Recognizing and Treating Five Shock States

Shock is a clinical condition that is life-threatening, yet early recognition and treatment of shock can save lives. Shock can result from several causes—injury, trauma, infection—and represents an imbalance between oxygen supply and demand. Shock is characterized by hypoxia and inadequate cellular function that can lead to organ system failure and death. An understanding of the pathophysiology, signs and symptoms, and treatment of shock are important for nurses, as the role of the bedside provider is key in identifying shock.

Five distinct types of shock are classified by etiology. These include cardiogenic, hypovolemic, anaphylactic, neurogenic, and septic shock. Generally, the causes of shock produce physiologic changes that can be distinguished from one another. However, all have manifestations of inadequate peripheral tissue perfusion, impaired cellular function, and impaired organ perfusion. Although compensatory mechanisms, including the sympathetic nervous system and neurohormonal responses, attempt to maintain cardiac output and perfusion, hypoxic injury and cellular and organ damage can occur. Recognizing the signs of shock and instituting treatment measures can help reestablish perfusion and prevent further deleterious effects. In monitoring patients and recognizing the signs of shock, the nurse plays a critical role in identifying and treating shock and, most importantly, helps positively influence outcomes for acutely ill patients.

Chapter 1
The Pathophysiology of Shock

Shock is a clinical syndrome that results from inadequate tissue perfusion.¹ Shock occurs when the blood supply to the organs, tissues, and cells of the body is decreased. Inadequate blood supply impairs cellular function. When shock occurs, systemic hypotension, acidosis, and impairment of vital organ functioning result.² An imbalance between the delivery and the uptake of oxygen leads to cellular dysfunction.

Shock is the body’s response to physiologic injury, trauma, or infection. The major types of shock include cardiogenic, hypovolemic, anaphylactic, neurogenic, and septic shock.¹ Regardless of the specific type and cause of shock, the end result is impaired tissue perfusion, which leads to inadequate oxygenation to the cell, causing cellular damage. Shock is defined by the presence of hypoperfusion to organs.³ Clinical signs include hypotension, tachycardia, tachypnea, cool skin, altered level of consciousness, and oliguria.³

Stages of shock

There are several distinct stages of shock. These include the initial, compensatory, progressive, and refractory stages of shock.^2,4

Initial

In the initial stage of shock, the cardiac output, or the amount of blood ejected from the heart per minute to perfuse the body, is decreased, leading to decreased blood supply. Clinical evidence of decreased cardiac output includes cool clammy skin, decreased urinary output, altered level of consciousness, cyanosis, pallor, and hypotension.² When tissue perfusion is impaired, changes in the normal functioning of the cell occur. As the blood supply to cells decreases, cells switch from aerobic to anaerobic metabolism as a source of energy. Anaerobic metabolism produces minimal energy and leads to a buildup of lactic acid, which is detrimental to the functioning of a cell. Lactic acidosis develops, causing more cellular damage as the body is unable to buffer the increased levels of acid. The degree of lactic acidosis can be determined by monitoring serum lactate levels. Normal serum lactate levels are less than 1 mmol/L.⁵ Lactic acidosis is associated with high levels of serum lactate (greater  than 4 mmol/L). In some patients with shock, neither the arterial pH nor bicarbonate may reflect the presence of lactic acidosis. Therefore, the most accurate assessment of the severity of lactic acidosis is the serum lactate level.⁵

Compensatory

In the compensatory stage of shock, the body’s homeostatic mechanisms attempt to improve tissue perfusion.^2,4 The compensatory mechanisms are mediated by the sympathetic nervous system (SNS) and consist of neural, hormonal, and chemical responses.

Neurohormonal responses maintain the cardiac output. The neurohormonal responses include the following:

• Catecholamines are released, causing increased contractility.
• Renin released by the kidneys causes the formation of angiotensin I, which is then converted to angiotensin II that causes vasoconstriction, shunting blood to vital organs. Aldosterone is released, causing water conservation.
• Capillary hydrostatic pressure decreases and shifts fluid to intravascular space.
• Antidiuretic hormone release causes conservation of sodium and water leading to decreased urine output.
• Release of epinephrine and norepinephrine by the sympathetic nervous system results in increased heart rate (HR).

The neuroendocrine to shock response includes several processes that attempt to compensate for the complications of decreased perfusion including hypotension and decreased circulating blood volume. When a change in perfusion occurs, volume-sensing mechanisms in the circulation including atrial stretch receptors, arterial baroreceptors, and intrarenal baroreceptors detect the change and stimulate several responses.^2,6,7 These include neuroendocrine and hormonal responses.

Following an insult, activation of the neuroendocrine system stimulates the release of numerous substances (“stress hormones”) into the circulation.^2,6,7 These include:

• Adrenocorticotropin hormone (ACTH) from anterior pituitary
• Glucocorticoids from adrenal cortex
• Epinephrine and norepinephrine from sympathetic nerves

Activation of the renin response results in the production of angiotensin II, which causes vasoconstriction and the release of aldosterone and antidiuretic hormone (ADH), leading to sodium and water retention.^2,6,7

Stimulation of the anterior pituitary results in secretion of adrenocorticotropic hormone (ACTH), which in turn stimulates the adrenal cortex to produce glucocorticoids, causing a rise in blood glucose levels. Stimulation of the adrenal medulla causes the release of epinephrine and norepinephrine, which further enhance the compensatory mechanisms.^2,6,7

These neurohormonal compensatory mechanisms are triggered in shock to help maintain arterial blood pressure despite a fall in cardiac output.^2,6,7

Hypoxic injury: A review

In shock, oxygen delivery to the mitochondria of the cell is decreased, leading to stalled energy production and failure of ion pumps (NA+, K+, and CA+). As a result, sodium accumulates within the cell, changing the osmotic gradient and causing cellular swelling.^6,7

Tissue hypoperfusion results in cellular hypoxia. At the cellular level, the body switches to metabolism that doesn’t require oxygen (anaerobic metabolism), which is insufficient to maintain cellular energy needs.^6,7 Anaerobic glycolysis results, with depletion of adenosine triphosphate (ATP) and intracellular energy reserves.^2,6,7 Energy that is required for cellular processes is stored in the phosphate bonds of the ATP molecule, and the breakdown of ATP results in the release of energy. With cellular hypoxia, the normal process of ATP breakdown is altered, resulting in increased hydrogen ion concentration.² Anaerobic glycolysis also causes accumulation of lactic acid, resulting in intracellular acidosis.

