Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and demand for oxygen and nutrients. The exchange of oxygen and nutrients at the cellular level is essential to life. When a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the microcirculatory level.
Classification of Shock
The four main categories of shock are
* absolute hypovolemia
* relative hypovolemia
* neurogenic shock
* anaphylactic shock
* septic shock
multiple organ dysfunction syndrome (MODS) target organs
* cardiovascular dysfunction
* lung dysfunction
* gastrointestinal dysfunction
* liver dysfunction
* CNS dysfunction
* Renal dysfunction
* Skin dysfunction
Although the cause, initial presentation, and management strategies vary for each type of shock, the physiologic responses of the cells to hypoperfusion are similar. Relationship of shock, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. CNS, Central nervous system.
cardiogenic shock shock occurring when either systolic or diastolic dysfunction of the myocardium results in compromised cardiac output either systolic or diastolic dysfunction of the pumping action of the heart results in reduced cardiac output (CO). Decreased filling of the ventricle will result in decreased stroke volume the heart’s inability to pump the blood forward is classified as systolic dysfunction. Systolic dysfunction primarily affects the left ventricle, because systolic pressure and tension are greater on the left side of the heart. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is reduced. The most common precipitating cause of systolic dysfunction is acute myocardial infarction (AMI). Cardiogenic shock is the leading cause of death from AMI patient experiences impaired tissue perfusion and impaired cellular metabolism because of cardiogenic shock. patient’s response may include tachycardia, hypotension, and a narrowed pulse pressure. An increase in systemic vascular resistance (SVR) increases the workload of the heart, thus increasing the myocardial oxygen consumption.
The heart’s inability to pump blood forward will result in a low CO (less than 4 L/min) and cardiac index (less than 2.5 L/min/m2). On examination, the patient will be tachypneic and have crackles on auscultation of breath sounds due to pulmonary congestion. Signs of peripheral hypoperfusion (e.g., cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) will be apparent. Decreased renal blood flow will result in sodium and water retention and decreased urine output. Anxiety, confusion, and agitation may develop as cerebral perfusion is impaired. Studies that are helpful in diagnosing cardiogenic shock include laboratory studies (e.g., cardiac enzymes, troponin levels, b-type natriuretic peptide [BNP]), electrocardiogram (ECG), chest x-ray, and echocardiogram. Hypovolemic shock occurs when there is a loss of intravascular fluid volume the volume is inadequate to fill the vascular space. The volume loss may be either an absolute or a relative volume loss. .
* Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. * In relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (e.g., interstitial or intracavitary space). This type of fluid shift is called third spacing. One example of relative volume loss is leakage of fluid from the vascular space to the interstitial space from increased capillary permeability, as seen in sepsis and burns A reduction in intravascular volume results in a decreased venous return to the heart, decreased preload, decreased stroke volume, and decreased CO A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, the hallmarks of shock A patient may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL).
Further loss of volume (15% to 30%) will result in a sympathetic nervous system (SNS)–mediated response. This response results in an increase in heart rate, CO, and respiratory rate and depth. The stroke volume, central venous pressure (CVP), and PAWP are decreased because of the decreased circulating blood volume. The patient may appear anxious and urine output will begin to decrease. If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible. If volume loss is greater than 30%, compensatory mechanisms may begin to fail and immediate replacement with blood products and albumin should be initiated.
Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks. The injury results in a massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can result in decreased vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock The most important clinical manifestations in neurogenic shock are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation) may not be able to regulate temperature. The inability to regulate temperature, combined with massive vasodilation, promotes heat loss. Initially, the patient’s skin will be warm due to the massive dilation.
As the heat disperses, the patient is at risk for hypothermia. Later, the patient’s skin may be cool or warm depending on the ambient temperature (poikilothermia—taking on the temperature of the environment). In either case, the skin will usually be dry Although spinal shock and neurogenic shock often occur in the same patient, they are not the same disorder. Spinal shock is a transient condition that is present after an acute spinal cord injury The patient with spinal shock will experience the absence of all voluntary and reflex neurologic activity below the level of the injury.7 Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). Usually an immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space.
