Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Chapter 54: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Shock • Complex syndrome • Alteration in compensatory mechanisms that results in: – Circulatory underperfusion – Respiratory underperfusion – Increased coagulation – Stimulation of the inflammatory responses leading to: • Multiple organs failing Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins The Delicate Balance • Tissue oxygenation and perfusion – Cells usually take up 25% of oxygen delivered. – This oxygen consumption is referred to as VO2. – Delivery of oxygen to the cellular tissue is the DaO2. – In stress VO2 depends upon DaO2. – Compensatory mechanisms ensure this takes place. – When cells can’t extract enough oxygen, the body turns to anaerobic metabolism, which can lead to lactic acidosis. – Cellular death can occur if this process isn’t reversed. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Compensatory Mechanisms: Autonomic Nervous System See Figure 54-1. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question The nurse suspects that a patient injured in a motor vehicle accident is going into hypovolemic shock. Which of the following compensatory mechanisms will help maintain a patient’s blood pressure? A. Increased urinary output B. Decreased respiratory effort C. Decreased preload D. Increase in systemic vascular resistance (SVR) Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer D. Increase in systemic vascular resistance (SVR) Rationale: The release of catecholamines causes a peripheral vasoconstriction and therefore an increase in the systemic vascular resistance (SVR) as well as venous vasoconstriction, which increases the preload. Respirations increase to supply more oxygen to the tissues. Urinary output decreases to conserve sodium and water under the influence of ADA. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Compensatory Mechanisms in Shock Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Shock Stages: A Progressive Downward Spiral Vital signs Cerebral perfusion Reversible STAGE I Nonprogressive stage Relatively normal Intact Yes STAGE II Progressive stage Noticeable changes; tachycardia and tachypnea Change in LOC Yes, if recognized and treated appropriately STAGE III Irreversible Temp down Pulse down Respirations down Hypotensive Profound decrease in cerebral perfusion No Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Classifications of Shock • Hypovolemic – Burns – Hemorrhage • Cardiogenic – Pump failure • Distributive – Spinal cord injury – Sepsis – Anaphylaxis Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Hypovolemic Shock Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pathophysiology • Decreased circulating volume stimulates SNS and hormonal responses. • Blood is shunted to the heart and brain at the expense of the kidney, liver, and gut. • If volume isn’t restored and compensatory mechanisms fail, the SNS increases myocardial demand and oxygen consumption (MvO2). • End-organ failure can result. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Signs/Symptoms Depend on the Volume Lost ASSESSMENT DATA LAB DATA • Change in LOC • Serum lactate • Tachypnea • Serial ABGs • Cool clammy skin • Hemoglobin and hematocrit • Tachycardia • Coagulation profiles • Hypotension (with >30% blood loss) • Decreased urinary output Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Treatment: Fluid Resuscitation Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Management During Fluid Resuscitation • Deliver warmed fluids through large-bore IVs • Monitor for pulmonary edema, which can occur if fluids are given too quickly • Elevate lower extremities • Monitoring – Vital signs – Oxygen saturation – Mentation (LOC) – Urinary output and labs Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Cardiogenic Shock • Decrease in oxygenation to the tissues from decreased heart pumping • Most significant cause is myocardial infarction – 40% of left ventricular mass infarction • Often occurs at home • Other causes include ruptured papillary muscle, ventricular septal defect/rupture, cardiomyopathy, valvular disease, and dsyrhythmias Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pathophysiology of Cardiogenic Shock Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Decreased cardiac output from cardiogenic shock leads to an increase in sodium and water retention, further leading to a downward spiral unless reversed. A. True B. False Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins ANSWER A. True Rationale: When the cardiac output drops, renin and angiotensin are secreted. Their ultimate response is to hold on to sodium and water. In hypovolemic and distributive shock, this is a beneficial mechanism because it helps keep water in the tubes. In cardiogenic shock, however, this increases edema, which puts more stress on the heart. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Signs/Symptoms ASSESSMENTS LABS/DIAGNOSTICS • Identify who is at high risk – MI • Elevated cardiac enzymes (troponin, CPK-MB) – Ejection fraction <35% • BNP – Diabetes mellitus • ECG changes – Elderly • Echocardiography • Pulmonary artery pressures • Chest pain • Thready rapid pulses • Distended neck veins • Pulmonary congestion (crackles, gurgles, hemoptysis) Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Treatment and Nursing Care • Judicious fluids with diuretics and nitrates • Monitor and replace electrolytes, especially K+, Ca, Mg • Narcotic analgesics, but watch the SaO2 • Treat rhythm disturbances • Possible cardioversion and pacing • Pulmonary artery pressure monitoring • Left ventricular assistive devices: IABP, LVA Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Medications • Medication administration (beta-blockers, dopamine, dobutamine, etc.) • Sodium nitroprusside, nitroglycerin • ACE inhibitors Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Distributive Shock: Blood Shunted From Core • Anaphylaxis – Allergens • Neurogenic – Loss of sympathetic tone from spinal cord injury • Septic – Sepsis Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Anaphylactic Shock • Life-threatening response to an allergen • Usually not with first exposure; antigens trigger a response with second exposure • Nurse should teach about prevention • Mostly due to insect venom (injected) – Drugs (injected or ingested) and foods are next most common; ASA and NSAIDs are common – Inhalation of antigens Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Antigen-Antibody Response See Figure 54-8. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient presents to the Emergency Care Unit and is thought to be having an anaphylactic reaction to a bee sting. Which of the following symptoms might the patient exhibit? A. Crackles B. Egophony C. Stridor D. Petechiae Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer C. Stridor Rationale: Patient with anaphylactic reactions can have stridor due to bronchoconstriction from the allergen. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Signs/Symptoms and Nursing Care • SIGNS/SYMPTOMS • NURSING CARE – Identify, remove offending allergen – Oxygen and possible intubation if not reversed Dyspnea, wheezing; can lead to stridor – Antihistamine such as diphenhydramine – Severe respiratory distress from laryngeal edema – Possible epinephrine – Hypotension and circulatory collapse – Rapid infusion of NSS if hypotensive – Circulatory support with vasoconstrictors prn – Generalized erythema – Urticaria and pruritus – Anxiety and restlessness – Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Septic Shock • High mortality rates • 1:4 patients in ICU will worsen from sepsis to septic shock – Worse in first 10 days of diagnosis • Initiated by an infection (gram – or + bacteria, fungi, etc.) • Inflammatory response that kills organism causes an increased permeability in the endothelial layer of the blood vessels. Fluid moves into interstitial spaces. • Stable fibrin clots form and adhere to the damaged endothelium. • Every organ system is affected. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Organ Effects of Septic Shock • CARDIOVASCULAR • RESPIRATORY – Vasodilation in response to nitric oxide release – Bronchoconstriction from cytokine activity – Other mediators cause vasoconstriction and clotting in microcirculation – Interstitial edema from inflammatory substances – Shunting – Impaired gas exchange – ARDS – Possible secondary infection from intubation/ventilation – Decreased CO, increased SVR – Lactic acidosis, which depresses myocardial contraction Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Organ Effects of Septic Shock (cont.) • HEMATOLOGICAL CHANGES – Platelet aggregation • METABOLIC CHANGES – Increased energy consumption – Obstructed flow decreases tissue metabolism – Hyperglycemia – Clotting factors depleted – Mitochondrial and cellular death – Result: DIC – Ketosis Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Findings and Treatment • PHYSICAL FINDINGS – Changes in LOC – Tachypnea – Fever; hypothermia – Decreased urinary output – – • TREATMENT – Antibiotics (“shotgun” approach until causative organism identified) – Restoring volume with crystalloid/colloids Decreased bowel sounds – Diminished peripheral pulses Monitoring for fluid overload with PA catheter – Dopamine/Levophed/ vasopressin/dobutamine Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question A patient is suspected of having septic shock. Which of the following medications improves outcomes in septic shock by decreasing the imbalance of clotting in the endothelium? A. Drotrecogin alfa (activated) (Xigris) B. Dobutamine C. Epinephrine D. Levophed Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer A. Drotrecogin alfa (activated) (Xigris) Rationale: Drotrecogin alfa (activated) (Xigris) decreases the clotting in the microvasculature that increases hypoxia in sepsis. Dobutamine, epinephrine, and Levophed are used to help increase cardiac contractions and improve vascular tone in septic shock. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Care and Treatment • Intubation and mechanical ventilation – PEEP may be used if ARDS • Drotrecogin alfa (activated) (Xigris) – Reestablishes homeostasis of clotting system • Nutritional support – Enteral feedings – TPN Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Systemic Inflammatory Response Syndrome (SIRS) • Should be suspected in any patient with shock or risk for shock • Inflammatory response that is systemic; microthrombic in vessels • Also caused by “leaky pipe syndrome” from released vasodilator • Management is similar to septic shock Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Multiorgan System Failure (MODS) • Cause is unknown • Inflammatory substances found in SIRS play a role in MODS • Multiple organs fail; usually lungs, heart, kidney, and lastly liver – Pulmonary hypoventilation and hypoxia – Decreased cardiac output; hypotension and dysrhythmias – Increased risk of DIC – Poor cerebral perfusion – Liver failure Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Signs/Symptoms and Treatment • Hypotension • Tachycardia • Tachypnea • Hypo- or hyperthermia • Treatment is supportive care and similar to septic shock Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins