Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Chapter 39 Care of Patients with Shock

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Learning Outcomes 1 Evaluate patient risk for hypovolemic shock or sepsis and septic shock. 2 Ensure vital sign measurements are accurate, and monitor them for changes indicating the presence of shock. 3 Apply principles of infection control to prevent infection and sepsis in susceptible patients, especially older adults. 4 Teach all people to avoid dehydration.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. 5 Teach all people to use safety devices to avoid trauma. 6 Instruct all patients going home after surgery or invasive procedures to seek immediate attention for persistent manifestations of early shock. 7. Compare the risk factors, causes, and manifestations of different types of shock. 8. Identify the manifestations associated with shock progression.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. 9. Describe the actions, side effects, and nursing implications of drug therapy for shock. 10. Explain the role of the systemic inflammatory response syndrome (SIRS) in the manifestations and progression of sepsis and septic shock. 11. Prioritize the nursing care for the patient with sepsis or septic shock.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Disorders Hypovolemic Shock Sepsis and Septic Shock

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Shock Overview Widespread abnormal cellular metabolism Oxygenation and tissue perfusion needs not met “Whole-body” response Any problem impairing oxygen delivery to tissues and organs can start shock, lead to life-threatening emergency

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. FIG Oxygenation and tissue perfusion affected by hypovolemic shock and adjustment/compensation. RBCs, Red blood cells.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Review of Oxygenation and Tissue Perfusion Oxygenation and perfusion depend on how much oxygen from the arterial blood perfuses the tissue. MAP is dependent on …. Total blood volume Cardiac output Size of vascular (capillary) bed FYI- 2 min video N9AU1GiQ

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. “Click on” the capillary bed.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc.

Questions to ponder or dig: FYI Which of the 5 images on the last slide is most severe? What may have caused it? How far back to do want to chase the cause? Do a RCA (root cause analysis). Could this have been prevented? How? The images described blood volume and size of the capillary beds. What would happen if you threw the Heart Rate variable in? What would happen to the MAP? What are factors that increase or decrease HR? What medications affect HR?

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Classification of Shock by Functional Impairment Hypovolemic Cardiogenic Distributive - Chemical-Induced Distributive Shock Obstructive

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Hypovolemic Shock Low circulating blood volume causes mean arterial pressure (MAP) decrease; inadequate total body oxygenation Commonly caused by hemorrhage (external or internal), dehydration

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. GIB- a bloody mess Family- a beautiful mess Priorities: S: B: A: R:

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Cardiogenic Shock Actual heart muscle is unhealthy; pumping is directly impaired Myocardial infarction most common cause FYI- Jen’s story- Cardiogenic shock 6 min anz0INzovs anz0INzovs (High quality “commercial”)

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Distributive Shock Blood volume distributed to interstitial tissues where it cannot circulate, deliver oxygen Caused by loss of sympathetic tone blood vessel dilation pooling of blood in venous & capillary beds capillary leak eg: Chemical-induced distributive shock

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Chemical-Induced Distributive Shock caused by…. Anaphylaxis Sepsis Capillary leak syndrome

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Obstructive Shock Impaired ability of normal heart muscle to pump effectively Conditions outside heart prevent either adequate filling of heart or adequate contraction of healthy heart muscle Pericarditis and Cardiac tamponade are the most common cause

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Pericarditis and Cardiac tamponade are the most common cause of obstructive shock The heart is surrounded by a sac called the pericardium. When this sac becomes filled with fluid, the liquid presses on the heart, preventing the lower chambers of the heart from properly filling with blood.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Pathophysiology of Hypovolemic Shock The basic problem of hypovolemic shock is a loss of blood volume from the vascular space The main trigger leading to hypovolemic shock is a sustained decrease in MAP that results from decreased circulating blood volume. Compensatory mechanisms to the rescue (if not too severe)

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Pathophysiology of Hypovolemic Shock (continued) If the initiating events continue and MAP decreases further, electrolyte and acid-base imbalances occur with tissue-damaging effects and depressed heart muscle activity. These effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. If shock continues, multiple organ dysfunction syndrome (MODS) occurs and recovery from shock is no longer possible.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Processes of Shock- 4 stages- Table Initial stage (early shock) 2.Nonprogressive (compensatory) stage 3. Progressive (intermediate) stage 4. Refractory (irreversible) stage

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Multiple Organ Dysfunction Syndrome (MODS) Sequence of cell damage More dead cells break open Microthrombi (small clots) form Liver, heart, brain, kidney function loss first

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Health Promotion and Maintenance Can usually be prevented Avoid trauma and hemorrhage Proper safety equipment Seat belts Awareness of hazards in home/workplace Secondary prevention Assess for early manifestations Patient teaching

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Cardiovascular Manifestations Decreased cardiac output Increased pulse Decreased blood pressure Narrowed pulse pressure

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. More Manifestations of SHOCK Increased respiratory rate Increased Thirst Decreased urine output Cool, cold or moist skin (clammy-next slide) Diminished or absent bowel sounds

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. What is clammy/ moist/ cool skin? Clammy skin occurs when your skin turns cooler than normal and is moist, despite a cooler surface temperature. Clammy skin is often pale. When the body is in any type of circulatory crisis, adrenaline prompts a decrease in the blood flow to peripheral areas of your body (such as your appendages and skin) in order to redirect more blood to the vital organs. This causes the cool and clammy skin. Frequent causes of clammy skin include acute allergic reaction; anxiety; hypoglycemia (low blood sugar); severe pain; and low blood oxygen levels from any of the following conditions: heart attack; heat exhaustion; pulmonary embolus (blockage of an artery within the lung due to a blood clot); heavy or internal bleeding, dehydration, or pneumonia; severe infection; or drug overdose that reduces heart function or blood pressure.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Assessment and Quality Care Psychosocial assessment Changes in mental status and behavior may be early signs of shock Laboratory tests H & H ABG pH Chart 39-3 Best Practice for Patient Safety & Quality Care-The Patient in Hypovolemic Shock

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Nonsurgical Management Goals: maintain tissue oxygenation increase vascular volume to normal range support compensatory mechanisms Oxygen therapy IV therapy- NS, RL, blood Drug therapy

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Drug Therapies- Chart 39-4 Goals: Increase venous return Improve cardiac contractility Improve cardiac perfusion by dilating coronary vessels Vasoconstrictors to increase venous return Dopamine (Intropin), Norepinephrine (Levophed), Phenylephrine HCL Agents enhancing contractility Dobutamine (Dobutrex), Milrinone (Primacor) Agents enhancing myocardial perfusion Sodim nitroprusside (Nitropress)

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Common progression of events leading to septic shock

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Sepsis and Septic Shock Pathophysiology Complex type of distributive shock— bacterial/fungal infection progresses to dangerous condition within days Sepsis is a condition where infectious microorganisms have entered the blood stream. Systemic inflammatory response (SIRS) triggered when number of organisms increase TABLE 39-4 CONDITIONS PREDISPOSING TO SEPSIS AND SEPTIC SHOCK

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. FIG Vicious cycle of SIRS and MODS in septic shock.- Figure is in the handouts too.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Clinical Manifestations vary with stages Cardiovascular Respiratory Skin Renal and urinary ** TABLE 39-3 SEPSIS WITH SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) CRITERIA **

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Interventions Oxygen therapy Drug therapy Chart 39-4 Blood replacement therapy clotting factors fresh frozen plasma whole blood packed red blood cells Teach about infection precautions- Chart 39-7

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. A 59-year-old male is 3 days postoperative after a colon resection. The nursing assistant is responsible for taking his morning vital signs. At 8:00 AM she reports that the patient’s oral temperature is 101.6° F. What is your best first action?

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. When the patient’s elevated temperature is reported by the nursing assistant, it is the nurse’s responsibility to determine what action should be taken. The nurse should proceed to his room for a complete assessment.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. (cont’d) Ten minutes later, your assessment reveals that the patient is flushed and slightly diaphoretic. He appears lethargic, but responds to simple questions. His vital signs are now BP 90/40, HR 134, R 26 and deep, temp 102.8° F. Lungs are clear throughout. His abdominal wound has a dressing that is moist with a moderate amount of purulent drainage. What is your best interpretation of this data?

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. The development of infection should be considered based on the patient’s operative history and vital signs. He has tachycardia and increased respirations, as well as a moderate amount of purulent drainage at the abdominal dressing site. Surgical dressings should not contain purulent drainage.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. (cont’d) Twenty minutes later, you call the health care provider to report the abnormal findings. The provider orders: A. Tylenol 650 mg PO prn q6h for temp above 101° F B. Blood cultures × 2, 5 min apart C. C & S of abdominal wound drainage D. Vancomycin 750 mg IVPB over 1 hr every 24 hr In what order should you implement these interventions?

