17 Emerg Med J: first published as 10.1136/emj.2003.012450 on 20 December 2004. Downloaded from REVIEW Critical care in the emergency department: shock and circulatory support C A Graham, T R J Parke ............................................................................................................................... Emerg Med J 2005;22:17–21. doi: 10.1136/emj.2003.012450 Effective resuscitation includes the rapid identification and will produce organ failure and, in the context of global hypoperfusion, multiple organ failure correction of an inadequate circulation. Shock is said to be ensues. The aim of resuscitation is to prevent present when systemic hypoperfusion results in severe shock worsening and to restore the circulation to dysfunction of the vital organs. The finding of normal a level that meets the body’s tissue oxygen requirements. haemodynamic parameters, for example blood pressure, Shock can arise through a variety of mechan- does not exclude shock in itself. This paper reviews the isms. Pump failure may be attributable to pathophysiology, resuscitation, and continuing inadequate preload (for example, severe bleed- ing), myocardial failure, or excessive afterload. management of the patient presenting with shock to the Shock can also occur with an adequate or emergency department. increased cardiac output as seen in distributive ........................................................................... shock (for example, septic or anaphylactic shock). Vital tissues remain ischaemic as much of the cardiac output is distributed inappropri- ately through vascular beds. The mechanisms producing shock may also be CLINICAL SCENARIO very complex involving combinations of these A 61 year old man is admitted to the resuscita- factors. For example, in septic shock, there may tion room with shortness of breath. He has a be reduced preload from increased vascular medical history of ischaemic heart disease permeability and venodilatation, impaired myo- treated with quadruple coronary artery bypass cardial contractility caused by inflammatory grafting five years ago. He has been unwell for mediators, and tissue hypoxia from inappropri- the past 48 hours with a productive cough, ate distribution of blood flow. lethargy, and fever. Compensatory mechanisms are activated in Vital signs on arrival include temperature of response to tissue hypoperfusion. Acutely, the 35.2˚C, respiratory rate 40/min, pulse 130 beats/ adrenergic autonomic nervous system is acti- min, non-invasive blood pressure 70/40 mm Hg, vated. Venoconstriction increases the preload to http://emj.bmj.com/ and oxygen saturation of 90% on 15 l/min face the heart; vasoconstriction of all non-essential mask oxygen using a non-rebreather bag. He is arterial beds sustains arterial blood pressure and poorly perfused, cold, and shut down. Initial myocardial contractility is maximised. This blood gas analysis shows a mixed respiratory and response attempts to optimise cardiac output metabolic acidosis. and maintain an adequate perfusion pressure to the coronary arteries and brain. Thus, the early Questions stages of uncomplicated shock are characterised N Is this patient suffering from shock? by tachycardia and a comparatively normal blood on September 30, 2021 by guest. Protected copyright. N What is the pathophysiology of the shock pressure. process? Further compensatory neuroendocrine mech- N What should the initial management in the anisms are activated in the kidney. This delayed first 15 minutes be for this patient? effect consists of rennin-angiotensin-aldosterone mediated renal retention of salt and water to further maximise preload and improve cardiac PHYSIOLOGY output. Shock is defined as acute circulatory failure with Hypotension occurs once the compensatory inadequate or inappropriately distributed tissue mechanisms have been overwhelmed, or the See end of article for perfusion resulting in generalised cellular autonomic nervous system is unable to respond authors’ affiliations ....................... hypoxia. Circulating blood must meet the tissues’ effectively. Reasons for this include advanced metabolic requirements rather than achieve set age, concurrent medication (for example b block), Correspondence to: haemodynamic variables (for example, a normal autonomic neuropathy, or adrenal insufficiency. Dr T R J Parke, Accident blood pressure). The presence of shock is best and Emergency In profound shock other autonomic mechan- Department, Southern detected by looking for evidence of compromised isms, primarily vagal, may come into play. In the General Hospital, end organ perfusion. presence of low cardiac filling pressures in severe Glasgow G51 4TF, UK; In early shock a switch from aerobic to hypovolaemia, the tachycardia response