Shock and Resuscitation

Hypovolaemic Shock (Preload Insufficiency)

This is the most common cause of shock encountered in hospital. 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 is inadequate intravascular volume and underfilling of the venous compartment. This can be caused by haemorrhagic or nonhaemorrhagic causes.

Haemorrhagic Hypovolaemic Shock

This can be further subdivided into:

• ‘Revealed’ haemorrhage—visually acknowledged blood loss, commonly seen in trauma, upper gastrointestinal (GI) and lower GI bleeding. Also occurs intraoperatively and postoperatively (from drains, etc.)

• ‘Concealed’ haemorrhage, for example intraabdominal bleeding from ruptured spleen or aortic aneurysm, haemorrhage from a duodenal ulcer into small intestine, intramuscular blood loss from fractures, or intracavity haemorrhage after operation.

In concealed haemorrhage, estimating blood loss is difficult. Even in the revealed form, a large proportion of blood loss may also be concealed. Fig. 15.1 (p. 211) shows the changes in vital signs associated with increasing amounts of blood loss.

Nonhaemorrhagic Hypovolaemic Shock

This is caused by loss of intravascular volume other than blood, for example:

• Loss of plasma in extensive burns, resulting in massive loss of serum into blisters or from the skin surface.

• Loss of body sodium and water resulting from severe vomiting or diarrhoea, prolonged fluid loss from a small bowel fistula or ileostomy, or third space loss secondary to acute pancreatitis or bowel obstruction.

Distributive Shock (Vasodilatory 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 vasodilatation 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. Molecules that mediate this initiation of vasodilatation vary between causative factors, but all result in severe peripheral vasodilatation. Causes are described subsequently.

Septic Shock

This is the most common form of distributive shock and occurs in response to an infective cause, resulting in impaired tissue perfusion in the setting of an uncontrolled immune response. Patients with septic shock will most likely have all the criteria for the systemic inflammatory response syndrome (SIRS, see later). Septic shock is a combination of distributive shock and organ dysfunction induced by mediators of the host inflammatory response (e.g., cytokines, complement) and sometimes directly by bacterial toxins, especially certain staphylococci or gram-negative bacilli, for example, from a colonic anastomotic leak. Bacterial toxins and cell wall components activate defensive mechanisms and the net result of this immune burst is that oxygen usage declines, metabolic acidosis and lactaemia develops and multiple organ dysfunction ensues. Failure of oxygen usage is the result of cardiorespiratory impairment, microcirculatory imbalance and, at cellular level, mitochondrial dysfunction. Septic shock itself can be thought of in three phases. In phase 1 there is extensive vasodilatation, causing relative hypovolaemia. In phase 2 there is widespread endothelial damage causing greatly increased capillary permeability and massive fluid leakage into the interstitial space. This manifests clinically as inadequate blood pressure in the presence of normal or increased cardiac output, until phase 3, when depression of myocardial contractility ensues.

The inflammatory burst also upsets normal blood coagulation by downregulating normal anticoagulants such as alpha-1-antitrypsin, and stimulating procoagulants such as tissue factor, as well as inhibiting fibrinolysis. The result may be disseminated intravascular coagulation (DIC) with microvascular occlusion, large vessel thrombosis and ischaemia, all contributing to organ dysfunction.

Toxic shock syndrome is a particular form of septic shock associated with staphylococcal or streptococcal infection associated with the use of superabsorbent tampons.

Anaphylactic Shock

This is an immunoglobulin E (IgE) mediated type 1 hypersensitivity response to a specific antigen resulting in release of mast cell mediators. The predominant effect is extensive dilatation of the venous compartment and rapid movement of fluid into the tissues. In addition, there can be bronchospasm, laryngeal oedema, rash and GI signs. Death can occur in minutes and prompt recognition is vital. First-line treatment is removal of potential causative agent, administered epinephrine (IM initially, but may need IV) and volume resuscitation.

In surgical practice, anaphylactic shock usually results from drug administration, particularly via the intravenous route. Antibiotics , particularly penicillins, and radiological contrast are the most common culprits. Anyone administering a drug must first check the patient is not sensitive. Insect bites (wasps, bees and hornets) and ingested nuts are also important causes and may be encountered in the emergency department.

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 (MI) or an acute ventricular arrhythmia . MI 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.

Obstructive Shock

This is caused by extracardiac causes of cardiac failure and circulatory flow. This can be caused by pulmonary problems (and consequent right-sided failure) or mechanical disruption resulting in reduced preload.

Pulmonary associated shock can be caused by:

• pulmonary embolism

• pulmonary hypertension

• valvular stenosis

Mechanical shock can be caused by:

• tension pneumothorax

• pericardial tamponade

• constrictive pericarditis

• restrictive cardiomyopathy

• abdominal compartment syndrome

Hypovolaemic Shock

Identifying the cause of the fluid loss is the top priority. Immediate measures should be taken to control blood loss, for example, pressure on a swab over a bleeding wound, endoscopic injection of bleeding peptic ulcer. Fluid replacement should be equivalent to estimated fluid loss but adjusted according to the response of pulse rate, blood pressure, observed jugular venous pressure (or CVP) and urine output. In trauma cases, focused assessment with sonography for trauma (FAST scan) can show evidence of intraabdominal mischief, which would not otherwise be revealed. Where possible, fluids of similar composition to those lost should be used: whole blood for haemorrhage, colloids after major burns. Fluids should be titrated in rapid boluses, for example, 250 mL at a time, and the response to each observed.

Cardiogenic Shock

Rapid diagnosis and resuscitation is key. Escalation to an enhanced care unit, respiratory support, correction of electrolyte and acid-base abnormalities, and prompt drug therapy to maintain blood pressure and cardiac output, along with urgent treatment of the underlying cause, are essential steps in optimising the outcome. The management of pulmonary embolism (which may present as cardiogenic shock) is discussed in Chapter 12 . Fluid overload is a significant hazard in cardiogenic shock.