Outcomes (NOC)	Interventions (NIC) and Rationales
Tissue Perfusion: Peripheral • Capillary refill fingers _____ • Capillary refill toes _____ • Extremity skin temperature _____ • Strength of peripheral pulses _____ Tissue Perfusion: Cellular • Systolic blood pressure _____ • Diastolic blood pressure _____ • Oxygen saturation _____ • Fluid balance _____ • Apical heart rate _____ • Heart rhythm _____ • Electrolyte and acid-base balance _____ • Capillary refill _____ • Urine output _____ • Creatinine clearance _____ Measurement Scale 1 = Severe deviation from normal range 2 = Substantial deviation from normal range 3 = Moderate deviation from normal range 4 = Mild deviation from normal range 5 = No deviation from normal range Tissue Perfusion: Cerebral • Restlessness _____ • Unexplained anxiety _____ • Agitation _____ • Impaired cognition _____ • Decreased level of consciousness _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	Shock Management • Monitor vital signs, mental status, and urinary output to assess trends in patient’s condition and evaluate patient’s response to treatment. • Monitor trends in hemodynamic parameters (e.g., CVP, APCO, CO, PAWP) to assess patient’s status and detect fluid deficits or excesses and to evaluate patient’s response to treatment. • Administer crystalloid or colloid intravenous fluids, as appropriate, to maintain blood pressure and CO. • Monitor laboratory evidence of inadequate tissue perfusion (e.g., increased lactic acid levels, decreased arterial pH levels) to assess trends in patient’s status and evaluate patient’s response to treatment. • Monitor determinants of tissue oxygen delivery (e.g., PaO₂, SpO₂, ScvO₂/SvO₂, MAP, hemoglobin levels, APCO, CO) to assess trends in patient’s status and evaluate patient’s response to treatment. • Monitor for symptoms of respiratory failure (e.g., low PaO₂, elevated PaCO₂ levels, respiratory muscle fatigue) to plan respiratory interventions. • Monitor fluid status, including intake and output and daily weights, to evaluate response to treatment. • Monitor renal function (e.g., BUN, Cr levels) to evaluate response to treatment. • Provide oxygen therapy and/or mechanical ventilation to maximize oxygenation and maintain SpO₂ ≥90%. • Monitor blood glucose levels, as indicated, to evaluate liver function. • Administer DVT and stress ulcer prophylaxis, as appropriate, because these conditions are common complications of shock. • Initiate early administration of antimicrobial agents and closely monitor their effectiveness to prevent progression of infection to septic shock. • Administer vasopressors, antidysrhythmic agents, antiinflammatory agents, diuretics, thrombolytics, inotropes, venodilators, and/or blood products as appropriate to maintain perfusion to vital organs. Shock Management: Cardiac • Monitor for symptoms of inadequate coronary artery perfusion (e.g., ST changes on ECG or angina). • Promote coronary artery perfusion (e.g., maintain mean arterial pressure >60 mm Hg and control tachycardia) to prevent myocardial ischemia. • Promote afterload reduction (with vasodilators, angiotensin-converting enzyme inhibitors or intraaortic balloon pumping) as appropriate. • Promote optimal preload to improve contractility while minimizing heart failure (e.g., administer nitroglycerin and maintain PAWP within prescribed range). • Promote adequate organ system perfusion (with fluid resuscitation and/or vasopressors) to maintain mean arterial pressure >60 mm Hg.
Tissue Perfusion: Cardiac • Pulmonary wedge pressure ____ • Ejection fraction _____ • Heart rhythm _____ • Oxygen saturation _____ • Cardiac index _____ • ECG findings _____ • Systolic blood pressure _____ • Diastolic blood pressure _____ Tissue Perfusion: Pulmonary • Pulmonary artery pressure _____ • Respiratory rate _____ • Respiratory rhythm _____ • PaO₂ _____ • PaCO₂ _____ • Arterial pH _____ • Oxygen saturation _____ Tissue Perfusion: Abdominal Organs • Urine output _____ • Fluid balance _____ • Electrolyte and acid-base balance _____ • Urine specific gravity _____ • BUN _____ • Plasma Cr _____ • Bowel sounds _____ • Liver function test findings _____ • Blood glucose _____ Measurement Scale 1 = Severe deviation from normal range 2 = Substantial deviation from normal range 3 = Moderate deviation from normal range 4 = Mild deviation from normal range 5 = No deviation from normal range	Shock Management: Vasogenic • Monitor for physiologic changes related to loss of vascular tone (e.g., note decreased BP, bradycardia, tachypnea, reduced pulse pressure, anxiety, oliguria) to evaluate response to treatment. • Place patient in a supine position with legs elevated to increase preload, as appropriate. • Maintain two large-bore intravascular access sites for administration of fluids and medications. • Administer isotonic crystalloids as bolus doses, keeping systolic pressure at 90 mm Hg or more to maintain perfusion to vital organs. • Administer antibiotics, antihistamines, epinephrine, and antiinflammatory drugs, if appropriate, to control symptoms. Shock Management: Volume • Monitor for sudden loss of blood, severe dehydration, or persistent bleeding as a cause of hypovolemic shock. • Check all secretions for frank or occult blood to identify source of volume loss. • Monitor for signs/symptoms of hypovolemic shock (e.g., increased thirst, increased HR, increased SVR, decreased UO, decreased bowel sounds, decreased peripheral perfusion, altered mental status, or altered respirations) to evaluate response to treatment. • Administer blood products (e.g., platelets or fresh frozen plasma) and/or isotonic crystalloids or colloids to replace lost volume. • Note hemoglobin and hemoglobin levels before and after blood administration to evaluate response to treatment.

Nursing Diagnosis

Patient Goals

1. Verbalizes feelings about the severity of condition

2. Reports decreased anxiety and increased psychological comfort

Outcomes (NOC)	Interventions (NIC) and Rationales
Anxiety Level • Restlessness _____ • Verbalized apprehension _____ • Increased pulse rate _____ • Increased respiratory rate _____ • Withdrawal _____ • Sleep pattern disturbance _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	Anxiety Reduction • Seek to understand the patient’s perspective of a stressful situation to validate patient’s feelings. • Use a calm, reassuring approach to reduce anxiety and fear. • Listen attentively to provide reassurance. • Administer medications if appropriate to reduce anxiety. • Stay with patient to promote safety and reduce fear. • Control stimuli for patient needs to reduce patient’s anxieties and oxygen need. • Provide factual information concerning diagnosis, treatment, and prognosis to patient and caregiver to reduce patient’s and caregiver’s fear of the unknown and assist them in making informed decisions. • Encourage caregiver to stay with patient to reduce anxiety level.

Outcomes (NOC)

Interventions (NIC) and Rationales

Anxiety Level

• Restlessness _____

• Verbalized apprehension _____

• Increased pulse rate _____

• Increased respiratory rate _____

• Withdrawal _____

• Sleep pattern disturbance _____

• Seek to understand the patient’s perspective of a stressful situation to validate patient’s feelings.

• Use a calm, reassuring approach to reduce anxiety and fear.

• Listen attentively to provide reassurance.

• Administer medications if appropriate to reduce anxiety.

• Stay with patient to promote safety and reduce fear.

• Control stimuli for patient needs to reduce patient’s anxieties and oxygen need.

• Provide factual information concerning diagnosis, treatment, and prognosis to patient and caregiver to reduce patient’s and caregiver’s fear of the unknown and assist them in making informed decisions.

• Encourage caregiver to stay with patient to reduce anxiety level.

ALT, Alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; CO, cardiac output; Cr, creatinine; CVP, central venous pressure; DVT, deep venous thrombosis; ECG, electrocardiogram; GGT, γ-glutamyl transferase; MAP, mean arterial pressure; PAWP, pulmonary artery wedge pressure; ScvO₂, percent oxygen saturation of hemoglobin in venous blood; SpO₂, percent oxygen saturation of hemoglobin measured by pulse oximetry; SvO₂, percent oxygen saturation of hemoglobin in mixed venous blood; UO, urine output.