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. ANS: C, B, D, A Based on the findings, this patient is possibly developing sepsis. The wound should be cultured immediately and the nurse should notify the laboratory that blood cultures must be obtained. All cultures must be drawn before administering the antibiotics. The first anti-infective should be started within 1 hour after the blood and wound cultures are obtained. The nurse may then give the patient Tylenol for his fever.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. (cont’d) Over the next hour, the patient continues to decline with a decreased level of consciousness and a temperature of 103.8° F. BP is 80/40, HR is 134, and RR is 34. You call the provider to report these findings and obtain orders for the patient to be transferred to ICU. When preparing for this transfer, you note that the O 2 saturation is 87% on room air. What intervention should you perform first? A. Apply oxygen at 2-3 L per nasal cannula B. Draw an arterial blood gas sample C. Administer acetaminophen 650 mg by mouth D. Place the patient on a cardiac telemetry monitor

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. ANS: A The patient is gravely ill. The first priority is his airway. He has a rapid respiratory rate and a low SaO 2, so supplemental oxygen should be applied first. His elevated temperature should also be addressed. You may choose to call the Rapid Response Team to help stabilize the patient, even though he is being transferred to the ICU.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. (cont’d) Within 30 minutes of the patient’s transfer to the ICU, his condition continues to deteriorate. His SaO 2 continues to fall, RR is 36/min, and you note blood oozing around his IV catheter sites. A Foley catheter is placed and his urine output is minimal. What is your best interpretation of these changes?

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. ANS: A The patient is gravely ill. The first priority is his airway. He has a rapid respiratory rate and a low SaO 2, so supplemental oxygen should be applied first. His elevated temperature should also be addressed. You may choose to call the Rapid Response Team to help stabilize the patient, even though he is being transferred to the ICU.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Question 1 A 37-year-old male is admitted with a severely abscessed tooth, BP 90/42, HR 136, RR 28, Sp O 2 90% on room air, T 38.7° C. The nurse suspects sepsis from the tooth. The priority intervention by the nurse would be to: A.Administer prescribed antibiotics prior to blood cultures B.Initiate intravenous fluid resuscitation C.Obtain a complete chemistry for laboratory analysis D.Insert an indwelling urinary catheter

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Answer: B Rationale: Initiating IV fluids is the primary intervention, followed by obtaining laboratory values, blood cultures, and providing oxygen. Antibiotics should be started ASAP, however, after blood cultures are obtained. An indwelling urinary catheter is lower in the list of necessary priority interventions. The Surviving Sepsis Campaign and IHI Sepsis Bundle provide guidelines for interventions for early resuscitation and treatment of patients with sepsis. Once a patient is suspected of sepsis, the following items (initiated within 6 hours and completed within the first 24 hours) have been found to enhance survival: (1) Obtain, monitor and treat serum lactate; (2) Obtain blood cultures prior to antibiotics; (3) Administer broad spectrum antibiotics as soon as possible; (4) Aggressively treat hypotension with IV fluids; (5) Apply vasopressor agents for hypotension that does not respond to fluids; and (6) Assess and maximize tissue oxygenation (monitor SVO 2 ). (See Table 39-6)

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Question 2 When assessing a patient for shock, the nurse knows that the earliest manifestation of shock is: A.A decrease in respiratory rate and depth B.A change in both systolic and diastolic blood pressure C.Anuria D.Increased heart rate

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Answer: D Rationale: The earliest clinical signs of hypovolemic shock are cardiovascular: increased heart rate and respiratory rate are the earliest manifestations of shock. Changes in systolic blood pressure are not always present in the initial stage of shock because of compensatory mechanisms and should not be used as the main indicator of shock presence or progression.

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Question 3 Which clinical manifestations would indicate a worsening in the condition of a patient in the refractory phase of shock? A. Warm, flushed skin B. Bleeding, oozing from IV sites C. Increasing respiratory rate D. Urine output of 20 mL/hr

Copyright © 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc. Answer: B Rationale: The onset of disseminated intravascular coagulation (DIC) as evidenced by bleeding to include oozing from IV sites indicates a consumption of clotting factors that occurs in the refractory stage of shock. The refractory stage or irreversible stage of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have overwhelming damage. The body can no longer respond effectively to interventions and shock continues. The patient usually requires full system support (e.g., mechanical ventilation, vasopressor agents, renal support [dialysis], etc.), rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation.