Module 8: Inflammation II - Unit 2: Shock Nursing Program PDF

Critical Care Nursing Program Module #8: Inflammation II Unit #2: Shock Introduction Shock is a very complete syndrome resulting in cellular an...

Critical Care Nursing Program Module #8: Inflammation II Unit #2: Shock Introduction Shock is a very complete syndrome resulting in cellular and tissue hypoxia. This can be caused by either reduced delivery of oxygen, increased oxygen consumption, inability to utilize oxygen or a combination of any of these processes. Regardless of the cause, the common denominator in all shock states is decreased cellular and tissue perfusion (Gaieski & Mikkelsen, 2020). If this altered cellular perfusion is not corrected the results are tissue injury (inflammatory response) and cell death. Critical care nurses are in a key position to improve patients’ survival rates from shock. Accurate, ongoing patient assessment provides the opportunity for early detection of the warning signs essential to the diagnosis and management of the shock state. This unit will build upon concepts learned in pumping and perfusion specifically preload (volume), afterload (resistance) and contractility (pump). This unit will focus on an overview of shock, its stages, and the anticipated assessment findings and treatment strategies for each stage. It will also present the specific assessment findings and treatment strategies for the major classifications of shock: hypovolemic, cardiogenic and distributive. Learning Outcomes On completion of this unit the learner will be able to: 1. Distinguish between the four stages of shock in relation to pathophysiology, assessment findings, and treatment strategies. 2. Discuss the etiology and pathophysiology of hypovolemic, cardiogenic, and distributive shock. 3. Describe the assessment findings and specific treatment strategies associated with hypovolemic, cardiogenic shock, and distributive shock in relation to each of the four stages of shock. Required Reading Please refer to your reading list for Inflammation II Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 1 of 10  Critical Care Nursing Program Stages of Shock A patient experiencing any form of shock will pass through four stages if untreated. These four stages are the initial stage, compensatory stage, progressive stage, and refractory (also called irreversible) stage. Progression through these stages can vary based on the patient’s prior health status, duration of the initiating event, response to treatment strategies, and correction of the underlying cause. Each patient’s response is highly individual and each patient may not experience each stage of shock. Thorough assessment and recognition of the early stages of shock can lead to early interventions and resolution of the underlying cause, thereby halting the progression of the shock state. Please refer to your reading list for Inflammation II Classifications of Shock Shock can be classified into three major categories depending on the underlying pathophysiology: hypovolemic, cardiogenic, and distributive. Hypovolemic shock occurs when the intravascular volume is depleted (preload). Cardiogenic shock is caused by an impaired ability of the heart to pump blood (contractility). Distributive shock results from a maldistribution of blood volume in the vascular system (afterload) and includes anaphylactic, neurogenic, and septic shock. In other words, all types of distributive shock result in a massive vasodilatory response and the associated assessment findings that result from this response. Although there are anticipated responses for any patient as they progress through the shock stages, the differences among these major categories of shock will influence the clinical presentation, the anticipated interventions, and the nursing care. Hypovolemic Shock Hypovolemic shock is characterized by a decrease in circulating or vascular blood volume. It usually manifests after a reduction of 15-25% in the volume of the intravascular compartment. Causes of Hypovolemic Shock Excessive loss of blood - from trauma, surgery, gastrointestinal bleeding, coagulopathies Excessive loss of body fluids - excess diuresis, vomiting, diarrhea, burns, sepsis Third spacing - ascites, bowel obstruction, peritonitis Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 2 of 10  Critical Care Nursing Program Clinical Manifestations With hypovolemic shock the general decrease in total blood circulating volume leads to a decreased oxygen/carbon dioxide exchange in the cells, decreased venous return and a decreased cardiac output. The patient may present with tachycardia, hypotension (less than 90 mmHg systolic), increased respiratory rate, decreased urine output, decreased CVP, cool, pale skin early, and clammy, mottled skin late in shock process. The patient may progress from restless to confused and disorientated. Treatment As in all acute scenarios, airway, breathing and circulation are the first priorities for the nurse to assess. The goal is to increase the supply of oxygen to the tissues without increasing the demand. Cardiac output can be optimized using fluid replacement and, if ineffective, medications. Oxygen-carrying capacity of the blood can be increased by administering packed red blood cells. Arterial oxygen saturation can be increased by supplemental O2 and/or mechanical ventilation. Plan nursing interventions to minimize O2 demands, such as bathing following treatment modalities and after the patient has rested. The hallmark of treatment for hypovolemic shock is fluid replacement. Generally isotonic crystalloids are given in the early stages, followed by colloids or hypotonic crystalloids. Crystalloids (Isotonic) - 0.9% NaCl, Lactated Ringers’ (careful in patients with liver failure), Normosol/Plasmalyte. No shift between the extracellular fluid (ECF) and the cell will occur Colloids – Albumin Blood, plasma (if fluid loss is from bleeding). Fluid is pulled from interstitial space into plasma. Please refer to your reading list for Inflammation II Cardiogenic Shock Cardiogenic shock, or severe ventricular failure (primarily left ventricular failure), is a complex syndrome characterized by systemic hypotension, arterial vasoconstriction, and impaired organ and tissue perfusion. Cardiogenic shock develops