Would you recognize the early signs of shock? Shock is a life-threatening condition, and early recognition and treatment can save lives.¹ Shock is a clinical condition that can have several causes, including infection, injury, severe bleeding, and trauma; it 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.^1,2 Several distinct types of shock exist, including anaphylactic, cardiogenic, hypovolemic, neurogenic, and septic. Despite having different etiologies, all of the shock states have similar manifestations of inadequate peripheral tissue perfusion, impaired cellular function, and impaired organ perfusion.
 
As blood supply to the cells decreases, hypoperfusion results in cellular hypoxia. At the cellular level, the body switches to a metabolism that doesn't require oxygen (anaerobic metabolism); because this metabolism is insufficient to maintain energy needs, irreversible cellular damage begins to occur.^3,4 Compensatory mechanisms — including the sympathetic nervous system response with release of catecholamines — attempt to improve tissue perfusion. Neurohormonal responses — such as vasoconstriction via renin-angiotensin release — attempt to maintain cardiac output and perfusion.² As shock progresses, these compensatory mechanisms can no longer sustain adequate perfusion to tissues, resulting in impaired oxygen delivery.⁴ Metabolic acidosis with severe electrolyte imbalance and respiratory acidosis with hypoxemia can occur. Irreversible cellular and organ damage begins. Death can result from impaired tissue perfusion, cellular necrosis, and organ system failure.^2-4

Signs of shock include tachycardia (heart rate greater than 100 beats per minute), hypotension (systolic blood pressure less than 90 mm Hg for at least 30 minutes), paleness, and cool, clammy skin.^1,2 In general, the different types of shock can be distinguished from one another.

Types of Shock

Hypovolemic, the most common form of shock, results from loss of blood or from loss of plasma volume of greater than 20% of the circulating volume, or from profound dehydration.¹ Causes include bleeding, burns, large amounts of GI losses, dehydration, or internal third spacing (fluid collection within a body space or cavity, e.g., from pancreatitis, bowel obstruction, or ascites).¹

Hypovolemic shock has four stages.^1,5 In the initial stage, about 15% (750 ml) of volume loss has occurred. The patient is asymptomatic as compensatory mechanisms maintain cardiac output and blood pressure.^1,5,6 In the second, or compensatory, stage, the volume loss increases from 15% to 30% (750 ml to 1,500 ml). In this stage, clinical symptoms begin to manifest, including tachycardia (heart rate greater than 100 beats per minute), increased respiratory rate (tachypnea, rate greater than 20), decreased capillary refill, and anxiety.^1,6 In the third, or progressive, stage, 30% to 40% volume loss (1,500 ml to 2,000 ml) has occurred. Patients can exhibit marked clinical signs of deterioration, including hypotension, tachycardia, cardiac arrhythmias, tachypnea, decreased urine output, and changes in mental status.^1,6 In the fourth, or refractory, stage, more than 40% volume loss (greater than 2,000 ml) has occurred. Such volume loss is life-threatening, and clinical signs of organ system failure, including severe hypotension, marked tachycardia, and hemodynamic instability are evident.^1,6

Treatment goals for hypovolemic shock target the underlying cause, control additional fluid loss, and replace fluid losses. Crystalloids (e.g., lactated Ringer's injection, normal saline) and colloids (e.g., hetastarch [Hespan]) are administered to replace fluid volume. Crystalloids are effective at expanding intravascular volume and interstitial fluid, and colloids expand the intravascular space by pulling fluid from the interstitial spaces.⁶ Although colloids are more effective than crystalloids at increasing intravascular fluid, data suggests an increased incidence of complications and risk of death with the use of colloids, particularly albumin.⁶ Blood and blood products are used for patients who are hemodynamically unstable, for patients with more than 1,500 cc blood loss, or for patients with uncontrolled sources of bleeding.⁶ Transfusion of blood and blood products is usually indicated for a hematocrit less than 28%.¹⁴ Whole blood is used to replace large blood loss volumes, while packed red blood cells (PRBCs) are used to replace moderate blood loss.^1,4 New artificial red blood cells termed red blood cell substitutes are in development.⁸ RBC substitute solutions are typically hypertonic colloids and expand blood volume more than the volume of the infused solution.⁴