A brief review of oxygen delivery can help explain the effects of altered tissue perfusion and impaired oxygen delivery in shock:

• Oxygen delivery (DO2) is defined as the amount of oxygen delivered to the tissues of the body per minute. DO2 is dependent upon the cardiac output (CO), or the amount of blood pumped per minute, and the arterial oxygen content of that blood (CaO2).⁸
• Oxygen delivery is defined by the following equation⁸: DO2 (mL O2/min) = CaO2 (mL O2/L blood) X CO (L/min)
• The CaO2 is dependent upon how much oxygen-carrying capacity is available in terms of hemoglobin (Hgb) content as well as by how much oxygen the patient’s hemoglobin contains, defined as the arterial oxygen saturation (SaO2).⁸ The CaO2 is defined by the following formula: CaO2 = Hgb (g/100 mL) X SaO2 X 1.34 mL O2/g
• A state of clinical shock may exist when CaO2 is impaired either by hypoxia, which decreases SaO2, or by anemia, which reduces the amount of Hgb and hence reduces the body’s total oxygen-carrying capacity.⁸ Often, this is why patients in shock are given increased oxygenation, many times through intubation and mechanical ventilation. In addition, blood transfusions can be used to increase the oxygen-carrying capacity of the blood.
• Cardiac output depends on the amount of blood pumped with each heartbeat, determined by the patient’s stroke volume (SV) and heart rate (HR). Cardiac output is defined by the following formula: CO = HR (beats/min) x SV (mL/beat).⁸
• SV is dependent upon the ventricular end-diastolic filling volume (commonly referred to as ventricular preload), myocardial contractility, and the afterload.⁸ These factors can be impaired in clinical shock states and impact the cardiac output.⁸

These principals are used to provide treatment measures to the patient in shock. Often, intravenous fluids are administered in order to increase preload, vasodilators are used to decrease afterload, and inotropes are given to improve contractility.

Progressive shock

As shock progresses, these compensatory mechanisms are no longer able to sustain adequate perfusion to tissues and impaired oxygen delivery results.

A decreased cardiac output results in impaired oxygenation that causes hypoxic injury to the cells. Metabolic acidosis with severe electrolyte imbalance and respiratory acidosis with hypoxemia can occur. Under anaerobic metabolism, toxic metabolites accumulate, including lactic acid.⁹ The acid-base status of the body (pH) is normally between 7.35 and 7.45.⁹ The blood pH decreases when lactic acid production increases (termed lactic acidosis).⁹ Profound acidosis (a pH less than 7.0) results in altered cellular functioning and cellular damage.

Refractory shock

In the refractory stage of shock, systemic hypoperfusion causes multiple organ damage.

• Shock becomes unresponsive to therapy.
• End-organ damage and cellular necrosis occur.
• Death occurs from impaired tissue perfusion because of the failure of the circulation to meet cellular oxygen demands.

Differentiating shock states

There are several types of shock states: cardiogenic, hypovolemic, anaphylactic, neurogenic, and septic. Each type of shock involves several clinical manifestations that are also characteristic of many other critical conditions, making diagnosis difficult. In addition, the body’s many compensatory mechanisms can initially mask many of the definitive signs of shock.

In summary, shock results from decreased tissue perfusion that affects the vital functioning of cells. Shock is characterized by hypotension and inadequate perfusion that can lead to organ system failure and death. Compensatory mechanisms, including the sympathetic nervous system release of catecholamines and neurohormonal responses including vasoconstriction via renin-angiotensin release and fluid conservation via antidiuretic hormone release attempt to maintain cardiac output and perfusion. If compensatory mechanisms fail to provide adequate perfusion to tissues, hypoxic injury, acidosis, severe electrolyte imbalance, and death can result.

Chapter 2
Cardiogenic Shock

Cardiogenic shock results when the heart no longer functions as an effective pump, often because of acute myocardial infarction. Other causes include pulmonary edema, cardiomyopathies, dysrhythmias, pericardial tamponade, or valvular regurgitation.^1,2 The estimated incidence of cardiogenic shock is 5%-10% of patients with myocardial infarction.^1,2

Cardiogenic shock results in decreased cardiac output, altered oxygen delivery, and reduced tissue perfusion. Specifically, cardiogenic shock is defined as a decrease in cardiac output along with evidence of tissue hypoxia in the presence of adequate blood volume.^1,2 In cardiogenic shock, the heart is unable to effectively contract, and right or left ventricular dysfunction can result because of diminished or ineffective contractility. Cardiogenic shock is often characterized by both systolic and diastolic myocardial dysfunction. Inadequate tissue perfusion results from myocardial dysfunction, which leads to cellular hypoxia and ischemia, the end results of shock.^3,4  Clinical signs and symptoms include^1,2,3 —

• Altered mentation
• Pale, cool clammy skin
• Hypotension
• Tachycardia
• Oliguria
• Distended neck veins
• Low cardiac output and cardiac index (less than 2.2 L/minute/m2)

Cardiogenic shock is diagnosed based on clinical signs and symptoms as well as specific hemodynamic criteria that indicate inadequate cardiac functioning. These include —

• Sustained hypotension (systolic blood pressure [SBP] less than 90 mm Hg or 40 mm Hg below baseline for at least 30 minutes)
• Reduced cardiac index (less than 2.2 L/minute/m2) with  pulmonary capillary wedge pressure (PCWP) more than 15 mm Hg.¹

In cardiogenic shock, the myocardial dysfunction is difficult to treat because the underlying cellular damage is often irreversible.^2,3 Treatment goals include —

• Enhanced contractility
• Decreased oxygen demands
• Increased myocardial oxygen supply
• Increased cardiac output

These goals are difficult to achieve, as interventions to increase CO tend to increase myocardial oxygen demands.^2,3,4 The management of cardiogenic shock is aimed at optimizing myocardial function.

Treatment components

Common treatments for cardiogenic shock include supplemental oxygen or endotrachael intubation and mechanical ventilation and hemodynamic support. The initial approach should include fluid resuscitation only if pulmonary edema is not present.^2,3,4 Other indicated aspects of treatment can include:

• Diuretic therapy to decrease preload and pulmonary congestion, thus improving oxygenation.
• Medications, such as intravenous inotropes (e.g., amrinone or dobutamine) to increase mycardial contractility.
• Vasodilator medications such as nitroglycerin or nitroprusside to decrease ventricular preload and afterload. But must be used with caution, after BP has stabilized.
• Use of vasopressors such as norepinephrine (Levophed) when hypotension remains refractory.
• Catecholamine infusions such as epinephrine must be carefully titrated in patients with cardiogenic shock to maximize coronary perfusion pressure with the least possible increase in myocardial O2 demand.
• Vasopressin, a hormone, has been used with a good response for refractory vasodilatory shock when administered as an intravenous infusion to promote vasoconstriction.⁵
• Mechanical support devices such as the intra-aortic balloon pump (IABP) can be used to augment coronary artery perfusion and systolic ejection. The IABP is inserted through the femoral artery and positioned in the descending thoracic aorta. It inflates during diastole to improve blood flow to the heart by supplying the coronary arteries with freshly oxygenated blood. The balloon then deflates at the end of diastole just prior to ventricular systole (contraction of the left ventricle) to decrease left ventricular afterload (resistance to ejection) to improve cardiac output.⁴ The IABP is used for temporary support for patients in cardiogenic shock until either myocardial function improves or surgical intervention can be performed. 
• Another assist device, a ventricular assist device, decreases the heart’s workload and increases cardiac output. However, VADs are not usually used for cardiogenic shock alone but as a bridge to transplant.
• Other indicated treatments may include reperfusion interventions such as percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery. These interventions reestablish perfusion to improve ventricular function after myocardial infarction. Reperfusion measures in patients with cardiogenic shock after myocardial infarction have increased survival rates.⁶  - Thrombolysis is the most common treatment for acute MI, but successful outcomes depend on drug delivery to the clot, which may be less likely in hypoperfused states/hypotension/cardiogenic shock.
      -  Studies have shown that thrombolytics can reduce the likelihood of shock after initial presentation, but no studies demonstrate that thrombolytics reduce mortality rate in patients presenting in cardiogenic shock.

