ITU

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12 ITU

Shock

Case history (1)

A 60-year-old bank manager presents with crushing central chest pain. This started 45 minutes ago and has remained constant ever since.

On examination he is pale and clammy. His pulse is 100/min, poor volume and BP 90/60.

Diagnosis.

Shock – cardiogenic; ECG shows evidence of anterior myocardial infarction.

Case history (2)

A 50-year-old man who works in a bar has been brought to hospital vomiting a large amount of blood. He gave no history of upper abdominal pain but did admit to drinking a bottle of whiskey a day and occasional beers as well.

He also admits to a previous hospital admission with abdominal swelling which was due to alcoholic liver disease. He was told that his liver disease was bad and that he must stop drinking and take propranolol regularly as he had varices on endoscopy. He had not stopped drinking, nor was he taking his propranolol.

On examination he is sweating profusely with visible shaking of his extremeties. His pulse rate is 120/min with a blood pressure of 90/60.

Diagnosis.

Shock – hypovolaemia due to blood loss, probably from oesophageal varices.

Remember

• Shock is a life-threatening condition in which the patient is suffering global hypoxic injury

• Establish clear airway

• Oxygen must be given immediately to all haemodynamically unstable patients.

Physiology (Fig. 12.1)

Shock is ‘inadequate tissue oxygenation’ where there is failure of the circulatory system due to:

• Failure of the heart to maintain an adequate cardiac output, e.g. myocardial infarction

• Reduction in the volume of blood within the circulation, e.g. haemorrhage

• Loss of vascular tone within the circulatory system, e.g. septicaemia

• Obstruction to the circulation, e.g. pulmonary embolism.

Figure 12.1 The sympatho-adrenal response to shock showing the effect of increased catecholamines on the left of the diagram and the release of angiotensin and aldosterone on the right. Both mechanisms result in maintaining the blood pressure and cardiac output in shock.

Causes of shock

• Cardiogenic: myocardial infarction, tamponade, aortic dissection, pulmonary embolism

• Sepsis: infective causes, e.g. pneumonia, urinary tract infection or meningococcal septicaemia or ‘systemic inflammation’, resulting from trauma, post-surgery or anaphylaxis

• Hypovolaemia: profound dehydration, haemorrhage.

Remember

A patient might have more than one cause of shock, e.g. Case 2 may have an alcoholic cardiomyopathy (pump failure) as well as his haematemesis (decreased blood volume).

Is the shock state in Case 1 due to myocardial infarction, an obstructed circulation or other shock-inducing factors?

A history in a shocked patient of chest pain associated with ECG evidence of a myocardial infarction makes the diagnosis in this case. However, be careful because ECG changes with tachyarrhythmias and some ST segment changes which look characteristic of myocardial ischaemia can also occur in other types of shock.

Is the shock state in Case 2 due to fluid loss? If so, what fluid and from where?

In this case the blood loss is obvious, i.e. haematemesis. Try and estimate from the patient how much was lost. In other cases blood loss might be concealed, e.g. pancreatitis.

Clinical examination

In assessing the shocked patient the following indices should be monitored:

• Pulse rate and respiratory rate

• Peripheral venous filling/capillary filling

• Limb temperature

• Arterial blood pressure

• Urinary output

• Mental status.

Investigations

• Haemoglobin and haematocrit, U&Es, LFTs, troponin estimation

• ECG and monitor

• Central venous pressure (see p. 225)

• If the CVP is low (< 5 mmHg) fluid replacement is necessary

• If 10 mmHg or more, fluid replacement is probably not required immediately

Case 1 – has a problem with the circulatory pump and probably needs no extra intravascular fluid administration.

Case 2 – the haematemesis patient – has lost circulating volume with a low central venous pressure. His problems are with the plumbing circuit not the heart pump but his condition might be compounded by coagulation and biochemical disturbances consequent upon hepatic insufficiency.

Other investigations (see Fig 12.2)

• Arterial blood gas analysis: in hypovolaemic shock (as in all shock states) there is a metabolic acidosis with a high hydrogen ion concentration and low bicarbonate concentration. In cases with respiratory complications the pO₂ and pCO₂ values will help indicate the need for ventilatory support.

• Lactate levels: blood lactate levels rise approximately in proportion to the severity of the shock.

• X-rays: these are usually of little value in the acute stages of shock management. A CXR will exclude any treatable pathology, such as a pneumothorax or haemothorax often complicating insertion of monitoring lines. A CT scan may be helpful in, for example, a case of trauma.

Figure 12.2 Management of shock. Patients require intensive nursing care.

How would you treat?

Both patients should be admitted to high-dependency nursing units in the first instance as their MEWS scores were > 5.

Case 1

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