Chapter 66 NURSING MANAGEMENT: shock and multiple organ dysfunction syndrome

This chapter provides an overview of precipitating factors, signs and symptoms and clinical management of the various types of shock and multiple organ dysfunction syndrome (MODS). Systemic illness defined by generic pathophysiological processes in response to a wide variety of insults has been termed systemic inflammatory response syndrome (SIRS). Shock, SIRS and MODS are serious and interrelated problems. Figure 66-1 shows the relationship between shock, SIRS and MODS.

Figure 66-1 The relationship between shock, systemic inflammatory response syndrome and multiple organ dysfunction syndrome. CNS, central nervous system.

Shock

Shock is a syndrome characterised by cellular ischaemia from decreased perfusion and impaired metabolism.¹^–³ The exchange of oxygen and nutrients at the cellular level is essential to life. Shock results in an imbalance between the supply of and the demand for oxygen and nutrients in the tissues.⁴ When a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply, and ischaemia and tissue death may result. Hypoperfusion from shock is at first reversible. Untreated, shock becomes irreversible and the consequence is death.^1,²

CLASSIFICATION OF SHOCK

The initial classification of shock (in the 1970s) included four categories: hypovolaemic, cardiogenic, obstructive and distributive.¹ However, these categories no longer accurately reflect the pathogenesis of shock, and shock is now classified as low blood flow shock (cardiogenic and hypovolaemic shock) or maldistribution of blood flow shock (septic, anaphylactic and neurogenic shock; see Table 66-1). Although the causes and initial presentation of various types of shock differ, the physiological responses of the cell to hypoperfusion have similarities. Management depends on the cause but relies on reversing hypoperfusion and targeted therapy.

TABLE 66-1 Classification and precipitating factors of shock

GI, gastrointestinal.

Low blood flow shock

Cardiogenic shock

Cardiogenic shock manifests as circulatory failure from cardiac dysfunction.⁵ Cardiogenic shock has an incidence of 6–10% in patients presenting with an acute myocardial infarction (MI) and usually occurs within 48 hours of infarction.^6,⁷ It has a mortality rate of approximately 60%.⁸^–¹¹ However, acute MI is not the only cause of cardiogenic shock. Although this type of shock occurs predominantly from left ventricular failure,^7,¹² it may occur with right heart failure and when systolic and diastolic dysfunction of the myocardium results in compromised cardiac output. (Heart failure is discussed in Ch 34.) Systolic dysfunction means that the heart ineffectively pumps blood forwards and is characterised by poor contractility of the myocardium. Systolic dysfunction primarily affects the left ventricle because systolic pressure and tension are greater on the left side of the heart. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is compromised. Precipitating factors for systolic dysfunction include MI, cardiomyopathies, severe systemic or pulmonary hypertension, blunt cardiac injury and myocardial depression from sepsis. Diastolic dysfunction is an impaired ability of the right or left ventricle to fill during diastole. Decreased filling of the ventricle results in decreased stroke volume (the amount of blood ejected from the heart with each contraction).

Figure 66-2 illustrates the pathophysiology of cardiogenic shock. Whether the initiating event is an MI, a structural problem (e.g. valvular abnormality, papillary muscle dysfunction, acute ventricular septal defect) or arrhythmias, the physiological responses are similar. The patient experiences impaired tissue perfusion and impaired cellular metabolism as a result of cardiogenic shock.¹²

Figure 66-2 The pathophysiology of cardiogenic shock.

Cardiogenic shock has been defined as the inability to maintain perfusion when there is adequate circulating volume,¹³ with the following clinical parameters: cardiac index <2.1 L/min/m² (normal range [NR] = 2.6–4.2 L/min/m²), systolic blood pressure <90 mmHg and pulmonary capillary wedge pressure >18 mmHg (NR = 2–15 mmHg). Additional invasive haemodynamic variables for cardiogenic shock include intrathoracic blood volume index >850 mL/m² (NR = 850–1000 mL/m²), global end-diastolic volume >700 mL/m² (NR = 680–800 mL/m²) and extravascular lung volume index >10 mL/kg (NR = 3–7 mL/kg).^3,⁴ These variables may be measured by invasive monitoring devices used to distinguish shock types. The measurements are not usually used in isolation: when combined, they support a clinical picture that is indicative of the patient’s volume status and cardiac functioning.

The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient with acute heart failure (see Ch 34). The patient usually presents with tachycardia, hypotension, a narrowed pulse pressure, dyspnoea and increased systemic vascular resistance (SVR), which increases the workload of the heart and thus increases myocardial oxygen consumption. On examination, the patient will be tachypnoeic and have pulmonary congestion, as evidenced by the presence of crackles. The haemodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure and pulmonary vascular resistance (see Table 66-2).

TABLE 66-2 Effects of shock, systemic inflammatory response syndrome and multiple organ dysfunction syndrome on haemodynamic parameters

Note: Haemodynamic effects in some illnesses are highly variable. The haemodynamic findings in MODS depend on the system failing.

Key: ↓, decrease; ↑, increase; <, no change. BP, blood pressure; CO, cardiac output; CVP, central venous pressure; HR, heart rate; MODS, multiple organ dysfunction syndrome; PAP, pulmonary artery pressure; PAWP, pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; SIRS, systemic inflammatory response syndrome; SvO₂, mixed venous oxygen saturation; SVR, systemic vascular resistance.

Signs of peripheral hypoperfusion (e.g. cyanosis, pallor, cool and clammy skin, decreased capillary refill time) will be apparent. Decreased renal blood flow will result in sodium and water retention and decreased urine output. Anxiety and delirium may develop as cerebral perfusion is impaired. Information that may be helpful in diagnosing cardiogenic shock includes laboratory studies (e.g. cardiac enzymes, troponin levels; see Table 66-3),¹⁴ electrocardiogram (ECG), chest X-ray and echocardiogram. The overall clinical presentation of a patient with cardiogenic shock is presented in Table 66-4.

TABLE 66-3 Laboratory abnormalities in shock

DIAGNOSTIC STUDIES

ADH, antidiuretic hormone; ALT, alanine aminotransferase; AST, aspartate aminotransferase; DIC, disseminated intravascular coagulation; GGT, gamma-glutamyl transferase; PT, prothrombin time; PTT, partial thromboplastin time.

TABLE 66-4 Clinical presentation of the major types of shock

ARDS, acute respiratory distress syndrome; BP, blood pressure; CO, cardiac output; ECG, electrocardiogram; GI gastrointestinal; HR, heart rate; LOC, level of consciousness; MvO₂, myocardial oxygen consumption; PAWP, pulmonary artery wedge pressure; SvO₂, mixed venous oxygen saturation; SVR, systemic vascular resistance; WBC, white blood cell.

Hypovolaemic shock

Hypovolaemic shock occurs when there is a loss of intravascular fluid volume leading to inadequate tissue perfusion.^15,¹⁶ In hypovolaemic shock, the intravascular volume is inadequate to fill the vascular space. The volume loss may be either an absolute loss or a relative loss. Absolute hypovolaemia results when fluid is lost through haemorrhage, gastrointestinal (GI) loss (e.g. vomiting, diarrhoea), fistula drainage, diabetes insipidus or diuresis. In relative hypovolaemia, fluid volume moves out of the vascular space into the extravascular space (e.g. interstitial or intracavitary space).¹⁷ This type of fluid shift is called third spacing. One example of relative volume loss is leakage of fluid from the vascular space to the interstitial space from increased capillary permeability, which is seen in sepsis. Other examples include sequestration of fluid into the colon from a bowel obstruction, loss of blood volume into a fracture site (e.g. pelvic fracture), burns (see Ch 24) and ascites (see Table 66-1).

In hypovolaemic shock, the physiological consequences are similar regardless of whether the loss of intravascular volume is absolute or relative.¹⁷ A reduction in intravascular volume results in a decreased venous return to the heart, decreased preload, decreased stroke volume and decreased cardiac output (see Table 66-2). A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, which are the hallmarks of shock (see Fig 66-3).¹⁸

Figure 66-3 The pathophysiology of hypovolaemic shock.