Cardiogenic shock is a decrease in cardiac output along with tissue hypoxia in the presence of adequate blood volume.⁷ Cardiogenic shock occurs when the effective contraction of the myocardium is lost, often after acute MI.⁹ Other causes include pulmonary edema, cardiomyopathies, dysrhythmias, pericardial tamponade, and valvular regurgitation.⁷ Despite advances in the treatment of acute MI, the in-hospital mortality associated with cardiogenic shock continues to be about 50%.⁷ In cardiogenic shock, decreased cardiac contraction results in ineffective emptying of blood from the left ventricle and congestion within the pulmonary circulation, leading to both left- and right-sided heart failure. The result is impaired cardiac output, altered oxygen delivery, and reduced tissue perfusion.^1,7 Hypotension and a low cardiac index (less than 2.2 liters/min per m²) are classic signs of cardiogenic shock.7 While the treatment of cardiogenic shock is to enhance contractility and increase cardiac output (by administering drugs to increase the force of ejection), these goals often are difficult to achieve because measures that increase cardiac output also tend to increase myocardial oxygen demands.^1,7 Common treatments include supplemental oxygen, hemodynamic support, diuretics for pulmonary congestion, and vasopressors for hypotension unresponsive to fluid therapy. Vasodilators such as nitroglycerin or nitroprusside sodium (Nipride) can decrease left ventricular afterload. For severely reduced tissue perfusion, a device called an intra-aortic balloon pump can be used. The IABP is placed in the descending thoracic aorta, with inflation and deflation of the balloon timed to the cardiac cycle. The balloon inflates in diastole, improving perfusion to the heart, and deflates at the end of diastole just before contraction of the left ventricle to decrease the resistance to ejection, thus improving cardiac output.⁷ In addition, the hormone vasopressin is beneficial for refractory cardiogenic shock. Revascularization procedures and emergent cardiac bypass surgery may be indicated for patients in cardiogenic shock.⁷

Anaphylactic shock is a whole-body allergic reaction.^1,8 It is an extremely life-threatening hypersensitivity reaction that can develop rapidly, within seconds of exposure, or after 12 hours or more.^1,8 Anaphylactic shock results from a reaction to an allergen that causes the release of immunoglobulin E (IgE), an antibody formed as part of the immune response. The release of IgE results in the activation of mast cells and the release of histamine, which causes profound vasodilation.^1,8 Other mediators, such as prostaglandins, kinins, and complement (plasma proteins), are released and cause increased vascular permeability with edema and bronchoconstriction with airway compromise.^1,8,9 Death in anaphylaxis can result from cardiovascular or respiratory distress. A variety of allergens can cause anaphylactic shock. Foods and food additives that have been known to cause anaphylaxis include eggs, peanut butter, nuts, fish, shellfish, milk, cheese, tomatoes, chocolate, and monosodium glutamate. Examples of medications include antibiotics, aspirin, vaccines, local anesthetics, narcotics, and contrast dyes. Other common allergens include latex, blood products, insect bites, and venom. The signs and symptoms of anaphylactic shock can include skin rash/flushing, pruritis (generalized itching), sneezing/coughing, wheezing, uticaria (hives), angioedema (edema of the lips/tongue), and restlessness. Life-threatening signs and symptoms can include respiratory stridor, bronchospasm, and laryngeal edema.^1,8,9 Signs and symptoms can be subtle (itching) or profound (wheezing, respiratory stridor, CV collapse).

Treatment goals include the ABCs (airway, breathing, circulation) of emergency care, along with volume expansion, vasoconstricting agents, epinephrine, and antihistamines. Epinephrine is a first-line agent for anaphylaxis because it promotes vasoconstriction, along with inhibiting the further release of mediators.^8,9 Antihistamines (e.g., diphenhydramine [Benadryl]), bronchodilators, and corticosteroids are considered second-line agents that reduce additional symptoms and late-phase reactions.¹³ Screening patients at risk and monitoring patient responses to drugs and blood products are important aspects of nursing care to prevent anaphylactic shock. An allergy history is also important in identifying potential allergens.^1,8,9 When patients experience an anaphylatic event, they should be instructed to avoid the allergen and related products. MedicAlert identification bracelets or necklaces are available for patients to wear. Iatrogenic patients should be educated about the signs and symptoms of anaphylaxis, the importance of seeking prompt medical care, and the use of self-administered agents, such as subcutaneous epinephrine.^8,9

Neurogenic shock results from the loss of normal sympathetic nervous system response, often from spinal cord injury in trauma or from regional anesthesia or autonomic blocking agents.^1,10 This results in massive vasodilation with severe hypotension and unopposed vagal tone that can result in bradycardia.^1,14 Neurogenic shock is considered the rarest form of shock.^10,11 It can occur immediately after spinal cord injury or weeks or months after injury.^1,10,11 Treatment goals include the ABCs, fluid resuscitation and vasoconstrictors to increase blood pressure, and agents to block vagal effects that cause bradycardia, such as atropine.^1,11,12

