Early detection and management of shock to reverse pathological processes improves patient outcomes.⁶ Although the traditional hallmark of shock is hypotension (SBP <90 mmHg) this can be a late or misleading sign and is considered a medical emergency.⁷ It is therefore critical that other signs and symptoms are identified early by frequent observations to detect a patient’s deteriorating state and respond before irreversible shock ensues.⁸ No one vital sign is adequate in determining the level or extent of shock⁶ nor is there a specific laboratory test which diagnoses the shock syndrome.

This chapter provides an overview of the pathophysiology of shock, the commonly described categories and associated pathologies, along with appropriate monitoring and interventions for managing a patient in shock.

Pathophysiology

Traditionally, shock is classified by aetiology: hypovolaemic, cardiogenic and distributive.^3,^4,⁹ Each has a specific mechanism of action that leads to altered tissue perfusion and oxygen and nutrient uptake at the cellular level (see Table 20.1). In practice, it is common to find overlap between different shock types (e.g. in sepsis there may also be hypovolaemia and/or myocardial dysfunction).

TABLE 20.1 Shock types ⁵

Shock type	Main characteristic
Hypovolaemic	a reduction in circulating blood volume through haemorrhage or dehydration or plasma fluid loss
Cardiogenic • obstructive shock	pump failure (impaired cardiac contractility) usually as result of myocardial infarction a sub category of cardiogenic shock characterised by blockage of circulation to the tissues by impedance of outflow or filling in the heart (e.g. due to cardiac tamponade or pulmonary emboli)
Distributive shock	a maldistribution of circulation from sepsis, anaphylaxis or neurogenic injury

Shock occurs when there is an inability of the body to meet metabolic demands of the tissues; hypoperfusion (decreased blood flow to the tissues) results in cellular dysfunction, as there is homeostatic imbalance between nutrient supply and demand,^4,¹⁰ and adaptive responses can no longer accommodate circulatory changes. These adaptive responses are moderated via numerous ‘sensors’ throughout the thorax and large vessels in particular, which detect subtle changes in pressure (baroreceptors) or biochemical changes (chemoreceptors). These receptors feed back to the hypothalamus which regulates through the pituitary gland (for the release of a number of hormones such as antidiuretic hormone [ADH] and adrenocorticoid trophic hormone [ACTH] to target organs such as the kidney) and the cortex of the adrenal gland to respond and counter the developing effects of shock. Concurrently direct feedback stimulates the sympathetic nervous system to act on blood vessel tone, particularly the arterioles, and also target organs such as the adrenal gland and kidney to respond via the release of endogenous catecholamines (adrenaline and noradrenaline), mineral and glucocorticoids (aldosterone, cortisol), and the renin–angiotensin–aldosterone system (RAAS). RAAS activation results in synthesis of angiotensin II, a powerful vasoconstrictor that further potentiates the reduction in peripheral blood vessel capacity.

Collectively, these responses form a sympatho–endocrine–adrenal–axis that moderates the systemic response to shock. The axis maintains circulation to the vital organ system and combines with the inflammatory response to limit local and systemic tissue damage and ultimately confer a survival advantage. Combined responses include profound vasoconstriction, oligoanuria (fluid retention), redirection of blood flow to vital organs, hyperglycaemia, immunomodulation and procoagulation. This universal response to impending shock is particularly effective in compensating for loss of circulating blood volume, but may be counterproductive when pump failure occurs or ‘uncoupled’ in distributive shock states.

As adaptive responses fail, cardiac output becomes insufficient to provide adequate organ perfusion despite increasing tissue oxygen consumption (see Chapters 9 and 10). When oxygen is ‘supply dependent’, oxygen delivery is decreased and, to compensate, increased extraction occurs to enable continued tissue consumption. However, when oxygen delivery falls below a critical threshold, and extraction demand rises above the available blood oxygen levels, this compensation mechanism fails and oxygen debt results.^6,^11,¹²

Hypoperfusion may also exist despite a relatively normal cardiac output, and may not be immediately evident clinically.⁶ This maldistribution of bloodflow to some tissues while other areas receive more blood flow than needed,^4,^7,^10,^13,¹⁴ is often referred to as distributive shock, and is typical of the shock types that affect vasomotor tone (e.g. septic, neurogenic and anaphylactic shock). This maldistribution may leave some organ systems ischaemic for long periods leading to persistent organ dysfunction and failure.⁶ There is also evidence supporting the presence of cytopathic hypoxia as a result of excessive nitric oxide and tumour necrosis factor-alpha (TNFα) production (cellular proinflammatory mediators), where there is impaired mitochondrial (the powerhouse of the cell) oxygen utilisation which leads to depleted stores of adenosine tri-phosphate (ATP)^4,^11,^13,^15,¹⁶ and interferes with electron transport and metabolism¹⁶ (see Chapter 19). Nitric oxide is associated with vascular relaxation and is a major contributor to alterations in microvasculature and capillary leak in sepsis.¹⁷

Organ systems have varying responses in shock and are not measured directly. Often surrogate markers of global hypoperfusion are used to indicate the severity of shock.¹⁸^–¹⁹ Lactate and acid–base disturbances, such as an increase in strong ion gap, have been suggested as early markers of mitochondrial dysfunction and cellular hypoperfusion.^8,²⁰ These ‘surrogate’ biochemical markers of hypoperfusion (pH, serum lactate and standard base excess) assess acidaemia and provide some insight into the degree of shock present.²¹ Lactate, a strong anion with normal production of 1500–4500 mmol/day, is a product of carbohydrate metabolism. Increased levels are present in tissue hypoxia, hypermetabolism, decreased lactate clearance, inhibition of pyruvate dehydrogenase and activation of inflammatory cells; all characteristics of developing shock (see Table 20.2). Increased lactate production is a warning sign of impending organ failure, as it is indicative of anaerobic metabolism. Blood lactate levels have been directly linked to deteriorating patient outcomes in shock.^21,²²

TABLE 20.2 Lactate production ⁹

Lactate production
Product of carbohydrate metabolism (1400–4500 mmol/day)	Glucose, glycolysis; pyruvate, lactate
Rise in lactate levels
Tissue hypoxia	Hypodynamic shock Organ ischaemia

Hypermetabolism

Increased aerobic glycolysis

Increased protein catabolism

Haematological malignancies

Decreased clearance of lactate

Liver failure

Shock

Inhibition of pyruvate dehydrogenase

Thiamine deficiency

Endotoxin

Activation of inflammatory cells Phagocytosis

Wounds (e.g. trauma/burns)

Liver

Gastrointestinal

Lungs (e.g. ARDS)

Major source in sepsis Phagocytes

Lungs

Wounds

Liver: neutrophil sequestration increased, glucose uptake increased

Gut: prone to hypoxia, phagocytes

As the shock state deteriorates and the body fails to compensate, organ systems begin to fail. This is complicated by a systemic inflammatory response (SIRS) which can be a direct cause of the shock state (see section on Distributive shock) or develop as a consequence of protracted shock. This results in ‘capillary leak’ or increased microvascular permeability which leads to interstitial oedema as a consequence of alterations to tissue endothelium. Many immune mediators including circulating cytokines, oxygen free-radicals and activated neutrophils alter the structure of the endothelial cells, creating space to allow larger intravascular molecules to cross into the extravascular space,²³ with proteins and water moving from the intravascular space into the interstitium.²⁴ This response mechanism improves the supply of nutrient-rich fluid to the site of local injury, however, systemically, fluid shifts lead to hypovolaemia, impaired organ function and development of acute organ injury such as acute lung injury (ALI) and acute kidney injury (AKI).²⁴ This developing organ injury is the precedent to organ failure (more fully described in Chapter 21).

The next sections describe the general assessment and management of shock, different classifications of shock and specific management principles to avoid, or at least limit, tissue injury and the eventual progression to organ failure.

Patient Assessment

Critically ill patients often exhibit signs of tissue hypoxia as a result of cardiovascular disturbances.²⁵ Table 20.3 provides an overview of the physiological changes in shock. Therapy is targeted to maintain oxygen delivery (DO₂) to vital organs to prevent ischaemia and cell death.^25,²⁶ Ideally, organ systems and tissues should be monitored individually,²⁵ however global measures such as perfusion pressure, cardiac output (CO) and DO₂, are commonly used as surrogates to assist in treatment decision making.¹⁹ Patient assessment and haemodynamic monitoring, including calculation of CO, are used to differentiate shock states and assess progress in relation to treatment.²⁶^–²⁸ CO is seen by many clinicians as an important assessment of shocked patients as it is a major determinant of DO₂.^25,²⁶ Critically ill patients are frequently assessed clinically, although cardiac output estimations from physical examination are generally unreliable and patient status may change quickly.²⁹ Therefore invasive techniques are most commonly used in critical care to measure CO (see also Chapter 9).

TABLE 20.3 Physiological changes in shock ³⁷

Non-Invasive Assessment

Perfusion status is determined clinically using gross organ function such as mental status, urine output and peripheral warmth and colour.⁶ Basic physical assessment of cardiovascular, central nervous system and renal function are essential when assessing a patient at risk of shock. Subtle changes in urine output, heart rate and capillary refill are all signs of physiological compensation in response to altered tissue perfusion associated with shock. Regular tracking of these vital signs and trend monitoring through careful documentation can alert clinicians to impending deterioration in the shock state. Level of consciousness may deteriorate; an early sign may be anxiety, and progress to restlessness, agitation or coma. Other assessment findings include cool, clammy skin, postural hypotension, tachycardia and decreased urine output.³ The reliability of these measures is questionable, particularly where multiple assessments by different clinicians are performed; in the ICU continuous ECG monitoring and invasive monitoring techniques are employed to assist in the objective assessment of changes in cardiovascular state.