Anaphylactic shock can lead to respiratory distress, because of laryngeal edema or severe bronchospasm, and circulatory failure, because of massive vasodilation. S/S: patient experiences a sudden onset of symptoms, including dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. In addition, the patient may become very anxious and confused and feel an impending sense of doom. patient can develop a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or injection with an antigen (allergen) to which the individual has previously been sensitized
Sepsis is a systemic inflammatory response to a documented or suspected infection. is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of inadequate tissue perfusion. The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also lead to the development of sepsis and septic shock When a microorganism enters the body, the normal immune/inflammatory cascade responses are initiated.
However, in severe sepsis and septic shock the body’s response to the microorganism is exaggerated. There is an increase in inflammation and coagulation, and a decrease in fibrinolysis. e combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium. Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients may be normovolemic but because of acute vasodilation, relative hypovolemia and hypotension occur. In addition, blood flow in the microcirculation is decreased causing poor oxygen delivery and tissue hypoxia.
Obstructive shock develops when a physical obstruction to blood flow occurs with a decreased CO. This can be caused from a restriction to diastolic filling of the right ventricle due to compression (e.g., cardiac tamponade, tension pneumothorax, superior vena cava syndrome). Other causes include abdominal compartment syndrome in which increased abdominal pressures compress the inferior vena cava decreasing venous return to the heart Pulmonary embolism and left ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. This leads to decreased blood flow to the lungs, as well as decreased blood return to the left atrium. Patients experience a decreased CO, increased afterload, and variable left ventricular filling pressures depending on the obstruction. Other clinical signs include jugular vein distention and pulsus paradoxus
Stages of Shock
In addition to understanding the underlying pathogenesis of the type of shock that the patient is experiencing, monitoring and management are guided by knowing where the patient is on the shock “continuum.” This continuum begins with the initial stage of shock that occurs at a cellular level and is usually not clinically apparent. Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid buildup. Lactic acid is a waste product that is removed by the liver. However, this process requires oxygen, which is unavailable because of the decrease in tissue perfusion. Shock is categorized into three clinically apparent but overlapping stages: the compensatory stage, the progressive stage, and the irreversible stage
In the compensatory stage, the body activates neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand classic signs of shock is a drop in blood pressure (BP), which occurs because of a decrease in CO and a narrowing of the pulse pressure. The baroreceptors in the carotid and aortic bodies immediately respond by activating the SNS. The SNS stimulates vasoconstriction and the release of the potent vasoconstrictors epinephrine and norepinephrine. Blood flow to the most essential (vital) organs, the heart and the brain, is maintained, while blood flow to the nonvital organs, such as the kidneys, GI tract, skin, and lungs, is diverted or shunted. myocardium responds to the SNS stimulation and the increase in oxygen demand by increasing the heart rate and contractility. However, increased contractility increases myocardial oxygen consumption.
The coronary arteries dilate in an attempt to meet the increased oxygen demands of the myocardium. Shunting blood away from the lungs has an important clinical effect in the patient in shock. Decreased blood flow to the lungs increases the patient’s physiologic dead space. Physiologic dead space is the anatomic dead space (the amount of air that will not reach gas-exchanging units) and any inspired air that cannot participate in gas exchange. The clinical result of an increase in dead space ventilation is a ventilation-perfusion mismatch. There will be areas of the lungs participating in ventilation that will not be perfused because of the decreased blood flow to the lungs. Arterial oxygen levels will decrease, and the patient will have a compensatory increase in the rate and depth of respirations The shunting of blood from other organ systems also results in clinically important changes. The decrease in blood flow to the GI tract results in impaired motility and a slowing of peristalsis.
This increases the risk for the development of a paralytic ileus. Decreased blood flow to the skin results in the patient feeling cool and clammy Decreased blood flow to the kidneys activates the renin-angiotensin system. Renin stimulates angiotensinogen to produce angiotensin I, which is then converted to angiotensin II (see Fig. 45-4). Angiotensin II is a potent vasoconstrictor that causes both arterial and venous vasoconstriction. The net result is an increase in venous return to the heart and an increase in BP. Angiotensin II also stimulates the adrenal cortex to release aldosterone. This results in sodium and water reabsorption, and potassium excretion by the kidneys.
The increase in sodium reabsorption raises the serum osmolality and stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH increases water reabsorption by the kidneys, thus further increasing blood volume. The increase in total circulating volume results in an increase in CO and BPA multisystem response to decreasing tissue perfusion is initiated in the compensatory stage of shock. At this stage, the body is able to compensate for the changes in tissue perfusion. If the cause of the shock is corrected, the patient will recover with little or no residual aftereffects. If the cause of the shock is not corrected and the body is unable to
The progressive stage of shock begins as compensatory mechanisms fail Changes in the patient’s mental status are important findings in this stage. he cardiovascular system is profoundly affected in the progressive stage of shock. CO begins to fall, resulting in a decrease in BP and coronary artery, cerebral, and peripheral perfusion. Continued decreased cellular perfusion and resulting altered capillary permeability are the distinguishing features of this stage. Altered capillary permeability allows leakage of fluid and protein out of the vascular space into the surrounding interstitial space. In addition to the decrease in circulating volume, there is an increase in systemic interstitial edema. The patient may have anasarca, or diffuse profound edema. Fluid leakage from the vascular space also affects the solid organs (e.g., liver, spleen, GI tract, lungs) and peripheral tissues by further decreasing perfusion. Sustained hypoperfusion results in weak peripheral pulses, and ischemia of the distal extremities eventually occurs. Myocardial dysfunction from decreased perfusion results in dysrhythmias, myocardial ischemia, and possibly AMI. The end result is a complete deterioration of the cardiovascular system. the pulmonary system is often the first system to display signs of critical dysfunction.
*** During the compensatory stage, blood flow to the lungs is already reduced. In response to the decreased blood flow and the SNS stimulation, the pulmonary arterioles constrict, resulting in increased pulmonary artery (PA) pressure. As the pressure within the pulmonary vasculature increases, blood flow to the pulmonary capillaries decreases and ventilation-perfusion mismatch worsens. Another key response in the lungs is the movement of fluid from the pulmonary vasculature into the interstitial space. As capillary permeability increases, the movement of fluid to the interstitial spaces results in interstitial edema, bronchoconstriction, and a decrease in functional residual capacity. With further increases in capillary permeability, the fluid moves to the alveoli, with resultant alveolar edema and a decrease in surfactant production. The combined effects of pulmonary vasoconstriction and bronchoconstriction are impaired gas exchange, decreased compliance, and worsening ventilation-perfusion mismatch. Clinically, the patient has tachypnea, crackles, and an overall increased work of breathing.
GI system is also affected by prolonged decreased tissue perfusion. As the blood supply to the GI tract is decreased, the normally protective mucosal barrier becomes ischemic. This ischemia predisposes the patient to ulcers and GI It also increases the risk of bacterial migration from the GI tract to the blood. The decreased perfusion to the GI tract also leads to a decreased ability to absorb nutrients. The effect of prolonged hypoperfusion on the kidneys is renal tubular ischemia. The resulting acute tubular necrosis may lead to the development of acute renal failure, which can be worsened by nephrotoxic drugs (e.g., certain antibiotics, anesthetics, diuretics) The patient will have a decreased urine output and an elevated blood urea nitrogen (BUN) and serum creatinine.
Metabolic acidosis occurs from the kidneys’ inability to excrete acids (especially lactic acid) and reabsorb bicarbonate. Other organ systems are also affected by the sustained hypoperfusion in the progressive stage of shock. The loss of the functional ability of the liver leads to a failure of the liver to metabolize drugs and waste products (e.g., lactate, ammonia). Jaundice results from an accumulation of bilirubin. As the liver cells die, enzymes become elevated (e.g., alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase). The liver also loses its ability to function as an immune organ. Bacteria that may move from the GI tract are no longer destroyed by the Kupffer cells. Instead, they are released into the bloodstream, thus increasing the possibility of bacteremia
Irreversible Stage rreversible stage: compensatory mechanisms are not functioning or are totally ineffective, leading to multiple organ dysfunction syndrome. In the final stage of shock, the irreversible stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism The accumulation of lactic acid contributes to an increased capillary permeability and dilation of the capillaries. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds secondary to the constricted venules and dilated arterioles.
The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO. Cerebral blood flow cannot be maintained, and cerebral ischemia results. The patient in this stage of shock will demonstrate profound hypotension and hypoxemia. The failure of the liver, lungs, and kidneys will result in an accumulation of waste products, such as lactate, urea, ammonia, and carbon dioxide. The failure of one organ system will have an effect on several other organ
no single diagnostic study to determine whether a patient is in shock.
