Nursing 4060 Study Guide for Exam #1 July 18, 2018
This exam includes the airway management,
... [Show More] Hemodynamic monitoring & care, and all types of shock. There will be 3-5 calculations, all types. There is a total of 50-55 questions, with multiple multiples. Know the nursing management of all types of shock, goals of treatment of shock, medical management, and stages of shock (include nursing management). Understand use of central lines and arterial lines for critically ill patients-know possible complications and priority of care for these patients. Good Luck studying.
Shock: (25 questions)
Anaphylactic: know signs/symptoms, nursing and medical management, prevention
⦁ An acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). The reaction quickly causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space.Anaphylactic shock can lead to respiratory distress due to laryngeal edema or severe bronchospasm, and circulatory failure from the massive vasodilation.
Signs/symptoms:
⦁ Dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. In addition, the patient may be anxious and confused and have a sense of impending doom.
Nursing and medical management:
⦁ The first strategy in managing patients at risk for anaphylactic shock is prevention. A thorough history is key to avoiding the risk factors for anaphylaxis (⦁ Table 66-1). The clinical presentation of anaphylactic shock is dramatic, and immediate intervention is required. IM epinephrine is the first drug of choice to treat anaphylactic shock. It causes peripheral vasoconstriction and bronchodilation and opposes the effect of histamine. Diphenhydramine and ranitidine (Zantac) are given as adjunctive therapies to block the ongoing 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, usually with crystalloids, is necessary. IV corticosteroids may be helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy (⦁ Tables 66-8 and ⦁ 66-9).
Oxygenation Circulation Drug Therapies Supportive Therapies
Anaphylactic Shock
• Maintain patent airway
• Optimize oxygenation with supplemental O2
• Intubation and mechanical ventilation, if necessary • Aggressive fluid resuscitation with colloids • Epinephrine (IM or IV)
• Antihistamines (e.g., diphenhydramine)
• Histamine (H2)-receptor blockers (e.g., ranitidine [Zantac])
• Bronchodilators: nebulized (e.g., albuterol)
• Corticosteroids (if hypotension persists) • Identify and remove offending cause
• Prevent via avoidance of known allergens
• Premedicate with history of prior sensitivity (e.g., contrast media)
Safety Alert
Preventing Allergic Reactions
• Always confirm the patient's allergies before giving drugs or starting diagnostic procedures (e.g., CT scan with contrast media).
• Premedicate (e.g., diphenhydramine, methylprednisolone) patients who need 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 device and report their allergies to their HCPs.
• Tell patients about the availability of kits that contain equipment and drugs (e.g., epinephrine [EpiPen]) for the treatment of acute allergic reactions.
Septic: know signs/symptoms, nursing and medical management, medications, labs
Sepsis: Constellation of symptoms or syndrome in response to an infection, characterized by a dysregulated patient response along with new organ dysfunction related to the infection.
Septic shock is characterized by persistent hypotension despite adequate fluid resuscitation requiring vasopressors, along with inadequate tissue perfusion resulting in tissue hypoxia. The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also cause sepsis and septic shock
⦁ When a microorganism enters the body, the normal immune or inflammatory responses are triggered. However, in sepsis and septic shock the body's response to the microorganism is exaggerated.
⦁ Both proinflammatory and antiinflammatory responses are activated, coagulation increases, and fibrinolysis decreases. Endotoxins from the microorganism cell wall stimulate the release of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through secondary mediators such as platelet-activating factor, IL-6, and IL-8. The release of platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature. The combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium.
⦁ In addition to the cardiovascular dysfunction that accompanies sepsis, respiratory failure is common. The patient initially hyperventilates as a compensatory mechanism, resulting in respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis develops. Respiratory failure develops in 85% of patients with sepsis, and 40% develop acute respiratory distress syndrome (ARDS). These patients may need to be intubated and mechanically ventilated.
Three Pathophysiological effects of Septic Shock: Vasodilation, maldistribution of blood flow, and myocardial depression.