In summary, cardiogenic shock results from altered ability of the heart to contract and eject blood, leading to a decreased cardiac output. Cardiogenic shock often results from acute MI and is characterized by systolic and/or diastolic dysfunction. Decreased contractility and low cardiac output lead to reduced tissue perfusion. Pulmonary edema can result from impaired left ventricular ejection and high filling pressures, leading to hypoxemia. Cardiogenic shock is a medical emergency and requires oxygenation, diuretics for pulmonary congestion, and vasopressor and inotropic support for hypotension refractory to fluid therapy. IABP counterpulsation may be needed to stabilize the patient, and therapeutic interventions such as revascularization procedures may be needed.

Chapter 3
Hypovolemic Shock

Hypovolemic shock is considered the most common form of shock.¹ Hypovolemic shock results from loss of blood, from loss of plasma volume of greater than 20% of the circulating volume, or from profound dehydration.¹

Commonly, hypovolemic shock is due to rapid blood loss.² Other causes of hypovolemic shock include massive gastrointestinal losses, burns, capillary leak, and tissue third spacing, which results in leakage of fluid out of the intravascular space into the interstitial tissues, which can occur in such conditions as pancreatitis, bowel obstruction, and ascites.^1,2

The clinical signs of hypovolemic shock include pale, cool, clammy skin; systolic blood pressure less than 90 mm Hg or 40 mm Hg below baseline; delayed capillary refill; tachycardia; tachypnea; oliguria; anxiety; and decreased level of consciousness.^2,3 There is wide variation in the clinical symptoms depending upon the amount of volume loss, the rate of loss, and the underlying illness or injury causing the loss.³ Hypovolemia results in shock caused by decreased blood volume, leading to decreased cellular oxygen supply and impaired tissue perfusion.^1,2,3,4

Stages of hypovolemic shock

There are several distinct stages of hypovolemic shock.^1,4

1. Initial stage: 15% (750 ml) volume loss
 - Compensatory mechanisms maintain cardiac output.
 - Patient is asymptomatic.

2. Second or compensatory stage: 15-30% (750-1500 ml) volume loss
 - Cardiac output falls, resulting in compensatory increase in heart rate and respiratory rate, low urine output, and altered level of consciousness.
 - Hypoxemia develops as perfusion to tissues is reduced as a result of the decreased cardiac output.
 - Sympathetic nervous system compensatory mechanisms are activated with resulting vasoconstriction.

3. Third or progressive stage: 30-40% (1500 to 2000 ml) volume loss
 - Compensatory mechanisms become overwhelmed, and impaired tissue perfusion develops.
 - Dysrhythmias caused by myocardial ischemia, metabolic acidosis. and respiratory distress occur.

4. Fourth or refractory stage: Over 40% (more than 2000 ml) volume loss
 - Overwhelming blood loss is immediately life-threatening.
 - Compensatory mechanisms deteriorate and organ failure occurs.
 - Severe tachycardia, hypotension, narrow pulse pressure, and cardiac arrest ensues.

Pathophysiology

In hypovolemic shock, venous return to the heart (preload) decreases, resulting in decreased cardiac output.³ Compensatory mechanisms respond by increasing heart rate, systemic vascular resistance (SVR), cardiac output, and tissue perfusion owing to catecholamine release.³ Blood volume is increased in several ways, including through neurohormonal mechanisms including the renin-angiotension-aldosterone system that promotes conservation of sodium and water and a shifting of the interstitial fluid into the vasculature in response to the decreased circulating volume. Additionally, the liver and spleen release stored red blood cells and plasma. With continued blood loss, the compensatory mechanisms are unable to maintain perfusion to the tissues and organs, and the end result of shock can result: profound acidosis, altered cellular functioning, and cellular damage.³

Treatment goals

The treatment goals for hypovolemic shock are to treat the underlying cause, control additional fluid loss, and replace fluid losses.^5-7 Volume expanders including crystalloid solutions (e.g., lactated Ringer’s solution, normal saline) and colloids (e.g., albumin, hetastarch [Hespan]) are used for fluid resuscitation of patients with hypovolemic shock. Crystalloids are effective at expanding intravascular volume and interstitial fluid.⁶ Lactated Ringer’s solution and normal saline are the two most commonly used isotonic solutions.⁸ The advantage of using lactated Ringer’s solution is that it is metabolized by the liver and kidneys to generate bicarbonate, which provides a buffer against the lactic acid generated by tissue hypoperfusion, thereby promoting normal pH balance.⁸ Colloids expand the intravascular space by pulling fluid from the interstitial spaces.⁹ Although colloids are more effective than crystalloids at increasing intravascular fluid, data suggest an increased incidence of complications and risk of death with the use of colloids, particularly albumin.¹⁰

Blood and blood products are used for patients who are hemodynamically unstable, for patients with greater than 1500 cc blood loss, and patients with ongoing uncontrolled sources of bleeding.^8,10 Transfusion of blood and blood products are usually indicated for a hematocrit less than 28%.¹ Whole blood is used to replace large blood loss, while packed red blood cells (PRBCs) are used to replace moderate blood loss.¹¹ Platelets are administered when platelet levels are decreased (thrombocytopenia), which occurs in hemorrhage. Fresh frozen plasma (FFP) is used to correct plasma deficits and restore osmotic pressure.¹¹

Type-O PRBCs are used for initial resuscitation in emergent situations, until cross-matched blood is available.⁸ In the presence of coagulopathy, hypothermia, or when PRBC transfusion exceeds six units, platelets and FFP should be administered.⁸

With massive hemorrhage, in which the volume of blood lost equals the patient’s total blood volume, a 70-kg adult may require 10 units of PRBCs in 24 hours.⁸

New artificial red blood cells that are more like RBCs are being developed.¹² Red blood cell (RBC) substitutes, often referred to as hemoglobin-based O2 carriers (HBOCs), consist of extracted hemoglobin from lysed RBCs.¹² Most RBC substitutes have a hemoglobin concentration of 10%-15%, compared to a typical hemoglobin concentration of PRBCs of 20-25 g/dl.¹² RBC substitute solutions are typically hypertonic colloids and expand blood volume more than the volume of the infused solution.¹²

Other aspects of treatment include determining the cause of blood or volume loss and preventing further volume loss.⁵ Vasopressor medications such as dopamine, phenylephrine, and dobutamine may be required to increase blood pressure and cardiac output. However, vasopressors should not be given without adequate fluid replacement because they can cause cardiac decompensation and hemodynamic deterioration, especially in patients with ischemic heart disease.¹³ Other interventions may include insertion of a urinary catheter to monitor urine output and invasive monitoring with a Swan-Ganz catheter to monitor cardiac output and metabolic consumption (SVO2).⁵ A central venous catheter may be inserted to monitor central venous pressure.

In summary, hypovolemic shock results from loss of blood, loss of plasma volume, and profound dehydration. It is the most common form of shock. Hypovolemic shock is categorized into several stages based on fluid loss. The goals of treatment for hypovolemic shock are to replace losses, prevent further fluid loss, and treat the underlying cause.

Chapter 4
Anaphylactic Shock

Anaphylactic shock results from an allergic reaction that causes systemic release of immunoglobulin E (IgE), an antibody formed as part of immune response, and causes mast cell activation and histamine release.^1,2 Anaphylaxis affects up to 15% of the U.S. population.³ It is estimated that 3.29 million to 40.9 million people are at risk of anaphylaxis.³

Many substances known as allergens can cause anaphylaxis (see Table 2).

Allergens may include foods, food additives, drugs, and insect stings. Insect stings present the greatest number of cases of anaphylaxis.³ Routes of entry for an allergen can include injection, ingestion, inhalation, and skin absorption.

Clinical signs of anaphylaxis include generalized pruritis, respiratory distress, hives, and restlessness (see Table 3).^4,5,6,7,8

The signs and symptoms of anaphylaxis can appear within several minutes of exposure to the antigen. The severity of the reaction is directly related to the onset of symptoms, with early signs appearing with a severe reaction. Occasionally, biphasic reactions occur in which symptoms recur several hours after the initial reaction.⁶

Anaphylaxis is a life-threatening hypersensitivity reaction that can develop rapidly (within seconds) or occur as a delayed reaction (12 or more hours after initial exposure).^4,5,6

Pathophysiology of anaphylaxis

Anaphylaxis, caused by an antibody-antigen response, results in an extensive immune and inflammatory response.^1,2,3 Anaphylactic shock results from an allergic reaction that causes release of IgE, an antibody that is formed as part of the immune response. Leukocytes, including mast cells, basophils, and eosinophils, release mediators such as histamine, prostaglandins, kinins, and complements that cause vasodilation, increased vascular permeability, hypotension, brochoconstriction, and coronary vasoconstriction.^1,2,3,4

The result is peripheral pooling of blood, tissue edema, airway constriction, and myocardial depression. A state of relative hypovolemia occurs, with altered tissue perfusion and impaired cellular metabolism. If untreated, anaphylaxis results in a shock state and can lead to cardiac, renal, pulmonary, and multisystem organ failure.^1,2,3,4 Death may result from cardiovascular or respiratory distress.

Treatment Goals

The treatment goals for anaphylactic shock include the “ABCs” (airway, breathing, and circulation) of emergency care, along with volume expansion.^1-4

Epinephrine is a first-line drug administered to patients with anaphylaxis to promote vasoconstriction and further inhibit mediator release. The standard dose of epinephrine is 1:1000, 0.3 ml given subcutaneously.⁹

Hypotension should be managed with intravenous fluids to promote intravascular volume expansion. Colloid solutions (e.g., 5% albumin, 6% hetastarch) better facilitate volume expansion than crystalloid solutions (e.g., lactated Ringer’s solution, 5% dextrose in normal saline). Vasoconstrictor agents such as norepinephrine (Levophed), phenylephrine (Neo-Synephrine), and dopamine HCL (Intropin) may be administered to reverse the effects of severe vasodilation and myocardial depression.^1,2,3,4

Antihistamines, such as diphenhydramine (Benadryl), are useful as second-line drug therapy to block the histamine response and stop the inflammatory reaction. Additional treatment measures include Amino-phylline and inhaled beta 2 agonists to reverse bronchospasm and corticosteroids to help stabilize capillary membranes and prevent a delayed reaction.^1,2,3,4,9

Prevention

Prevention of anaphylactic shock through identification of patients at risk and careful monitoring of patient response to drugs, blood products, and blood is an important component of nursing care (see Table 4).⁸

Important measures include obtaining a complete allergy history and identifying potential allergens. Patients experiencing an episode of anaphylaxis should be instructed to avoid the allergen. Teaching about the importance of seeking prompt medical attention when symptoms of anaphylaxis occur is an important part of patient education.⁸ Early identification and prompt medical treatment are essential in preventing a life-threatening reaction. The American Academy of Allergy, Asthma, and Immunology stresses that education of the lay and professional public will help promote the prompt administration of epinephrine for the emergency treatment of anaphylaxis.⁹

Chapter 5
Neurogenic Shock

Neurogenic shock results from loss of peripheral sympathetic vasomotor tone. Neurogenic shock is commonly seen in trauma and results from a change in systemic vascular resistance, mediated by a neurologic injury (e.g., head injury or high thoracic or cervical spinal cord injury).^1,2 Neurogenic shock, sometimes called vasogenic shock, is considered the rarest form of shock³ and results from the disruption of autonomic nervous system control over vasoconstriction.⁴ After spinal cord injury, neurogenic shock can occur immediately after injury or can exhibit a delayed response for up to weeks after the initial injury.¹

Although the terms are sometimes used interchangeably, neurogenic shock is not spinal shock, which refers to an acute, transient neurologic syndrome of motor, sensory, and reflex dysfunction that develops below the level of injury.⁵ Neurogenic shock is a hemodynamic syndrome associated with upper thoracic and cervical spinal cord injury or head injury and is characterized by bradycardia and decreased systemic vascular resistance. The two patterns may or may not occur concurrently.⁵ Neurogenic shock is distinguished by a pattern of decreased heart rate, blood pressure, and systemic vascular resistance.⁵

The classic signs of shock may not be present in neurogenic shock because of alteration in sympathetic tone.⁵ As a result, bradycardia is commonly seen and the skin is warm, dry, and pink, rather than cool and pale — at least below the level of spinal cord injury.⁵

Pathophysiology

In neurogenic shock, sympathetic nervous system dysregulation occurs. As vasomotor tone is lost, systemic arteriolar resistance decreases profoundly and venous pooling increases, resulting in decreased preload and afterload and subsequent massive vasodilation and decreases in cardiac output.^1,2,3 Unopposed vagal tone results in significant bradycardia.

The loss of normal sympathetic tone also results in an inability to shunt blood from the periphery to the core, and heat loss through the skin becomes excessive, resulting in hypothermia.^1,2,3,4 Decreased tissue perfusion results primarily from arterial hypotension caused by a reduction in systemic vascular resistance.^1,2,3,4 In addition, a reduction in effective circulating plasma volume often occurs because of a decrease in venous tone and subsequent venous pooling of blood and loss of intravascular volume into the interstitium because of increased capillary permeability.⁶ As a result, a decrease in cardiac output leads to decreased cellular oxygen supply and impaired cellular metabolism.

The clinical signs and symptoms of neurogenic shock include hypotension and pale, cool, clammy skin with warm extremities below the level of injury. Bradycardia, hypothermia, and decreased level of consciousness can also be present.^1,2,3,4

Treatment

The diagnosis of neurogenic shock is often one of exclusion.⁷ Priorities of treatment include the ABCs of emergency care. The Trendelenburg position can be used temporarily to increase the blood pressure. Fluid resuscitation is given with caution, as the blood volume is sufficient but blood distribution is altered.^1-4 The administration of a large volume of IV fluids to increase central venous return may cause heart failure. Insertion of a Foley catheter may be required as bladder function may be lost. Atropine may be administered to block dominant vagal effects that cause bradycardia.^{1,2,3,4,5,6,7}

Vasoconstrictive intravenous agents may be used to increase blood pressure that is resistant to fluid replacement.^1,2,3,4 Positive inotropic agents such as dopamine and dobutamine at lower dosages (1-5 mcg/kg/min) can enhance cardiac output, increase perfusion pressure, and improve renal hemodynamics.^5,6,7 However, vasopressors are used with caution, as vasoconstriction may decrease spinal cord blood flow, which can ultimately influence the extent of secondary cord injury. In rare cases, a pacemaker may be required for refractory bradydysrthythmias.^6,7  Venous pooling puts patients at risk for DVT and PE.

In summary, neurogenic shock results from loss of peripheral sympathetic tone, often because of spinal cord injury from trauma or regional anesthesia. The loss of normal sympathetic tone results in massive vasodilation with severe hypotension and unopposed vagal tone that can result in bradycardia. Treatment goals include the ABCs of emergency care, fluid resuscitation, and vasocontrictive agents to increase blood pressure and agents to block vagal effects causing bradycardia.

Chapter 6
Septic Shock

Sepsis is a complex syndrome that results from an infectious process. Hypovolemia and vasodilation result from the effects of inflammatory mediators that are released during the immune system response to infection. As with the other shock states, tissue perfusion is impaired, but the process is more complex as in sepsis microcirculatory clot formation further impairs perfusion to the tissues and cells.^1,2

In addition, damage to the lining of the blood vessels, or the endothelium, occurs. This causes fluid to leak from the intravascular and intracellular spaces into the interstitial spaces, causing edema. The combination of fluid leak from increased capillary membrane permeability, microemboli, and vasodilation from the effect of mediators results in decreased perfusion that can be detrimental to vital organs.^1,2,3,4

Overview of sepsis

Sepsis with acute organ dysfunction (severe sepsis) is common and frequently fatal. Risk factors include a compromised immune system, chronic illness, and age of under 1 or over 65. (See Table 5, “Risk Factors for Sepsis.”)

Each year, approximately 215,000 deaths occur from severe sepsis.⁵ Severe sepsis, which is sepsis with malfunctioning of one or more organs, is common, affecting 750,000 Americans annually.^5,6 Severe sepsis is associated with a mortality rate of 28%-50% or greater.^5,6

Epidemiology

In the United States, severe sepsis is the most common cause of death in noncardiac ICUs and the 10th leading cause of death overall.⁷ A number of factors has led to an increased incidence of sepsis: the  rise in the number of elderly patients in health care facilities; an increased number of patients with compromised immune status, chronic illness, or malnutrition; an increased number of patients having invasive and surgical procedures; and an increased number of resistant microorganisms.^1,2

Pathophysiology of severe sepsis

The pathophysiology of sepsis is complex and is associated with three integrated responses: activation of inflammation, activation of coagulation mediators, and procoagulant factors and impairment of fibrinolysis.⁹

Inflammation in severe sepsis

Inflammation represents the body’s normal response to infection. White blood cells, specifically monocytes and macrophages, generate and release cytokines, nonspecific mediators of inflammation.^1,9

Inflammatory cytokines including tumor necrosis factor-a (TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), and platelet-activating factor (PAF) are released.¹⁰ These early response cytokines play a critical role in the immune system response to infection by attracting activated neutrophils to the site of infection.

Activation of coagulation

Several mechanisms activate clot formation in patients with severe sepsis. Cytokines stimulate the release of tissue factor, a cell surface glycoprotein, from monocytes and endothelial cells. Tissue factor directly stimulates the extrinsic coagulation pathway.¹¹ The result is the formation of the enzyme thrombin, which converts fibrinogen to fibrin, producing a clot.  Continued thrombin production leads to the formation of microthrombi, which can affect blood flow and organ perfusion.

Sepsis-associated coagulopathy

Alterations in coagulation that occur in sepsis can lead to sepsis-associated coagulopathy and death. Abnormalities in fibrinolysis, in addition to coagulation, frequently occur in patients with sepsis. Thrombocytopenia can also occur and is often a result of disseminated intravascular coagulation (DIC), inhibition of thrombopoiesis, or increased destruction or margination of activated platelets into the peripheral circulation.³

Impairment of fibrinolysis

Fibrinolysis, or clot breakdown, is a part of the body’s normal response to the formation of clots. While the fibrinolytic system is activated in sepsis, inhibition of the fibrinolytic system follows because of the release of several mediators that suppress fibrinolysis. These include plasminogen activator inhibitor-1 (PAI-1) and thrombin activatable fibrinolysis inhibitor (TAFI). Plasminogen activator inhibitor-1 is produced by endothelial cells and platelets and serves as the major inhibitor of tissue plasminogen activator (t-PA), which promotes conversion of plasminogen to plasmin to break down clots.¹¹

While PAI-1 and TAFI have a protective function in limiting excessive fibrinolysis, increased levels of PAI-1 and TAFI suppress fibrinolysis to the point of creating a state of coagulopathy.¹¹ The imbalance between inflammation, coagulation, and fibrinolysis that occurs results in systemic inflammation, widespread coagulopathy, and microvascular thrombosis, which can lead to multiple organ dysfunction.^1,2,3,4

The endothelium in severe sepsis

The endothelium is a one-cell layer lining all of the blood vessels. The endothelium plays a role in facilitating blood flow and the movement of cells within the blood. It was once thought that the endothelium merely separated the blood and underlying tissue.^11,13 Research on the endothelium has demonstrated that the endothelium is a metabolically active organ that plays a significant role in many homeostatic processes, including controlling vasomotor tone, promoting movement of cells and nutrients, and maintaining the fluid movement of blood.¹³

The endothelium plays a key role in the inflammatory, procoagulation, and impaired fibrinolytic processes of sepsis. The endothelium is the largest organ in the body, having a surface area estimated to exceed l000 m2, significantly more than the skin.¹⁴

Physiologically, the normal endothelium has an anticoagulant phenotype.¹¹ In sepsis, injury to the endothelium results when proinflammatory mediators are released from monocytes and macrophages responding to the infection.

While mediator release promotes recruitment of neutrophils and accumulation of platelets to wall off a site of infection, continued cytokine release can result in endothelial damage.

Physical disruption of the endothelium then allows inflammatory fluid and cells to move from the intravascular space into interstitial spaces, further adding to altered endothelial cell dysfunction, inflammation, and edema formation.¹⁵ As sepsis progresses, alterations in vasoregulation can result in vasodilation, severe hypotension, and impaired microcirculatory blood flow. In severe sepsis, progression of endothelial damage can lead to endothelial dysfunction.

Symptoms of sepsis

While early recognition of sepsis is important and influences survival, the clinical signs of sepsis can be difficult to identify. Signs of sepsis include changes in vital signs (blood pressure, heart rate, respiratory rate, temperature), along with signs of altered perfusion to vital organs (e.g., decreasing urine output from the development of acute renal failure).

Often, patients with sepsis exhibit signs of the systemic inflammatory response or SIRS criteria: alteration in temperature (most often elevation), elevated heart rate (more than 90 beats/minute), elevated respiratory rate (more than 20 breaths/ minute or a PCO2 less than 32 mm Hg), and an altered white blood cell count (greater than 12,000 cells/mm3, less than 4000 cells/mm3, or more than 10% immature (band) forms.⁸ Several terms specifically define the progression from infection to severe sepsis to septic shock and are outlined in Table 6.

Organ system dysfunction in sepsis

As sepsis continues, organ system dysfunction can occur because of altered perfusion and changes within the cell that lead to cell death. Multiple organ dysfunction syndrome (MODS) is a major cause of mortality in sepsis.¹⁶

Patients with severe sepsis have an average of two organ systems that are affected or become dysfunctional.⁴ This is associated with a mortality of up to 40%. As other organ systems are affected, mortality rates increase by 15%-20% with each additional failure.⁴ The implication for clinical practice is significant, as early detection and treatment of organ system dysfunction can prevent increasing rates of mortality in patients with severe sepsis.

Organ system dysfunction: cardiovascular

The clinical signs and symptoms of cardiovascular system dysfunction include tachycardia (heart rate greater than 100 beats per minute) and hypotension. Sepsis-induced hypotension is defined as a systolic blood pressure less than 90 mm Hg or a reduction of 40 mm Hg or greater from baseline without other obvious causes of hypotension.⁸

Clinical evidence of cardiovascular dysfunction in sepsis:

• Tachycardia 
• Restlessness, anxiety
• Hypotension
• Palpitations
• Elevated cardiac output and low systemic vascular resistance initially, then cardiac output decreases: anxiety
• Poor capillary refill
• Chest pain
• Dysrhythmias
• Cardiac arrest

Alteration in the cardiovascular system is often seen in sepsis because of the profound vasodilation, changes in vascular permeability, and direct myocardial depressant effects that result from cytokine release.¹⁶ Hypotension is considered a hallmark of the systemic inflammatory response, which results from mediator release and altered endothelial vasoregulation.^1,16 Septic shock occurs when hypotension is refractory to fluid resuscitation, and emergent stabilization requires aggressive therapy with vasopressors and inotropes.¹⁷

Patients at risk for developing sepsis should be monitored for alterations in cardiovascular functioning. Key areas of nursing assessment include blood pressure, heart rate, heart rhythm, heart sounds, capillary refill, skin color, and skin temperature.¹²

Additional information about cardiovascular functioning can be obtained with CVP monitoring and pulmonary artery catheter monitoring, but only when indicated. Various newer methods of monitoring cardiovascular functioning including esophageal Doppler are also being used to measure hemodynamic parameters.¹⁸

Organ system dysfunction: respiratory system

As hypotension occurs and perfusion status is altered in severe sepsis, impaired oxygenation often results. Signs and symptoms of altered respiratory status include an increase in respiratory rate, shortness of breath, anxiety, and restlessness. Nearly 85% of patients with severe sepsis require mechanical ventilation for respiratory failure, and up to 40% of patients develop acute lung injury or acute respiratory distress syndrome (ARDS).^4,16

Clinical evidence of respiratory dysfunction in sepsis:

• Tachypnea
• Restlessness/anxiety
• Dyspnea/cyanosis
• Abnormal blood gases
• Decreased oxygen saturation via pulse oximetry 
• Abnormal chest X-ray
• Need for mechanical ventilation
• Need for positive end expiratory pressure (PEEP) greater than 7.5

Nursing assessment of respiratory rate, breath sounds, pulse oximetry, and arterial blood gas results is an important part of monitoring for respiratory failure in sepsis. Along with assessment of respiratory function, providing supplemental oxygen and monitoring changes in pulse oximetry and oxygenation levels are important aspects of nursing care.¹²

Organ system dysfunction: renal system

Alterations in renal function are common in sepsis, as approximately 20% of the cardiac output perfuses the kidneys. Therefore, with decreases in blood pressure, cardiac output and perfusion, the kidneys are prone to renal failure. Changes in renal system functioning are reflected in decreased urine output and increased levels of blood urea nitrogen and creatinine.¹⁷

Renal failure develops in 15%-40% of patients with sepsis, and as many as 5% of patients require dialysis.^4,16 Many are unable to tolerate hemodialysis, so continuous renal replacement therapy is necessary. The factors that contribute to the development of acute renal failure include hypotension that leads to loss of autoregulation, decreased renal blood flow, and acute tubular necrosis.

Clinical evidence of renal dysfunction in sepsis:

• Increased BUN
• Increased creatinine
• Decreased creatinine clearance
• Decreased urine output. Oliguria is less than 0.4 mL/kg/hr. Anuria is less than 50 mL/day.

Nursing assessment should include monitoring urine output and laboratory values such as creatinine and blood urea nitrogen (BUN) levels to detect alterations in renal function. Hourly urine output should be monitored via a Foley catheter for decreasing trends, with the awareness that decreases to less than 0.5 mL/kg/hour indicate oliguria.¹⁹ The administration of fluid therapy, perfusion strategies, and renal replacement therapies may be indicated for patients with worsening renal function.

Organ system dysfunction: hematologic system

Alterations in hematologic function can occur in sepsis, owing in part to the increased coagulation and impaired fibrinolysis that result. Impaired perfusion, microcirculatory clot formation, and bleeding tendencies can occur. Patients with sepsis are also at increased risk for microvascular thrombus formation, which further compromises tissue perfusion.²⁰ While clinical disseminated intravascular coagulation (DIC) is found in about 20% of patients with severe sepsis, the majority of patients have some alteration in coagulation.²¹

Clinical evidence of hematologic dysfunction in sepsis include:

• Abnormal WBC count
• Left shift (increase in bands or immature neutrophils seen on the CBC and differential count, signifying release of immature WBCs by the bone marrow in an attempt to fight infection)
• D-dimer is positive
• Fibrin split products are increased
• Thrombocytopenia (low platelet count [less than 100,000/mm3])
• Increased bleeding times: protime (PT), partial thromboplastin time (PTT), international normalized ratio (INR)
• Bruising
• Bleeding
• Petechial hemorrhages

Important nursing considerations include monitoring laboratory parameters and monitoring patients for bleeding or bruising tendencies.¹² Deep vein thrombosis (DVT) and thromboembolism prophylaxis are also necessary for patients with severe sepsis, as they are commonly at increased risk because of critical illness, prolonged bed rest, and circulatory stasis.

Organ system dysfunction: hepatic and GI systems

Alterations in perfusion can also affect liver and GI functioning. Hypotension can precipitate intestinal ischemia, which can impair the barrier function of the intestinal mucosa, increasing the risk for bacterial translocation.²² Decreased hepatic blood flow can precipitate liver failure.

Clinical evidence of hepatic/GI dysfunction in sepsis include:

• Ileus
• Increased hepatic enzymes
• Increased amylase and lipase enzymes
• Nausea and vomiting
• Abdominal distention
• Change in bowel sounds
• Diarrhea or constipation

Organ system dysfunction: metabolic and endocrine

Metabolic derangements can be seen in severe sepsis including the development of lactic acidosis and altered glycemic control.¹⁶

Clinical evidence of metabolic and endocrine dysfunction in sepsis include:

• Metabolic acidosis results from anaerobic metabolism. Low pH (pH under 7.30)
• High lactate (above upper limit of normal)
• Serum protein consumption leads to decrease in capillary osmotic pressure with resultant edema
• Glycogenolysis, gluconeogensis, and insulin-resistant hyperglycemia initially; then glucose levels fall
• Increased catecholamine release (compensatory mechanism); adrenal insufficiency can result

Nursing assessment of GI function includes monitoring bowel sounds and laboratory values, and checking for residuals during enteral feedings. Patients may develop gastroparesis, which limits the ability to tolerate gastric feedings. Ileus formation may also compromise GI function. Clinical signs may include nausea, vomiting, and decreased or absent bowel sounds. Ensuring adequate nutrition is important in promoting cellular function as well as enhancing overall immune function.²³ Early initiation of enteral nutrition in critically ill patients has been shown to reduce infections and length of hospital stay.²⁴

Organ system dysfunction: neurologic system

Changes in neurologic status can occur in severe sepsis and can indicate alteration of an additional organ system.²⁵ Although mental status changes are common in acutely ill patients, their presence is not often recognized as a sign of severe sepsis.

Clinical evidence of neurologic dysfunction in sepsis include:

• Confusion
• Restlessness
• Disorientation: Altered consciousness, restlessness, and confusion
• Coma
• Psychosis
• Reduced Glasgow Coma Score

Multiple organ dysfunction syndrome

Alteration of organ function can result from the progression of sepsis. Multiple organ dysfunction syndrome (MODS) is a major cause of mortality in sepsis. Clinical criteria and laboratory markers can be used to assess the development and progression of MODS in severe sepsis. (See Table 7.)

Treatment goals

Essential treatment goals for severe sepsis include antibiotic therapy, supportive treatment with oxygenation and ventilation, and circulatory support with fluid and inotropic administration. The goal of fluid resuscitation is to restore tissue perfusion, and fluid infusion should be titrated to clinical end points, such as heart rate, blood pressure, and urine output.²⁶

Vasopressive agents such as dopamine, phenylephrine, or norepinephrine are indicated if volume infusions do not normalize blood pressure and organ perfusion, as judged by a mean arterial pressure (MAP) of greater than 60 mm Hg and adequate urine output.²⁶

The Surviving Sepsis Campaign Guidelines¹⁹ provide strategies for targeting treatment of patients at risk of developing severe sepsis and septic shock. The guidelines outline several evidence-based guidelines for the treatment of patients with severe sepsis. The recommendations are graded based on the degree of support from research.

Appendix A outlines the treatment strategies and grading for severe sepsis based on the Surviving Sepsis Campaign guidelines.

Because nurses are often involved in providing treatment measures, the ramifications of the guidelines for nursing care are important considerations. Appendix B outlines strategies for integrating the guidelines in nursing practice.

Progress has been made in decreasing the mortality rates of severe sepsis.³ Advances in the treatment of sepsis include goal-directed therapy to maximize perfusion, glucose control with the use of intravenous insulin to maintain serum glucose levels less than 150/dL (suggested range of 80-110 mg/dL), and use of activated protein C, an endogenous protein with antiinflammatory, antithrombotic, and pro-fibrinolytic effects.^3,27,28 Drotrecogin alfa (activated), or Xigris, is indicated for patients with severe sepsis with three or more SIRS criteria and evidence of organ system dysfunction.^29,30 Contraindications include active or recent bleeding, presence of an epidural catheter, trauma, being within 12 hours after major invasive procedures or surgery, intracranial neoplasm, or risk of bleeding.^29,30 Appendix C outlines nursing care considerations for Xigris therapy.

Role of the nurse

As the nurse is involved in the continuous bedside care of acutely ill patients, the nurse’s role in assessing and managing patients with shock and sepsis is an important one. Key areas include monitoring patients for evidence of developing shock and organ dysfunction, identifying patients at risk for shock and sepsis, promoting early identification, and instituting treatment measures.^31,32 Appendix D outlines nursing measures for patients with severe sepsis.

Keeping abreast of new evidence-based practices for nursing care is also important in ensuring adequate care for acutely ill patients. Research has highlighted the role of oral care in critically ill patients as a way to prevent colonization of bacteria in oral plaque that can lead to microaspiration and seeding of pneumonia.^33,34

Supine body position has been identified as a risk factor for nosocomial pneumonia, and raising the head of the bed to more than 30 degrees has beneficial effects.³⁵ Oral care and turning and positioning are direct nursing care measures and evidence-based practices that help prevent infection and promote optimal care.

Chapter 7
Case Studies

Case Study 1

Mr. G, a 45-year-old male with no significant medical history, presents to the ED with complaints of chest pain and syncope. His blood pressure is 90/50 mm Hg and his heart rate is 110 beats per minute. He has noted jugular vein distension and bilateral pedal edema. He is transferred to the intensive care unit and his heart rhythm is noted to be sinus tachycardia with some premature ventricular contractions.

1. What condition might be suspected?

2. Is he demonstrating signs of shock?

3. If so, what type?

Case Study 2

Mr. T, a 65-year-old male with a history of high blood pressure and asthma, was dining out with friends at a local restaurant when he suddenly became dizzy. The emergency medical system was activated and when the ambulance arrived, he was having difficulty breathing.  The emergency medical technician noted that he had a rash and hives on his neck.

1. What type of shock might be suspected?

2. Is Mr. T exhibiting any life-threatening signs and symptoms?

Case Study 3

A 69-year-old woman is brought to the ED by a neighbor, who reports that she found the patient in an incoherent state in her apartment after neighbors had noticed that the patient had not checked her mail for three days. The patient is currently awake and responsive, but is lethargic. She is Russian and speaks little English.

Current vital signs: BP: 88/50 mm Hg  Hr: 125 beats/min  Temp: 97.4 F (orally)   Respirations: 34 breaths/min

The initial physical exam reveals a thin white female, ill in appearance. Her skin is cool to touch, and the skin and mucous membrane color are pale. Lungs have bibasilar crackles to auscultation posteriorly. Abdomen is soft with hyperactive bowel sounds. She has no JVD. Slight pedal edema is present, capillary refill is sluggish. The EKG reveals sinus tachycardia. A Foley catheter was inserted for 60 cc dark yellow urine return.

Details about her past medical history are unavailable. An IV is started and lab work is drawn. A Russian translator arrives in the emergency room and begins interpretation. The patient relates that she is very weak and dizzy but denies pain. She states that she has had a “flu bug” for the past week, has not kept much food down and has been having diarrhea.

1. What additional questions should be asked?

2. What type of shock might be an initial differential diagnosis?

A rectal exam revealed red blood without masses and the stool culture is guiac positive. An NG is inserted and returns bright red blood and lavage is begun. IV fluid replacement and transfer to the ICU are initiated.

3. What additional testing may be indicated?

4. What stage of hypovolemic shock is present?

Case Study 4

Mr. H. is a 77-year-old male with a 16-year history of hypertension and a 30 pack/year cigarette history who is hospitalized in the intensive care unit after an emergency exploratory laparotomy and cholecystectomy. He remains intubated with mechanical ventilation. Attempts at weaning have been delayed by periodic hypoxemia.

He currently has an arterial line, central line, T-tube drain, and Foley catheter. He is alert and oriented, moving in bed with little assistance. His physical exam reveals that his skin is pale pink, warm to touch, lungs have a few bibasilar crackles, and 1+ pedal edema is present bilaterally. His abdomen is nondistended, with no active bowel sounds. His 5 inch midline abdominal wound requires dressing changes three times a day and is approximated with retention sutures. His temperature is 101.0 F rectally, heart rate is 122 beats/min, respiratory rate 34 breaths/min, and blood pressure 112/70 mm Hg. His postoperative lab results reveal a WBC count of 22,000 with 65 neutrophils, 50 segs, and 12 bands.

