Ch. 34 Flashcards
Shock is a complex pathophysiologic process that often results in MODS and death. All types of shock involve ineffective tissue perfusion and acute circulatory failure.
shock syndrome is a pathway involving a variety of pathologic processes that may be categorized in four stages: initial, compensatory, progressive, and refractory
Progression through each stage varies with the patient’s prior condition, duration of initiating event, response to therapy, and correction of the underlying cause
Shock can be classified as hypovolemic, cardiogenic, or distributive, depending on the pathophysiologic cause and hemodynamic profile.
Hypovolemic shock results from a loss of circulating or intravascular volume. Cardiogenic shock results from the impaired ability of the heart to pump.
Septic shock is the result of the host’s dysregulated response to microorganisms entering the body. Anaphylactic shock is the result of a severe antibody antigen reaction. Neurogenic shock is the result of the loss of sympathetic tone.
Description and Etiology - SHOCK SYNDROME
occurs from inadequate fluid volume in the intravascular space. The lack of adequate circulating volume leads to decreased tissue perfusion and initiation of the general shock response.
most commonly occurring form of shock can result from absolute or relative hypovolemia
Absolute hypovolemia occurs when there is a loss of fluid from the intravascular space.
can result from an external loss of fluid from the body or from internal shifting of fluid from the intravascular space to the extravascular space.
Fluid shifts can be due to a loss of intravascular integrity, increased capillary membrane permeability, or decreased colloidal osmotic pressure. Relative hypovolemia occurs when vasodilation produces an increase in vascular capacitance relative to circulating volume
Description and Etiology - HYPOVOLEMIC SHOCK
clinical manifestations of hypovolemic shock depend on the severity of fluid loss and the patient’s ability to compensate for it
Assessment of the hemodynamic parameters of a patient in hypovolemic shock varies by stage but commonly reveals a decreased CO and cardiac index (CI). Loss of circulating volume leads to a decrease in venous return to the heart, which results in a decrease in the preload of the right and left ventricles.
decline in the CVP or right atrial pressure (RAP) and pulmonary artery occlusion pressure (PAOP).
Vasoconstriction of the arterial system results in an increase in the afterload of the heart, as evidenced by an increase in the SVR. This vasoconstriction may produce inaccurate systolic and diastolic blood pressure values when measured by arterial catheter or noninvasive oscillometry. MAP is more accurate in this low-flow state.
Assessment and Diagnosis - HYPOVOLEMIC SHOCK
The major goals of therapy for a patient in hypovolemic shock are to correct the cause of the hypovolemia, restore tissue perfusion, and prevent complications. This approach includes identifying and stopping the source of fluid loss, administering fluid to replace circulating volume, and administering vasopressor therapy to maintain tissue perfusion until volume is restored.
Fluid administration can be accomplished with use of a crystalloid solution, a colloid solution, blood products, or a combination of fluids.
Limited or hypotensive (systolic blood pressure 60 to 80 mm Hg or MAP 40 to 60 mm Hg) volume resuscitation in patients with uncontrolled hemorrhage has been shown to lessen bleeding and improve survival.
type and amount of solutions used for fluid resuscitation and the rate of administration influence immune function; inflammatory mediator release; coagulation; and the incidence of cardiac, pulmonary, renal, and GI complications.
Medical management - HYPOVOLEMIC SHOCK
Prevention of hypovolemic shock is one of the primary responsibilities of the nurse in the critical care unit. Preventive measures include the identification of patients at risk and frequent assessment of the patient’s fluid balance. Accurate monitoring of intake and output and daily weights are essential components of preventive nursing care. Early identification and treatment result in decreased mortality.
requires continuous evaluation of intravascular volume, tissue perfusion, and response to therapy.
include minimizing fluid loss, administering volume replacement and vasopressor agents (if needed), assessing response to therapy, providing comfort and emotional support, and preventing and maintaining surveillance for complications.
minimize fluid loss include limiting blood sampling, observing lines for accidental disconnection, and applying direct pressure to bleeding sites
facilitate the administration of volume replacement include insertion of large-bore peripheral intravenous catheters and rapid administration of prescribed fluids
adequate tissue perfusion and for clinical manifestations of fluid overload or complications related to fluid and blood product administration is essential for preventing further problems.
monitor the patient for organ failure, which may occur for up to several days after resuscitation.