⦁ Patients may be euvolemic, but because of acute vasodilation, relative hypovolemia and hypotension occur. In addition, blood flow in the microcirculation is decreased, causing poor O2 delivery and tissue hypoxia. The ejection fraction is decreased for the first few days after the initial insult. Because of a decreased ejection fraction, the ventricles dilate to maintain the SV. The ejection fraction typically improves, and ventricular dilation resolves over 7 to 10 days. Persistence of a high CO and a low SVR beyond 24 hours is an ominous finding and is often associated with an increased development of hypotension and MODS. Coronary artery perfusion and myocardial O2 metabolism are not primarily altered in septic shock.
Signs/Symptoms:
⦁ Fever(100.9F), hypothermia, HR (>90), Tachypnea, SBP(<100), altered Mental status, hyperglycemic
⦁ Other clinical signs of septic shock include alteration in neurologic status; decreased urine output; and GI dysfunction, such as GI bleeding and paralytic ileus.
Nursing Management:
⦁ Patients in septic shock require large amounts of fluid replacement. Volume resuscitation of 30 to 50 mL/kg is usually done with isotonic crystalloids to achieve adequate fluid resuscitation. Albumin 4% to 5% may be added when patients require substantial volumes.
⦁ A fluid challenge technique (e.g., to achieve a minimum of 30 mL/kg of crystalloids) is used and repeated until hemodynamic improvement (e.g., increase in MAP and/or CVP, change in SVV) is noted. ⦁ Table 66-9 presents predetermined end points of fluid resuscitation along with methods to reassess volume status.
⦁ One of these methods is a passive leg raise (PLR) challenge along with hemodynamic measures to monitor response. A PLR challenge provides a transient increase in fluid volume of 150 to 500 mL by placing the patient supine and raising the legs to 45 degrees. Response is monitored within 1 to 2 minutes by measuring CO, CI, SV, SVV, or other parameters for improvement. If the response is positive, then the patient is fluid responsive and should receive additional fluids. To optimize and evaluate large-volume fluid resuscitation, hemodynamic monitoring with various noninvasive or invasive monitors is necessary. The overall goal of fluid resuscitation is to restore the intravascular volume and organ perfusion.
⦁ If the patient remains hypotensive after initial volume resuscitation with minimally 30 mL/kg and the patient is no longer fluid responsive, vasopressors may be added. The first drug of choice is norepinephrine. Vasodilation and low CO, or vasodilation alone, can cause low BP in spite of adequate fluid resuscitation. Vasopressin may be added for patients refractory to initial vasopressor therapy. Exogenous vasopressin is used to replace the stores of physiologic vasopressin that are often depleted in septic shock.
⦁ Vasopressor drugs may increase BP but may also decrease SV. An inotropic agent (e.g., dobutamine) may be added to offset the decrease in SV and increase tissue perfusion. IV corticosteroids may be considered for patients in septic shock who cannot maintain an adequate BP with vasopressor therapy despite fluid resuscitation. 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 O2 demands, the CO may have to be increased using drug therapy (e.g., dopamine). ScvO2or SvO2 monitoring is used to assess the balance between O2 delivery and consumption, and the adequacy of the CO. If balance is maintained, the tissue demands will be met.
⦁ Antibiotics are an important and early component of therapy. They should be started within the first hour of severe sepsis or septic shock. Every hour delay has shown to significantly decrease survival. Obtain cultures (e.g., blood, wound exudate, urine, stool, sputum) before antibiotics are started. However, this should not delay the start of antibiotics within the first hour. Broad-spectrum antibiotics are given first. More specific antibiotics may be ordered once the organism has been identified.
⦁ Glucose levels should be maintained below 180 mg/dL (10.0 mmol/L) for patients in shock. Intensive glucose control (81 to 108 mg/dL) actually increases mortality. Monitor glucose levels in all patients in septic shock according to agency policy.
⦁ Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole) for patients with bleeding risk factors and venous thromboembolism prophylaxis (e.g., heparin, enoxaparin [Lovenox]) are also recommended for these patients.
