Shock and resuscitation
The pathophysiology of shock
There are several mechanisms of shock:
• Cardiogenic shock occurs when the pump function of the heart is impaired
• Septic shock arises as a result of microvascular changes and cardiac depression caused by systemic inflammation
• Anaphylactic shock is an acute hypersensitivity reaction to an allergen
The classical symptoms and signs of shock include hypotension, hyperventilation, a rapid weak pulse, cold clammy cyanotic skin and oliguria. Mental changes also occur, most commonly anxiety, confusion and combativeness. Investigations reveal metabolic acidosis, low oxygen saturation and low central venous pressure. Notably, in septic shock there is peripheral vasodilatation rather than vasoconstriction.
Early recognition of shock
To help recognise these patients early, structured scoring systems have been developed, seeking to emulate the simplicity, reliability and clinical value of the Glasgow Coma Scale (Table 16.1, p. 219). These generally employ routinely recorded physiological data and most are modifications of the Early Warning Score (Table 4.1). These have proved extremely useful for spotting those at risk of deterioration needing urgent medical attention and have become part of standard care for surgical patients.
Table 4.1
Modified Early Warning Score (MEWS)*
*MEWS is one form of bedside scoring that can help early identification of patients likely to need urgent assessment (score 3 or more). A score of 5 or more indicates that the patient is likely to require critical care, usually in a high-dependency or intensive care unit
Types of shock
Hypovolaemic shock (preload insufficiency): Preload is defined as the rate of venous return of blood to the heart. Preload insufficiency reduces the diastolic filling pressure and volume and leads to low cardiac output. The underlying problem may be inadequate total blood volume and underfilling of the venous compartment, i.e. absolute hypovolaemia (hypovolaemic shock) or else may be relative hypovolaemia (distributive shock) caused by an increase in capacity of the venous compartment or capillary beds relative to blood volume. Hypovolaemia is responsible for the majority of cases of shock encountered in hospital. Figure 15.1 (p. 200) shows the changes in vital signs associated with increasing amounts of blood loss.
The main causes of fluid loss leading to hypovolaemic shock are:
• ‘Revealed’ haemorrhage, e.g. massive haematemesis from peptic ulcer, deep lacerations, large haematemeses (vomiting of blood), continued loss from a wound drain indicating internal bleeding
• ‘Concealed’ haemorrhage, e.g. intra-abdominal bleeding from ruptured spleen or aortic aneurysm, haemorrhage from a duodenal ulcer into small intestine, intramuscular blood loss from fractures
• Extensive burns, resulting in massive loss of serum into blisters or from the skin surface
• Severe vomiting or diarrhoea, or prolonged fluid loss from a small bowel fistula or ileostomy
• Excessive urinary fluid loss, e.g. diabetic ketoacidosis, recovering acute tubular necrosis
• Sequestration of fluid in bowel caused by bowel obstruction
• Massive loss of fluid into interstitial tissues (‘third space losses’) as occurs in sepsis
• Major accumulation of fluid in the peritoneal cavity, e.g. acute pancreatitis
Distributive shock: Relative hypovolaemia occurs if there is inappropriate expansion of the circulatory capacity in relation to blood volume; it may result from failure of normal peripheral resistance and/or venodilatation of large veins. Peripheral resistance normally maintains cardiac afterload and is controlled by the tone of smooth muscle arteriolar and capillary sphincters. About 80% of capillaries are normally closed, and any mechanism that causes inappropriate opening greatly expands circulatory capacity. In septic shock, both arteriolar dilatation and an increase in venous volume play a part.
Septic shock: Septic shock is impaired tissue perfusion in the context of an inflammatory response. The aetiology is frequently infective but not always; it may be traumatic or surgical, or it may involve local inflammation, infection, severe burns or the presence of necrotic tissue, e.g. a gangrenous leg. If immune responses escape local control, this spill over provokes a complex cellular response and mediator cascade that leads to progressive clinical manifestations including the systemic inflammatory response syndrome (SIRS) and, later, multiple organ dysfunction (MODS). Mediator responses involve the complement system, acute phase proteins and cytokines (particularly TNF-alpha and the interleukins IL1-beta and IL6); once triggered, the inflammatory response cascade is difficult to control or suppress.
Pump failure (cardiogenic shock): Cardiogenic shock describes a drastic reduction in cardiac output resulting from any form of ‘pump failure’ caused by direct myocardial damage, mechanical abnormality or malfunction of the heart. This most commonly arises from an acute myocardial infarction or an acute ventricular arrhythmia. Myocardial infarction may cause ischaemia or infarction of papillary muscles which produces acute mitral regurgitation. Another cause is when a large pulmonary embolus obstructs blood flow through the lungs and causes secondary cardiac failure. Other causes include cardiac (pericardial) tamponade and tension pneumothorax.
Anaphylactic shock: Anaphylactic shock is a generalised form of type I hypersensitivity reaction. The stimulatory antigen binds with antibodies attached to the surface of mast cells, triggering degranulation and release of histamine and other vasoactive amines. The predominant effect is extensive dilatation of the venous compartment and rapid movement of fluid into the tissues. The systemic effects are compounded by hypoxia due to bronchoconstriction and often laryngeal oedema.