Nursing management - HYPOVOLEMIC SHOCK
result of failure of the heart to effectively pump blood forward.
can occur with dysfunction of the right or the left ventricle, or both.
lack of adequate pumping function leads to decreased tissue perfusion and circulatory failure with an ST segment myocardial infarction (MI), and it is the leading cause of death of patients hospitalized with MI.
can result from problems affecting the muscular function or the mechanical function of the heart or the cardiac rhythm.
can occur with ST segment elevation or non ST segment elevation MI
damage to the myocardium may occur after one massive MI (usually of the anterior wall), or it may be cumulative as a result of several smaller MIs or a small MI in a patient with preexisting ventricular dysfunction
Cardiomyopathy may cause cardiogenic shock as left ventricular function becomes unable to maintain adequate CO.
problems affecting the mechanical function of the heart to fill and eject adequately include severe valvular disease; acute papillary muscle, chordal, or septal rupture; cardiac tamponade; and massive pulmonary embolus
Description and Etiology - CARDIOGENIC SHOCK
Various clinical manifestations occur in patients in cardiogenic shock depending on etiologic factors, the patient’s underlying medical status, and the severity of the shock state.
Although some clinical manifestations are caused by failure of the heart as a pump, many are related to the overall shock response include systolic blood pressure less than 90 mm Hg, MAP less than 65 mm Hg, or an acute drop in systolic or mean blood pressure of 30 mm Hg or more; decreased sensorium; cool, pale, moist skin; and urine output of less than 30 mL/h.
The patient also may complain of chest pain. Tachycardia develops to compensate for the decrease in CO.
A weak, thready pulse develops, and diminished S1 and S2 heart sounds may occur as a result of the decreased contractility. The respiratory rate increases to improve oxygenation. ABG values at this point indicate respiratory alkalosis, decrease in urine sodium level and an increase in urine osmolality and specific gravity as the kidneys start to conserve sodium and water. Serum B-type natriuretic peptide levels are likely to be elevated
the left ventricle fails, auscultation of the lungs may disclose crackles and rhonchi, indicating the development of pulmonary edema
Jugular venous distention is evident with right-sided failure.
Assessment of the hemodynamic parameters of a patient in cardiogenic shock reveals decreased CO with CI less than 2.2 L/min/m2 in the presence of an elevated PAOP
Increased filling pressures are necessary to rule out hypovolemia as the cause of circulatory failure.
increase in PAOP reflects an increase in the left ventricular end-diastolic pressure and left ventricular end-diastolic volume resulting from decreased SV.
Compensatory vasoconstriction typically results in an increase in the afterload of the heart, as evidenced by an increase in the SVR, unless inflammation produces vasodilation and a normal or decreased SVR. Echocardiography confirms the diagnosis of cardiogenic shock, provides noninvasive estimates of PAOP and ejection fraction, and often clarifies etiologic factors
Myocardial ischemia progresses, as evidenced by continued increases in heart rate, dysrhythmias, and chest pain. Pulmonary function deteriorates, which leads to respiratory distress. ABG values during this phase reveal respiratory and metabolic acidosis and hypoxemia,
Renal failure occurs, as exhibited by the development of anuria and increases in blood urea nitrogen and serum creatinine levels. Cerebral hypoperfusion manifests as a decreasing level of consciousness
Assessment and Diagnosis - CARDIOGENIC SHOCK
The major goals of therapy are to treat the underlying cause, enhance the effectiveness of the pump, and improve tissue perfusion. This approach includes identifying and treating the etiologic factors of heart failure and administering pharmacologic agents or using mechanical devices to enhance CO. Inotropic agents are used to increase contractility and maintain adequate blood pressure and tissue perfusion.37 Dobutamine is the inotrope of choice.