Collaborative Care General Measures
Critical factors in the successful management of a patient experiencing shock relate to the early recognition and treatment of the shock state. Prompt intervention in the early stages of shock may prevent the decline to the progressive or irreversible stage. Successful management of the patient in shock includes the following: 1.Identification of patients at risk for developing shock
2.Integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis 3.Interventions to control or eliminate the cause of the decreased perfusion 4.Protection of target and distal organs from dysfunction
5.Provision of multisystem supportive care general management strategies for a patient in shock begin with ensuring that the patient has a patent airway. Once the airway is established, either naturally or with an endotracheal tube, oxygen delivery must be optimized. Supplemental oxygen and mechanical ventilation may be necessary to support the delivery of oxygen to maintain an arterial oxygen saturation greater than or equal to 90% (PaO2 greater than 60 mm Hg) to avoid hypoxemia
Oxygen and Ventilation
Oxygen delivery is dependent on CO, available hemoglobin, and arterial oxygen saturation (SaO2). Methods to optimize oxygen delivery are directed at increasing supply and decreasing demand. Supply is increased by (1) optimizing the CO with fluid replacement or drug therapy, (2) increasing the hemoglobin by the transfusion of whole blood or packed red blood cells (RBCs), and/or (3) increasing the arterial oxygen saturation with supplemental oxygen and mechanical ventilation. You must plan care that will not disrupt the balance of oxygen supply and demand. Space activities that increase oxygen consumption (e.g., endotracheal suctioning, position changes) appropriately for oxygen conservation
Except for cardiogenic and neurogenic shock, all other types of shock involve decreased circulating blood volume. In obstructive shock, the treatment involves alleviating or repairing the obstruction. The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with the administration of the appropriate fluid. Before beginning fluid resuscitation, you should insert two large-bore (e.g., 14- to 16-gauge) intravenous (IV) catheters, preferably in the antecubital veins. Both crystalloids (e.g., normal saline solution) and colloids (e.g., albumin) have a role in fluid resuscitation The choice of fluid for resuscitation remains controversial.
Currently, isotonic crystalloids, such as normal saline, are used in the initial resuscitation of shock. Lactated Ringer’s solution is used cautiously in all shock situations because the failing liver cannot convert lactate to bicarbonate. Thus serum lactate levels increase. In some cases, hypertonic saline may be administered to expand plasma volume.21 Colloids are effective volume expanders because the size of their molecules keeps them in the vascular space for a longer period of time. Despite this fact, colloids are costly and no definitive studies demonstrate that using colloids for resuscitation improves patient outcomes
The choice of fluid for resuscitation must also be based on the type and volume of fluid lost and the patient’s clinical status. If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous or PA pressure monitoring may be started monitor urine output will also assist in monitoring the patient’s fluid status. When large amounts of fluids are required, you must protect the patient against two major complications: hypothermia and coagulopathy. vasopressor (e.g., norepinephrine [Levophed], dopamine [Intropin]) and/or an inotrope (e.g., dobutamine [Dobutrex]) may be added. The goal for fluid resuscitation remains the restoration of tissue perfusion. Thus decisions on which agent to use should be based on the physiologic goal. Although BP helps determine whether the patient’s CO is adequate, an assessment of end-organ perfusion (e.g., urine output, neurologic function, peripheral pulses) provides information that is more relevant.
•Warm crystalloid and colloid solutions during massive fluid resuscitation. •When administering large volumes of packed RBCs, remember that they do not contain clotting factors. Replace these factors based on the clinical situation and laboratory studies. Drug Therapy
The primary goal of drug therapy for shock is the correction of decreased tissue perfusion. Medications used to improve perfusion in shock are administered intravenously via an infusion pump and central venous line. One main reason for administering these medications via a central line is that many of them have vasoconstrictor properties that may have harmful effects if administered peripherally and the drug extravasates
Many of the drugs used in the treatment of shock have an effect on the SNS. Drugs that mimic the action of the SNS are termed sympathomimetic. The effects of these drugs are mediated through their binding to α-adrenergic or β-adrenergic receptors. Many of the sympathomimetic drugs cause peripheral vasoconstriction and are called vasopressor drugs (e.g., norepinephrine, dopamine, phenylephrine [Neo-Synephrine]). These drugs have the potential to cause severe peripheral vasoconstriction and an increase in SVR The increased SVR increases the workload of the heart. This can be harmful to a patient in cardiogenic shock by causing further myocardial damage. Use of vasopressor drugs is limited to patients who do not respond to fluid resuscitation. Adequate fluid resuscitation must be achieved before starting vasopressors because the vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion.