Although CO estimations based on physical assessment findings are unreliable, physical examination using an estimation of vascular resistance has shown reasonable accuracy.³⁰ Clinical assessment may determine CO using the rearranged equation of systemic vascular resistance (SVR = MAP − CVP/CO) where vascular resistance is measured through peripheral skin temperature changes.³⁰ A reliable and accurate non-invasive clinical assessment technique of estimating cardiac output would be clinically useful²⁷ allowing assessment of patients without invasive monitoring, or used to verify accuracy from invasive devices. While a number of non-invasive cardiac output measuring devices are available, further research and refinement is required before widespread application is considered in critical care.³¹

Invasive Assessment

Continuous assessment of heart rate and blood pressure by an intra-arterial catheter also enables circulatory access for frequent blood sampling to assess serum lactate levels, electrolytes and blood gas estimation including pH level.

The indicator dilution method using a thermal (thermodilution) signal (cold or hot) is the customary clinical standard for measuring CO ²⁶ in ICU. This is usually achieved by placement of a pulmonary artery catheter (PAC), or a central line in conjunction with a thermistor-tipped arterial cannula (transpulmonary aortic thermodilution). Other invasive techniques measure CO continuously using pulse contour or arterial pressure analysis and ultrasound doppler methods use an oesophageal probe. All methods have degrees of invasiveness, can be time-consuming to yield measurements of acceptable accuracy³², may be expensive and are not without risk of complications.^27,³³ The PAC is a controversial assessment tool^26,^28,³³ due to the risk associated with the invasive line versus benefits for the measurement of CO³⁴. This has led to increased interest in less or non-invasive measures of CO.

A further invasive assessment approach is the continuous estimation of mixed venous oxygen saturation using a light-emitting sensor in a PAC. As tissue oxygen delivery fails to meet demand and oxygen extraction rises, the residual oxygen content of blood returning to the lungs will fall; in effect a surrogate indicator of failure to meet body tissue oxygen demand. This technology was used in the landmark study by Rivers and colleagues.³⁵ to monitor early deterioration of septic shock patients presenting to the ED in need of resuscitation and was part of a goal-directed approach to managing patients. This single-centre US study has been the subject of much interest for its claimed improvement in patient outcome, with this goal-directed approach being assessed in a major multicentre study in an effort to verify its findings within an international context and varying approach to critical care delivery.³⁶

Management Principles

Managing a patient in shock focuses on treating the underlying cause, and restoration and optimisation of perfusion and oxygen delivery; this includes relevant activities using the acronym VIP ³⁷ (see Box 20.1). It is also suggested that giving critically ill patients a daily ‘FASTHUG’ improves the quality of care for patients in ICU.³⁸ Specific management of patients with shock are discussed separately below depending on the cause.

Box 20.1

VIP acronym ³⁷

• Ventilation, including airway, added oxygen and ventilation

• Infusion of appropriate volume expanders

• Improved heart Pumping with drug therapy such as antiarrhythmics, inotropes, diuretics, and vasodilators.

Practice tip

Fast hug mnemonic:³⁸

Feeding (prevent malnutrition, promote adequate caloric intake)

Analgesia (reduce pain, improve physical and psychological wellbeing)

Sedation (titrate to the 3Cs – calm, cooperative, comfortable)

Thromboembolic prophylaxis (prevent DVT)

Head of bed elevated (up to 45° to reduce reflux and VAP)

Ulcer prophylaxis (to prevent stress ulceration)

Glycaemic control (to maintain normal blood glucose levels)

Hypovolaemic Shock

Hypovolaemia is a common primary cause of shock and also a factor in other shock states. Insufficient circulating blood volume is the underlying mechanism, leading to decreased cardiac output and altered perfusion.^39,⁴⁰ Death related to haemorrhage is most likely in the first few hours after injury.⁴⁰ The most obvious cause is direct injury to vessels leading to haemorrhage, but there are more insidious causes such as dehydration from prolonged vomiting or diarrhoea, sepsis and burns.⁴¹ Hypovolaemic shock is classified as mild, moderate or severe, depending on the amount of volume loss (see Table 20.4). As the shock state worsens, associated compensatory mechanisms will be more pronounced,³ and hypovolaemic shock may deteriorate to Multi Organ Dysfunction Syndrome (MODS) if poor oxygen delivery is prolonged³⁹ (see Chapter 21).

TABLE 20.4 Signs and symptoms of hypovolaemic shock ³

Clinical Manifestations

Symptoms of haemorrhage may not be present until more than 15–30% of blood volume is lost, and will deteriorate as the shock state worsens.^3,⁴¹ Estimating blood or plasma loss is difficult and dilutional effects of resuscitation fluids may be evident when assessing haemoglobin and hematocrit.⁴¹ As the body compensates for the reduced circulating volume, widespread vasoconstriction occurs in most body systems apart from the heart and CNS; SVR rises markedly in an attempt to retain a viable circulatory system (this accounts for many of the signs and symptoms associated with circulatory compensation). However, as tissues are starved of oxygen and nutrients over a prolonged ischaemic time, local mediators are released as part of the inflammatory responses, leading to organ microvasculature vasodilation and capillaries re-open to maintain oxygen delivery and reduce hypoxia.⁴¹ This is a hallmark of developing MODS.

Nursing Practice

Clinical management of hypovolaemia centres on minimising fluid loss and rapid restoration of circulating blood volume ⁴¹ once the airway and breathing are secure. More than one large-bore intravenous cannulae are usually inserted and lost circulating volume is replaced by colloids, isotonic crystalloids or blood products to achieve haemodynamic endpoints (e.g. MAP >65 mmHg). Body heat can be lost rapidly due to blood loss, the rapid infusion of room temperature fluids and exposure in the pre-hospital setting or during repeated physical examination. It is therefore important to institute measures to maintain patient temperature >35°C to avoid coagulopathies and loss of thermoregulation.⁴² The aim is to ameliorate the lethal triad of anaemia, coagulopathy and hypothermia.⁴⁰^–⁴²

Debate surrounds early surgical intervention prior to aggressive fluid resuscitation.⁴⁰ The premise is that allowing a lower perfusion pressure prior to achieving haemostasis with controlled or no fluid infusion results in less blood loss, due to the compensatory mechanisms described above.⁴⁰ Use of medications such as Factor IVa and EPO also remains controversial in the setting of critical haemorrhage.⁴² Guidelines for ‘massive transfusion’ currently being finalised by the National Blood Authority (NBA) do not recommend use of Factor IVa beyond licensed indications, although there may be an indication when conventional therapy has failed to secure haemostasis following massive blood loss and transfusion of blood products. The current debate also includes dosage and thromboembolic complications associated with its use.⁴² The NBA is a statutory agency established in 2003 to improve and enhance the management of the Australian blood banks and plasma product sector. Current initiatives of the agency include development and promulgation of evidence based guidelines for both massive transfusion and intensive care.

Fluid resuscitation

Fluid resuscitation is a first-line treatment for hypovolaemic shock; providing fluid volume increases preload and therefore cardiac output (Starling’s law) and organ perfusion. A related principle is that the fluid infused should reflect fluid loss, e.g. plasma replacement in burns, fresh blood in massive haemorrhage. Giving a ‘fluid challenge’ is not always appropriate; the determining factors will be assessment of volume responsiveness, and whether the infusion will not be deleterious, causing overload, fluid shifts and perpetuating inflammatory responses.⁶ The fluid type, volume, rate and targeted endpoints is documented;⁴¹ often this is structured as a bolus dose in volume/kg to achieve a measured haemodynamic variable. When massive transfusion is required, attention should be given to product selection and hence a protocol can be employed.

Independent Practice

Critical care nurses must be efficient and practised at initial patient assessment to establish the degree of compensation occurring in a hypovolaemic patient. Figure 20.1 highlights clinical manifestations of haemorrhage. Careful consideration of a patient’s clinical picture will establish a hierarchy and priority of needs. Most hospitals have some level of track and trigger response that escalates care to appropriate levels (e.g. MET calling criteria), however nurses are in a position to establish first line management such as intravenous access where this is a required skill. There are also many examples of protocols and guidelines for nurses to initiate fluid resuscitation where a patient has indications of inadequate circulating blood volume; e.g. a fluid bolus up to 20 mL/kg of colloidor 30–40 mL/kg crystalloid may be recommended (depending on organisational guidelines).

FIGURE 20.1 Physiological derangements of massive blood transfusion.

Collaborative Management

Selection of the appropriate fluid indications for surgical management and ‘permissive hypotension’ (deliberate limiting or minimising resuscitation until after adequate surgical control of haemorrhage).^40,⁴² will be assessed by the multidisciplinary team. Goal-directed therapy includes prevention of tissue hypoxia, typically through rigorous fluid resuscitation with either crystalloids or colloids to achieve specific haemodynamic endpoints (e.g. a CVP of 8–12 mmHg, MAP >70 mmHg, urine output >0.5 mL/kg/h). Vasopressor and inotrope therapy may be then added to maintain adequate perfusion pressure; noradrenaline is the vasopressor of choice because of vasoconstrictor effects.⁴³

Preload management

The colloid versus crystalloid fluid resuscitation debate (use of albumin-based solutions or colloids) continues despite findings from the SAFE study conducted in Australasia; crystalloids (isotonic saline based solutions) were as effective as colloids for fluid resuscitation.⁴⁴^–⁴⁶ The scientific rationale for using colloids over crystalloids is to preserve plasma oncotic pressure so as to retain intravascular fluid and minimise oedema. Colloids may also attenuate the inflammatory response.²⁰ If moderate to severe hypovolaemia is suspected then blood is often used to improve oxygen-carrying capacity. Further dilution of blood by volume expanders increases hypoxia (otherwise known as isovolaemic anaemia) and red cells are usually needed. Use of isotonic saline as a volume expander is common, although resuscitation with large volumes of saline solutions can be associated with hyperchloraemic acidosis.⁴⁰ Blood and blood components are usually considered necessary where patients exhibit signs of moderate to severe haemorrhage (see Figure 20.2). There is no perfect resuscitation fluid, and selection is guided by patient condition and the type of fluid lost.

FIGURE 20.2 Indications for massive transfusion.

There are a number of factors to consider when administering blood products in massive volume. Massive transfusion is defined as replacement of a patient’s total blood volume in less than 24 hours (approximately 10 units of red cells);^47,⁴⁸ although the literature is inconsistent.⁴⁸ A number of complications are evident (e.g. transfusion reactions, coagulopathies, hypothermia, sepsis)³ and is associated with high mortality.⁴⁸ Patients receiving massive blood transfusions require careful monitoring for signs of metabolic derangements, hypothermia, citrate toxicity, hyperkalaemia and coagulopathies (due to depletion of clotting factors). Dilution and clotting factor consumption cause microvascular bleeding, often manifesting as oozing from multiple sites even after surgical correction.^47,⁴⁸ Massive transfusion of stored blood with high oxygen affinity adversely affects oxygen delivery to the tissues. It is therefore preferable to transfuse blood cells that are less than 1 week old; 2,3-diphosphoglycerate levels rise rapidly after transfusion, and normal oxygen affinity is usually restored within a few hours of transfusion.⁴⁷

Each unit of blood contains approximately 3 g of citrate, which binds to ionised calcium. A healthy adult liver metabolises 3 g of citrate every 5 minutes. If blood is transfused rapidly or the liver is impaired, citrate toxicity and hypocalcaemia may develop. The patient should therefore be monitored for signs of tetany, hypotension and electrocardiographic evidence of hypocalcaemia.⁴⁷ As stored blood ages, plasma potassium levels rise (possibly to over 30 mmol/L). Hypokalaemia may be more common as red cells begin active metabolism and intracellular uptake of potassium restarts with transfusion.⁴⁷

Acid–base disturbances may also be evident due to the stored blood lactic acid levels and the citric acid. Citrate metabolises to bicarbonate, and a profound metabolic alkalosis may result from massive blood transfusion. As hypothermia causes reduced citrate and lactic acid metabolism, an increase in the affinity of haemoglobin to oxygen, platelet dysfunction and an increased tendency for cardiac dysrhythmias,⁴⁷ the patient and the blood transfused should be warmed to avoid complications.

Leucocyte depletion occurs during donation in Australia and decreases up-regulation of the inflammatory immune response associated with transfusion. Current clinical practice guidelines for the administration of blood products and red cells to stable adult patients are listed in Tables 20.5 and 20.6. A new structure with multiple guidelines has been developed and the massive transfusion guideline is complete and will be followed by a number of other specialised guidelines. All guidelines will be available to download from the National Blood Authority website as they are completed (see Online resources).

TABLE 20.5 Clinical practice guidelines for red blood cell and platelet administration

Appropriate Use of Blood Components For Stable Adults & Children >4 months (corrected) age Adapted from NHMRC/ASBT guidelines (www.anzsbt.org.au) Haemoglobin is NOT the sole deciding factor for transfusion – consider other patient factors e.g. signs of hypoxia and ongoing blood loss.
Red Cells
Hb	Considerations
<70 g/L	Transfusion is often clinically useful unless early Hb recovery is expected. A threshold of <60 g/L may be appropriate for children.
70–100 g/L	Likely to be appropriate during surgery with major blood loss or if there are signs or symptoms of impaired oxygen transport.
>80 g/L	May be appropriate to control anaemia-related symptoms in a patient on a chronic transfusion regimen or during marrow suppressive therapy.
>100 g/L	Not likely to be appropriate unless there are specific indications
	WHAT DOSE? Red Cells (mL) = 0.4 × wt (kg) × (desired – actual) Hb (g/L)
Platelets
	Use of platelets is likely to be appropriate as prophylaxis for:
Indication	Considerations
Bone Marrow Failure	At a platelet count of <10 Ö 109/L in the absence of risk factors and <20 Ö 109/L in the presence of risk factors (e.g. fever, antibiotics, evidence of haemostatic failure)
Surgery/Invasive	To maintain platelet count at >40 Ö 109/L. For surgical procedures with high risk of bleeding (e.g. ocular or neurosurgery) it may be procedure appropriate to maintain at 100 Ö 109/L
Platelet Function Disorders	May be appropriate in inherited or acquired disorders, depending on clinical features and setting. In this situation, platelet count is not a reliable indicator
	Use of platelets is likely to be appropriate as therapy for:
Bleeding	Any patient in whom thrombocytopenia is considered a major contributory factor.
Massive Bleeding/Transfusion	Confined to patients with thrombocytopenia and/or functional abnormalities who have significant bleeding. Often with platelet count <50 Ö 109/L (<100 Ö 109/L with diffuse microvascular bleeding).

TABLE 20.6 Adverse reactions to blood products

Cardiogenic Shock

Cardiogenic shock manifests as circulatory failure from cardiac dysfunction,⁴⁹ and is reflected in a low cardiac output (CI <2.1 L/min/m²), hypotension (SBP <90 mmHg) and severe pulmonary congestion, high central vascular filling pressures (CVP; PAOP >18 mmHg).⁵⁰ Additional invasive parameters are: intrathoracic blood volume index >850 mL/m²; global end-diastolic volume >700 mL/m²; and extravascular lung volume index >10 mL/kg.^51,⁵² Cardiogenic shock is commonly associated with AMI and manifests when 40% or more of the left ventricle is ischaemic. It is also related to mechanical disorders (e.g. acute cardiac valvular dysfunction or septal defects), deteriorating cardiomyopathies or congestive cardiac failure,^53,⁵⁴ trauma and obstruction or inhibition of left ventricular ejection (referred to as obstructive shock e.g. pulmonary emboli, dissecting aneurysm, tamponade)^37,⁵³ (see Chapter 10). Myocardial depression from non-cardiac causes such as sepsis, acidosis, myocardial depressant factor, hypocalcaemia or drug impact⁵⁵ may be so severe as to present as cardiogenic shock.

Incidence has been estimated at 3% of patients presenting with AMI, and mortality remains high (50–80%),⁵⁶ given death from AMI overall is 7%. This is despite treatment advances including emergency revascularisation.^57,⁵⁸ Wider distribution of interventional cardiac revascularisation services has likely improved outcome for patients who present early in the course of their acute disease.

Clinical signs include poor peripheral perfusion, tachycardia and other signs of organ dysfunction such as confusion, agitation, oliguria, cool extremities, dyspnoea, many of which are present in hypovolaemic shock.⁴⁹ Compensatory mechanisms are conflicting for a patient with cardiogenic shock, as cardiac workload is increased on an already-failing heart yet cardiac muscle oxygen delivery may be compromised.⁵⁴ A careful but rapid assessment of the clinical history is helpful in differentiating the precipitant cause of this shock.

Managing patients with heart failure as a result of cardiogenic shock can be challenging and is often undertaken simultaneously with preparation for definitive treatment. Maintaining perfusion is difficult, as compensatory mechanisms usually cause further harm to the heart. While judicious administration of fluid is considered in terms of optimising remaining cardiac function (Starling’s Principle), administration of pharmacological agents that reduce cardiac workload and improve function is paramount: dobutamine for inotropic and afterload-reducing effects via vasodilation; and morphine to reduce pain, improve coronary perfusion and reduce oxygen demand. Treatment of the underlying cause is again critical; this may include surgery to repair obstruction to flow or percutaneous resolution of a coronary artery blockage.

Clinical Manifestations

The clinical features of cardiogenic shock are reflective of congestive cardiac failure, although with greater severity:^50,^51,⁵⁸

Features consistent with the cause of the cardiogenic shock may also be present, including chest pain and ST segment changes, murmurs, features of pericardial tamponade and arrhythmias.

In the absence of invasive monitoring, the profile of hypotension, peripheral hypoperfusion, and severe pulmonary and venous congestion are evident although this ‘classic’ profile is not universal. On initial examination, 30% of patients with shock of left ventricular aetiology had no pulmonary congestion and 9% had no hypoperfusion.⁵⁹

Based on the underlying pathology of an acute left ventricular myocardial infarction, the structural or contractile abnormality impairs systolic performance resulting in incomplete left ventricular emptying.⁵⁰ This results in subsequent progressive congestion of first the left atrium, then the pulmonary circulation, right ventricle, right atrium and finally the venous circulation.^50,^60,⁶¹ When invasive haemodynamic monitoring is available, sequence of changes exist as illustrated in Figure 20.3.

FIGURE 20.3 Sequence of haemodynamic changes in cardiogenic shock ( ↑ = increase, ↓ = decrease).

