maintain CVP despite hypovolaemia; indeed, CVP may fall in response to fluid. The response to a fluid challenge is the safest method of assessment.

The aim of a fluid challenge is to produce a significant (200mL) and rapid increase in plasma volume. Colloid fluids are ideal; a gelatin solution is recommended for short‐term plasma volume expansion in simple hypovolaemia. Consider hydroxyethyl starch when there is a probability of capillary leak. Packed red cells have a high haematocrit and do not adequately expand the plasma volume. Crystalloid fluids are rapidly lost from the circulation and give a less reliable increase in plasma volume.

Ideally, the response of CVP, PAWP or, preferably, stroke volume should be monitored during a fluid challenge. Fluid challenges should be repeated if the response suggests continuing hypovolaemia. However, if such monitoring is not available, it is reasonable to assess the clinical response to up to two fluid challenges (200mL each).

The change in CVP/PAWP after a 200mL fluid challenge depends on the starting blood volume (see figure opposite). A ≥3mmHg rise in CVP/PAWP represents a significant increase and suggests an adequate circulating volume. A positive response may sometimes occur in the vasoconstricted patient with a lower blood volume. It is also important to assess clinical response; if inadequate, it may be appropriate to monitor stroke volume before further fluid challenges or considering further circulatory support (see figure 21.1.).

In the inadequately filled left ventricle, a fluid challenge will increase stroke volume. Failure to increase stroke volume may be due to a well‐filled ventricle (usually accompanied by a ≥3mmHg rise in filling pressure), ongoing rapid fluid loss (e.g. massive haemorrhage), right heart failure or obstruction (e.g. pericardial tamponade, massive PE, mitral stenosis). It is important to monitor stroke volume rather than cardiac output during a fluid challenge. If the heart rate falls appropriately in response to a fluid challenge, the cardiac output may not increase despite an increase in stroke volume (see figure 21.1).

Central venous catheter—insertion, p168; Central venous catheter—use, p170; Cardiac output—central thermodilution, p178; Cardiac output—peripheral thermodilution, p180; Cardiac output—indicator dilution, p182; Cardiac output—Doppler ultrasound, p184; Cardiac output—pulse contour analysis, p186; Cardiac output—other techniques, p188; Pressure and stroke volume variation, p190; Echocardiography, p192; Colloids, p246; Basic resuscitation, p338.