The goals of vasopressor therapy are to achieve and maintain an MAP of greater than 65 mm Hg.14,19 You must continuously monitor end-organ perfusion (e.g., urine output, level of consciousness) and serum lactate levels (e.g., every 2 hours for the first 6 hours) to ensure that tissue perfusion is adequate.
Patients in cardiogenic shock have decreased myocardial contractility and vasodilators may be needed to decrease afterload. This reduces myocardial workload and oxygen requirements. Although generalized sympathetic vasoconstriction is a useful compensatory mechanism for maintaining systemic pressure, excessive constriction can reduce tissue blood flow and increase the workload of the heart. The goal of vasodilator therapy, as in vasopressor therapy, is to maintain the MAP greater than 65 mm Hg. Also monitor hemodynamic parameters (e.g., CVP, CO, ScvO2/SvO2, PA pressures) so that fluids can be increased or vasodilator therapy decreased if a serious fall in CO or BP occurs. The vasodilator agent most often used for the patient in cardiogenic shock is nitroglycerin (Tridil). Vasodilation may be enhanced with nitroprusside (Nipride) or nitroglycerin in noncardiogenic shock.
Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock. Nutrition is vital to decreasing morbidity. Enteral nutrition should be started within the first 24 hours. parenteral nutrition is used if enteral feedings are contraindicated or fail to meet at least 80% of the patient’s caloric requirements. Start the patient on a slow continuous drip of very small amounts of enteral feedings (e.g., 10 mL/hr). Early enteral feedings enhance the perfusion of the GI tract and help maintain the integrity of the gut mucosa. A patient in shock should be weighed daily on the same scale at the same time of day. If the patient experiences a significant weight loss, you should rule out dehydration before adding more calories. Large weight gains are common because of third spacing of fluids. Therefore daily weights serve as a better indicator of fluid status than caloric needs Serum protein, total albumin, BUN, serum glucose, and serum electrolytes are all used to assess nutritional status.
Collaborative Care Specific Measures
For a patient in cardiogenic shock, the overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand. Definitive measures to restore blood flow include thrombolytic therapy, angioplasty with stenting, emergency revascularization, and valve replacement Hemodynamic management of a patient in cardiogenic shock aims to reduce the workload of the heart through drug therapy and/or mechanical interventions. Drug selection is based on the clinical goal and a thorough understanding of the pharmacodynamics of each drug. Drugs can be used to decrease the workload of the heart by dilating coronary arteries (e.g., nitrates), reducing preload (e.g., diuretics), reducing afterload (e.g., vasodilators), and reducing heart rate and contractility (e.g., β-adrenergic blockers).
The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume. Fluid resuscitation in hypovolemic shock initially is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss) Septic Shock
Patients in septic shock require large amounts of fluid replacement. At times as much as 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids are needed in the first 6 hours to achieve a target CVP of 8 to 12 mm Hg To optimize and evaluate large-volume fluid resuscitation, hemodynamic monitoring with a minimum of a central venous catheter is necessary. The overall goals of fluid resuscitation are to restore the intravascular volume deficit and organ perfusion. Once the CVP is greater than or equal to 8 mm Hg, vasopressors may be added. Norepinephrine and dopamine are the initial drugs of choice. Vasodilation and low CO, or vasodilation alone, can cause low BP in spite of adequate fluid resuscitation DRUG ALERT
•Infuse at low doses (e.g., 0.01 to 0.03 units/min).
•Do not titrate infusion.