A patient with cardiogenic shock is also assessed and monitored for their oxygen delivery and tissue oxygen requirements (oxygen consumption). Systemic DO₂ falls in proportion to a declining cardiac output, and is further worsened as hypoxaemia develops due to pulmonary oedema. Initially, VO₂ may be sustained by an increase in tissue oxygen extraction ratio (O₂ER).⁶² Normally 25% of delivered oxygen is extracted by tissues, but as delivery falls, tissues extract proportionally more oxygen to meet metabolic needs. Oxygen consumption can therefore be sustained until the severity of oxygen delivery deficit exceeds the ability to increase extraction. Maximal extraction is approximately 50%, and consumption falters when oxygen delivery falls to around 500–600 mL/min (cardiac index <2.2 L/min/m²).⁶²^–⁶⁴ While use of a PAC is a well-described measure of severity in cardiogenic shock (as with hypovolaemic shock), evidence of improved patient outcome is unclear.^28,⁶⁵

Once oxygen consumption falls below tissue needs, resulting anaerobic metabolism causes lactate generation and the subsequent lactic acidosis.^50,⁶² Progressive tissue ischaemia and injury ensues, along with worsening metabolic acidosis unless oxygen delivery can be restored. Myocardial contractile performance further worsens when myocardial ischaemia develops or when existing ischaemia or infarction is worsened, and a vicious cycle of ischaemia and dysfunction ensues.⁶²

Compensatory responses effective in lessening severity of hypovolaemic shock are initially advantageous, but may ultimately be counterproductive when cardiogenic shock is due to myocardial infarction:

• Tachycardia offsets low stroke volume but increases myocardial oxygen consumption and decreases diastolic duration, reducing coronary perfusion time.

• Vasoconstriction limits the severity of hypotension but increases resistance to left ventricular emptying and may contribute to worsening of the cardiac output, in particular when cardiogenic shock is due to contractile dysfunction.

• An increase in cardiac workload to overcome the rise in systemic afterload increases myocardial oxygen demand, but cannot be met due to coronary artery occlusion.

• Developing pulmonary congestion is no longer contained within the pulmonary capillary and moves into the alveolar capillary space, creating pulmonary oedema, further impeding oxygen delivery to the circulation.

Nursing Practice

Treatment of cardiogenic shock includes haemodynamic management, respiratory and cardiovascular support, biochemical stabilisation and reversal or correction of the underlying cause. This complex presentation requires a coordinated approach to the multiple aspects of care of a patient with cardiogenic shock.

• IV diuretics (frusemide)⁶⁸ given usually as intermittent boluses or if necessary as a continuous infusion

• venodilation (glyceryl trinitrate infusions at 10–200 µg/min titrated to blood pressure)⁶⁹

• continuous haemofiltration (might be considered to rapidly reduce circulating volume)

• continuous positive airway pressure (indicated for pulmonary relief, with the additional benefit of reducing venous return).

Additional measures to reduce pulmonary hypertension may be employed. Morphine is useful to lessen the anxiety and oxygen demands during cardiogenic shock, and may offer additional benefits by reducing pulmonary artery pressure and pulmonary oedema.⁶⁸ Other treatment options include correction of hypercapnoea if present, and nitric oxide by inhalation.

Inotropic therapy

Intravenous positive inotropes promote myocardial contractility to improve cardiac output and blood pressure. Currently available inotropes are not uniform in their beneficial effect on cardiac output and blood pressure because of additional vasoactive actions (either vasodilation or constriction) (see Table 20.7). Selection of an inotropic agent is therefore partly based on inotropic potency as well as the desired effect on vascular resistance:

• vasodilation in addition to inotropy (inodilator effect) favours cardiac output, but may compromise blood pressure ⁷⁰

• vasoconstriction in addition to inotropy (inoconstrictor effect) improves blood pressure, but may at times compromise left ventricular emptying and cardiac output.

TABLE 20.7 Inotrope drug actions and characteristics ⁷⁰^–⁷³

All inotropes present a paradox in the treatment of cardiogenic shock, as they have the potential to raise heart rate, increase myocardial oxygen demands, and increase the frequency of arrhythmias to a greater or lesser extent. Monitoring is used to identify heart rate, rhythm and the development of ST segment or T wave changes.

The vasodilation seen with inodilator agents may reduce both preload and afterload, leading to more effective myocardial pumping and an increased cardiac output. The effect on blood pressure is variable, as the opposing actions of increased contractility and vasodilation are not uniform in potency, and occur with differing effects between patients. Inodilators are generally selected when a patient has an elevated afterload and low cardiac output.⁷⁰ By reducing afterload, left ventricular emptying is favoured with a reduction in cardiac contractility, reducing myocardial oxygen demand. Inodilators are therefore preferred in ischaemic cardiogenic shock.⁷¹^–⁷³

In contrast, inoconstrictors constrict the vasculature, resulting in increased preload and afterload while also increasing myocardial contractility.⁷⁰ These increases, particularly in afterload, generally result in a raised blood pressure, but the impact on cardiac output is less predictable. An increase in cardiac output is often seen with these agents, but the increase in afterload may become limiting to left ventricular emptying when there is significant contractile impairment. Inoconstrictors are therefore generally selected when the afterload and resultant blood pressure are more severely compromised than the cardiac output. Vasoconstriction also further increases myocardial work and myocardial oxygen demand, and may worsen ischaemia.⁷⁴

Dobutamine has traditionally been the inodilator of choice,⁷⁵ although accumulating evidence for levosimendan, a calcium-sensitising agent, suggests improved outcomes.^71,⁷³ However, the slow onset of action time of levosimendan (hours) makes it a less suitable drug for acute resuscitation; other inotropes are therefore currently used initially and if required, levosimendan is then introduced. The long half-life (>5 days) of levosimendan confers a lasting impact on contractility after cessation of the infusion. Milrinone is also an effective inodilator,⁷⁰ but excessive vasodilation may contribute to significant hypotension; in practice a concurrent vasoconstrictor (e.g. noradrenaline) may be administered. Close management of intravascular fluid volume is critical when using these agents.

Dopamine and adrenaline are the major agents in the inoconstrictor class, and are more effective at raising blood pressure than inodilators. Both agents also increase cardiac output, but when there is significant impairment of contractility the increase in afterload may cause cardiac output to suffer. Importantly, inoconstrictors increase myocardial work and oxygen demands, raise heart rate, and increase the risk of tachyarrhythmias; these impacts are stronger with adrenaline than for dopamine.

Afterload control

Specific management of afterload, independent of contractility, is sometimes necessary, although caution is needed as the maintenance of blood pressure often provides little scope for further afterload reduction. Arteriodilators such as sodium nitroprusside reduce afterload and increase cardiac output, although with limitations due to hypotension.⁷⁶ The introduction of oral angiotensin-converting enzyme (ACE) inhibitors as soon as possible after stabilisation of the patient with infarct-related cardiogenic shock is strongly recommended.^77,⁷⁸

Adjunctive therapies

A range of adjunctive therapies are available for refractory shock, when first-line treatments are not effective, and can include insertion of an intraaortic balloon pump, initiation of mechanical ventilation and correction of metabolic disturbances. These strategies are discussed below in relation to cardiogenic shock.

Intra-aortic balloon pumping

Low cardiac output, pulmonary congestion, reduced MAP, and myocardial ischaemia from cardiogenic shock may all be improved by the introduction of intra-aortic balloon pump (IABP) therapy (see Chapter 12). Balloon inflation during diastole raises MAP and promotes coronary and systemic blood flow, while balloon deflation in advance of systole reduces afterload. This afterload reduction improves cardiac output and reduces left ventricular systolic pressure, lessening the oxygen demands of the ischaemic ventricle by reducing the necessary contractile force of the left ventricle.

Respiratory support

Varying degrees of pulmonary oedema accompany cardiogenic shock, causing hypoxaemia due to intrapulmonary shunt, decreased compliance and increased work of breathing (WOB). Hyperventilation with respiratory alkalosis may initially compensate for hypoxaemia and lactic acidosis, but fatigue during this increased WOB may cause patient progression to hypoventilation and respiratory acidosis. Oxygen is administered for hypoxaemia, but responses may be limited as the primary gas exchange defect is an intrapulmonary shunt. Non-invasive ventilatory approaches may be sufficient, but a wary eye for the need to intubate and mechanically ventilate should be maintained in the acute phase of treatment. CPAP at conventional levels of 5–15 cmH₂O is well established as a support for the spontaneously breathing patient with pulmonary oedema.⁷⁹ CPAP improves hypoxaemia, lessens WOB, reduces left ventricular afterload and provides additional benefit by impeding venous return, an effect that may lessen pulmonary congestion. These benefits are weighed against the potential for hypotension.

If hypoventilation and dyspnoea continue despite the use of CPAP, non-invasive bi-level positive airway pressure (BiPAP) is considered. Additional pressure support is applied during inspiration, above existing CPAP, improving inspiratory efficiency, with increased tidal volume and less work of breathing.^66,⁸⁰ Endotracheal intubation and ventilation should be undertaken when neither CPAP nor BiPAP result in improvement, or when the patient continues to deteriorate or tire. Many clinicians prefer to intubate and ventilate early, even in the absence of a specific respiratory need, to decrease the cardiovascular demands of the greater ventilatory effort. However this approach is controversial as mechanical ventilation is associated with poorer patient outcomes⁸¹ and disturbs cardiovascular balance as it exerts changes to intrathoracic pressures, particularly at inspiratory initiation.

Ventilation strategies largely reflect those for other compliance disorders (e.g. ARDS), and are described in more detail in Chapter 15. Initially, full mechanical ventilation with little or no contribution from the patient is appropriate to correct arterial blood gases and lessen the cardiovascular demands of the ventilatory burden. Subsequent reduction of ventilatory support, as the patient’s respiratory ability improves, follows conventional processes.