A vasopressor, preferably norepinephrine, may be necessary to maintain blood pressure when hypotension is severe
Diuretics may be used for preload reduction.Antidysrhythmic agents should be used to suppress or control dysrhythmias that can affect CO. Intubation and mechanical ventilation are usually necessary to support oxygenation
The cause of pump failure should be identified as quickly as possible so that measures can be taken to correct the problem if possible.
The cause of pump failure should be identified as quickly as possible so that measures can be taken to correct the problem if possible.
Medical Management - CARDIOGENIC SHOCK
Prevention of cardiogenic shock is one of the primary responsibilities of the nurse in the critical care unit. Preventive measures include the identification of patients at risk, facilitation of early reperfusion therapy for acute MI, and frequent assessment and management of the patient’s cardiopulmonary status.
include limiting myocardial oxygen demand, enhancing myocardial oxygen supply, maintaining adequate tissue perfusion, providing comfort and emotional support, and preventing and maintaining surveillance for complications
Measures to limit myocardial oxygen demand include administering analgesics, sedatives, and agents to control afterload and dysrhythmias; positioning the patient for comfort; limiting activities; providing a calm and quiet environment and offering support to reduce anxiety; and teaching the patient about the condition. Measures to enhance myocardial oxygen supply include administering supplemental oxygen, monitoring the patient’s respiratory status, administering prescribed medications, and managing device therapy.
Effective nursing management of cardiogenic shock requires precise monitoring and management of heart rate, preload, afterload, and contractility.
through accurate measurement of hemodynamic variables and controlled administration of fluids and inotropic and vasoactive agents.
Dysrhythmias are common and require immediate recognition and treatment.
require mechanical device therapy (IABP, VAD, or extracorporeal membrane oxygenator) need to be observed frequently for complications.
Complications of mechanical circulatory assist devices include infection, bleeding, thrombocytopenia, hemolysis, embolus, stroke, device malfunction, circulatory compromise of a cannulated extremity, and sepsis.
Nursing Management - CARDIOGENIC SHOCK
type of distributive shock, is the result of an immediate hypersensitivity reaction. It is a life-threatening event that requires prompt intervention. The severe and systemic response leads to decreased tissue perfusion and initiation of the general shock response
is a systemic reaction caused by an immunologic antibody antigen response or nonimmunologic activation of mast cells and basophils.
reactions can be IgE-mediated or non IgE-mediated responses.
reaction triggers the release of bio-chemical mediators from the mast cells and basophils and initiates the cascade of events that precipitates anaphylactic shock. Some immunologic anaphylactic reactions are non IgE-mediated. These can be IgG mediated, occur as a result of direct activation of the mast cells, or be mediated by activation of the complement system.
Nonimmunologic direct activation of the mast cells and basophils may occur with exercise or exposure to cold, heat, sunlight, ethanol, or medications.
Description and Etiology - ANAPHYLACTIC SHOCK
is a severe systemic reaction that can affect multiple organ systems. Various clinical manifestations occur in a patient in anaphylactic shock, depending on the extent of multi-system involvement.
usually start to appear within minutes of exposure to the antigen, but they may not occur for hours
Symptoms may also reappear after a 1- to 72-hour window of resolution in what is termed a biphasic reaction.
These late-phase reactions may be similar to the initial anaphylactic response, milder, or more severe. In protracted anaphylaxis, symptoms may last 32 hours.
cutaneous effects may appear first and include pruritus, generalized erythema, urticaria, and angioedema.
may appear restless, uneasy, apprehensive, and anxious and may complain of being warm. Respiratory effects include the development of laryngeal edema, bronchoconstriction, and mucous plugs.
inspiratory stridor, hoarseness, a sensation of fullness or a lump in the throat, and dysphagia. Bronchoconstriction causes dyspnea, wheezing, and chest tightness. GI and genitourinary (GU) manifestations, which may develop as a result of smooth muscle contraction, include vomiting, diarrhea, cramping, and abdominal pain
Hypotension and reflex tachycardia may develop quickly in response to massive vasodilation and rapid loss of circulating volume. Jugular veins appear flat as right ventricular end-diastolic volume is decreased. The eventual outcome is circulatory failure and ineffective tissue perfusion. The patient’s level of consciousness may deteriorate to unresponsiveness.
decreased CO and CI.
decrease in preload
Vasodilation of the arterial system results in a decrease in the afterload of the heart, as evidenced by a decrease in the SVR.