Septic shock is a complex condition occurring when overwhelming infection leads to low blood pressure, low blood flow, altered coagulation (with the formation of clots that impair blood perfusion), and impaired clot breakdown (altered fibrinolysis).^1,13,14 Septic shock results from vasodilation because of mediator release from WBCs during an infectious state as well as increased capillary permeability and altered response of the endothelium.¹³ In response to infectious organisms and their products, WBCs, specifically monocytes and macrophages, generate and release cytokines, or nonspecific mediators of inflammation.^1,13,14

Septic shock has the highest mortality rate of any type of shock — from 28% to more than 50%.¹⁵ Despite advances in treatment, the incidence of sepsis and septic shock is growing because of factors such as an increased risk of nosocomial infections and an increased number of immunocompromised patients and resistant organisms.¹⁵

Sepsis with acute organ dysfunction (severe sepsis) and septic shock (sepsis with hypotension) result from a systemic inflammatory response from infection.^14,15 As sepsis progresses, continued inflammation and edema and impaired circulation lead to cellular dysfunction and altered organ functioning.^1,14,15 Multiple organ failure can result. Vital sign changes may be the first indication of an infection, with temperature elevation, increased heart rate, or increased respiratory rate occurring as subtle signs of developing sepsis. The signs and symptoms of sepsis include the systemic inflammatory response syndrome (SIRS), which includes tachycardia, tachypnea, altered temperature (greater than 38 C or less than 36 C), and abnormal WBC count (usually elevated WBC greater than 12,000 or less than 10% immature [band] forms). Other signs and symptoms include hypotension, hypoxemia, and signs of impaired perfusion (poor capillary refill, decreased urine output, cardiac arrhythmias, and altered mentation).^14,15
 
Organ system dysfunction can result as sepsis progresses. Patients often exhibit alterations in CV status (tachycardia, hypotension) and respiratory compromise (tachypnea, hypoxemia). As a result of decreased tissue perfusion, other organ system failure, such as renal failure evidenced by decreased urine output or hematologic dysfunction with coagulopathy, also can occur.^14,15 As the number of organ system failures increases, mortality rates also increase. Goals of treatment include hemodynamic support (e.g., fluids, inotropes, and vasopressors to increase blood pressure), oxygenation support (e.g., mechanical ventilation), and antibiotics.^13-15 For organ system dysfunction, specific organ support treatment strategies may be used (e.g., renal replacement therapies). As with other states of shock, the goal is to restore tissue and organ perfusion.

New guidelines for managing patients with sepsis, The Surviving Sepsis Campaign Guidelines,¹⁵ provide strategies for treatment of patients at risk for severe sepsis and septic shock. The guidelines outline several evidence-based measures for the treatment of patients with severe sepsis, including goal-directed initial resuscitation for hypoperfusion, appropriate cultures for diagnosis before antibiotic therapy, mechanical ventilation therapy, glucose control, renal replacement therapy, deep vein thrombosis prophylaxis, and use of drotrecogin alfa (activated). Drotrecogin alfa (activated), or Xigris, is indicated for patients with severe sepsis with three or more SIRS criteria and evidence of organ system dysfunction.¹⁵ Contraindications for use of the drug include active or recent bleeding or risk of bleeding.¹⁵

Proper Care

Early identification of patients at risk for shock facilitates diagnosis and treatment. Nurses can assess patients for the clinical signs of shock by frequently monitoring vital signs, including urinary output, skin color, and perfusion, and noting signs of organ system dysfunction.

Care measures for patients with shock –^17,18

• Hand hygiene measures, including anti-microbials
• Universal precautions
• Assessment for signs of infection
• Appropriate culture specimens
• Measures to prevent nosocomial infections
• Oral care
• Proper positioning (semi-recumbent position during mechanical ventilation)
• Wound care
• Invasive catheter care
• Antibiotics

Comprehensive shock treatment often includes administering IV fluids, blood products, or vasoconstrictive agents like norepinephrine (Levophed) to maintain perfusion. Supplemental oxygenation and measures to maximize respiratory function (e.g., positioning, use of incentive spirometry, and deep breathing) often are indicated in shock, as alterations in respiratory status also are common. Other treatment includes administering medications, monitoring laboratory values, and providing therapies (e.g., renal replacement therapies). Monitoring patient response to treatment, such as changes in blood pressure, is important to determine the effects of treatment.

Promoting patient comfort and providing patient and family education about shock and its treatment are other important aspects of nursing care. Enforcing infection control techniques can reduce nosocomial infections, a common source of sepsis for acutely ill patients.^16-18 Providing oral care, turning and positioning patients to reduce the risk of pneumonia, and using sterile technique (e.g., for dressing changes and catheter insertions) help reduce infection risk.^17,18 As key members of the healthcare team, nurses play an important part in the management of patients with shock.
 
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