Biochemical normalisation

Frequent biochemistry measurement is necessary to detect and monitor the following aspects of care:

• arterial blood gases to identify the adequacy of ventilation and oxygenation and the presence of metabolic acidosis

• lactic acid measurement to assess the level of shock and changes in patient response to treatment

• hypokalaemia or hypomagnesaemia due to aggressive diuretic use

• hyperkalaemia due to severe acidosis, especially in the presence of renal failure

• hyperglycaemia due to the stress response to acute illness, and in response to sympathomimetic administration

• bicarbonate levels decline due to pH buffering, but replacement therapy is not routinely undertaken unless the arterial pH is life-threatening

• urea and creatinine to detect the onset of acute renal failure due to renal hypoperfusion.

Haemofiltration-based therapies (as slow continuous ultrafiltration, continuous veno-venous haemofiltration or haemodialysis) are used for fluid and electrolyte control when renal function suffers or as acute method for unloading fluid from the circulation (see Chapter 18).

Distributive Shock States

Distributive shock states result in impaired oxygen and nutrient delivery to the tissues as a result of failure of the vascular system (the blood distribution system). While there may be additional factors (e.g. infection) beyond simple failure to provide sufficient perfusion to the capillary bed due to widespread vascular dilation, the common factor for all underlying causes of distributive shock is widespread failure of the vasculature. The most common categories of distributive shock are associated with systemic inflammatory response syndrome, anaphylaxis and neurogenic shock.

Sepsis and Septic Shock

Systemic Inflammatory Response Syndrome (SIRS) was a term developed to describe the clinical manifestations of many processes characterised by systemic inflammation including sepsis, burns, pancreatitis and trauma.⁸² This definition was however limited and problematic as it described general signs and was non-specific.^83,⁸⁴ Despite a revision in 2001,⁸⁴ SIRS was viewed as a valid descriptor but not useful for clinical diagnosis in that form. It was however noted that the use of the SIRS definition in sepsis to aid in early identification was important. Signs and symptoms were subsequently added to SIRS in response to infection (sepsis): hyperglycaemia, altered mentation, generalised oedema, as well as a number of inflammatory, haemodynamic, organ dysfunction and tissue perfusion variables. A staging system (PIRO) was also introduced to profile the processes in septic patients⁸⁵ (see Table 20.8).

TABLE 20.8 PIRO acronym ⁸⁵

Predisposition	Factors that dispose certain patient groups to be more susceptible to infection and organ dysfunction, including genetic predisposition, age, and comorbidities like alcohol use and diabetes.
Infection	Type of infecting organism. How is it diagnosed? How severe is the infection? Is it local or general? What is the site of infection and the related outcomes? Hospital/ICU or community-acquired?
Response	Stratify severity, using biomarkers (e.g. IL-6 or procalcitonin) to gauge severity of the inflammatory/immune responses, and to predict how patients will respond and potential outcomes. Also assess ABGs, lactate levels, WBC, temperature, C reactive protein.
Organ dysfunction	Describe using either physiological levels or level of intervention. Use scoring systems to quantify level (mild, moderate, severe) and predict outcomes.

Severe sepsis and septic shock is a leading cause of admission to ICU and has an associated high mortality. The terms ‘severe sepsis’ and ‘septic shock’ were defined and then refined during international consensus meetings that also described SIRS ^82,⁸⁴ (see Table 20.9 and Chapter 21). The incidence of severe sepsis in Australia and New Zealand was 11.8% of ICU admissions, with median ICU and hospital stays of 6 days and 18 days respectively, and corresponding mortality rates of 32% at 28 days and an in-hospital mortality of 40%.⁸⁶ A Victorian epidemiological study reflected similar results.⁸⁷ More recent Australian data shows mortality remaining relatively high but in decline.^36,⁸⁸ The consequence of this high mortality focused attention on sepsis and its associated sequelae in the critical care literature, and led to a worldwide campaign in 2002 to reduce the mortality from sepsis.

TABLE 20.9 Sepsis, severe sepsis and MODS definitions ^82,⁸⁴

Term	Definition
Infection	• Characterised by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms. • Bacteraemia: the presence of viable bacteria in the blood.

SIRS

• A non-specific syndrome that results from a wide variety of severe clinical insults; present with two or more of the following:

• temperature >38°C or <36°C

• heart rate >90 beats/min

• respiratory rate >20 breaths/minute or PaCO₂ <32 mmHg

• WBC count >12 000/mm³ or >10% immature (band) forms.

• Other signs include: altered mental status, positive fluid balance or significant oedema, hyperglycaemia in the absence of diabetes, raised procalcitonin and/or C reactive protein, hypotension, hypoxaemia, acute oliguria, raised serum creatinine, coagulation abnormalities, ileus, thrombocytopenia, hyperbilirubinaemia, hyperlactaemia, decreased capillary refill/mottling.

Sepsis

• Systemic inflammatory response to infection. Manifestations of sepsis are the same as defined for SIRS. Determine if symptoms are a result of a direct systemic response to an infectious process and represent an acute alteration from baseline in the absence of other known causes for the abnormalities.

Severe sepsis

• Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Hypoperfusion abnormalities and perfusion abnormalities may include but are not limited to lactic acidosis, oliguria or acute alteration in mental status.

Septic shock

• A subset of severe sepsis; sepsis-induced hypotension (a systolic blood pressure <90 mmHg or a reduction of ≥40 mmHg from baseline) in the absence of other causes, despite adequate fluid resuscitation, and perfusion abnormalities (e.g. lactic acidosis, oliguria, acute alteration in mental status). Patients receiving vasopressor or inotropic agents may not be hypotensive by the time they manifest hypoperfusion abnormalities or organ dysfunction, but are still considered to have septic shock.

• Acute circulatory failure with persistent arterial hypotension unexplained by other causes and despite adequate fluid resuscitation (see also sepsis-induced hypotension).

MODS

• Presence of altered organ function in an acutely ill patient where homeostasis cannot be maintained without intervention.

MODS = multiple organ dysfunction syndrome; SIRS = systemic inflammatory response syndrome.

The Surviving Sepsis Campaign

The Surviving Sepsis campaign is an international collaborative formed after the Barcelona Declaration in 2002 to reduce the mortality of sepsis by 25% over a 5-year period, by increasing awareness and developing treatment guidelines for severe sepsis and shock, including a comprehensive list of graded recommendations.^89,⁹⁰

Various recommendations were combined to form ‘care bundles’ (‘a group of interventions related to a disease process that, when executed together, result in better outcomes than when implemented individually’)⁹¹^{, p.5} and promulgated through professional organisations (e.g. Institute of Healthcare Improvement [IHI]). Bundles have been introduced to change processes of care and as quality or benchmarking measures (see Chapter 3). Although the first version of the sepsis guidelines was supported by ANZICS, the subsequent and much expanded version was not,⁸⁸ as many of the recommendations were based on research involving non-ICU and/or non-sepsis patients. Further research and evaluation is needed as mortality benefits of ‘care bundles’ may be a result of increased clinician awareness rather than the impact of treatment changes.⁹²

An example of a refuted bundle relates to tight glycaemic control. The recommendation in the surviving sepsis guidelines supported tight glycaemic control and originated from research where the glycaemic control practice differed from Australia and New Zealand.⁹³ The NICE-SUGAR study subsequently concluded that measures to maintain blood glucose level of ≤10 mmol/L increased mortality particularly in relation to severe hypoglycaemia.⁹⁴ A recent meta analysis of 26 ICU related ‘tight glycaemic control’ studies, suggested that the practice could increase risk to ICU patients.⁹⁵ The more pragmatic approach of maintaining blood glucose levels close to normal without inducing hypoglycaemia and other metabolic imbalances is therefore appropriate.⁹⁶ The guideline was subsequently modified in 2009 to include findings from NICE-SUGAR.⁹⁷

Clinical Manifestations

Septic shock results when infectious agents or infection-induced mediators in the blood stream produce haemodynamic compromise. Primarily a form of distributive shock, it is characterised by ineffective tissue oxygen delivery and extraction associated with inappropriate peripheral vasodilation, despite preserved or increased cardiac output.⁹⁸ Hypovolaemia is also associated with septic shock due to the characteristic increased vasodilatation. This presents a clinical picture of a warm, pink and apparently well-perfused patient in early stages of septic shock with an elevated cardiac output, in contrast to that seen in hypovolaemic or cardiogenic shock patients.

Unchecked, cellular dysfunction in the presence of a failing compensatory process leads to cellular membrane damage, loss of ion gradients, leakage of lysosomal enzymes, proteolysis due to activation of cellular proteases and reductions in cellular energy stores which may result in cell death. Once enough cells from vital organs have reached this stage, shock becomes irreversible and death can occur despite eradication of the underlying septic focus. About half of the patients who succumb to septic shock die of failure of multiple organs.⁹⁸

The effect of sepsis and septic shock on the cardiovascular system is profound; the haemodynamic hallmark is generalised arterial vasodilation with an associated decrease in systemic vascular resistance. Arterial vasodilation is mediated in part by cytokines that upregulate the expression of inducible nitric oxide synthase in the vasculature. Vascular response to the vasodilatory effect of nitric oxide and the activation of ATP-sensitive potassium channels combine to cause closure of the voltage-gated calcium channels in the cell membrane. As the vasoconstrictor effect of noradrenaline and angiotensin II depend on open calcium channels, lack of response to these pressor hormones that are central to compensatory mechanisms in shock can occur with the inevitable failure of delivery of oxygen to the functional mitochondria resulting in lactic acidosis in patients with sepsis.⁹⁹ With high circulating levels of endogenous vasoactive hormones during sepsis, downregulation of their receptors occurs.

Nursing Practice and Collaborative Management

As with other forms of shock, initial management includes not only acting to correct physiological deterioration by initiating fluid management and frequent observation and assessment, but also addressing the underlying cause of sepsis through source (of infection) control.

Initial Management: Fluid Resuscitation

Measuring surrogate markers of preload as an indicator of volume status is a contentious issue, as CVP as a measure of preload is not a good marker of volume responsiveness.^32,¹⁰⁰ While CVP was used in sepsis trials of early goal-directed therapy (EGDT) protocols^35,¹⁰¹^–¹⁰³ and is an often documented endpoint of resuscitation, EGDT has been widely discussed and criticised in the literature. Australian data indicates that the incidence of patients meeting the criteria and mortality is lower than the treatment group in the original EGDT trial.³⁶ This is currently the focus of a large trial by the ANZICS Clinical Trials Group (ARISE).³⁶

Fluid resuscitation with crystalloid or colloid has long been controversial in the critical care literature. The landmark Saline versus Albumin Fluid Evaluation (SAFE) study ⁴⁴ demonstrated that in the adult intensive care patient population, albumin can be considered safe, without demonstrating any clear advantage over saline. In the study conducted in 14 Australian and 2 New Zealand ICUs, 6997 patients were randomised to receive either saline (n = 3500) or albumin (n = 3497). No significant differences were noted between the two treatment groups for 28-day all-cause mortality, days in intensive care, days in hospital, days on mechanical ventilation and days of renal replacement therapy.⁴⁴ The Surviving Sepsis Campaign guidelines do not advocate one preferred resuscitation fluid.⁸⁹ Irrespective of fluid selection, the disruption of the vascular bed in early septic shock through widespread vasodilatation results in increased capillary permeability and rapidly developing interstitial oedema. Large amounts of fluid can be administered without seemingly improving oxygen delivery whilst adding to developing generalised oedema which further impairs cellular delivery of oxygen and nutrients. Fluid resuscitation alone is therefore of limited value in septic shock and other measures must be considered.

Initial Management: Diagnosis, Source Control and Antimicrobial Therapy

Identifying and removing the source of infection and treating the infection with appropriate antimicrobial therapy are the mainstays of therapy for a patient with sepsis. Australian data indicate that in the ICU setting the most prevalent site of primary infection is pulmonary, followed by abdominal, together accounting for 70% of cases.⁸⁶ Similar epidemiology is reported in international sepsis studies.^104,¹⁰⁵ In 2005, ICU pneumonia practices were studied in 14 ICUs and demonstrated a ventilator associated pneumonia (VAP) incidence of 28%.¹⁰⁶ A further cohort study comparing Australian and Danish hospitals noted a lower incidence of VAP with a concomitant increase in broad spectrum antibiotics prescribed based on clinical signs and multiresistant organisms at the Australian site.¹⁰⁷

To provide patients with appropriate antimicrobial treatment for targeting the infecting organism, obtaining appropriate samples prior to instigating antimicrobial therapy is the clinical standard, although any prescribed treatment should not be delayed as time to antibiotic administration is important in severe sepsis.¹⁰⁸ In one large retrospective study, every additional hour to effective antimicrobial initiation in the first 6 hours after onset of hypotension was associated with >7% decrease in survival.^108,¹⁰⁹ Optimising dosage to achieve a therapeutic concentration is also important. Current practice is to continuously infuse glycopeptides to maintain a serum concentration above the minimum inhibitory concentration and therefore kill microbes more effectively. More recently there has been evidence that β-lactams should also be infused.¹¹⁰ Recently a paradigm shift has been suggested in relation to antimicrobial therapy; to get it right the first time with high doses, while limiting the duration of therapy and the potential to increase resistance.¹¹¹

Where a patient is able to respond appropriately during history and physical assessment, timelines of the infective process should be documented. Sites considered as infective sources include decubitus ulcers, invasive lines, drains, wounds, sinuses, ears, teeth, throat, chest, blood, lungs, back, abdomen, perianal, genital/urinary tract, bones and joints. More invasive sampling may include bronchioalveolar lavage, CSF, pleural fluid, abdominal collections or biopsy of other sites as clinically appropriate. X-rays, CT Scans and surgical consultation will also be a priority.

Minimum continuous monitoring includes ECG, blood pressure, pulse oximetry and other measures to assess preload and volume responsiveness, along with regular assessment of lactate, oxygenation and markers of inflammation and coagulation.

Ongoing Collaborative Management: Drug Therapy

A range of drug therapies aimed at supporting and ameliorating the signs and symptoms of septic shock are available and whilst inotropes in particular provide an important adjunct in managing the acute shock phase, other drug therapies remain controversial.

Inotropes and vasopressors

A goal of maintaining MAP greater than 65 mmHg is common, with inotropes and vasopressors commenced when fluid resuscitation is considered adequate. Administration of these drugs requires continuous blood pressure monitoring and enables effective titration to meet the treatment goal. Australian practice preferences noradrenaline (for its specific alpha-receptor effects) and adrenaline as the vasopressors of choice. Dobutamine (2.5–10 mcg/kg) is often added to support patients with myocardial dysfunction to increase myocardial contractility and oxygen delivery to the tissues.⁹⁰ Refractory hypotension, resistant to vasopressors, has been linked to downregulation of receptors. Vasopressin (0.4–0.6 units/hour) has been shown to reduce the requirements of other vasopressor agents.

Administration of arginine vasopressin in vasodilatory shock may help maintain blood pressure despite the relative ineffectiveness of other vasopressor hormones.⁹⁹ Specifically, arginine vasopressin may inactivate the KATP channels and thereby lessen vascular resistance to noradrenaline and angiotensin II. It also decreases the synthesis of nitric oxide (as a result of a decrease in the expression of nitric oxide synthase) as well as cyclic guanosine monophosphate (cGMP) signalling by nitric oxide.⁹⁹ The sites of major arterial vasodilation in sepsis – the splanchnic circulation, the muscles and the skin – are vascular beds that contain abundant arginine vasopressin receptors. In sepsis, vasopressin stores are quickly depleted. Administration of exogenous arginine vasopressin (0.04–0.06 units/min) can raise blood pressure by 25–50 mmHg by returning plasma concentrations of antidiuretic hormones to their earlier high levels.⁹⁹

Steroids

The use of steroid therapy in severe sepsis remains controversial. At times, steroid replacement therapy may be used when patients display resistance to increasing doses of adrenergic agonists, i.e. adrenal insufficiency. Some research indicates that patients with septic shock that are unable to increase cortisol levels in response to a challenge may benefit from administration of low-dose corticosteroids ¹¹² (see Chapters 19 and 21 for further information).

Recombinant human activated protein C

Activated protein C is a plasma protease produced in response to thrombin formulation. Actions of activated protein C include:

• decreased inflammation through reduced levels of TNFα and NFKβ

• decreased thrombin production leading to anticoagulation

• profibrinolytic action through modulation of fibrinolysis inhibitors.

Drotrecogin alfa-activated (rhu), a recombinant form of activated protein C, was developed using DNA recombinant technology as a treatment for sepsis. Previous drug trials had targeted particular aspects of the host response to sepsis but had not yielded positive results. Preclinical studies devised dose-dependent reductions in the markers of fibrinolysis (d-dimer) and inflammation (Interleukin 6) leading to a Phase III clinical trial which resulted in drotrecogin alfa-activated rhu being the first drug approved for the treatment of severe sepsis. The published phase III trial was a large multi-centre, double-blind randomised controlled trial (PROWESS);¹¹³ this landmark study was the first drug trial to demonstrate a positive result in the treatment of severe sepsis. PROWESS was conducted in 11 countries with the hypothesis that administration of drotrecogin alfa at 24 mcg/kg/min for 96 hours would reduce 28-day all-cause mortality in patients with severe sepsis, with an acceptable safety profile.

Controversy followed publication of the PROWESS paper and licensing of drotrecogin alfa. A further study, ADDRESS, mandated by the Food and Drug Administration in the USA to investigate the effect of the drug on patients with a low risk of death, was stopped prematurely due to futility and an increased risk of significant bleeding. Studies on children were also stopped due to the unacceptable risk profile. An open label trial, ENHANCE,¹¹⁴ was then conducted to replicate the results of PROWESS; the Australian data indicated that depending on the selection criteria used, up to 8% of patients may be eligible for treatment with drotrecogin alfa (activated).¹¹⁵ Evidence for use remains equivocal. Use is currently rare and where used in severe sepsis, preparation and administration requires additional education and continual assessment and specific attention to signs of bleeding including cerebral haemorrhage.

Other adjuncts

Adequate nutritional support to offset high caloric and protein demands is relevant with enteral feeding preferred. Translocation of gut bacteria due to splanchnic hypoperfusion and increased permeability is a factor in secondary septic insults and stress ulceration.¹¹⁶ Equally important to patient-specific measures is institution of diligent infection control practices in ICU.¹¹⁷ For more information on organ support refer to the relevant chapters in Section II and Chapter 21.