to shock [email protected] anaerobic metabolism compensates temporarily. Accepted for publication Lactate accumulates as a result of this anaerobic Abbreviations: ED, emergency department; IV, 8 April 2004 metabolism. Hypoxia eventually causes cellular intravenous; ECG, electrocardiography; CVP, central ....................... and then tissue necrosis. Loss of sufficient tissue venous pressure www.emjonline.com 18 Graham, Parke Emerg Med J: first published as 10.1136/emj.2003.012450 on 20 December 2004. Downloaded from may be replaced with a reflex bradycardia. As shock INITIAL MANAGEMENT OF THE CIRCULATION progresses, cells in ischaemic tissues switch to anaerobic Is a fluid challenge indicated? metabolism and lactic acidosis stimulates compensatory This can be a difficult decision to make on clinical grounds hyperventilation. and often depends on the context in which the patient has Identification and treatment of shock in the emergency presented. Conditions that are associated with actual or department is based on sound knowledge of these physiolo- relative hypovolaemia respond well to restoration of vascular gical principles. volume. Such conditions should be identified early. Blood loss can be assumed to be the cause of shock after trauma, at CLINICAL FEATURES OF SHOCK least initially, while a search is carried out for haemorrhage Clinical features of acute circulatory failure are usually those into the chest, pelvis, abdomen, or externally. of tissue hypoperfusion. This is most easily detected in the In conditions such as diabetic ketoacidosis, bowel obstruc- skin as central pallor, peripheral cyanosis, and sluggish tion, or severe diarrhoea and vomiting, it is reasonable to capillary return. Other clinical evidence could include a raised assume initially that salt and water depletion have caused respiratory rate, confusion, or coma. Renal hypoperfusion is hypovolaemic shock. indicated by a diminished urine output. Cardiac ischaemia If it is clear that shock has been caused by hypovolaemia, may be manifest on electrocardiographic monitoring. Arterial IV fluids should be started. Patients should receive an initial blood gas analysis may show a metabolic (lactic) acidosis. bolus of one to two litres of IV fluid rapidly and be reassessed. The traditional vital signs are less reliable indicators of The choice of fluid remains controversial, but crystalloids, 1 shock. The interplay between the sympathetic and para- particularly Ringer’s lactate, have become widely supported. sympathetic autonomic nervous system can produce pulse There is no place for inotropes in the management of severe rates and blood pressures that are normal, high, or low. hypovolaemia unless the patient is in established cardiac Shock cannot be excluded solely on the basis of normal vital arrest, as they may precipitate severe arrhythmias that may in signs. turn worsen the shock state. Blood sugar measurement can identify patients with shock In other circumstances fluid therapy can be harmful. A secondary to hyperglycaemia (diabetic ketoacidosis and patient with acute myocardial infarction or compromising hyperosmolar states) and with hypoglycaemia, which may arrhythmia may progress to cardiogenic shock with left resemble shock clinically. ventricular failure and pulmonary oedema. Such patients may be identified by a previous cardiac history, recent chest pain, or ECG changes together with the clinical and INITIAL MANAGEMENT OF SHOCK IN THE radiological signs of acute pulmonary oedema. Additional EMERGENCY DEPARTMENT fluid loading in these patients may increase an already Ideally, patients suffering from shock are identified at triage increased left ventricular end diastolic pressure and worsen and transferred to the resuscitation room. All patients should pulmonary oedema with no useful gain in terms of cardiac be given high flow oxygen, have intravenous (IV) access output. This is attributable to the flat nature of the Starling secured, and have basic monitoring instituted (non-invasive curve in the failing heart. Initial mangement in these blood pressure, pulse oximetry, and continuous ECG). circumstances is targeted at immediate treatment of any arrhythmia and early inotropic support, together with MANAGEMENT OF AIRWAY AND BREATHING aggressive management of pulmonary oedema. Does the patient require intubation and ventilation? A second scenario in which fluids may be harmful is Consider early intubation and ventilation for severe shock if where there is severe shock associated with ongoing non- http://emj.bmj.com/ there is respiratory distress, severe hypoxaemia, pronounced compressible haemorrhage, for example, penetrating trauma acidosis, or coma. Intubation ensures protection from to the torso or a leaking aortic aneurysm. There