The patient’s response to acute volume loss is dependent on a number of factors, including the extent of the injury or insult, their age and their general state of health (see Table 66-4). An overall assessment of physiological reserve may indicate the patient’s ability to compensate. A healthy young adult can compensate for a sudden loss of up to 15% of total blood volume (or approximately 750 mL out of the average 5 L of total blood volume in a 70-kg person) and only a slight tachycardia and delayed capillary refill may be seen. Further loss of volume (15–30%) results in a sympathetic nervous system mediated response, with tachycardia of more than 100 beats/min, tachypnoea, decreased pulse pressure, cool clammy skin and anxiety.^19,²⁰ The stroke volume and pulmonary artery wedge pressure are decreased because of the decreased circulating blood volume. The patient will be anxious and urine output will begin to decrease. If hypovolaemia is corrected immediately, tissue dysfunction is generally reversible. If volume loss is greater than 30%, blood volume must be replaced aggressively with blood or blood products, as the compensatory mechanisms become overwhelmed.²¹ Clinical signs of volume depletion will be profound. Loss of more than 40% of total blood volume is characterised by loss of autoregulation in the microcirculation and usually results in irreversible tissue destruction.²⁰ Tests that may be done include measurements of serial haemoglobin and haematocrit levels, urine specific gravity, and serum electrolyte and lactic acid levels (see Table 66-3). Large volume resuscitation may confound interpretation of the results due to haemodilution.¹⁷

Maldistribution of blood flow shock

Neurogenic shock

Neurogenic shock is a form of distributive shock caused by loss of vasomotor (sympathetic) tone, which is generally thought to occur due to inhibition of neural output. Table 66-1 lists the causes of neurogenic shock. The primary cause is spinal cord injuries above T6, secondary to the disruption of the sympathetic outflow from T1–L2 and to unopposed vagal tone, leading to a decrease in vascular resistance with associated vascular dilation and pooling of blood in the blood vessels.²¹ It may also develop after anaesthesia, particularly spinal, or cerebral medullary ischaemia, or when the spinal cord suffers a complete or partial injury above the midthoracic region (thoracic outflow tract).

Hypoperfusion associated with neurogenic shock results in impaired tissue perfusion. The pathophysiology of neurogenic shock is described in Figure 66-4 and includes systolic blood pressure <90–100 mmHg and heart rate <80 bpm without other obvious causes.²² Most often it includes hypotension, bradycardia and hypothermia. Tables 66-2, 66-3 and 66-4 further describe the clinical presentation of a patient with neurogenic shock. Spinal shock (see Ch 60) is a form 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. Spinal shock can occur with a spinal cord laceration or cord contusion, and may be associated with varying degrees of motor and sensory deficit. Trauma is frequently the reason for primary injury and simultaneous injuries may also be responsible for haemodynamic compromise.²² The onset of neurogenic shock can begin as soon as 30 minutes after the injury and may last from days to weeks following spinal cord injury.

Figure 66-4 The pathophysiology of neurogenic shock.

Hypothalamic dysfunction may result in alterations to temperature control. The patient will often have poikilothermia (taking on the temperature of the environment) which, combined with massive vasodilation, promotes heat loss, often resulting in hypothermia.²³ In poikilothermia the skin will be cool or warm depending on the ambient temperature. In either case, the skin will usually be dry. Initially, the skin will be warm due to the massive dilation without compensation. As the heat dissipates, the skin loses heat and the patient is at risk of hypothermia.²⁴

Anaphylactic shock

Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitising substance (e.g. drug, vaccine, food or insect venom). Anaphylaxis is an immunoglobulin E (IgE)-mediated hypersensitivity reaction to an allergen. The allergic response is via a host mast-cell reaction mediated by IgE and an antibody produced in response to the allergen that is attached to mast cells. Subsequent exposure leads to mast-cell–allergen complexes and the release of histamine.^25,²⁶ Subsequent response to an allergen cannot be predicted.²⁷

The physiological response is related to release of many vasoactive mediators leading to vasodilation and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space. Anaphylactic shock can lead to respiratory distress, as a result of laryngeal oedema or severe bronchospasm, and circulatory failure. The patient will experience a sudden onset of symptoms, including hypotension, chest pain, swelling of the lips and tongue, wheezing and stridor. Skin changes include flushing, pruritus and urticaria. In addition, the patient may feel an impending sense of doom and become very anxious and confused. Immediate treatment focuses on airway, breathing and circulation.²⁶

An individual can develop a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion or injection with an antigen (allergen) to which the person has previously been sensitised (see Table 66-1). Parenteral administration of the antigen (allergen) is the route most likely to cause anaphylaxis. However, oral, topical and inhalation routes can also cause anaphylactic reactions. Tables 66-2, 66-3 and 66-4 describe the clinical presentation of a patient in anaphylactic shock. Quick and decisive action by the nurse is critical in preventing the progression of an anaphylactic reaction to anaphylactic shock. (Anaphylaxis is discussed in Ch 13.)

Septic shock

Sepsis is a systemic inflammatory response to a documented or suspected infection,^28,²⁹ which may be bacterial, viral, fungal or parasitic. Septic shock is the presence of sepsis with hypotension, despite fluid resuscitation, along with the presence of tissue perfusion abnormalities. The pathogenesis of septic shock is complex and is outlined in Figure 66-5.

Figure 66-5 The pathophysiology of septic shock. CNS, central nervous system.

Australasian epidemiological data of septic shock are limited. Intensive care unit (ICU) data in 2004 indicated hospital mortality due to sepsis was around 37.5%,³⁰ and in 2005 the incidence of sepsis was found to be 1.1% of hospital admissions with a mortality of 18.4%, with 23.8% requiring treatment in ICU.³¹ More recently, septic shock mortality was reported to be 60% in Australasia.³²

Infective organisms leading to septic shock include Gram-positive bacteria and Gram-negative, fungal, viral and parasitic organisms. Infective agents stimulate biochemical pathways and the release of multiple cytokines from leucocytes through various mechanisms.³³ Cytokines are peptides with multiple actions that are released with SIRS and are integral to the inflammatory and coagulation cascades producing the detrimental effects seen in sepsis.³⁴ The cascade often begins with the release of several key pro-inflammatory cytokines, including tumour necrosis factor (TNF) and interleukin-1 and -6 (IL-1, IL-6). These mediators stimulate the release of other inflammatory mediators, such as platelet-activating factor, thromboxanes, leukotrienes, prostaglandins and interleukin-8 (IL-8). (See Chs 12 and 13 for a discussion of the inflammatory response.) The combined effects of the mediators result in damage to the endothelium, coagulation, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium.^33,³⁵

Tissue injury and damage to the endothelium lead to coagulation via the expression of tissue factor and factor VIIa complex,^18,³³ and coagulation amplification via factor Xa and Va, leading to massive thrombin formation and fibrin clots.^15,²⁹ The formation of microthrombi leads to obstruction of the microvasculature. These alterations manifest in the cardiovascular and respiratory systems; however, derangements also occur in the metabolic pathways, with catabolic metabolism and insulin resistance a feature.^33,³⁶

The clinical presentation of septic shock includes decreased SVR, with a compensatory increase in cardiac output, hypotension, tachypnoea, alterations in blood count and loss of temperature control (high or low). Tables 66-2 and 66-4 further delineate the clinical presentation of a patient with septic shock.

The combination of TNF and IL-1 are thought to have a role in sepsis-induced myocardial dysfunction. The ejection fraction is decreased for the first few days after the initial insult. Because of a decreased ejection fraction the ventricles will dilate in order to maintain the stroke volume. The ejection fraction typically improves and the ventricular dilation resolves over 7–10 days. Persistence of a high cardiac output and a low SVR beyond 24 hours is an ominous finding and is often associated with an increased development of hypotension and MODS. Coronary perfusion and myocardial oxygen metabolism are generally normal in septic shock.³³

STAGES OF SHOCK

In addition to understanding the underlying pathogenesis of the type of shock the patient is experiencing, monitoring and management are also guided by knowing where the patient is on the shock continuum. This continuum begins with the initial stage of shock, followed by the compensatory and progressive stages. If tissue perfusion is not restored, and the progression of shock is not halted, the patient will deteriorate to the refractory (final) stage of shock, from which recovery is unlikely. Although there are no clear-cut divisions between the stages, they provide a framework for understanding the shock process.

Initial stage

The initial stage of shock may not be clinically apparent. The patient will have no outward signs of decreased tissue perfusion despite the fact that the body begins to respond to the imbalance of oxygen supply and demand at the cellular level. Metabolic changes include increased energy requirements and increased anaerobic metabolism and hyperglycaemia.³⁶ Anaerobic metabolism leads to a build-up of lactic acid, which accumulates as a waste product and may lead to a metabolic acidosis. The lactic acid must be removed via the circulation and metabolised by the liver. This process also requires oxygen, which is unavailable at the cellular level in shock. Unresolved lactic acidosis has been linked to an increased mortality.²⁴

Compensatory stage

The next stage is the compensatory stage. In this stage, the body activates several compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis (see Fig 66-6). Neuroendocrine compensatory mechanisms occur. The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand (see Table 66-5).

Figure 66-6 The compensatory stage of shock: reversible stage during which compensatory mechanisms are effective and homeostasis is maintained. ADH, antidiuretic hormone; GI, gastrointestinal.

TABLE 66-5 Clinical manifestations of the stages of shock

ALT, alanine aminotransferase; ARDS, acute respiratory distress syndrome; AST, aspartate aminotransferase; BP, blood pressure; DIC, disseminated intravascular coagulation; GGT, gamma-glutamyl transferase; GI, gastrointestinal; HR, heart rate; MAP, mean arterial pressure; MvO₂, myocardial oxygen consumption.

One of the first clinical signs of shock may be a fall in blood pressure and increased heart rate, which occur as a result of a decrease in cardiac output. Baroreceptors and chemoreceptors in the carotid and aortic bodies immediately respond by activating the autonomic nervous system, which stimulates vasoconstriction and the release of adrenaline and noradrenaline, both of which are potent vasoconstrictors. Blood flow to the most essential (vital) organs (the heart, lungs and brain) is maintained, whereas blood flow to the non-vital organs (e.g. the GI tract and reproductive organs) is diverted or shunted.³¹

Decreased blood flow to the kidneys activates the renin–angiotensin system. Renin is released, which activates angiotensinogen to produce angiotensin I, which is then converted to angiotensin II (see Ch 44). Angiotensin II is a potent vasoconstrictor and causes both arterial and venous vasoconstriction. The net result is an increase in venous return to the heart and an increase in blood pressure. Angiotensin II also stimulates the adrenal cortex to release aldosterone, which results in sodium and water reabsorption and potassium excretion by the kidneys. The increase in sodium reabsorption raises the serum osmolality and stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH works by increasing water reabsorption by the kidneys, thus further increasing blood volume. The increase in total circulating volume results in an increase in cardiac output and blood pressure.

The shunting of blood from other organ systems also results in clinically important changes. Decreased blood flow to the GI tract results in impaired motility and reduced peristalsis, which increases the risk of paralytic ileus and the potential for translocation of gut flora. Decreased blood flow to the skin results in the patient feeling cool and clammy. The exception is the patient in early septic shock, whose skin may feel warm and flushed.

The myocardium responds to the sensory nervous system stimulation and the increase in oxygen demand by increasing the heart rate and contractility. However, increased contractility also increases myocardial oxygen consumption (MvO₂) and the coronary arteries dilate in an attempt to meet the increased oxygen demands of the myocardium.

A multisystem response to decreasing tissue perfusion is initiated in the compensatory stage of shock. At this stage, the body is able to compensate for the changes in tissue perfusion. If the perfusion deficit (the cause of the shock) is corrected, the patient will recover with little or no residual sequelae. If the perfusion deficit is not corrected, however, and the body is unable to compensate, the patient enters the progressive stage of shock.

Progressive stage

The progressive stage of shock begins as compensatory mechanisms fail (see Fig 66-7). In this stage, aggressive interventions are necessary to prevent the development of MODS. The hallmarks of this stage of shock are decreased cellular perfusion and altered capillary permeability. The altered capillary permeability allows leakage of fluid and protein out of the vascular space into the surrounding interstitial space (oedema). In addition to the decrease in circulating volume, there is an increase in systemic interstitial oedema.⁵ The patient may have anasarca (diffuse profound oedema). Fluid leakage from the vascular space affects the solid organs (e.g. liver, spleen, GI tract, lungs), as well as the peripheral tissues.

Figure 66-7 The progressive stage of shock: compensatory mechanisms are becoming ineffective and fail to maintain perfusion to vital organs.

The adaptive responses of the compensatory stage are unable to adjust to circulatory changes. Cardiac output becomes insufficient to provide adequate organ perfusion despite increasing tissue oxygen consumption. Oxygen delivery is decreased and, to compensate, increased extraction occurs to enable continued tissue consumption. When delivery falls below a critical threshold, this compensation mechanism fails.³⁷ Clinically, the patient shows signs of worsening hypoxia, becomes more tachypnoeic, and has crackles and increased work of breathing.

The cardiovascular system is profoundly affected in the progressive stage of shock.³⁷ Cardiac output begins to fall, with a resultant decrease in blood pressure and peripheral perfusion, including a decrease in coronary artery perfusion. Capillary permeability continues to increase, enhancing the movement of fluid from the vascular space into the interstitial space. Sustained hypoperfusion results in weak peripheral pulses, and ischaemia of the distal extremities eventually occurs. Myocardial dysfunction from decreased perfusion results in arrhythmias, myocardial ischaemia and, potentially, MI. Shock is a medical emergency usually characterised by hypotension.¹⁰

Hypotension and shock are established risk factors for acute kidney injury. Renal function is markedly impaired during the progressive stage of shock.³⁸ The patient will have a decreased urine output and elevated serum urea and serum creatinine levels. Metabolic acidosis occurs from an inability to excrete acids and reabsorb bicarbonate.

The GI system is also affected by prolonged decreased tissue perfusion. As the blood supply to the GI tract decreases, the normally protective mucosal barrier becomes ischaemic. This ischaemia predisposes the patient to erosive ulcers and GI bleeding, and increases the risk of translocation of bacteria from the GI tract to the blood. The decreased perfusion also leads to an inability to absorb nutrients from the GI system.

Other systems are also affected by the sustained hypoperfusion in the progressive stage of shock. The loss of the functional ability of the liver leads to a failure of the liver to metabolise drugs and waste products such as ammonia and lactate. Jaundice results from an accumulation of bilirubin. As the liver cells die, enzymes become elevated, in particular alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transpeptidase (GGT). The liver also loses its ability to function as an immune organ. The Kupffer cells are unable to scavenge the bacteria that have translocated from the GI system. Instead, bacteria are released into the bloodstream, thus increasing the possibility of the development of bacteraemia.

Dysfunction of the haematological system adds to the complexity of the clinical picture. The patient is at risk of developing disseminated intravascular coagulation (DIC). In DIC, there is a consumption of platelets and clotting factors with secondary fibrinolysis.^39,⁴⁰ This results in clinically significant bleeding from many sites, including, but not limited to, the GI tract, lungs and puncture sites. Altered laboratory values in DIC include decreased platelet count, prolonged prothrombin time, prolonged partial thromboplastin time, decreased fibrinogen and increased fibrin degradation products (FDPs) or fibrin split products (FSPs) (see Tables 66-3 and 66-5).⁴⁰

Refractory stage

In the final stage of shock, the refractory stage, decreased perfusion from unabated peripheral vasoconstriction and decreased cardiac output exacerbates anaerobic metabolism (see Fig 66-8). The accumulation of lactic acid contributes to capillary dilation and increased capillary permeability. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds secondary to the constricted venules and dilated arterioles. The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow further depresses myocardial function and reduces cardiac output. Cerebral blood flow cannot be maintained and cerebral ischaemia results.

Figure 66-8 The irreversible or refractory stage of shock: compensatory mechanisms are not functioning or are totally ineffective, leading to multiple organ dysfunction syndrome.

The patient in this stage of shock will demonstrate profound hypotension and hypoxaemia. The failure of the liver, lungs and kidneys will result in rapid accumulation of waste products, such as lactate, ammonia and carbon dioxide. The failure of one organ system will have an effect on several other organ systems. In this final stage of shock, recovery is unlikely. The organs are in failure and the body’s compensatory mechanisms are overwhelmed (see Table 66-5).

DIAGNOSTIC STUDIES

There is no single diagnostic study to determine whether or not a patient is in shock. Assessing end-organ perfusion is the key to diagnosing shock states. The decreased tissue perfusion seen in shock will lead to metabolic acidosis, often with an elevated lactate level from anaerobic metabolism (indicative of hypoxia) and a base deficit.⁴¹ Table 66-3 summarises the laboratory findings that may be seen in shock. High lactate levels in shock are indicative of a poor outcome.^42,⁴³

The process of establishing a diagnosis begins with a thorough history and physical examination. The history may be obtained from the patient, family or friends and will provide information that is invaluable in differentiating shock states. Important diagnostic studies include a 12-lead ECG, continuous cardiac monitoring, chest X-ray, haemodynamic monitoring (e.g. arterial pressure monitoring, pulmonary artery [PA] pressure monitoring), continuous pulse oximetry and baseline blood results.⁴³

MULTIDISCIPLINARY CARE: GENERAL MEASURES

Critical factors in the successful management of the patient experiencing shock relate to the early recognition and treatment of the shock state. Prompt intervention in the early stages of shock (initial and compensatory stages) may prevent the decline to the progressive or refractory stages. Successful management of the patient in shock is multidisciplinary and includes the following:

Table 66-6 provides an overview of the initial assessment findings and interventions for the emergency care of the patient in shock. Management of medical emergencies begins with airway, breathing and circulation. General management strategies for the patient in shock begin with ensuring that the patient has a patent airway. Once the airway is established and secure, oxygen delivery must be optimised. Mechanical ventilation may be necessary to ensure the delivery of oxygen to target arterial oxygen saturation of at least 90% or greater (PaO₂ >60 mmHg [>8 kPa]) to avoid hypoxaemia. The circulating blood volume is optimised with fluid replacement, and when necessary drug therapy may also be required to support perfusion.

TABLE 66-6 Shock

EMERGENCY MANAGEMENT

IV, intravenous.

* See Table 66-1 for additional aetiologies of shock.

Oxygen and ventilation

Oxygen delivery is dependent on cardiac output and arterial oxygen content (including haemoglobin level, SaO₂ and PaO₂). Methods to optimise oxygen delivery are directed at increasing supply and decreasing demand. Oxygen supply can be increased by: (1) optimising the cardiac output with intravenous (IV) fluid volume challenge to ensure adequate circulating blood volume and/or initiating drug therapy to increase perfusion pressure; (2) increasing the haemoglobin level by the transfusion of blood or packed red blood cells (RBCs); and/or (3) increasing the arterial oxygen saturation with supplemental oxygen and optimising lung function through respiratory support, such as mechanical ventilation.

Care must be planned so as not to disrupt the balance of oxygen supply and demand. The nurse must evaluate interventions that increase the patient’s oxygen demand and appropriately space those interventions so that the patient’s supply and demand balance is not disrupted. The use of a PA catheter that includes a sensor to measure the mixed venous oxygen saturation (SvO₂) may be useful in determining the adequacy of tissue oxygenation. The SvO₂ reflects the dynamic balance between oxygenation of the arterial blood, tissue perfusion and tissue oxygen consumption. The SvO₂, when considered in conjunction with the arterial oxygen saturation, is useful in analysing the patient’s haemodynamic status and response to treatments or activities (see Ch 65).

Fluid replacement

Except for cardiogenic shock, all other types of shock usually feature decreased circulating blood volume. The cornerstone of therapy for these shock states is volume expansion via administration of an appropriate fluid. The rationale for this is based on the Frank–Starling law to increase preload and contractility by stretching the myocytes, thus optimising stroke volume (see Ch 31). Before beginning fluid resuscitation, two large-bore (e.g. 14–16 gauge) IV catheters must be inserted, preferably into the antecubital veins: as well as providing central access, large bore cannulas allow rapid infusion of fluid as needed. They may also be used for central venous pressure (CVP) measurement, and routine fluid and drug administration.

Crystalloids (e.g. normal saline solution) and colloids (e.g. albumin) have a role in fluid resuscitation (see Table 66-7). The best fluid for resuscitation remains controversial and both crystalloids and colloids are used. A large Australian study comparing the administration of saline versus albumin solution for fluid resuscitation showed neither fluid to have a clear advantage. More saline was required to achieve the same end point and all-cause mortality at 28 days showed no significant difference.⁴⁴

TABLE 66-7 Fluid therapy in shock

NSA, normal serum albumin; TGA, Therapeutic Goods Administration.

The choice of fluid for resuscitation must also be based on the type and volume of fluid lost and the patient’s clinical status. A widely held principle is to replace what the patient has lost—for example, in massive haemorrhage, blood will be required. Administration of blood and blood products should be considered carefully. In Australia and New Zealand, the national blood authority provides guidelines for blood product use in the setting of massive transfusion, and guidelines are currently being developed for use in ICU.

There are a number of additional factors to consider when administering blood products in massive volumes. Massive transfusion has been defined as the replacement of the patient’s total blood volume in less than 24 hours (approximately 10 units of red cells).^45,⁴⁶ It is associated with a number of complications, such as transfusion reactions, coagulopathies, hypothermia and sepsis.¹⁸ Massive transfusion is generally associated with high mortality.⁴⁶

Patients receiving massive blood transfusions require careful monitoring for signs of metabolic derangements, hypothermia, citrate toxicity and hyperkalaemia. Coagulation abnormalities, due to the depletion of clotting factors, may also be present. Dilution and clotting factor consumption are the major causes of microvascular bleeding, often manifesting as oozing from multiple sites.^42,⁴⁷

Selection of the appropriate fluid and indications for surgical management and ‘permissive hypotension’⁴⁸ require assessment by the multidisciplinary team. Permissive hypotension is the deliberate strategy of limiting or minimising resuscitation until after adequate control of haemorrhage.^17,⁴⁹ Supportive vasopressor and inotrope therapy may be commenced to maintain adequate perfusion pressure, with noradrenaline usually the vasopressor of choice as its primary action is to cause vasoconstriction.⁴⁷

If the patient does not respond to fluid challenge, other monitoring may be instituted. Patients in shock, as defined by low blood pressure, will usually require continuous blood pressure monitoring via an arterial catheter. An indwelling urinary catheter is likely to be inserted to enable monitoring and assessment of fluid balance.

When large amounts of fluid replacement are required, the patient must be protected against complications. The major complications are hypothermia, coagulopathy and acidosis.⁴⁴ For example, the patient can be protected from hypothermia by warming the crystalloid and colloid solutions used during massive fluid resuscitation and ensuring that the patient remains covered as much as possible.

If the patient does not respond to volume replacement, more intensive monitoring, such as a PA catheter, may be considered to assist in evaluating the status of the intravascular volume. A PA catheter facilitates measurement and/or calculation of cardiac output, vascular resistance, pulmonary pressures and SvO₂. If the patient has persistent hypotension after adequate volume resuscitation, a vasopressor agent, such as noradrenaline, may be introduced. Therapies are goal oriented to measures of haemodynamic status. Mean arterial pressure (MAP) is commonly used as a global guide of perfusion to the tissues, as it is the driving force of flow to the microvasculature.⁴⁸ The objective for resuscitation remains the restoration of tissue perfusion. Decisions on which vasopressor or inotrope to use should be based on the physiological goal. An assessment of end-organ perfusion (e.g. urine output, neurological function, peripheral pulses) provides relevant information about the adequacy of resuscitation.

Vasoactive drug therapy

The primary goal of drug therapy for shock is the correction of decreased tissue perfusion by increasing MAP.⁴⁹ Medications used to improve perfusion in shock should be administered via central venous access using a controlled infusion device. Because these medications often have vasoconstrictor properties, administration via a large vein reduces the risk of damage to smaller vessels. If drugs are administered peripherally, there may be deleterious effects if the drug extravasates into surrounding tissue (see Table 66-8).

TABLE 66-8 Shock

DRUG THERAPY

BP, blood pressure; CO, cardiac output; CVP, central venous pressure; HR, heart rate; MAP, mean arterial pressure; MvO₂, myocardial oxygen consumption; PAWP, pulmonary artery wedge pressure; SVR, systemic vascular resistance.

* Consult individual facility’s guidelines, pharmacist, pharmacology references and drug manufacturer’s administration materials for additional information and exact dosing.

Sympathomimetic drugs

Many of the drugs used in the treatment of shock have an effect on the sympathetic nervous system. These drugs are termed sympathomimetic. The effects of these drugs are mediated through binding to α-adrenergic or β-adrenergic receptors. The various drugs differ in their relative α-adrenergic and β-adrenergic effects.^50,⁵¹

Many of the sympathomimetic drugs cause peripheral vasoconstriction and are referred to as vasopressor drugs because of the observed α-adrenergic effects (e.g. adrenaline, noradrenaline). These drugs are used to increase MAP and thereby improve oxygen delivery and tissue perfusion.⁴³ At high doses, though, these vasopressor drugs have the potential to cause severe peripheral vasoconstriction and further jeopardise tissue perfusion, either directly or indirectly. The increase in SVR raises cardiac workload, which can be detrimental to a patient in cardiogenic shock by causing further myocardial damage. These drugs, particularly adrenaline, often have metabolic consequences by increasing oxygen consumption and glucose production, and therefore have implications for care.

Currently, there is no recommendation to use one drug over another in shock, so practical and patient considerations are the key to decision making.⁴⁹^–⁵¹ Shock states that have profound peripheral vasoconstriction, decreased cardiac output and arterial pressure (low flow shock states) will require slightly different drug therapy than vasodilatory shock states (maldistribution shock states). Use of vasopressor drugs is generally reserved for patients who are unresponsive to fluid challenge. Adequate volume replacement must be administered before the use of any vasopressor drugs, because peripheral vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion. Other drugs may be used for their β-adrenergic or inotropic effects (e.g. dobutamine). Often, more than one drug is used synergistically. For example, the combination of noradrenaline and dobutamine has been suggested to be of benefit in the treatment of patients with septic shock.^36,⁵⁰ Dobutamine is recommended for myocardial dysfunction in sepsis.^49,⁵² Drugs such as vasopressin and the longer acting terlipressin may also have a role in the treatment of shock states.⁵⁰

The goals of vasopressor and inotropic therapy are to improve cardiac output and achieve and maintain the MAP of at least 65 mmHg.⁵¹ The nurse must continuously monitor end-organ perfusion (e.g. urine output, neurological function) to ensure that the blood pressure is providing adequate perfusion. Drugs of this type are usually administered via a central catheter and a controlled infusion device to maintain stable serum concentrations.

Vasodilator drugs

Some patients in shock show evidence of excessive vasoconstriction and poor tissue perfusion in spite of volume replacement and normal or even high systemic blood pressures. Use of vasodilators is most likely in patients with cardiogenic shock. Although generalised sympathetic vasoconstriction is a useful compensatory mechanism for maintaining systemic pressure, excessive constriction can reduce tissue blood flow and increase the workload of the heart. The rationale for using vasodilator therapy for a patient in shock is to improve coronary perfusion and reduce myocardial oxygen demand and consumption. The goal of vasodilator therapy, as in vasopressor therapy, is to maintain the MAP at 65 mmHg or greater. It is also important to monitor PA pressures to assess pulmonary congestion along with the MAP, so that fluid administration can be increased or the dose of the vasodilator decreased if a serious fall in blood pressure occurs. Nitrites are the vasodilator agents most often used for the patient in cardiogenic shock.

Nutritional therapy

Protein–energy malnutrition and insulin resistance are manifestations of hypermetabolism in shock and critical illness.⁵³ Adequate nutrition is vital to decreasing morbidity and mortality. Early enteral nutrition (within 24–48 hours) has been advocated for critically ill patients and evidence-based guidelines have been developed (see Ch 65), although the evidence is variable and ICU practice is inconsistent.⁵⁴ Parenteral feeding may be used where enteral feeding is difficult to establish. (Total parenteral nutrition and enteral tube feedings are discussed in Ch 39.) Early enteral feedings are thought to enhance perfusion of the GI tract and prevent translocation of gut bacteria.

MULTIDISCIPLINARY CARE: SPECIFIC MEASURES

Cardiogenic shock

For the patient in cardiogenic shock, the overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand. Early reperfusion therapy (angioplasty with stenting and emergency revascularisation) is associated with improved outcomes.¹² Supportive measures to restore blood flow include thrombolytic therapy, although results vary (particularly if therapy is given after shock develops), and invasive devices to support circulation (see Ch 33).^6,⁷ Cardiac catheterisation should be performed as soon as possible after the initial insult, and coronary angioplasty with or without stenting may be performed at the same time. Until these interventions can be performed, the heart must be supported to optimise stroke volume and cardiac output in an effort to facilitate optimal perfusion (see Table 66-9).

TABLE 66-9 Specific measures for the treatment of shock

MULTIDISCIPLINARY CARE

ACE, angiotensin-converting enzyme; BP, blood pressure; CI, cardiac index; CVP, central venous pressure; GI, gastrointestinal; IABP, intra-aortic balloon pump; IV, intravenous; PAWP, pulmonary artery wedge pressure; SVR, systemic vascular resistance; VAD, ventricular assist device.

Haemodynamic management of the patient is geared towards reducing the workload of the heart through drug therapy or mechanical interventions. Drug selection is based on the clinical goal and a thorough understanding of the pharmacodynamics of each drug. Drugs can be used to decrease the workload of the heart and improve coronary blood flow by dilating coronary arteries (e.g. nitrates), reducing preload (e.g. diuretics) and reducing afterload (e.g. inodilators). Levosimendan, a novel calcium-sensitiser and inodilator, provides positive inotropic effects without increasing myocardial oxygen demand.¹⁰

The patient may also benefit from a circulatory assist device, such as an intraaortic balloon pump (see Ch 33) or a ventricular assist device (see Ch 65). The intraaortic balloon pump is inserted into the femoral artery and positioned in the descending thoracic aorta just distal to the left subclavian artery. The goal of this intervention is to increase myocardial oxygen supply and decrease myocardial oxygen demand by reducing afterload and improving coronary perfusion. The ventricular assist device may be used on a temporary basis, in specialised units, for the patient in cardiogenic shock and/or awaiting cardiac transplantation. Cardiac transplantation is an option for a small and select group of patients with cardiogenic shock. While thrombolysis can be attempted with inotropic support or augmentation of blood pressure with an intraaortic balloon pump, the greatest reduction in mortality has been seen after urgent coronary angiography and early revascularisation.⁹

Hypovolaemic shock

The underlying principles of managing the patient with hypovolaemic shock focus on halting the loss of fluid and restoring the circulating volume. Table 66-7 delineates the different types of fluid used for volume resuscitation, the mechanisms of action and specific nursing implications for each fluid type.

Septic shock

Improving mortality and the management of patients with septic shock has been the subject of many publications, as can be evidenced by release of the Surviving Sepsis Guidelines.^53,⁵⁵ These guidelines provide graded recommendations for many treatment strategies and are worth reading. However, the most recent version from 2008 is not supported by the Australian and New Zealand Intensive Care Society.⁵⁶ There are many gaps in the research and quality research is still needed.⁵⁷ The mainstays of care for septic shock include blood cultures to determine the type of infecting organism, source control and appropriate antibiotics as soon as possible^58,⁵⁹ to kill and remove the invading pathogens, and organ support (e.g. fluid resuscitation, vasoactive drug administration).^33,⁶⁰

Patients in septic shock often require large amounts of fluid replacement due to relative hypovolaemia. Aggressive fluid replacement to achieve predetermined resuscitation end points is recommended. Table 66-9 includes some guidelines. To optimise and evaluate resuscitation and obtain surrogate measures of perfusion, invasive haemodynamic monitoring is usually necessary. This may include arterial and central lines and some form of cardiac output monitoring. Other organ supportive therapies may be necessary, such as mechanical ventilation and renal replacement therapy.

Drotrecogin alfa (activated) rhu, a recombinant form of activated protein C (APC), is the first drug to demonstrate (at 28-day mortality) benefit in treating patients with severe sepsis.⁶¹ The drug acts directly on pathophysiological processes present in severe sepsis and septic shock. APC is a plasma protease usually produced in response to thrombin formation. Its functions include a reduction in inflammation by decreasing TNF and nuclear factor-kappa B (NF-κB) production, anticoagulant properties, reducing thrombin production when activated via thrombin–thrombomodulin complexes, and profibrinolytic responses by inhibiting thrombin-activatable fibrinolytic inhibitor and plasminogen activator inhibitor-1. Bleeding is the most common serious adverse effect associated with the administration of the drug.^58,^61,⁶²

Neurogenic shock

The specific treatment of neurogenic shock is dependent on the cause. If the cause is spinal cord injury, general measures to promote spinal stability (e.g. spinal precautions, cervical stabilisation with a collar) are used.²⁴ This generally requires the patient to be placed supine, with the legs positioned in alignment with the torso. Elevation of the head may cause pooling of blood in the lower limbs, exacerbating the hypotension, and makes the patient sensitive to sudden position changes.⁶³ Once the spine is stabilised, definitive treatment of the hypotension and bradycardia is essential to prevent further spinal cord damage. Hypotension, which occurs as a result of a loss of sympathetic tone, is associated with peripheral vasodilation and decreased venous return. The usual response to reduction in cardiac output (a raised heart rate) does not occur due to the dominance of the parasympathetic nervous system and blockage of sympathetic compensatory responses.²² The skin may be warm and dry.

If the venous return is not optimised by administration of IV fluids, addition of an α-adrenergic agonist may be indicated (see Table 66-8). Symptomatic bradycardia due to the loss of sympathetic outflow may require cardiac pacing if unresponsive to atropine. Therapies include inotropes for vasomotor tone and fluid resuscitation to increase preload and maintain the MAP >80–85 mmHg.²² The aim is to restore spinal cord perfusion to prevent secondary neuronal hypoperfusion.⁶⁴

In addition, the patient with a spinal cord injury will need to be monitored for hypothermia due to hypothalamic dysfunction (see Table 66-9). It is also useful to remember that any spinal cord injury above T11 will lead to some respiratory compromise and requires vigilant monitoring.

Anaphylactic shock

The first strategy in managing patients at risk of anaphylactic shock is prevention. A thorough history is the key to avoiding the risk factors for anaphylaxis (see Table 66-1). The clinical presentation of anaphylactic shock is dramatic and immediate intervention is required. Adrenaline is the drug of choice.^26,^27,^65,⁶⁶ It induces peripheral vasoconstriction and bronchodilation and opposes the effect of histamine. Adjunctive drugs may include H₂-antagonists, antihistamines, corticosteroids and other β_-2 agonists for airway symptoms. Blocking both H₁ and H₂ receptors has been suggested to be an advantage in the treatment of urticaria. Corticosteroids may be beneficial in the treatment of persistent bronchospasm, asthma and severe cutaneous reactions and are not usually beneficial for acute management. Glucagon and noradrenaline may be required for patients who have been taking β-blockers.⁶⁶ Glucagon exerts positive inotropic and chronotropic effects on the heart, independently of catecholamines. Patients taking β-adrenergic blockers may have resistant severe hypotension and bradycardia. Atropine may be required to reverse the bradycardia. Vasopressin has also been suggested where shock is refractory to adrenaline.⁶³

Maintaining a patent airway is important because the patient can quickly develop airway compromise from laryngeal oedema or bronchoconstriction and this is the reason for most anaphylaxis-related deaths. Nebulised bronchodilators are highly effective. Aerosol adrenaline can also be used to treat laryngeal oedema. Endotracheal intubation or tracheostomy may be necessary to secure and maintain a patent airway.

Hypotension results from the leakage of fluid from the intravascular space into the interstitial space as a result of increased vascular permeability and vasodilation. Aggressive fluid replacement, predominantly with colloids, may be necessary (see Tables 66-7 and 66-9).

NURSING MANAGEMENT: SHOCK

Nursing assessment

The role of the nurse is vital in caring for patients who are at risk of developing shock or are in a shocked state. The initial assessment should be geared towards the ABCs: airway, breathing and circulation. Further assessment should focus on tissue perfusion and includes evaluation of vital signs, peripheral pulses, level of consciousness, capillary refill, skin characteristics (e.g. temperature, colour, moisture) and urine output. As shock progresses, the patient’s skin will become cooler and mottled, urine output will decrease and neurological status will continue to deteriorate.

To understand and manage the patient’s clinical status, the nurse must integrate all assessment data. As care is initiated (see Tables 66-6 and 66-9), it is essential for the nurse to obtain a brief history from the patient, if able, or from another knowledgeable person. This information should include a description of the events leading to the shock condition, the time of onset and duration of the symptoms, and a health history (e.g. medications, allergies, date of last tetanus). In addition, details regarding any care that the patient received prior to hospitalisation are equally important.

It is important for nurses to become involved in the prevention of shock. To prevent shock, nurses need to identify patients at risk. In general, patients who are older, those with comorbidities and those who are immunocompromised are at an increased risk.³³ Any person who sustains surgical or accidental trauma is at high risk of shock resulting from haemorrhage, spinal cord injury and other conditions (see Table 66-1). Patients who have had any procedure that breaches normal host defence barriers (e.g. line insertion) must also be monitored for signs of infection. Essentially, any patient who is at risk of decreased oxygen delivery or tissue hypoxia is also at risk of developing shock.

Planning is essential to help prevent shock after a susceptible individual has been identified. For example, a person with an acute MI, especially an anterior wall MI, is at risk of cardiogenic shock. The primary goal for the patient with an acute MI is to limit the size of the infarction by restoring coronary blood flow through thrombolytic therapy, coronary artery interventions or surgical revascularisation. Morphine, oxygen, nitrates and anticoagulants can improve perfusion and reduce myocardial oxygen demand. The nurse can modify the patient’s environment to provide care at intervals that will not increase the patient’s oxygen demand. For example, if the patient becomes anxious when washing, that activity can be planned at a time so as not to interfere with X-rays or other activities that may also increase oxygen demand.

A person with a severe allergy to substances such as drugs, shellfish and insect bites is at an increased risk of developing anaphylactic shock. This risk can be decreased if the patient is carefully questioned about allergies before administering a new drug (even if the patient has received this drug in the past) or before undergoing diagnostic procedures involving the use of contrast media. Patients with severe allergies should wear a medical alert tag and report their allergies to their healthcare provider. These patients should also be instructed about the availability of special kits that contain equipment and medication (e.g. adrenaline [Epipen]) for the treatment of acute hypersensitivity reactions.⁶⁵ If a patient’s condition warrants receiving a medication to which they are at high risk of developing an allergic reaction (e.g. contrast media), they should receive a premedication or participate in a desensitising process.

Careful monitoring of fluid balance can help to prevent hypovolaemic shock. Ongoing monitoring of intake and output and daily weights are important in patients at risk. In addition, monitoring of the patient’s clinical status is essential because trends in clinical findings and compiling a complete picture of clinical status are more meaningful than any single piece of clinical information.

All patients must be carefully monitored for the development of infection. Progression from infection to sepsis and septic shock is dependent on the patient’s host defence mechanisms. Patients who are immunocompromised or immunosuppressed are at especially high risk of developing hospital-acquired infections. Interventions to decrease the risk of infection for hospitalised patients include always employing standard precautions and strict use of contact precautions when resistant organisms have been identified. Other measures include decreasing the number of indwelling lines (e.g. central lines, indwelling urinary catheters), judicious use of antibiotics and meticulous hygiene standards. In addition, all equipment must be changed according to institutional policy, or thoroughly cleaned or discarded (if disposable) between each patient use.

NURSING RESEARCH

Thirty-four patients with no, unilateral and bilateral pulmonary infiltrates on chest X-ray were assessed by ABG, respiratory mechanics and haemodynamics with the patients supine, then were assessed again 30 minutes and 2 hours after lateral positioning and then again 30 minutes post-return to the supine position.

Results and conclusions

There were no changes to the PaO₂/FiO₂ (P:F) ratio, blood pressure or heart rate with the position changes; the cardiac index increased and dynamic lung compliance decreased; 21% had minor adverse events. Lateral positioning had no beneficial effect on gas exchange.

Implications for nursing practice

Repositioning critically ill patients to prevent or limit the complications of immobility is essential. In ventilated patients who are haemodynamically stable, repositioning is well-tolerated and not associated with significant serious adverse events.

In addition to monitoring the patient’s cardiovascular status, the nurse must administer the prescribed therapy that is designed to correct the alterations to cardiovascular function. The response to fluid and medication administration is assessed progressively after intervention. Appropriate adjustments should be made as needed; for example, vasoactive drugs are titrated to maintain established goals, such as the MAP ≥65 mmHg. Once tissue perfusion is restored, the patient is slowly weaned off the medications being used to support blood pressure and tissue perfusion.

Respiratory status

The patient’s respiratory status must be assessed frequently to ensure adequate oxygenation, detect complications early and provide data regarding the patient’s acid–base status. The rate, depth and rhythm of respirations are monitored regularly. Increased respiratory rate and depth provide information regarding the patient’s effort to increase alveolar ventilation. Breath sounds should be assessed for any changes, which may indicate fluid overload, atelectasis and/or accumulation of secretions.

Pulse oximetry is used to continuously monitor the oxygen saturation of haemoglobin. Pulse oximetry using peripheral sites may not be accurate in an advanced shock state because of poor peripheral circulation. In this situation, the probe should be attached to the nose, ear or forehead (according to the manufacturer’s guidelines) to increase accuracy. Arterial blood gases (ABGs) provide definitive information on oxygenation status and acid–base balance. Initial interpretation of ABGs is often the nurse’s responsibility. The first step is to assess oxygenation, looking at both the PaO₂ (NR = 80–100 mmHg [11–13.5 kPa]) and SaO₂ (NR = 94–100%). A PaO₂ below 60 mmHg (<8 kPa) (in the absence of chronic lung disease) indicates the presence of hypoxaemia and the need for the administration of higher oxygen concentrations or the addition of therapies to improve lung function, such as continuous positive airway pressure. The next step is to assess the pH (NR = 7.35–7.45) to look for the overall change to the acid–base status. A pH <7.35 indicates acidaemia and is often the result of acute changes. It is then important to assess the respiratory component (PaCO₂ NR = 35–45 mmHg [4–6 kPa]) and the metabolic component (standard base excess [SBE] –2 to +2) of the ABG and the magnitude of the change. It is important to remember that there may be both respiratory and metabolic symptoms leading to the change in pH or that one system may be compensating for the other. Where it is evident that hypoxia and respiratory acidosis (high carbon dioxide) are both affecting patient status, mechanical ventilation will most likely be required. The nurse may then need to assist with inserting and securing an artificial airway, maintaining the patency of the airway, monitoring ventilatory status and minimising the potential for ventilator-related complications. (Artificial airways and mechanical ventilation are discussed in Ch 65.)

Renal status

Hourly measurements of urinary output are used as a proxy assessment of the adequacy of renal perfusion. An indwelling urinary catheter is inserted to facilitate measurement. Urine output of less than 0.5 mL/kg/hour despite adequate fluid resuscitation may indicate inadequate perfusion of the kidneys. Serum urea and serum creatinine values are additional indicators used to assess renal function. The serum creatinine level is a better indicator of renal function because serum urea levels can be influenced by the catabolic state of the patient. Protein and muscle breakdown will increase urea levels.

Body temperature and skin changes

In the presence of an elevated or a subnormal temperature, it is important to measure core temperature. Many indwelling lines (e.g. cardiac output devices) are available with a thermistor that allows constant core temperature to be measured. In most circumstances fever is a normal homeostatic mechanism to improve host defence and does not require intervention unless the patient is uncomfortable, the temperature is leading to haemodynamic compromise or the temperature rises to a point that is damaging and uncontrollable and becomes life-threatening (>40°C). The patient’s skin should be monitored for pallor, flushing, cyanosis, diaphoresis or piloerection, and shivering should be avoided as it increases metabolic demand substantially. In addition, the rapidity of capillary refill should be monitored as an indicator of peripheral perfusion (NR = <2 seconds). Delayed refill (>3 seconds) may indicate poor perfusion or dehydration.

Gastrointestinal status

Bowel sounds should be auscultated at least every 4 hours and abdominal distension should be assessed. Bowel sounds are usually auscultated in each quadrant of the abdomen and it usually takes several minutes to make an appropriate assessment. Some drugs, such as opioids, slow peristalsis and this should be taken into consideration. Hypoactive or absent sounds may be indicative of ileus or obstruction. Hyperactive sounds are sometimes present with diarrhoea, constipation and early obstruction. Abdominal distension may be present for many reasons and should be addressed to limit effects on the respiratory system. If a nasogastric tube is used, the drainage should be measured as part of the fluid output as well as being tested for occult blood. If the patient has a bowel movement, the stool should be checked for occult blood. Where possible, feeding should be established to promote gut integrity and provide for energy demands.

Personal hygiene

Hygiene is especially important to the patient in shock because impaired tissue perfusion predisposes the patient to skin breakdown and infection. However, bathing and other nursing measures must be carried out judiciously because the patient is experiencing problems with oxygen delivery to tissues. The nurse must use clinical judgement in determining priorities of care in order to limit the demands for increased oxygen. Pressure area care is particularly important to reduce patient morbidity.

Oral care is essential because mucous membranes may become dry and fragile in the volume-depleted patient. In addition, the intubated patient usually has difficulty swallowing, resulting in pooled secretions in the mouth that have a high bacterial load. A water-soluble lubricant applied to the lips prevents drying and cracking. Moist swabbing of the tongue and oral mucosa with saline solution may be beneficial. Lemon–glycerine swabs should not be used because they can cause further drying of the mucosa; however, various other mouthwashes are available and selective decontamination is gaining popularity. Teeth brushing and antimicrobial mouth washes have been suggested to reduce complications.

Passive range of motion should be performed three to four times per day to maintain joint mobility. The patient should be turned at least every 2–4 hours (if haemodynamic stability permits) and positioned in good body alignment to help prevent pressure ulcers. Use of a pressure-relieving mattress or a specialty bed may also be needed. Nursing interventions should be monitored to ascertain the patient’s tolerance to activity.

Emotional support and comfort

The effects of anxiety and fear on the patient and family in the face of a critical, life-threatening situation are frequently overlooked or underestimated. Anxiety, fear and pain may aggravate respiratory distress and increase the release of catecholamines. When implementing care, the nurse should assess and monitor the patient’s anxiety and pain. Medications to decrease anxiety and pain are common modes of therapy. Infusions of a benzodiazepine (e.g. midazolam) or short-acting sedative (e.g. propofol) and an opioid (e.g. morphine) are extremely helpful in decreasing anxiety, pain and oxygen utilisation. There is increasing evidence that infusion of these drugs requires regular assessment based on an agreed protocol and daily breaks, to reduce length of hospital stay.^67,⁶⁸

The nurse should always talk to the patient when providing care, even if the patient is intubated, sedated or appears comatose. Hearing is often the last sense to be diminished and even if the patient cannot respond, they may still be able to hear. If the intubated patient is capable of writing, ways of communication should be sought so that patient care needs are collaboratively agreed.

Keeping patient diaries may also help alleviate posttraumatic stress. A marker and paper is sufficient and alphabet boards or signboards with common requests (e.g. turn, lights) are also useful. The patient should always receive explanations of procedures before they are carried out, as well as information regarding the current plan of care and its rationale. If the patient asks questions about progress and prognosis, simple and honest answers should be given.

Family and significant others can have a therapeutic effect on the patient. Family needs have been identified in the literature and it is evident that critical care nurses’ perceptions of needs and family-reported needs are not always the same.⁶⁹ It is important for the nurse to remember that compassionate understanding is as essential as scientific and technical expertise in the total care of the patient and family. Family time with the patient should be facilitated, provided that this time is perceived as comforting by the patient. The nurse should explain in simple terms the purpose of tubes and equipment surrounding the patient, and the family should be informed of what they may and may not touch. If desired, the family may be encouraged to perform simple comfort measures. Privacy should be provided as much as possible, but the patient and family should be assured that assistance is readily available should it be required. The call bell should be in reach at all times.

Ambulatory and home care

Intensive care has a long and varied effect on patients and can increase mortality rates beyond hospital discharge; however, treatment in the ICU is beneficial and severity of illness is the key indicator of predicted outcome.^70,⁷¹ Rehabilitation of the patient who has experienced a critical illness necessitates correction of the precipitating cause and prevention or early treatment of complications. The nurse should continue to monitor the patient for indications of complications throughout the recovery period. Complications may include decreased range of motion, polyneuropathies leading to weakness syndromes, muscle wasting and decreased physical endurance, chronic renal failure (see Ch 46) and ongoing lung disease as a result of acute respiratory distress syndrome (ARDS; see Ch 67). Thus, patients recovering from shock may require diverse services on discharge. These can include admission to transitional care units (e.g. for weaning), rehabilitation centres (inpatient or outpatient) or home healthcare agencies. The nurse should begin to anticipate and facilitate a safe transition from the hospital to home on admission.

Evaluation

Expected outcomes for the patient with shock are addressed in NCP 66-1.

Systemic inflammatory response syndrome and multiple organ dysfunction syndrome

AETIOLOGY AND PATHOPHYSIOLOGY

Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults, including infection, ischaemia, infarct and injury (see Box 66-1).²⁹ SIRS is characterised by an imbalance of inflammatory mediators, leading to damage in organs remote from the initial insult.⁷² Normally, the inflammatory process is contained within a confined environment. A systemic inflammatory response can be triggered by many mechanisms (see Fig 66-1). Examples include the following:

BOX 66-1 Definitions of sepsis, severe sepsis, septic shock and multiple organ dysfunction syndrome ^*

Infection

• Disease caused by an invasion of the body by pathogenic organisms

Bacteraemia

• Presence of viable bacteria in the blood; demonstrated by positive blood cultures

Sepsis

• Systemic inflammatory response to a documented or suspected infection

Severe sepsis

• Sepsis associated with organ dysfunction, hypoperfusion or hypotension

Septic shock

• Sepsis with hypotension despite adequate fluid resuscitation along with the presence of tissue perfusion abnormalities (e.g. lactic acidosis, oliguria, alteration in mental status)

Hypotension

• A systolic BP of <90 mmHg or a reduction of >40 mmHg from baseline and in which BP is not adequate for normal perfusion

^*These definitions are from the American College of Chest Physicians and the Society of Critical Care Medicine.

Multiple organ dysfunction syndrome (MODS) is defined as two or more dysfunctional organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention (see Box 66-1 and Fig 66-1).^21,²² MODS can develop as a result of a primary injury (primary MODS) or a secondary injury (secondary MODS). Primary MODS occurs early and results from a well-defined illness or injury (e.g. pulmonary contusion, aspiration or inhalation injury). Secondary MODS results from uncontrolled systemic inflammation with resultant organ dysfunction. MODS related to sepsis or shock states is a common cause of admission to the ICU.⁷³ The incidence of MODS is increasing as critical care units are able to support more organ systems and sicker patient populations. The mortality rate from MODS is estimated to be 40–60% and increases with subsequent organ dysfunction.^32,⁷³^–⁷⁵ Cellular damage in various organs in patients who develop MODS begins with the onset of local injury, which is then thought to be compounded by activation of the innate immune system. This includes activation and release of mediators at the microcellular level, leading to episodes of hypotension or hypoxaemia.^73,⁷⁴ The therapeutic goal for the healthcare team is to identify pre-existing factors that may lead to subsequent organ damage away from the initial site of injury and to maintain adequate tissue perfusion and prevent the onset of MODS. Nurses are ideally placed to recognise early signs of clinical deterioration and to act to prevent further organ dysfunction.

Organ and metabolic dysfunction

It is evident that metabolic and subsequent organ dysfunction results from reduced cellular performance in shock states.⁷¹ Metabolic changes are pronounced in SIRS and MODS. Both syndromes trigger a hypermetabolic response. Glycogen stores are rapidly converted to glucose (glycogenolysis). Once glycogen is depleted, amino acids are converted to glucose (gluconeogenesis), reducing protein stores. Fatty acids are mobilised for fuel. Catecholamines and glucocorticoids are released and result in hyperglycaemia and insulin resistance.³⁶ The net result is a catabolic state and lean body mass (muscle) is lost.

The hypermetabolism that is associated with SIRS and MODS may last for several days and prompt liver dysfunction. Liver dysfunction in MODS may exist long before clinical evidence is present. Protein synthesis is impaired. The liver is unable to synthesise albumin, one of the key proteins that has an essential role in maintaining plasma oncotic pressure. Consequently, plasma oncotic pressure decreases and fluid and protein leak from the vascular spaces to the interstitial space. As the state of hypermetabolism persists, the patient is unable to convert lactate to glucose and lactate accumulates (lactic acidosis).

Failure of the coagulation system manifests as DIC. DIC is an exaggeration of a normal response to tissue or vessel wall injury, occurring in many patients with MODS. Endothelial inflammation and damage as a result of SIRS produce a procoagulant state, and tissue injury and mediators that are released can lead to platelet aggregation and activation of clotting factors and fibrin formation. Obstruction of the microvasculature leads to ischaemic injury and the progression of multiple organ failure.

Electrolyte imbalances, which are common, are related to hormonal and metabolic changes and fluid shifts. These changes exacerbate mental status changes, neuromuscular dysfunction and cardiac arrhythmias. The release of ADH and aldosterone results in sodium and water retention. Aldosterone increases urinary potassium loss and catecholamines cause potassium to move into the cell, resulting in hypokalaemia. Hypokalaemia is associated with arrhythmias and muscle weakness. Metabolic acidosis results from impaired tissue perfusion, hypoxia, altered metabolism and electrolyte disturbances. Progressive renal dysfunction also contributes to metabolic acidosis. Hypocalcaemia, hypomagnesaemia and hypophosphataemia are common.

CLINICAL MANIFESTATIONS

The defining manifestations of SIRS and MODS are delineated in Box 66-1. The clinical manifestations of MODS are presented in Table 66-10.

TABLE 66-10 Multiple organ dysfunction syndrome: clinical manifestations and management

ALT, alanine aminotransferase; ARDS, acute respiratory distress syndrome; AST, aspartate aminotransferase; CO, cardiac output; ECG, electrocardiogram; GGT, gamma-glutamyl transferase; GI, gastrointestinal; HR, heart rate; MAP, mean arterial pressure; PA, pulmonary artery; PAWP, pulmonary artery wedge pressure; PT, prothrombin time; PTT, partial thromboplastin time; SVR, systemic vascular resistance.

NURSING AND COLLABORATIVE MANAGEMENT: SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE ORGAN DYSFUNCTION SYNDROME

Multidisciplinary care for the patient with SIRS or MODS focuses on: (1) prevention and treatment of infection; (2) maintenance of tissue oxygenation; (3) nutritional and metabolic support; and (4) appropriate support of individual failing organs. Table 66-10 summarises the management for the patient with MODS.

Prevention and treatment of infection

Aggressive infection control strategies are essential to decrease the risk of hospital-acquired infections. Despite aggressive strategies, host dysfunction may lead to the development of an infection. Once an infection is suspected, interventions to control the source are recommended.^43,⁵² Appropriate cultures should be sent to the laboratory and broad-spectrum therapy should be initiated, followed by directed antibiotic therapy.⁵² Early, aggressive surgery is recommended to remove necrotic tissue (e.g. early debridement of burn tissue) that may provide a culture medium for microorganisms.

Maintenance of tissue oxygenation

Hypoxaemia frequently occurs in patients with SIRS or MODS. These patients have increased oxygen needs and decreased oxygen supply to the tissues. Interventions that decrease oxygen demand and increase oxygen delivery are essential. Sedation, mechanical ventilation and analgesia may decrease oxygen demand and should be considered. Early goal-directed therapy aimed at maintaining normal levels of haemoglobin (e.g. transfusion of packed RBCs) and optimising cardiac output with inotropes (e.g. dobutamine) has been found to improve oxygen delivery and resuscitation, but this is under investigation in Australia as mortality rates for non-treatment groups have been shown to be lower than those reported in the landmark study.^31,^32,^72,^73,⁷⁶

Nutritional and metabolic needs

Hypermetabolism in SIRS or MODS can result in profound weight loss, cachexia and further organ failure. The goal of nutritional support is to preserve organ function. Providing adequate nutrition decreases morbidity and mortality rates in patients with SIRS and MODS. The use of the enteral route is preferable to parenteral nutrition as it preserves gut mucosal function and may limit translocation of gut bacteria and reduce other complications. (Enteral and parenteral nutrition are discussed in Ch 39; see Fig 65-1 for ICU nutrition guidelines.)

Support of failing organs

Support of any failing organ is a primary goal of therapy. For example, the patient with ARDS requires aggressive oxygen therapy and mechanical ventilation (see Ch 65). DIC should be treated appropriately (e.g. administration of blood products and clotting factors; see Ch 30). Renal failure may require renal replacement therapy. Continuous renal replacement therapy is better tolerated than haemodialysis, especially in a patient with haemodynamic instability (see Ch 46).

The patient in shock

CASE STUDY