^*The outcomes and related interventions are not all inclusive and will vary based on the type of shock that the patient is experiencing.

Classification of Shock

The four main categories of shock are cardiogenic, hypovolemic, distributive, and obstructive 1,2 (Table 67-1). Although the cause, initial presentation, and management strategies vary for each type of shock, the physiologic responses of the cells to hypoperfusion are similar.

TABLE 67-1

CLASSIFICATION OF SHOCK STATES

Types and Causes	Examples
Cardiogenic Shock
• Systolic dysfunction: inability of the heart to pump blood forward	Myocardial infarction, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, myocardial depression from metabolic problems
• Diastolic dysfunction: inability of the heart to fill	Cardiac tamponade, ventricular hypertrophy, cardiomyopathy
• Dysrhythmias	Bradydysrhythmias, tachydysrhythmias
• Structural factors	Valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax
Hypovolemic Shock
*Absolute Hypovolemia*
• External loss of whole blood	Hemorrhage from trauma, surgery, GI bleeding
• Loss of other body fluids	Vomiting, diarrhea, excessive diuresis, diabetes insipidus, diabetes mellitus
*Relative Hypovolemia*
• Pooling of blood or fluids	Bowel obstruction
• Fluid shifts	Burn injuries, ascites
• Internal bleeding	Fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis
• Massive vasodilation	Sepsis
Distributive Shock
*Neurogenic Shock*
• Hemodynamic consequence of spinal cord injury and/or disease at or above T5 • Spinal anesthesia • Vasomotor center depression	Severe pain, drugs, hypoglycemia, injury
*Anaphylactic Shock*
• Hypersensitivity (allergic) reaction to a sensitizing substance	Contrast media, blood or blood products, drugs, insect bites, anesthetic agents, food or food additives, vaccines, environmental agents, latex
*Septic Shock*
• Infection	Pneumonia, peritonitis, urinary tract, invasive procedures, indwelling lines and catheters
• At-risk patients	Older adults, patients with chronic diseases (e.g., diabetes mellitus, chronic kidney disease, heart failure), patients receiving immunosuppressive therapy or who are malnourished or debilitated
Obstructive Shock
• Physical obstruction impeding the filling or outflow of blood resulting in reduced cardiac output	Cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, pulmonary embolism

Cardiogenic Shock.

Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart’s pumping action results in reduced cardiac output (CO). Causes of cardiogenic shock are listed in Table 67-1. Mortality rates for patients with cardiogenic shock approach 60%.³ Decreased filling of the heart results in decreased stroke volume.

The heart’s inability to pump the blood forward is called systolic dysfunction. Systolic dysfunction primarily affects the left ventricle, since systolic pressure is 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 reduced. The most common cause of systolic dysfunction is acute myocardial infarction (MI). Cardiogenic shock is the leading cause of death from acute MI.⁴ Causes of diastolic dysfunction are listed in Table 67-1.

Fig. 67-2 describes the pathophysiology of cardiogenic shock. Whether the initiating event is myocardial ischemia, a structural problem (e.g., valvular disorder, ventricular septal rupture), or dysrhythmias, the physiologic responses are similar: the patient experiences impaired tissue perfusion and cellular metabolism.

FIG. 67-2 The pathophysiology of cardiogenic shock.

The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated heart failure (see Chapter 35). The patient may have tachycardia and hypotension. Pulse pressure may be narrowed due to the heart’s inability to pump blood forward during systole and increased volume during diastole. An increase in systemic vascular resistance (SVR) increases the workload of the heart, thus increasing the myocardial oxygen consumption. The heart’s inability to pump blood forward also results in a low CO (less than 4 L/minute) and cardiac index (less than 2.5 L/min/m²).

On assessment, the patient is tachypneic and has crackles on auscultation of breath sounds because of pulmonary congestion. The hemodynamic profile demonstrates an increase in the pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular resistance.

Signs of peripheral hypoperfusion (e.g., cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) are seen. Decreased renal blood flow results in sodium and water retention and decreased urine output. Anxiety, confusion, and agitation may develop as cerebral perfusion is impaired. Tables 67-2 and 67-3 describe the laboratory findings and clinical presentation of a patient with cardiogenic shock.

TABLE 67-2

DIAGNOSTIC STUDIES
Laboratory Changes in Shock

Laboratory Study	Finding	Significance of Finding
Red blood cells
RBC count, hematocrit, hemoglobin	Normal	Remains within normal limits in shock because of relative hypovolemia and pump failure and in hemorrhagic shock before fluid resuscitation.
	↓	Hemorrhagic shock after fluid resuscitation when fluids other than blood are used.
	↑	Nonhemorrhagic shock caused by actual hypovolemia and hemoconcentration.
White blood cells
WBC count, bands	↑	Infection, septic shock.
DIC screen		Acute DIC can develop within hours to days after an initial assault on the body (e.g., shock).
• Fibrin split products (FSP)	↑
• Fibrinogen level	↓
• Platelet count	↓
• PTT and PT	↑
• INR	↑
• Thrombin time	↑
• D-dimer	↑
Creatine kinase	↑	Trauma, myocardial infarction in response to cellular damage and/or hypoxia.
Troponin	↑	Increases in myocardial infarction.
BUN	↑	Indicates impaired kidney function caused by hypoperfusion as a result of severe vasoconstriction, or occurs secondary to catabolism of cells (e.g., trauma, infection).
Creatinine	↑	Indicates impaired kidney function caused by hypoperfusion as a result of severe vasoconstriction. Is more sensitive indicator of renal function than BUN.
Glucose	↑	Found in early shock because of release of liver glycogen stores in response to sympathetic nervous system stimulation and cortisol. Insulin insensitivity develops.
	↓	Occurs because of depleted glycogen stores with hepatocellular dysfunction possible as shock progresses.
Serum electrolytes
• Sodium	↑	Found in early shock because of increased secretion of aldosterone, causing renal retention of sodium.
	↓	May occur iatrogenically when excess hypotonic fluid is administered after fluid loss.
• Potassium	↑	Results when cellular death liberates intracellular potassium. Also occurs in acute kidney injury and acidosis.
• Potassium	↓	Found in early shock because of increased secretion of aldosterone, causing renal excretion of potassium.
Arterial blood gases	Respiratory alkalosis	Found in early shock secondary to hyperventilation.
Arterial blood gases	Metabolic acidosis	Occurs later in shock when lactate accumulates in blood from anaerobic metabolism.
Base deficit	>−6	Indicates acid production secondary to hypoxia.
Blood cultures	Growth of organisms	May grow organisms in patients who are in septic shock.
Lactate level	↑	Usually increases once significant hypoperfusion and impaired oxygen utilization at the cellular level have occurred. By-product of anaerobic metabolism.
Liver enzymes (ALT, AST, GGT)	↑	Elevations indicate liver cell destruction in progressive stage of shock.

ALT, Alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; DIC, disseminated intravascular coagulation; GGT, γ-glutamyl transferase; INR, international normalized ratio; PT, prothrombin time; PTT, partial thromboplastin time.

TABLE 67-3

CLINICAL PRESENTATION OF TYPES OF SHOCK

Cardiogenic Shock	Hypovolemic Shock	Distributive Shock			Obstructive Shock
Cardiogenic Shock	Hypovolemic Shock	Neurogenic Shock	Anaphylactic Shock	Septic Shock	Obstructive Shock
Cardiovascular System
Tachycardia ↓ BP ↓ Capillary refill Chest pain may or may not be present	↓ Preload ↓ Stroke volume ↓ Capillary refill	↓ BP ↓/↑ Temperature Bradycardia	Chest pain Third spacing of fluid	↓/↑ Temperature Myocardial dysfunction Biventricular dilation ↓ Ejection fraction	↓ BP ↓ Preload
Pulmonary System
Tachypnea Crackles Cyanosis Rhonchi	Tachypnea → bradypnea (late)	Dysfunction related to level of injury	Shortness of breath Edema of larynx and epiglottis Wheezing Stridor Rhinitis	Hyperventilation Crackles Respiratory alkalosis → respiratory acidosis Hypoxemia Respiratory failure ARDS Pulmonary hypertension	Tachypnea → bradypnea (late) Shortness of breath
Renal System
↑ Na⁺ and H₂O retention ↓ Renal blood flow ↓ Urine output	↓ Urine output	Bladder dysfunction	Incontinence	↓ Urine output	↓ Urine output
Skin
Pallor Cool, clammy	Pallor Cool, clammy	↓ Skin perfusion Cool or warm Dry	Flushing Pruritus Urticaria Angioedema	Warm and flushed → cool and mottled (late)	Pallor Cool, clammy
Neurologic System
↓ Cerebral perfusion: • Anxiety • Confusion • Agitation	↓ Cerebral perfusion: • Anxiety • Confusion • Agitation	Flaccid paralysis below the level of the lesion Loss of reflex activity	Anxiety Feeling of impending doom Confusion ↓ LOC Metallic taste	Alteration in mental status (e.g., confusion) Agitation Coma (late)	↓ Cerebral perfusion: • Anxiety • Confusion • Agitation
Gastrointestinal System
↓ Bowel sounds Nausea, vomiting	Absent bowel sounds	Bowel dysfunction	Cramping Abdominal pain Nausea Vomiting Diarrhea	GI bleeding Paralytic ileus	↓ to absent bowel sounds
Diagnostic Findings*
↑ Cardiac markers ↑ b-Type natriuretic peptide (BNP) ↑ Blood glucose ↑ BUN ECG (e.g., dysrhythmias) Echocardiogram (e.g., left ventricular dysfunction) Chest x-ray (e.g., pulmonary infiltrates)	↓ Hematocrit ↓ Hemoglobin ↑ Lactate ↑ Urine specific gravity Changes in electrolytes		Sudden onset History of allergies Exposure to contrast media	↑/↓ WBC ↓ Platelets ↑ Lactate ↑ Blood glucose ↑ Urine specific gravity ↓ Urine Na⁺ Positive blood cultures	Specific to cause of obstruction

ARDS, Acute respiratory distress syndrome; BUN, blood urea nitrogen; LOC, level of consciousness;

^*Also see Table 67-2.

Hypovolemic Shock.

Hypovolemic shock occurs after a loss of intravascular fluid volume (see Table 67-1). The volume is inadequate to fill the vascular space. The volume loss may be either an absolute or a relative volume loss. Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. In relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (e.g., intracavitary space). 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, as seen in burns (see Chapter 25).

In hypovolemic shock the size of the vascular compartment remains unchanged while the volume of blood or plasma decreases. Whether the loss of intravascular volume is absolute or relative, the physiologic consequences are similar. A reduction in intravascular volume results in a decreased venous return to the heart, decreased preload, decreased stroke volume, and decreased CO. A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, the hallmarks of shock (Fig. 67-3).

FIG. 67-3 The pathophysiology of hypovolemic shock.

The patient’s response to acute volume loss depends on a number of factors, including extent of injury, age, and general state of health. However, the clinical presentation of hypovolemic shock is consistent (see Table 67-3). An overall assessment of physiologic reserves may indicate the patient’s ability to compensate. A patient may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL). Further loss of volume (15% to 30%) results in a sympathetic nervous system (SNS)–mediated response. This response results in an increase in heart rate, CO, and respiratory rate and depth. The stroke volume, central venous pressure (CVP), and PAWP are decreased because of the decreased circulating blood volume.

The patient may appear anxious, and urine output begins to decrease. If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible. If volume loss is greater than 30%, compensatory mechanisms may begin to fail and immediate replacement with blood products should be started. Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of the total blood volume.5,6 Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, mixed central venous oxygen saturation (SvO₂), and hourly urine outputs (see Table 67-2).

Distributive Shock

Neurogenic Shock.

Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above; it can last up to 6 weeks. The injury results in a massive vasodilation without compensation because of the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism (Fig. 67-4).

In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock (see Table 67-1).

The most important clinical manifestations in neurogenic shock are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).⁷ The patient may not be able to regulate body temperature. Combined with massive vasodilation, the inability to regulate temperature promotes heat loss. Initially, the patient’s skin is warm due to the massive dilation. As the heat disperses, the patient is at risk for hypothermia. Later, the patient’s skin may be cool or warm depending on the ambient temperature (poikilothermia—taking on the temperature of the environment). In either case, the skin is usually dry. Tables 67-2 and 67-3 further describe the laboratory findings and clinical presentation of a patient with neurogenic shock.

Although spinal shock and neurogenic shock often occur in the same patient, they are not the same disorder. Spinal shock is a transient condition that is present after an acute spinal cord injury (see Chapter 61). The patient with spinal shock experiences the absence of all voluntary and reflex neurologic activity below the level of the injury.

Anaphylactic Shock.

Anaphylactic shock is an acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). The reaction quickly causes massive vasodilation, release of vasoactive mediators, 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 due to laryngeal edema or severe bronchospasm, and circulatory failure from the massive vasodilation.⁸ The patient has a sudden onset of symptoms, including dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. In addition, the patient may be anxious and confused and have a sense of impending doom.

A patient can have a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or injection with an antigen (allergen) to which the individual has previously been sensitized (see Table 67-1). 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 67-2 and 67-3 describe the laboratory findings and clinical presentation of a patient in anaphylactic shock. Quick and decisive action is critical to prevent the progression of an allergic reaction to anaphylactic shock. (Anaphylaxis is discussed in Chapter 14.)

Septic Shock.

Sepsis is a systemic inflammatory response to a documented or suspected infection (Table 67-4). In as many as 10% to 30% of patients with sepsis, the causative organism is not identified. Severe sepsis, defined as sepsis complicated by organ dysfunction, is diagnosed in more than 750,000 patients per year and has mortality rates as high as 28% to 50%.^9–11

TABLE 67-4

DIAGNOSTIC CRITERIA FOR SEPSIS

Infection, documented or suspected, and some of the following.

General Variables

• Fever (temperature >100.9° F [38.3° C])

• Hypothermia (core temperature <97.0° F [36° C])

• Heart rate >90 beats/min

• Tachypnea

• Altered mental status

• Significant edema or positive fluid balance (>20 mL/kg over 24 hr)

• Hyperglycemia (blood glucose >140 mg/dL) in the absence of diabetes

Inflammatory Variables

• Leukocytosis (WBC count >12,000/µL)

• Leukopenia (WBC count <4000/µL)

• Normal WBC count with >10% immature forms

• Elevated C-reactive protein

• Elevated procalcitonin

Hemodynamic Variables

• Arterial hypotension (SBP <90 mm Hg, MAP <70 mm Hg, or a decrease in SBP >40 mm Hg)

Organ Dysfunction Variables

• Arterial hypoxemia (PaO₂/FIO₂ <300)

• Acute oliguria (urine output <0.5 mL/kg/hr for at least 2 hr despite adequate fluid resuscitation)

• Serum creatinine increase >0.5 mg/dL

• Coagulation abnormalities (INR >1.5 or PTT >60 sec)

• Ileus (absent bowel sounds)

• Thrombocytopenia (platelet count <100,000/µL)

• Hyperbilirubinemia (total bilirubin >4 mg/dL)

Tissue Perfusion Variables

• Hyperlactatemia (>1 mmol/L)

• Decreased capillary refill or mottling

FIO₂, Fraction of inspired oxygen; INR, international normalized ratio; MAP, mean arterial pressure; PaO₂, partial pressure of arterial oxygen; PTT, partial thromboplastin time; SBP, systolic blood pressure.

Source: Dellinger RP, Levy MM, Rhodes A, et al: Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012, Crit Care Med 41:580, 2013.

Septic shock is the presence of sepsis with hypotension despite adequate fluid resuscitation, along with inadequate tissue perfusion resulting in tissue hypoxia. The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also cause sepsis and septic shock.¹² Fig. 67-5 presents the pathogenesis of septic shock.

FIG. 67-5 The pathophysiology of septic shock. *CNS,* Central nervous system.

When a microorganism enters the body, the normal immune or inflammatory responses are started. However, in severe sepsis and septic shock the body’s response to the microorganism is exaggerated. Inflammation and coagulation increase, and fibrinolysis decreases. Endotoxins from the microorganism cell wall stimulate the release of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through secondary mediators such as platelet-activating factor, IL-6, and IL-8.¹² (See Chapter 12 for discussion of the inflammatory response.) The release of platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature. The combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium.

Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients may be euvolemic, but because of acute vasodilation, relative hypovolemia and hypotension occur. In addition, blood flow in the microcirculation is decreased, causing poor oxygen delivery and tissue hypoxia. The combination of TNF and IL-1 is 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 dilate to maintain the stroke volume. The ejection fraction typically improves, and ventricular dilation resolves over 7 to 10 days. Persistence of a high CO and a low SVR beyond 24 hours is an ominous finding and is often associated with an increased development of hypotension and MODS. Coronary artery perfusion and myocardial oxygen metabolism are not primarily altered in septic shock.

In addition to the cardiovascular dysfunction that accompanies sepsis, respiratory failure is common. The patient initially hyperventilates as a compensatory mechanism, resulting in respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis develops. Respiratory failure develops in 85% of patients with sepsis, and 40% develop acute respiratory distress syndrome (ARDS) (see Chapter 68). These patients need to be intubated and mechanically ventilated. Other clinical signs of septic shock include alteration in neurologic status; decreased urine output; and GI dysfunction, such as GI bleeding and paralytic ileus. Table 67-3 gives the clinical presentation of a patient with septic shock.

Obstructive Shock.

Obstructive shock develops when a physical obstruction to blood flow occurs with a decreased CO (Fig. 67-6). This can be caused by restricted diastolic filling of the right ventricle from compression (e.g., cardiac tamponade, tension pneumothorax, superior vena cava syndrome). Other causes include abdominal compartment syndrome in which increased abdominal pressures compress the inferior vena cava, thus decreasing venous return to the heart (see Chapter 43). Pulmonary embolism and right ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. This leads to decreased blood flow to the lungs and decreased blood return to the left atrium.

Patients experience a decreased CO, increased afterload, and variable left ventricular filling pressures depending on the obstruction. Other clinical signs include jugular venous distention and pulsus paradoxus (see Table 37-5). Rapid assessment and treatment are important to prevent further hemodynamic compromise and possibly cardiac arrest (see Fig. 67-6).

Stages of Shock

In addition to an understanding of the underlying pathogenesis of the type of shock that the patient is experiencing, monitoring and management are guided by knowing where the patient is on the shock “continuum.” This continuum begins with the initial stage of shock that occurs at a cellular level and is usually not clinically apparent. Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid buildup. Lactic acid is a waste product that is removed by the liver. However, this process requires oxygen, which is unavailable because of the decrease in tissue perfusion. Shock is categorized into three clinically apparent but overlapping stages: compensatory stage, progressive stage, and irreversible stage.⁵

Compensatory Stage.

In the compensatory stage the body activates neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. (See eFig. 67-1 on the website for this chapter.) The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand (Table 67-5).

TABLE 67-5

MANIFESTATIONS OF STAGES OF SHOCK *

Compensatory Stage	Progressive Stage	Irreversible Stage
Neurologic System
Oriented to person, place, time Restless, apprehensive, confused Change in level of consciousness	↓ Cerebral perfusion pressure ↓ Cerebral blood flow ↓ Responsiveness to stimuli Delirium	Unresponsive Areflexia (loss of reflexes) Pupils nonreactive and dilated
Cardiovascular System
Sympathetic nervous system response: • Release of epinephrine/norepinephrine (vasoconstriction) • ↑ MVO₂ • ↑ Contractility • ↑ HR Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Introduction Nursing Management: Sexually Transmitted Infections Nursing Assessment: Cardiovascular System Nursing Management: Musculoskeletal Problems Stay updated, free articles. Join our Telegram channel Tags: Medical-Surgical Nursing Assessment and Management of Clinical P Nov 17, 2016 \| Posted by admin in NURSING \| Comments Off on Nursing Management: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access

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Nursing Management: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome

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