•Use cautiously in patients with coronary artery disease. Vasopressor drugs may increase BP but may also decrease stroke volume. An inotropic agent (e.g., dobutamine) is often added to offset the decrease in stroke volume and increase tissue perfusion (see Table 67-9). IV corticosteroids are only recommended for patients in septic shock who cannot maintain an adequate BP with vasopressor therapy despite fluid resuscitation.19 In an attempt to meet the increasing tissue demands coupled with a low SVR, the patient initially demonstrates a normal or high CO. If the patient is unable to achieve and maintain an adequate CO and has unmet tissue oxygen demands, the CO may need to be increased using drug therapy (e.g., dopamine) Antibiotics are an important and early component of therapy.
They should be started within the first hour of septic shock. Obtain cultures (e.g., blood, wound exudate, urine, stool, sputum) before antibiotics are started, but this should not prevent the initiation of antibiotics within the first hour. Broad-spectrum antibiotics are given initially, followed by antibiotics that are more specific once the organism has been identified.19 Mortality rates from septic shock remain high. Drotrecogin alfa (Xigris), a recombinant form of activated protein C, has helped patients with severe sepsis and a high risk of death (e.g., multiorgan failure).18-20,23 Activated protein C is a naturally occurring substance whose exact mechanism of action is unclear. It is thought to have antithrombotic and antiinflammatory effects. Activated protein C is found in subnormal levels in patients with sepsis. Drotrecogin interrupts the body’s response to severe sepsis, including bleeding and clotting abnormalities.
Drotrecogin alfa (Xigris)
•Administer to appropriate patients within the first 24 to 48 hours for best results. •Monitor the patient for bleeding (the most common side effect of the drug). Glucose levels should be maintained below 150 mg/dL (8.33 mmol/L) for patients in shock.19 Early research showed improved survival rates when continuous infusions of insulin and glucose were used to keep glucose levels between 80 and 110 mg/dL Frequent monitoring of glucose levels of all patients in septic shock is necessary. Stress ulcer prophylaxis (e.g., famotidine [Pepcid], pantoprazole [Protonix]) and venous thromboembolism prophylaxis (e.g., heparin, enoxaparin [Lovenox]) are also recommended for these patients.19 Neurogenic Shock
he specific treatment of neurogenic shock is dependent on the cause. If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal precautions, cervical stabilization with a collar) are initially used. Once the spine is stabilized, definitive treatment of the hypotension and bradycardia is essential to prevent further spinal cord damage. Hypotension, which occurs as a result of a loss of sympathetic tone, is associated with peripheral vasodilation and decreased venous return.
Treatment involves the use of vasopressors (e.g., phenylephrine) to maintain BP and organ perfusion (Bradycardia may be treated with atropine (Atro-Pen). Fluids are administered cautiously because the cause of the hypotension is not related to fluid loss.2 The patient with a spinal cord injury will also need to be monitored for hypothermia due to hypothalamic Although corticosteroids do not have an effect in neurogenic shock, methylprednisolone (Solu-Medrol) is used for patients with a spinal cord injury to prevent secondary spinal cord damage caused by the release of chemical mediator
The first strategy in managing patients at risk for anaphylactic shock is prevention. A thorough history is key in avoiding the risk factors for anaphylaxis (The clinical presentation of anaphylactic shock is dramatic, and immediate intervention is required. Epinephrine is the drug of choice to treat anaphylactic shock.9 It causes peripheral vasoconstriction and bronchodilation and opposes the effect of histamine. IV diphenhydramine (Benadryl) is given to block the massive release of histamine from the allergic reaction.
Maintaining a patent airway is important because the patient can quickly develop airway compromise from laryngeal edema or bronchoconstriction. Nebulized bronchodilators are highly effective. Aerosolized epinephrine can also be used to treat laryngeal edema. Endotracheal intubation or cricothyroidotomy may be necessary to secure and maintain a patent airway Hypotension results from leakage of fluid out of the intravascular space into the interstitial space as a result of increased vascular permeability and vasodilation. Aggressive fluid resuscitation, predominantly with colloids, is necessary
The primary strategy in treating obstructive shock is early recognition and treatment to relieve or manage the Mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by needle or tube insertio compression or obstruction of the outflow tract of the mediastinum, may be treated by radiation, debulking, or removing the mass or cause. A decompressive laparotomy may be indicated for abdominal compartment syndrome for patients with high intraabdominal pressures and hemodynamic instability. Obstructive shock from a pulmonary embolism may require thrombolytic therapy to restore circulation to the lungs and left side of the heart via the pulmonary artery. Nursing Management
Your role is vital in caring for patients who are at risk for developing shock or are in a state of shock. Focus your initial assessment on the ABCs: airway, breathing, and circulation. Next, focus on the assessment of tissue perfusion and include an evaluation of vital signs, level of consciousness, peripheral pulses, capillary refill, skin (e.g., temperature, color, moisture), and urine output. shock progresses, the patient’s skin will become cooler and mottled, the urine output will decrease, the peripheral pulses will diminish, and the neurologic status will decline. description of the events leading to the shock condition, time of onset and duration of symptoms, and a health history (e.g., medications, allergies, date of last tetanus vaccination, recent travel)
Ineffective and/or risk for ineffective perfusion: peripheral, renal, cerebral, cardiopulmonary, gastrointestinal, and hepatic related to low blood flow or maldistribution of blood as evidenced by the following possible findings: Anxiety related to severity of condition as evidenced by verbalization of anxiety about condition and fear of death, or withdrawal with no communication; restlessness; sleeplessness; increase in heart and respiratory rate
PLANNING The overall goals for a patient in shock include (1) evidence of adequate tissue perfusion, (2) restoration of normal or baseline BP, (3) return/recovery of organ function, and (4) avoidance of complications from prolonged states of hypoperfusion. Nursing Implementation
To prevent shock, you need to identify patients at risk. In general, patients who are older, those with debilitating illnesses, and those who are immunocompromised are at an increased risk. Any individual who sustains surgical or accidental trauma is at high risk for shock resulting from hemorrhage, spinal cord injury, sepsis, and other conditions (see Any patient who is at risk for decreased oxygen delivery is also at risk for the development of shock. example, an individual with an acute anterior wall MI is at high risk for cardiogenic shock primary goal for this patient is to limit the size of the infarction.
The infarct size can be limited by restoring coronary blood flow through thrombolytic therapy, percutaneous coronary intervention, or surgical revascularization. Rest, analgesics, and sedation can reduce the myocardial demand for oxygen. You should modify the patient’s environment to provide care at intervals that will not increase the patient’s oxygen demand. An individual with a severe allergy to such substances as drugs, shellfish, and insect bites is at increased risk to develop anaphylactic shock. The risk of anaphylactic shock can be decreased if the patient is carefully questioned about allergies
SAFETY ALERT•Always confirm the patient’s allergies before administering medications or beginning diagnostic procedures (e.g., computed tomography [CT] scan with contrast media). •Premedicate (e.g., diphenhydramine, methylprednisolone) patients who require a drug to which they are at high risk for an allergic reaction (e.g., contrast media). •Encourage patients with allergies to obtain and wear a medical alert tag and report their allergies to their health care providers. •Instruct patients about the availability of kits that contain equipment and medication (e.g., epinephrine [EpiPen]) for the treatment of acute hypersensitivity reactions.
Patients who are immunocompromised are at especially high risk to develop opportunistic infections. Interventions to decrease the risk of infection for hospitalized patients include decreasing the number of indwelling catheters (e.g., central lines, urinary catheters), using aseptic technique during invasive procedures, and strict attention to hand washing. In addition, all equipment must be changed according to institutional policy, or thoroughly cleaned or discarded (if disposable) between patient use. Acute Intervention
Your role in shock involves (1) monitoring the patient’s ongoing physical and emotional status, (2) identifying trends to detect changes in the patient’s condition, (3) planning and implementing nursing interventions and therapy, (4) evaluating the patient’s response to therapy, (5) providing emotional support to the patient and caregiver, and (6) collaborating with other members of the health team to coordinate care
Assess the patient’s neurologic status, including orientation and level of consciousness, at least every hour or more often. The patient’s neurologic status is the best indicator of cerebral blood flow. Be aware of the clinical manifestations that may indicate neurologic involvement (e.g., changes in behavior, restlessness, hyperalertness, blurred vision, confusion, paresthesias). Orient the patient to time, place, person, and events on a regular basis. If the patient is in an ICU, orientation to the environment is particularly important. You should minimize noise and light levels to control sensory input. Maintain a day-night cycle of activity and rest as much as possible.
Most of the therapy for shock is based on information about the patient’s cardiovascular status. If the patient is unstable, you should continuously assess heart rate and rhythm, BP, CVP, and PA pressures including CO, SVR, and stroke volume (if available)
Frequently assess the respiratory status of the patient in shock to ensure adequate oxygenation, detect complications early, and provide data regarding the patient’s acid-base status. Initially monitor the rate, depth, and rhythm of respirations as frequently as every 15 to 30 minutes. Increased rate and depth provide information regarding the patient’s attempts to correct metabolic acidosis. Assess breath sounds every 1 to 2 hours and as required for any changes that may indicate fluid overload or accumulation of secretions. pulse oximetry to monitor oxygen saturation continuously. Pulse oximetry using a patient’s finger may not be accurate in a shock state because of poor peripheral circulation.
In this situation, attach the probe to the ear, nose, or forehead (according to the manufacturer’s guidelines) to increase accuracy. Arterial blood gases (ABGs) p Low PaCO2 in the presence of a low pH and low bicarbonate level may indicate that the patient is attempting to compensate for a metabolic acidosis from increasing lactate levels. A rising PaCO2 in the presence of a persistently low pH and PaO2 may indicate the need for intubation and mechanical ventilation. renal Status
Obtain hourly measurements of urinary output to assess the adequacy of renal perfusion. Inserting an indwelling bladder catheter will facilitate measurements. Urine output below 0.5 mL/kg/hr may indicate inadequate perfusion of the kidneys. Also use trends in serum creatinine values to assess renal function
Body Temperature and Skin Changes
Monitor the temperature every 4 hours if normal. In the presence of an elevated or subnormal temperature, obtain hourly core temperatures (e.g., urinary, central line, PA catheter). Use light covers and control the environmental temperature to keep the patient comfortably warm. If the patient’s temperature rises above 101.5° F (38.6° C) and the patient becomes uncomfortable or experiences cardiovascular compromise, manage the fever with antipyretic drugs (e.g., ibuprofen [Motrin], acetaminophen [Tylenol]), and/or by removing some of the patient’s covers.
Auscultate bowel sounds at least every 4 hours, and monitor for abdominal distention. If a nasogastric tube is present, measure drainage and check for occult blood. Similarly, check all stools for occult blood.
Hygiene is especially important to the patient in shock because impaired tissue perfusion predisposes the patient to skin breakdown and infection. You need to perform bathing and other nursing measures carefully because a patient in shock is experiencing problems with oxygen delivery to tissues. oral care for the patient in shock is essential because mucous membranes may become dry and fragile in the volume-depleted patient. In addition, the intubated patient usually has difficulty swallowing, resulting in pooled secretions in the mouth. Apply a water-soluble lubricant to the lips to prevent drying and cracking. Brush the patient’s teeth with a soft toothbrush every 12 hours and swab the lips and oral mucosa with a moisturizing solution every 2 to 4 hours.29 Perform passive range of motion three or four times a day to maintain joint mobility.
Emotional Support and Comfort
Do not overlook or underestimate the effects of fear and anxiety in the face of a critical, life-threatening situation on the patient and caregiver. Fear, anxiety, and pain may aggravate respiratory distress and increase the release of catecholamines. When implementing care, monitor the patient’s emotional state and level of pain. Provide medications to decrease anxiety and pain as appropriate. Continuous infusions of a benzodiazepine (e.g., lorazepam [Ativan]) and an opioid or anesthetic (e.g., morphine, propofol [Diprivan]) are extremely helpful in decreasing anxiety and pain. A neuromuscular blocking agent (e.g., cisatracurium [Nimbex]) may be added when these medications are not adequate.
Talk to the patient and encourage the caregiver to talk to the patient, even if the patient is intubated, is sedated, or appears comatose. Hearing is often the last sense to be reduced, and even if the patient cannot respond, he or she may still be able to hear. If the intubated patient is capable of writing, provide a “magic slate” or a pencil and paper. Caregivers can have a therapeutic effect on the patient. To perform this role, they need to be supportive and comforting.
(1) link the patient to the outside world, (2) facilitate decision making and advise the patient, (3) assist with activities of daily living, (4) act as liaisons to advise the health care team of the patient’s wishes for care, and (5) provide safe, caring, familiar relationships for the patient