when there is an insufficient amount of healthy myocardium to adequately support systemic Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 3 of 10  Critical Care Nursing Program perfusion. It is generally understood that cardiogenic shock will develop if 40% or more of the ventricular myocardium, particularly the left ventricle, is damaged. Cardiogenic shock carries an 85% mortality rate. The primary etiology leading to cardiogenic shock is impaired cardiac muscle function associated with a massive myocardial infarction. Remember back to pumping and perfusion when we discussed the concepts of impaired contractility. Understanding cardiogenic shock comes from a fundamental concept that the pump (heart) doesn’t work effectively. Please refer to your reading list for Inflammation II Distributive Shock Distributive shock results from profound vasodilation resulting in compromise circulation of blood flow and compromised perfusion to the tissues and organs (Allen, & Gilbert, 2019). There are three types of distributive shock: neurogenic, anaphylactic, and septic shock. Despite their differing etiologies, they initially present a clinical picture reflective of profound peripheral vasodilation leading to an increase in the size of the vascular bed and a resulting decreased systemic vascular resistance (afterload). Anaphylactic Shock Anaphylactic shock is a severe hypersensitive (allergic) reaction between an antigen and an antibody that if not treated promptly and accurately, results in death. Please refer to your reading list for Inflammation II Neurogenic Shock Neurogenic shock is characterized by massive vasodilation, impairment of the baroreceptor response, and impairment of thermoregulation as a result of an interruption or loss of sympathetic innervation. This type of shock is usually transitory and is most commonly seen in persons who have suffered a spinal cord injury. Other etiologies associated with neurogenic shock include: Disease of the spinal cord High levels of spinal anaesthesia Emotional stress Severe pain Drug overdose other than anaesthetic agents (e.g., barbiturates). Please refer to your reading list for Inflammation II Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 4 of 10  Critical Care Nursing Program Septic Shock Sepsis is now defined as a “life threatening organ dysfunction caused by a dysregulated host response to infection shock is a complex condition that results from an infectious process” (Singer et al, 2016). It is the leading cause of in-hospital deaths (Urden et al., 2022). Sepsis is an intense bloodstream infection that can easily progress to multi-organ failure and death. The body’s systemic inflammatory response to the severe infection results in altered circulation, coagulation processes and impaired tissue perfusion. Septic shock, is now defined as “a subset of sepsis in which underlying circulatory and metabolism abnormalities are profound enough to substantially increase mortality” (Singer et al., 2016). Septic shock carries a 23% to 50% mortality rate (Urden et al., 2022). Septic shock, often begins subtly, progresses rapidly, and results in death if not recognized and aggressively treated in its early stages. Although both gram- negative and gram- positive can both cause sepsis, over the last two decades it has been shown that gram-positive bacteria are the most common cause of sepsis (Urden et al., 2022). Septic shock actually occurs as a result of the body’s attempt to destroy these invading organisms and not as a direct result of the bacteria per se. Just like neurogenic and anaphylactic shock, septic shock is characterized by massive vasodilation, decreased tissue perfusion and a loss of cellular energy. Pathophysiology A severe infection will cause serious damage to cells and trigger the body to mount a strong immune system response (inflammation), as it attempts to fight the infection. This inflammatory response begins with vasodilation (body attempting to bring WBCs to source of infection) and increased permeability of cells (to allow immune system phagocytes to attack infectious organisms). The body also begins to clot, an important function in containing the infection and repairing the tissue. In sepsis this response is exaggerated as an excessive inflammatory process pervades the entire body. Normally the body contains the inflammatory response locally, close to the source of the infection. With sepsis the immune response affects the entire body. Cells damaged from infection release inflammatory mediators (e.g., histamine, cytokines) that cause widespread vasodilation. These grossly dilated blood vessels drop the blood pressure, decreasing tissue perfusion. The permeability of the cell walls also increases allowing fluid to leave the blood vessels, dropping the blood pressure even more (from hypovolemia). The coagulation system is over stimulated and tiny blood clots form, interfering with the blood flow to organs and tissues. The body is unable to reverse the process as it is overwhelmed by the inflammatory and coagulation response. Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 5 of 10  Critical Care Nursing Program Clinical Manifestations Quick Sequential Organ Failure Assessments (qSOFA) can promptly identify those at risk for sepsis: Alteration in mental status Systolic blood pressure 22/min In the presence of an infection, two or more of the following symptoms may indicate the patient is septic:  High or low temperature >38 o C or 90 beats per minute.  