1. Why might Mr. H be at risk for developing sepsis?

2. What clinical signs and symptoms may be evidence of early sepsis?

3. Does he demonstrate any SIRS criteria? If so, which ones?

Case Study 5

A 55-year-old man presented to the ED with severe right upper quadrant pain. The initial diagnosis was possible intestinal obstruction. He was immediately taken to surgery for repair of perforated bowel. The estimated blood loss was 1200 cc, which was replaced with 2 units of PRBCs and 3 liters of crystalloid. His intraoperative course was stable, surgery was however prolonged by the presence of adhesions.

His past medical history includes obesity and he is a two pack-a-day smoker. Past surgical history includes a tonsillectomy as a child and a recent repair of right shoulder rotator cuff injury. His current blood pressure is 120/60 mm Hg, heart rate of 122 beats/min, temperature 96.4 F orally and respirations of 36 breaths/min.

Although he was stable immediately after surgery, his blood pressure suddenly decreased to 92/60 mm Hg and his heart rate increased to 130 beats/min.

Postoperative labs are drawn and intravenous fluids are increased. 

1. What type of shock might be an initial differential diagnosis?

2. What additional assessment findings might be helpful in differentiating the type of shock?

Lab work reveals a stable hemoglobin and hematocrit. However, a 12-lead EKG reveals ischemia in leads II, III, and AVF, indicating an inferior wall MI. 

3. What type of shock might now be suspected?

4. What treatment may be indicated?     

Case Study 6

Mrs. R is a 62-year-old female with chronic renal failure who is receiving dialysis three times a week. During dialysis, her blood pressure suddenly decreases and she becomes faint. Her family relates that she has been feeling ill the past several days and has had an upper respiratory infection. Her chest x-ray reveals a right lower lobe pneumonia and she is admitted for intravenous antibiotic therapy.

1. Is she at risk for developing sepsis?

2. What might be some nursing care measures that can be instituted?

Answers: Case Study 1

1. A myocardial infarction should be suspected as the patient is presenting with chest pain and syncope. He has noted jugular vein distension and bilateral pedal edema.

2. He is exhibiting signs of early shock as his blood pressure is 90/50 mm Hg and his heart rate is 110 beats/min. Tachycardia is a compensatory response in shock and hypotension is a hallmark sign of shock.

3. Cardiogenic shock should be suspected as the patient is exhibiting a low blood pressure along with jugular vein distension and bilateral pedal edema. In cardiogenic shock, systolic and diastolic myocardial dysfunction result, leading to a decreased cardiac output, increased left ventricular end diastolic pressure, pulmonary congestion, and fluid retention.

Answers: Case Study 2

1. The patient presented with sudden dizziness, difficulty breathing, hives and a rash, all signs and symptoms of anaphylaxis, possibly precipitated by ingesting an allergen while eating at the restaurant.

2. The patient is exhibiting difficulty breathing, which can be a life-threatening condition in anaphylactic shock as it could indicate laryngeal edema, airway constriction, and impaired oxygenation.

Answers: Case Study 3

1. The patient should be questioned about her past medical history, allergies, current medications, as well as additional information about her recent illness – any fever, chills, amount and characteristics of her emesis, any diarrhea or melena.

2. Based on the patient’s symptoms, both hypovolemic or cardiogenic shock should be suspected. She has crackles and pedal edema, but no jugular vein distention. However, she could have some cardiac origin to her condition. Further work-up of the patient is required to determine the specific cause of her signs of shock. 

3. Laboratory testing should be performed, including a hemoglobin and hematocrit and possibly a type and cross-match in case a transfusion is required. 

4. Based on the patient’s signs and symptoms, she is in the second or compensatory stage of hypovolemic shock as she is exhibiting an increase in heart rate and respiratory rate and a decrease in blood pressure, signs of a decreased cardiac output. In the second or compensatory stage of hypovolemic shock, 15% to 30% (750-1500 ml) volume loss occurs, but compensatory mechanisms are activated to promote vasoconstriction to increase the cardiac output. With treatment, she has a relatively good prognosis as she is currently not exhibiting signs of decompensation or impaired tissue perfusion.

Answers: Case Study 4

1. Mr. H. is at risk for developing sepsis due to his age, recent surgery, intubation and invasive lines including an arterial line, central line, T-tube drain, and Foley catheter, which can be sources of infection. In addition, he has a 5-inch midline abdominal wound that requires dressing changes three times a day, further increasing the risk for infection.

2. Clinical signs and symptoms that are evidence of early sepsis include an elevated temperature, tachycardia, tachypnea and an elevated total white blood cell count and increase in bands, or left shift, indicating the release of immature white blood cells by the bone marrow to combat infection.

3. The SIRS criteria include elevated temperature, tachycardia, tachypnea, increased total white cell count, and left shift. He demonstrates all of these.

Answers: Case Study 5

1. The patient is most likely experiencing shock caused by hypovolemia, due to postoperative bleeding or dehydration from surgical losses without sufficient replacement or possible septic shock caused by his intestinal perforation with a possible infection.

2. Additional assessment findings that might be helpful in differentiating the type of shock include laboratory work – including hemoglobin, hematocrit, white blood count and differential. Intake and output data, and response to intravenous fluids would further help to assess the patient status.

3. After gaining the information from the lab results and EKG, it is now evident that cardiogenic shock should be suspected as the patient has sustained a myocardial infarction. Cardiogenic shock occurs in 5%-10% of hospitalized patients with myocardial infarction and is due to loss of effective myocardial contractile function that results in impaired cardiac output, altered oxygen delivery, and reduced tissue perfusion.

4. Indicated treatment includes increasing tissue perfusion, decreasing oxygen demands, decreasing afterload, and enhancing contractility. Intravenous fluid administration should be used with caution so as not to promote fluid overload to an already taxed myocardium. Cardiovascular support with inotropic agents, diuretics for pulmonary congestion, and vasodilators to reduce ischemia by reducing left ventricular filling pressure and redistributing coronary blood flow may by used for treatment of cardiogenic shock. Intra-aortic balloon pump counterpulsation and reperfusion strategies may also be indicated for advancing shock.

Answers: Case Study 6

1. The patient is at risk for developing sepsis as she has a right lower lobe pneumonia and requires hospitalization for intravenous antibiotic therapy. Pneumonia is a known condition that can lead to sepsis. Intravenous therapy presents an additional risk for infection. Broad spectrum antibiotic therapy and chronic illness (renal failure) are additional risk factors for sepsis.

2. Nursing care measures that can be instituted to prevent infection include measures to prevent infection (handwashing, universal precautions, sterile technique with intravenous antibiotic administration, pulmonary hygiene measures) as well as astute clinical assessment of the patient to promote early detection of developing sepsis. Monitoring for temperature elevation, altered respiratory status indicating worsening pneumonia, and signs of systemic infection – i.e., SIRS criteria — are specific parameters to be monitored closely in the patient. Reporting signs of infection to promote early recognition and treatment of sepsis is also important in the care of this patient.