Anaphylaxis

Anaphylaxis is the most severe, potentially life-threatening form of an allergic reaction,¹¹⁸^–¹²¹ usually as a type I hypersensitivity classification (IgE-mediated hypersensitivity).¹²¹ Anaphylaxis appears rare,¹²⁰ although data are sporadic in the literature; 0.01–0.02% of the general population is affected.¹²¹ Anaphylaxis appears more common in Western countries, but this may be related to more thorough reporting mechanisms.¹²² The prevalence of allergy with anaphylaxis has been documented as high as 7% in one Australian study of children, with insect stings, oral medications or food the most often cited causes. However, in this study, less than 1% of the population actually suffered an anaphylactic reaction manifesting with generalised multisystem allergic reaction, including evidence of airway involvement, rashes, GIT and cardiovascular dysfunction.¹²³

This allergic response is via a host mast-cell reaction mediated by immunoglobulin E (IgE),¹¹⁸ and an antibody produced in response to the allergen that is attached to basophils (mast cells). Once sensitised to an allergen, subsequent exposure may lead to an anaphylactic reaction in affected individuals. The mechanism is that subsequent exposure leads to mast-cell–allergen complexes and the release of histamine.¹²⁴ Reactions to an allergen cannot be predicted in anaphylaxis, with a subsequent exposure leading to an amplified or lesser response.¹¹⁹ There can be an initial reaction, which subsides with treatment over about 24 hours, but often described is a second or rebound reaction up to 8–10 hours after initial exposure to an allergen.^118,¹²²

Clinical Manifestations

Exposure to an allergen causes release of histamine and other mediators, with subsequent vasodilation and increased microvascular permeability – a distributive form of shock. Histamine acts, and is metabolised, rapidly while other mediators have a sustained effect.¹²¹ The antigen–antibody reaction may directly damage vascular walls, while release of vasoactive mediators such as histamine, serotonin, bradykinins and prostaglandins trigger a systemic response, resulting in vasodilation and increased capillary permeability, with widespread loss of fluid into the interstitial space and hypovolaemia. Blood pressure and cardiac output/index may fall with a compensatory rise in heart rate. Severe bronchospasm may also occur from mediator-induced bronchial oedema and pulmonary smooth muscle contraction.⁹ Abdominal pain is thought to be due to the inflammation of Peyer’s patches (clusters of lymphatic tissue containing B-lymphocytes, located in the mucosa and submucosa of the small intestine).¹²⁴ A list of signs and symptoms for anaphylaxis appears in Table 20.10. Anaphylaxis should be considered when there are two or more organ systems involved.¹²⁵

TABLE 20.10 Clinical manifestations of anaphylaxis ^119,^122,¹²³

System	Clinical manifestations
Nervous	Syncope, dizziness, weakness, seizures, anxiety
Respiratory	Stridor, wheeze, cough, pharyngeal/laryngeal oedema, dyspnoea, bronchospasm, tachypnoea, cyanosis, use of accessory muscles
Cardiovascular	Tachycardia, hypotension, arrhythmias
Abdominal	Nausea, vomiting, cramps, pain, diarrhoea
Other	Flushed skin, pruritus, urticaria, angiooedema, erythema, rash, lacrimation, conjunctival injection, warmth, itching

Of note is the high mortality in patients with asthma and those on beta-blocker or ACE inhibitor medications;^119,¹²⁶ these medications may limit the effectiveness of adrenaline therapy. Age and preexisting lung disease are the most important factors in relation to severity; older people and those with asthma or airways disease have a higher risk of a life-threatening reaction.¹²⁴

Nursing Practice and Collaborative Care: Initial Management

Diagnosis of an anaphylactic reaction requires an appropriate assessment and history, including acute onset, history of allergic reaction and initial measures instituted to support airway, breathing and circulation (ABC). Removal of the causative agent (if possible) and early treatment (within 30 minutes of exposure to an allergen) results in improved outcomes. ABC measures are important considering the rapid impact of circulating mediators and potential decline in respiratory and cardiovascular function. Securing the airway is vital as most anaphylactic related deaths are due to asphyxiation.¹²¹ Adrenaline is recommended as first-line drug treatment^119,^121,^122,¹²⁴ often as an IM injection.

Nursing Practice and Collaborative Care: Airway Management

Early elective intubation is recommended for patients with airway oedema, stridor, or any oropharyngeal swelling. Patients with airway swelling and/or angiooedema are at high risk for rapid deterioration and respiratory compromise.¹²⁵ Late presentation to hospital or delayed intubation when airway swelling is present may mean that intubation and other emergency airway procedures may be extremely difficult. Multiple attempts at intubation increase laryngeal oedema or cause trauma to the airway. Early recognition of the potentially difficult airway allows planning for alternative airway management by experts in difficult airways.¹²⁵

Nursing Practice and Collaborative Care: Adjunctive Support

Adjunctive drugs include H₂-antagonists, antihistamines, corticosteroids and other beta₂-agonists for airway symptoms. The H₂-antagonists are competitive antagonists of histamine at the parietal cell H₂ receptor. Blocking both H₁ and H₂ receptors is an advantage with urticaria present. Corticosteroids may be beneficial for persistent bronchospasm, asthma and severe cutaneous reactions but not in acute management. Glucagon and noradrenaline may be required for patients on beta-blockers who may have resistant severe hypotension and bradycardia.¹²⁷ Glucagon exerts positive inotropic and chronotropic effects, independently of catecholamines, while atropine may reverse bradycardia. Vasopressin is also suggested where shock is refractory to adrenaline.¹²¹ Given that a second reaction may occur after the initial allergic response, monitoring should continue for up to 48 hours.¹²¹

Preventative Care

Individuals with known allergies are taught avoidance of allergens, and the use of emergency kits with adrenaline for IM injection.^120,¹²⁴ Desensitisation therapy may reduce severity of symptoms.

Neurogenic/Spinal Shock

Neurogenic shock is a form of distributive shock caused by loss of vasomotor (sympathetic) tone from disruption to or inhibition of neural output. Characteristics include SBP <90–100 mmHg and a HR <80 bpm without other obvious causes.¹²⁸ Note that the HR is within otherwise accepted normal limits. Most often it is described as a triad of hypotension, bradycardia and hypothermia. The primary cause is a spinal cord injury above T6, secondary to disruption of sympathetic outflow from T1–L2 and to unopposed vagal tone, leading to decreased vascular resistance and associated vascular dilation.¹²⁹ It may also develop after anaesthesia, particularly spinal, cerebral medullary ischaemia or when there is spinal cord complete or partial injury above the midthoracic region (thoracic outflow tract).

Spinal shock is a subclass of neurogenic shock, with a transient physiological (rather than anatomical) reflex depression of cord function below the level of injury and associated loss of sensorimotor functions. Incidence has been reported at 14% of patients presenting to the ED within 2 hours of injury and predominantly affects patients with cervical damage.¹²⁸ Spinal shock can also occur with a spinal cord laceration or contusion, and is associated with varying degrees of motor and sensory deficit (see also Chapters 17 and 23). Trauma is frequently the reason for primary injury and simultaneous injuries may also be responsible for haemodynamic compromise.¹²⁸ Haemorrhagic shock in combination with neurogenic shock has a poor outcome.

Clinical Manifestations

Inhibited sympathetic outflow results in dominance of the parasympathetic nervous system, with a reduction in systemic vascular resistance and lowered blood pressure. Preload to the right heart is reduced, which lowers stroke volume and subsequent cardiac output/index. The usual response to reduction in cardiac output (a raised heart rate) does not occur due to the parasympathetic nervous system and blockage of sympathetic compensatory responses, and the patient may be bradycardic and hypotensive,¹²⁹ with their skin warm and dry.

In spinal shock there may be an initial rise in blood pressure due to release of catecholamines, followed by hypotension.¹²⁹ Flaccid paralysis, including that of the bladder and bowel, is observed and sustained priapism may develop. Symptoms may last hours to days, until the reflex arcs below the level of injury begin to regain function. This is a result of damage to the spinal cord, and results in pale, cold skin above the site of injury, and warm, pink skin below the site of injury. Anhidrosis (absence of sweating) may be present. Heart rate may be slow, requiring intervention.

Nursing Practice and Collaborative Management

The extent of injury, whether complete (no sensory or motor function) or incomplete (some sensory or motor function), determines clinical medical management. Priority focuses on airway, breathing and circulation.

After neck and torso stabilisation, a patient is placed in a position that supports spinal precautions (neutral neck positioning) with the spinal boards removed within 20 minutes if possible. Caution for spinal instability remains despite medical imaging clearance, due to the potential for spinal ligament damage. The patient is positioned supine, with their legs in alignment with the torso. Elevation of the head may cause pooling of blood in the lower limbs, exacerbating hypotension,¹³⁰ and makes the patient sensitive to sudden position changes.

Loss of sympathetic outflow requires close cardiac and haemodynamic monitoring for bradycardia and hypotension. Symptomatic bradycardia is treated and may require cardiac pacing if unresponsive to atropine. Therapies include fluid resuscitation with the addition of inotropes if necessary to improve vasomotor tone to increase preload and maintain a MAP >80–85 mmHg ¹²⁹ to restore spinal cord perfusion and to prevent secondary neuronal hypoperfusion.¹³¹ A higher (supranormal) MAP may be targeted to improve recovery and prevent secondary injuries.¹³¹ Volume expansion with colloids and crystalloids or blood products will vary depending on patient situation, however subgroup analysis in the SAFE trial indicated that colloids and hypotonic solutions may not be the best options.⁴⁴

Respiratory function is closely monitored to prevent or minimise atelectasis, pneumonia ¹³¹ and secretion retention. The level of injury is indicative of the potential for respiratory muscle weakness (see Table 20.11). The diaphragm is innervated by the phrenic nerve (originating at C3–C5); any injury above C3 leads to complete respiratory muscle paralysis and patients will require ventilatory support.¹³¹ Incomplete injuries between C3 and C5 may also require ventilation initially but subsequently recover some respiratory function.

TABLE 20.11 Respiratory muscle innervation by cord level

Cord level innervation	Accessory muscle
C3–C5 (mostly C4)	Diaphragm
C6	Serratus anteriorLatissimus dorsiPectoralis
T1–11	Intercostals
T6–L1	Abdominals

Hypothermia may be present, resulting from dilated peripheral blood vessels allowing radiant loss of heat. A patient is monitored for core temperature changes, and external warming devices may be required.