Oxygenation Circulation Drug Therapies Supportive Therapies
Septic Shock
• Provide supplemental O2
• Intubation and mechanical ventilation, if necessary
• Monitor ScvO2 or SvO2 • Aggressive fluid resuscitation (e.g., 30 mL/kg of crystalloids repeated as long as hemodynamic improvement is noted)
• End points of fluid resuscitation are based on:
1. Focused physical examination including vital signs, cardiopulmonary assessment, capillary refill, peripheral pulses, and skin or any 2 of the following:
• ScvO2 >70 or SvO2 >65
• CVP 8-12 mm Hg
• Cardiovascular ultrasound
2. Assessment of fluid responsiveness with passive leg raise or fluid challenge • Antibiotics as ordered
• Vasopressors (e.g., norepinephrine)
• Inotropes (e.g., dobutamine)
• Anticoagulants (e.g., low-molecular-weight heparin) • Obtain cultures (e.g., blood, wound) before beginning antibiotics
• Monitor temperature
• Control blood glucose
• Stress ulcer prophylaxis
Drug Alert
Vasopressin
• Given along with norepinephrine.
• Infuse at low doses (e.g., 0.03 U/min) using an IV pump.
• Do not titrate infusion.
• Use cautiously in patients with coronary artery disease.
Neurogenic: know signs/symptoms, nursing and medical management
⦁ Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury and can last up to 6 weeks,generally associated with a cervical or high thoracic injury.The injury results in a massive vasodilation without compensation because of the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism
⦁ In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock (⦁ Table 66-1).
Signs/Symptoms:
⦁ The most important clinical manifestations in neurogenic shock are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).⦁ 6 The patient may not be able to regulate body temperature. Combined with massive vasodilation, the inability to regulate temperature promotes heat loss. Initially, the patient's skin is warm due to the massive vasodilation.
⦁ As the heat disperses, the patient is at risk for hypothermia. Later, the patient's skin may be cool or warm depending on the ambient temperature (poikilothermia, taking on the temperature of the environment). In either case, the skin is usually dry. ⦁ Tables 66-2and ⦁ 66-3 further describe the laboratory findings and clinical presentation of a patient with neurogenic shock.
Nursing and medical management:
⦁ The specific treatment of neurogenic shock is based 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 (⦁ Table 66-8). Bradycardia may be treated with atropine. Infuse fluids cautiously as the cause of the hypotension is not related to fluid loss.
⦁ The patient with a spinal cord injury also needs to be monitored for hypothermia caused by hypothalamic dysfunction (⦁ Table 66-9). Corticosteroids do not have an effect in neurogenic shock, and current guidelines no longer recommend the use of methylprednisolone (Solu-Medrol) for patients with a spinal cord injury.
Oxygenation Circulation Drug Therapies Supportive Therapies
Neurogenic Shock
• Maintain patent airway
• Provide supplemental O2
• Intubation and mechanical ventilation (if necessary) • Cautious administration of fluids • Vasopressors (e.g., phenylephrine)
• Atropine (for bradycardia) • Minimize spinal cord trauma with stabilization
• Monitor temperature
Cardiogenic: know signs/symptoms, nursing and medical management
Table 66-1
Classification of Shock States
Types and Causes Examples
Cardiogenic Shock
• Systolic dysfunction: inability of the heart to pump blood forward Myocardial infarction, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, myocardial depression from metabolic problems
• Diastolic dysfunction: inability of the heart to fill Cardiac tamponade, ventricular hypertrophy, cardiomyopathy
• Dysrhythmias Bradydysrhythmias, tachydysrhythmias
• Structural factors Valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax
⦁ Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart's pumping action results in reduced cardiac output (CO). Causes of cardiogenic shock are listed in ⦁ Table 66-1. Mortality rates for patients with cardiogenic shock approach 60%. Decreased filling of the heart results in decreased stroke volume (SV).
⦁ The heart's inability to pump the blood forward is called systolic dysfunction. Systolic dysfunction primarily affects the left ventricle, since systolic pressure is greater on the left side of the heart. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is reduced. The most common cause of systolic dysfunction is acute myocardial infarction (MI).
Fig. 66-2 describes the pathophysiology of cardiogenic shock. Whether the first event is myocardial ischemia, a structural problem (e.g., valvular disorder, ventricular septal rupture), or dysrhythmias, the physiologic responses are similar: the patient experiences impaired tissue perfusion and cellular metabolism. [Show Less]