Respiratory rate >20 breaths per minute or PaCO2 12,000 or 2mmol/L. These signs and symptoms can be plotted out using the SOFA criteria in your text reading. Treatment Evidence informed practice when caring for a patient with septic shock has been divided into bundles of care. Initial treatment for septic shock involves the Hour 1- Bundle: Obtaining a lactate level Obtaining blood cultures prior to antibiotic administration Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 6 of 10  Critical Care Nursing Program Starting broad spectrum antibiotics Treating poor tissue perfusion with fluid resuscitation with 30 mls/kg Vasopressors (Norepinephrine/Levophed) are used when hypotension does not respond to fluid therapy. Blood cultures are preferably drawn from two sites: peripherally and from any central venous access device. Cultures are also obtained from other sites such as urine, wounds and respiratory secretions. Diagnostic studies that also seek to determine source of infection include x-rays, ultrasound and CT scans. Antibiotics should be administered, preferably within one hour of diagnosis of sepsis. Once the source of infection is identified treatment may also include removal of a device (e.g., urinary catheter or central venous catheter) or infectious source (e.g., debridement of infected wound or surgical removal of abscess). Guidelines for treatment also include oxygenation support (e.g., mechanical ventilation), renal replacement therapy (e.g., dialysis), if warranted. Glucose control has been shown to improve outcomes for patients who are septic. Corticosteroid therapy may be started if the patient shows signs of adrenal insufficiency. Stress ulcer prophylaxis, VTE prophylaxis, adequate nutrition and setting goals of care round out the management guidelines. Please refer to your reading list for Inflammation II Points of Clarification You may have noticed that some of the literature is very confusing with regards to the signs and symptoms associated with septic shock. The following statements may help you understand this information more clearly. 1. Cardiac Output Hyperdynamic (warm) Phase: The increased CO and CI observed in the hyperdynamic phase of septic shock are compensatory responses that occur due to the reduction in left ventricular afterload. This decreased afterload is caused by the massive vasodilation and decreased SVR. The degree of increase will depend greatly on the individual’s normal hemodynamic parameters and pre-shock state of health. You may also be wondering why the patient will experience a normal or increased cardiac output and cardiac index when your readings have described depressed myocardial functioning as an integral pathophysiologic process with the septic cascade. Remember cardiac output is determined by myocardial contractility, preload, afterload, and heart rate. Although contractility is Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 7 of 10  Critical Care Nursing Program impaired, the vasodilation associated with the warm phase of septic shock causes the compensatory mechanisms of reduced SVR and afterload to allow for the normal or increased cardiac output. Hypodynamic (cold) Phase: The reduced CO and CI, and increased SVR that are characteristic of the cold phase of septic shock are caused by the profound hypotension, intense vasoconstriction and decreased venous return to the heart. CO and CI are further impaired by the reduced myocardial contractility. 2. Oxygen Supply and Demand Hyperdynamic (warm) Phase: With septic shock the oxygen demand is actually quite high. However, in the hyperdynamic phase of septic shock, cell dysfunction prevents cellular extraction of oxygen even though cardiac output has increased tremendously. In essence, more oxygen remains in the venous blood. Hypodynamic (cold) Phase: Oxygen levels in the venous blood decreases in the cold or hypodynamic phase of septic shock, due largely to the poor cardiac output, decreased circulating volume, and continued increase in oxygen demand. 3. Renal Perfusion Vasoconstriction of the renal bed occurs throughout the clinical continuum of septic shock. However, urine output may increase or remain normal during the hyperdynamic phase of septic shock. The compensatory mechanism of increased cardiac output will, for a short time, allow for sufficient renal perfusion. As the shock state progresses, the renal ischemia and formation of micro emboli predispose the patient to experience acute kidney injury. Multiple Organ Dysfunction Syndrome The end phase of septic shock, as with all types of shock, is known as multiple organ dysfunction syndrome (MODS). In this phase, the person can exhibit the signs and symptoms associated with cardiac, renal, hepatic, pancreatic, hematological, gastrointestinal and neurological failure. ARDS, DIC, anuria, and hypoxemia refractory Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 8 of 10  Critical Care Nursing Program to oxygen therapy are common. Progression to this stage is gradual and extremely difficult for the patient, the family, and critical care health care workers. Treatment becomes palliative. Nursing care in this stage is frequently directed toward providing support for the family and ensuring that their patient’s physical, spiritual, and psychosocial needs are met. Please refer to your reading list for Inflammation II Hemodynamic Parameters in Shock Recall from the unit on advanced hemodynamic monitoring that assessing data from a pulmonary artery catheter provides information on a patients volume status (preload), vascular resistance (afterload) and pumping ability of the heart (contractility). This information assists clinicians to guide treatment. The following table outlines hemodynamic parameters in shock. Try to distinguish between the various types of shock based on their hemodynamic profile. Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic Septic Early Late RAP       PAWP       CO/CI     N  SVR       BP       MAP       HR       Conclusion Shock, regardless of the type, has serious consequences for the patient if not recognized early and treated aggressively. The acute care specialty nurse’s astute observation and assessment skills play a major role in the early recognition of the Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 9 of 10  Critical Care Nursing Program shock state and the implementation of appropriate therapeutic interventions. Inflammatory responses like sepsis, if untreated, can progress to MODS and death. The nurse’s ability to quickly prioritize as well as intervene appropriately could make the difference with a patient’s disease progression. Your assessment and critical thinking skills are being developed as you progress through the program by applying your acquired knowledge in the clinical setting. This does not have to be limited to your clinical practicum. Take the opportunity to apply your new knowledge on shock and practice your assessment skills in your present working environment. Module #8: Inflammation II Unit #2: Shock Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 10 of 10