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Shock overview


Essentials

  • 1

    Broad categories of shock include disorders of intravascular volume, vascular resistance, cardiac filling and the myocardial pump. Overlapping aetiologies are commonly encountered.

  • 2

    Hypotension is only one characteristic of shock, which should be considered a late and concerning finding.

  • 3

    Hypovolaemia and hence the need for volume resuscitation is a concern in every patient with shock.

  • 4

    Interventions in any form of shock are initially directed at the physiological deficit and act as a test of the underlying clinical hypothesis. Continuous reassessment is required.

  • 5

    Common errors in management are late diagnosis, inadequate control of the primary problem, inadequate fluid loading, delayed ventilatory assistance and excessive reliance on inappropriate adjuncts. There is not sufficient evidence that any one of the investigated vasopressors is clearly superior to others.

  • 6

    Mortality following cardiogenic shock is improved by revascularization strategies and cardiothoracic surgical intervention. Thrombolysis alone is unproven, as is intra-aortic balloon counterpulsation.

  • 7

    Currently no adjunctive therapies are of benefit in septic shock over adequate fluid resuscitation, vasopressors and inotropes, timely and appropriate antibiotics and/or source control.

Introduction

Shock is a clinical syndrome where tissue perfusion, and hence oxygenation, is inadequate to maintain normal metabolic function of the cells and organs. Although the effects of inadequate perfusion are initially reversible, prolonged oxygen deprivation leads to generalized cellular hypoxia with disruption of critical biochemical processes, eventually resulting in cell membrane ion pump dysfunction, inadequate regulation of intracellular pH, intracellular oedema and cell death.

Shock is traditionally classified and managed according to the presumed aetiology, but a common approach in practice is to attend urgently to the cardiorespiratory physiological abnormalities and to assess the response to adjust the working diagnosis, with later attention to the underlying diagnosis.

Recognizing shock may be difficult, particularly at the extremes of age. Pre-existing disease and the use of medications modify the compensatory mechanisms that safeguard perfusion of vital organs. Consider the possibility of inadequate tissue perfusion (‘shock’) in any emergency presentation with symptoms, signs or laboratory findings of abnormal end-organ function. Early, aggressive and targeted treatment of shock is associated with an improved outcome.

Aetiology and epidemiology

Shock is due to malfunction of components of the cardiovascular system, not uncommonly with more than one contributing mechanism. If the aetiology is apparent, classification based on the mechanism—such as hypovolaemic, cardiogenic, septic, neurogenic or anaphylactic shock—will guide therapy.

When the aetiology is unclear or the shock fails to respond to therapy, the following physiologically based classification assists in decision making ( Boxes 2.4.1–2.4.4 ).

Box 2.4.1
Volume loss contributing to shock: ‘ hypovolaemic shock ’

Intravascular compartment

Blood loss

  • External bleeding

    • Trauma

    • Gastrointestinal tract bleeding

  • Internal (concealed) bleeding

    • Haemothorax

    • Haemoperitoneum (ruptured abdominal aortic aneurysm, ruptured ectopic pregnancy)

    • Retroperitoneum (ruptured abdominal aortic aneurysm, pelvic trauma)

  • Plasma loss

    • Burns

    • Sweating/dehydration

    • Pancreatitis

    • Ascites (peritonitis, liver disease)

    • Toxic epidermal necrolysis (TEN), erythroderma, pemphigus

Extravascular loss

  • Gastrointestinal tract

    • Vomiting

    • Diarrhoea

    • Bowel obstruction

  • Renal tract

    • Adrenal insufficiency (aldosterone deficiency)

    • Diabetes mellitus (polyuria)

    • Diabetes insipidus (polyuria)

    • Diuretics

    • Polyuric intrinsic renal disease

Box 2.4.2
Shock resulting from altered venous capacitance and/or reduced vascular tone: ‘ distributive shock ’

  • Septic shock

  • Anaphylactic shock

  • Neurogenic shock

  • Vasoactive drugs (vasodilators, sedatives or toxins)

  • Adrenal insufficiency (cortisol deficiency)

  • Thyrotoxicosis/thyroid storm

  • Liver failure

  • Systemic inflammatory response features (e.g. pancreatitis, trauma, burns)

  • Prolonged shock from any cause—’decompensated shock’

Box 2.4.3
Inadequate filling due to extrinsic obstruction: ‘ obstructive shock ’

  • Tension pneumothorax

  • Pericardial tamponade/other pericardial disease

  • Pulmonary hypertension (large pulmonary embolus, chronic pulmonary hypertension)

  • Atrial myxoma and left atrial mural thrombus

Box 2.4.4
Myocardial dysfunction resulting in shock: ‘ cardiogenic shock ’

  • Reduced contractility (systolic dysfunction)

    • Ischaemia (acute myocardial infarction)

    • Myocarditis (infectious, hypersensitivity)

    • Myocardial contusion

    • Cardiomyopathy

    • Toxins/drugs (calcium channel blockers, doxorubicin)

  • Inadequate filling (due to intrinsic problem)

    • Diastolic dysfunction

    • Right ventricular infarction

  • Arrhythmia

    • Ventricular tachycardia

    • Atrial fibrillation (when cardiac output is dependent on atrial priming)

    • Bradycardia (heart block, drugs)

  • Failure of forward flow

    • Ruptured ventricular septum or free wall

    • Chordae tendineae rupture or papillary muscle dysfunction (post-myocardial infarction)

    • Critical mitral or aortic stenosis

    • Mitral or aortic regurgitation

    • Prosthetic valve thrombus/dysfunction

Reduced return to the heart—reduced preload— hypovolaemia (see Box 2.4.1 )

  • Intravascular compartment

  • Extravascular loss

Reduced total peripheral resistance—reduced afterload— distributive (see Box 2.4.2 )

  • Arterial vasodilatation

  • Altered venous capacitance

Obstruction to filling— obstructive (see Box 2.4.3 )

  • Tension pneumothorax

  • Pericardial tamponade

  • Large pulmonary embolism/pulmonary hypertension

  • Atrial myxoma

Pump dysfunction— cardiogenic (see Box 2.4.4 )

  • Reduced contractility—systolic dysfunction

  • Impaired relaxation—diastolic dysfunction/right ventricular (RV) infarction

  • Abnormal cardiac rate or rhythm

  • Forward flow failure—valvular dysfunction

No classification is exhaustive, and contributory causes may feature in more than one category.

Pathophysiology

Most organs and tissues are able to autoregulate or adjust their flow according to metabolic demand as long as flow is adequate. This flow is dependent on a gradient between an area of higher pressure (mean arterial pressure [MAP]) and the lower-pressure side of the venous system (represented by a central venous pressure [CVP]).

The MAP may fall if the cardiac output (CO) is reduced or if the total peripheral resistance (TPR) in the arterial tree falls; that is,


MAP = CO × TPR

CO is determined by the stroke volume (SV) and heart rate (HR). The heart is a relatively simple pump and hence preload (the volume of blood in the left ventricle at the end of filling or the amount of stretch of the left ventricle) determines SV until disease states intervene, as represented by


CO = SV × HR

Relaxation of the arterial and venous tone by vasoactive mediators or lack of vasotonic mediators results in reduced resistance and increased capacitance as well as lower pressures in both the arterial and venous systems. Any injury to the endothelium will result in loss of volume and the failure of vascular autoregulation. Additionally, if there is a defective valve causing regurgitation of blood and repumping or a fixed narrow orifice, there is a failure in forward flow.

Compensatory mechanisms

Compensatory mechanisms are provoked by the combination of lowered pressure and inadequate perfusion of tissues and contribute to the symptoms and signs of shock. Neurohumoral stimulation produces increased circulating catecholamines, angiotensin, aldosterone and vasopressin, manifesting clinically with anxiety, thirst, restlessness, tachycardia, diversion of blood from the skin bed and a reduction in urinary output and urinary sodium. Blood flow to the brain and heart is maintained at the expense of renal, splanchnic, skin and muscle blood flow. Significant fluid shifts occur from the interstitium to the intravascular compartment, which may falsely maintain haematocrit.

Decompensated shock

The ultimate consequence of shock, if tissue perfusion is not returned by compensatory measures or resuscitation, is inadequate regeneration of adenosine triphosphate (ATP), causing failure of membrane ion pumps to maintain the function and structural integrity of the cell.

This cellular dysfunction manifests in the myocardium as systolic contractile dysfunction (also due in part to reduction in sensitivity to catecholamines and circulating myocardial depressant factors) and impaired ventricular relaxation (lusitropy). This myocardial failure, along with failure of vascular beds despite the increased circulating catecholamines, contributes to what is described as ‘decompensated shock’.

Clinical features

The clinical features in the initial diagnosis of shock are due to inadequate perfusion of tissues and resulting multiorgan dysfunction of the body’s compensatory mechanisms. Clinicians should not wait for physical observations to trigger a preconceived blood pressure (BP) limit before considering shock but should actively look for signs of inadequate perfusion in any patient presenting with abnormal organ function:

  • Mental state reflecting reduced cerebral perfusion, which may range from anxiety or confusion to coma.

  • Patients may describe thirst, coldness or impending doom and have presyncopal symptoms including nausea, yawning and preferring to lie down.

  • Retrospectively, the patient may have been a challenge to assess, with vital signs hard to elicit or variable and venepuncture or intravenous access difficult.

  • Peripheral circulation reveals venoconstriction, with decreased peripheral temperature, pallor and mottling. Capillary return may be prolonged beyond 4 seconds, although peripheral mottling and central cyanosis are late signs. However, with vascular tone failure—such as spinal, anaphylactic, neurogenic shock and sepsis—the skin may initially be warm and dry and capillary refill indeterminate as a consequence of vasodilatation.

  • Hypotension is a cardinal clinical sign, defined as a systolic blood pressure (SBP) less than 90 mm Hg or a reduction of more than 30 mm Hg in a previously hypertensive patient. Shock can be present despite an elevated BP, and a low SBP may not be associated with other signs of shock or be physiological in young thin females.

  • A low SBP should be considered a highly significant if not late finding in shock. MAP is increasingly considered more relevant and accurate as a measured parameter. Tachycardia is frequently present but may be masked by drugs or advanced age.

  • The trend with serial observations is more significant than absolute values. Bradycardia can occur in younger patients or following an inferior myocardial infarction (MI).

  • Tachypnoea is regarded as a sensitive but non-specific predictor of deterioration and is part of the shock syndrome.

  • Core temperature may be low, normal or elevated and will be affected by age, environment, volume status, coexisting disease, drug therapy and pre-hospital interventions.

  • Oliguria.

Initial management of shock

A structured framework, such as that advocated by early management of severe trauma (EMST/advanced trauma life support [ATLS]) or advanced cardiac life support (ACLS), promotes both a systematic survey and effective therapy to occur simultaneously. Treatments based on an initial working diagnosis are modified by the observed responses to therapy and/or the results of investigations. Frequent reassessment of status and adequacy of response is vital. Once shock has been recognized as present, a high chance of death is implied; thus urgent escalation to management by a multidisciplinary team in a monitored resuscitation area is indicated, with a designated team leader and communication being vital.

Primary survey

  • Assess and support airway and ventilation. Give supplemental high-flow oxygen to ensure maximal arterial oxygen saturation. Consider tracheal intubation and mechanical ventilation in the significantly shocked patient for reasons over and above the standard indications of airway protection and intractable hypoxaemia in order to divert needed CO to other hypoperfused organs, reduce oxygen consumption from respiratory musculature, maximize arterial oxygenation, manage respiratory acidosis, facilitate invasive monitoring procedures and guard against sudden catastrophic respiratory decompensation. The role of non-invasive ventilation is unproven in this setting. Positive-pressure ventilation and anaesthesia will have a significant effect in the setting of inadequate preload, so prior fluid resuscitation is vital (see Chapter 2.1, Fig. 2.1.3).

  • Circulation with haemorrhage control. Within the skill level of the operator, obtain and secure intravenous access in more than one site with short, large-bore peripheral cannulae. Central venous access is rarely required in an emergency and may increase delay and morbidity. Consider a supine/head-up position and elevation of the legs if tolerated.

  • Draw blood for investigations, including immediate bedside glucose level and venous or arterial blood gases.

  • Infuse fluid as the initial correction of shock with hypotension. Hypovolaemia and hence the need for volume resuscitation should be assumed in every patient with shock, until proven otherwise. Close observation of the response to fluid boluses will guide further boluses.

  • The usual initial fluid is isotonic normal saline or Hartmann (lactated Ringer) solution.

  • Use immediately available blood products (O-negative or group-specific) warmed by a cartridge-warming device for haemorrhagic shock or where haemoglobin may fall to a point where oxygen carriage is compromised (7 to 9 g/dL except in patients with acute haemorrhage or significant coronary artery disease).

  • Add an effective vasopressor/inotrope, such as epinephrine (adrenaline), by infusion if, despite ongoing rapid fluid volume resuscitation, hypotension and inadequate perfusion persist (see ‘Goal-directed resuscitation’, further on). However, this may achieve an adequate BP only at the expense of correct fluid volume replenishment.

Secondary survey

  • Review vital signs and any available history followed by a directed physical examination. Cardiac rhythm and pulse oximetry (SaO 2 ) are monitored continuously. All observations, including temperature, are recorded regularly.

  • At this point, obtain a chest x-ray, electrocardiogram (ECG) and other bedside emergency testing, such as ultrasound, that may point to the aetiology (e.g. a ruptured aortic aneurysm or ectopic pregnancy, cardiac tamponade or RV failure).

  • Place an indwelling urinary catheter in any shocked patient.

  • Anticipate complications and interventions and organize definitive care and disposal. Liaise with surgeons, radiologists and other specialists early. The complications of hypothermia, coagulopathy, hypoglycaemia, hypokalaemia and respiratory failure should be actively sought, prepared for and prevented. The need to move the patient to imaging or theatre should be anticipated and communicated to team members to allow for early preparation of the patient and monitoring setup.

Guidance for interventions and treatments

A key goal in the treatment of shock during and after the initial resuscitation is correction of the underlying problem. Methods used to guide resuscitation are discussed in the following text.

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