Assessment and Diagnosis - ANAPHYLACTIC SHOCK
Treatment of anaphylactic shock requires an immediate and direct approach to prevent death. The goals of therapy are to remove the offending antigen, reverse the effects of the biochemical mediators, and promote adequate tissue perfusion.
Reversal of the effects of the biochemical mediators involves the preservation and support of the patient’s airway, ventilation, and circulation. This is accomplished through oxygen therapy, intubation, mechanical ventilation, and administration of medications and fluids.
Epinephrine is the first-line treatment of choice for anaphylaxis and should be administered when initial signs and symptoms occur.
promotes bronchodilation, vasoconstriction, and increased myocardial contractility and inhibits further release of biochemical mediators.
Rapid volume replacement with crystalloid or colloid solutions is also used for patients with hypotension.
Several medications are used as second-line or third-line adjunctive therapy but are not to be used as substitutes for epinephrine. Inhaled beta-adrenergic agents are used to treat bronchospasm unresponsive to epinephrine. Diphenhydramine (Benadryl), 1 to 2 mg/kg (25 to 50 mg) given by a slow intravenous push, is used to block histamine response. Ranitidine or cimetidine given in conjunction with diphenhydramine has been found helpful to control cutaneous reactions. Corticosteroids are not effective in the immediate treatment of acute anaphylaxis but may be given with the goal of preventing a prolonged or delayed reaction.
Medical Management - ANAPHYLACTIC SHOCK
Prevention of anaphylactic shock is one of the primary responsibilities of the nurse in the critical care unit. Preventive measures include the identification of patients at risk and cautious assessment of the patient’s response to the administration of medications, blood, and blood products.
Complete and accurate history of the patient’s allergies is an essential component of preventive nursing care. In addition to a list of the allergies, a detailed description of the type of response for each allergy should be obtained. include administering epinephrine, facilitating ventilation, administering volume replacement, providing comfort and emotional support, maintaining surveillance for recurrent reactions, and preventing and maintaining surveillance for complications.
Measures to facilitate ventilation include positioning the patient to assist with breathing and instructing the patient to breathe slowly and deeply. Airway protection through prompt administration of prescribed medications is essential. Measures to facilitate the administration of volume replacement include inserting large-bore peripheral intravenous catheters and rapidly administering prescribed fluids. Measures to promote comfort include administering medications to relieve itching and applying warm soaks to skin. Observing the patient for clinical manifestations of a delayed or recurrent reaction is critical. Patient education about how to avoid the precipitating allergen is essential for preventing future episodes of anaphylaxis. Education about how to recognize and respond to a future episode including self-administration of epinephrine is essential to prevent a future life-threatening event.
Nursing Management - ANAPHYLACTIC SHOCK
Another type of distributive shock, is the result of the loss or suppression of sympathetic tone. The lack of sympathetic tone leads to decreased tissue perfusion and initiation of the general shock response most uncommon form of shock.
can be caused by anything that disrupts the SNS
problem can occur as the result of interrupted impulse transmission or blockage of sympathetic outflow from the vasomotor center in the brain. The most common cause is spinal cord injury (SCI)
Description and Etiology - NEUROGENIC SHOCK
hypotension, bradycardia, and warm, dry skin. The decreased blood pressure results from massive peripheral vasodilation. The decreased heart rate is caused by inhibition of the baroreceptor response and unopposed parasympathetic control of the heart.
The warm, dry skin occurs as a consequence of pooling of blood in the extremities and loss of vasomotor control in surface vessels of the skin that control heat loss.
reveals a decreased CO and CI. Venous vasodilation leads to a decrease in preload, a decline, and PAOP.
Vasodilation of the arterial system causes a decrease in the afterload of the heart, as evidenced by a decrease in the SVR.
Assessment and Diagnosis - NEUROGENIC SHOCK