Paralytic ileus is a concern in the acute phase of injuries above T5, where disruption of integrative innervation pathways leads to unmodulated colonic functioning ¹³² and peristaltic hypomotility. Ileus may lead to respiratory compromise and should be managed. The patient should remain ‘nil by mouth’ and treatment includes gastric decompression, adequate IV hydration and electrolyte balance. Drug therapy with prokinetics, probiotics, aperients and IV neostigmine or lignocaine has been reported to be useful.

Pressure care is attended every second hour and where Jordan frames are used, slats are removed between use. The patient is susceptible to deep venous thrombosis (DVT), so sequential calf compression devices and other prophylaxis are initiated early with D-dimers monitored regularly.

Summary

Shock is a generic term describing a syndrome and pervasive set of potentially life-threatening symptoms. The pathophysiological changes associated with shock feature a complex interaction of generic compensatory mechanisms which attempt to sustain perfusion and particularly oxygen delivery to the vital organ systems of the body. These protective responses are particularly strong in supporting cerebral perfusion and combine responses from the SNS, endocrine and adrenal/renal systems. As shock develops cellular dysfunction occurs in response to the release of a large collection of systemic and local inflammatory mediators which inevitably overwhelm cell function and lead to diffuse organ injury if shock continues unabated. The classification system described here differentiates shock into categories including hypovolaemic, cardiogenic and distributive; classification is dependent on aetiology. Clear assessment is required to distinguish the type of shock aids in appropriate treatment decisions, targeting the cause and managing associated symptoms. Critical care nurses are in a position to provide clear assessment and first-line emergency management of the various shock states. Collaborative integrated care is important to provide the patient with the best possible outcome.

Case study

Locally and internationally, there are many reports that demonstrate systematic hospital challenges for in-patients that develop shock. Identified issues include failure to recognise or respond to deteriorating patients, inadequate or delayed treatment, unstable patient transfers and a lack of clinical supervision. This has led to the implementation of track and trigger systems and development of various standards and performance indicators aimed at improving patient care. The following case study highlights some of these issues.

An independent 80-year-old female, Ellen, presented to the emergency department (ED) at 2200 h. The ED was very busy and short-staffed. Ellen was prescribed antibiotics for a urinary tract infection (UTI) 10 days ago but stopped taking them 6 days ago because of thrush. She started to feel very sick this evening and called an ambulance. Relevant medical history includes hypertension and a recent diagnosis of chronic renal failure which is currently being investigated. On arrival, the triage nurse recorded Ellen’s blood pressure at 104/37. An initial fluid bolus of 500 mL of normal saline was administered by the receiving ED nurse as per the local policy. The ED was very busy and no further observations were recorded until 0100h when her blood pressure was noted to be 82/60. The ED workflow was interrupted by the arrival of multiple patients from a nearby traffic accident that diverted nursing and medical staff to the resuscitation bays.

Only two further sets of observations were documented over the next four hours and recorded as 82/60 and then SBP 60. A further fluid bolus of 500 mL of normal saline was administered. The medical registrar was notified at 0540h by the team leader. After examination, antibiotics were prescribed and an indwelling catheter inserted. There was no residual volume. Ellen was then seen by the ICU registrar at 0620h. Central and arterial lines were inserted and it was recommended that the patient be transferred to ICU.

Unfortunately, prior to transfer, Ellen died. The case was investigated through a root cause analysis process as it was allocated the highest severity code. Recommended system improvements included processes to improve early recognition of deterioration and sepsis.

Research vignette

Harrison GA, Jacques T, McLaws ML, Kilborn G. Combinations of early signs of critical illness predict in-hospital death- the SOCCER study (signs of critical conditions and emergency responses). Resuscitation 2006; 71(3): 327–34.

Abstract

Background

Medical emergency team (MET) call criteria are late signs of a deteriorating clinical condition. Some early signs predict in-hospital death but have a high prevalence so their use as single sign call criteria could be wasteful of resources. This study searched a large database to explore the association of combinations of recordings of early signs (ES), or early with late signs (LS) with in-hospital death.

Methods

A cross-sectional survey was undertaken of 3046 non-do not attempt resuscitation adult admissions in 5 hospitals without MET over 14 days. The medical records were reviewed for recordings of 26 ES and 21 LS and in-hospital death. Combinations of ES with or without LS were examined as predictors of death. Global modified early warning scores (GMEWS) were calculated.

Results

ES with LS, plus LS only, had higher odds ratios than ES alone. Four combinations of ES were strongly associated with death: cardiovascular plus respiratory with decrease in urinary output, cardiovascular plus respiratory with a decrease in consciousness, respiratory with decrease in urinary output, and cardiovascular plus respiratory. In other combinations, recordings of SpO₂ 90–95%, systolic blood pressure 80–100 mmHg or decrease in urinary output in turn occurring with one or more disturbed blood gas variable were associated with death. Compared with admissions whose GMEWS were 0–2, admissions with GMEWS 5–15 were 27.1 times more likely to die while those with GMEWS 3–4 were 6.5 times more likely.Conclusions

The results support the inclusion of early signs of a deteriorating clinical condition in sets of call criteria.

Critique

It has long been recognised that vital signs falling out of ‘normal ranges’ are associated with adverse events for patients. This large scale study reviewed the case notes of 3160 patients from five NSW hospitals in late 2000 for early and late physiological signs of clinical deterioration. It is considered a landmark Australian study given the magnitude of the review and the rigorous application of categories to define patient deterioration. Twenty-six early signs and symptoms and 21 late signs and symptoms were defined prior to the review that was initially carried out by two ICU trained nurses and then verified by two of the investigators. The participant hospitals were chosen for their representativeness of ‘typical’ acute case mix and excluded those with do not resuscitate orders, under 14 years of age, day only admissions, non admitted ED patients, deaths in O.R. prior to ward transfer, ICU patients (whilst in ICU) and specific specialties such as palliative care or psychiatry. The carefully selected sites for investigation and exclusion criteria all contributed to ensuring the findings were both representative and generalisable to the broader Australian and international context.

Early signs of deterioration included, but were not limited to, SBP 80–100 mmHg, heart rate 40–49 or 121–140 b/min, respiratory rate 5–9 or 31–40 b/min, SPO₂ 90–95%, altered mentation, GCS 9–11 or fall >2, urine output <200 mL in 8 hrs, amongst others. Likewise, late signs include cardiac arrest, SBP <80 mmHg, GCS ≤8, PaO₂ <50 mmHg, pH <7.2, along with others. An ‘other’ category was included.

Not surprisingly, early signs, when combined with late signs, were more strongly predictive than early signs alone of risk of death. Having noted this, many of the early signs listed did not result in death so any system of response based on the early signs alone could be expensive in terms of demand with limited benefit, at least in reduction in mortality. So whilst this study further indentifies both early and late signs of deterioration that will allow for more refined calling criteria, it does fail to deliver the definitive set of calling criteria for clinical emergency response systems. Weaknesses include the retrospective nature of the review and the reliance on charted records. The original sample is now over 10 years old and care practices may have moved on since then. It does acknowledge the MERIT study,¹³⁴ the only large-scale prospective assessment of the MET system in Australia but does not discuss in detail why this research failed to show a difference where a MET system was in place.

Of note, parameters in the cardiovascular category most consistently feature in the combination of signs closely associated with clinical deterioration. This emphasises both the value and the importance of these measures in defining clinical deterioration in patients, and provides a strong message for all clinicians working in acute care as to the risks of ignoring these signs or failing to fully assess patients on a regular basis. Many other signs not listed specifically as cardiovascular are not mutually exclusive, with changes in mentation, urine output and blood pH inextricably linked to perfusion of specific organ systems and tissues as a whole. It is also clear that as the patient in shock deteriorates, the chances of successful intervention and recovery are reduced.

The SOCCER study continues to support the value of close, frequent clinical observation and the linking of signs and symptoms within the patient’s overall physiologic system that provides the astute clinician with numerous indicators of the health or otherwise of the cardiovascular system and the impending shock syndrome. It also supports less-experienced clinicians in seeking help to interpret the patient’s clinical state and gaining support to avoid deterioration to the point where late signs become an all-too-obvious message of imminent patient mortality.

Although there are more signs included in the SOCCER study than would be available on a standard bedside observation chart,¹³³ research such as this has led to initiatives to standardise observation charts and highlight appropriate calling criteria and escalation procedures. Standardisation in this way supports organisations to provide equitable service to patients. In NSW there has been statewide implementation of the ‘Between the Flags’ program¹³⁵ which includes a colour-coded chart, escalation procedure and indepth online training modules. This program enables clinicians to respond appropriately and communicate effectively when patients deteriorate. The Australian Commission on Safety and Quality in Healthcare has also developed a program to support organisations in increasing structures for hospital patients to receive comprehensive care regardless of location and time of day.¹³⁶ These are important initiatives to combat avoidable in-hospital complications and deaths.

Learning activities

The following reflective questions prompt analysis of the systems in place where you work, to reinforce appropriate care and identify areas for improvement. After reading the case study consider the following questions:

1. What assessments are important to obtain appropriate information for a patient presenting with signs of hypoperfusion?

2. What systems are in place where you work to ensure adequate processes are in place to assess patients presenting in shock?

3. How could the patient in the case study have been managed differently?

4. What are the clinical escalation processes in the facilities you have worked in?

Reflect on a case of a patient with shock that you have been involved in, and consider the following:

5. What elements of care or ‘care bundles’ were effective in managing symptoms of shock?

6. What processes would you use in future to syste-matically assess, manage and evaluate care of a patient in shock?