Week 12 - Multi-System Dysfunction - Student PDF

Multi-System Dysfunction SLIDES BY KARA SEALOCK RN EdD MEd BN CNCC(C) CCNE November 2024 WITH CONTRIBUTIONS FROM KIM HELLMER RN BN MN (SHOCK)  Putting “It” All Together Shock Types of Shock ▪Hypovolemic ▪Cardiogenic ▪Distributive ▪Sepsis ▪Anaphylaxis ▪Neurogenic Acid Base Analys...

Multi-System Dysfunction SLIDES BY KARA SEALOCK RN EdD MEd BN CNCC(C) CCNE November 2024 WITH CONTRIBUTIONS FROM KIM HELLMER RN BN MN (SHOCK)  Putting “It” All Together Shock Types of Shock ▪Hypovolemic ▪Cardiogenic ▪Distributive ▪Sepsis ▪Anaphylaxis ▪Neurogenic Acid Base Analysis  Types Shock Types of shock ▪Hypovolemic shock ▪Cardiogenic shock ▪Obstructive ▪Distributive shock ▪Septic shock ▪Anaphylactic shock ▪Neurogenic shock  What is Shock? “A complex clinical syndrome resulting in cellular hypoxia, accumulation of cellular metabolic wastes, cellular destruction, and organ and system failure. Begins as an adaptive response, progresses to multi-system organ failure. Multiple interactive mechanisms lead to: ▪Decreased intravascular volume ▪Decreased myocardial contractility ▪Increased venous capacitance.” Christine Schulman, 2003  What is Shock ▪Occurs when the CV system fails to perfuse tissues, cells, and organs adequately, resulting in widespread impairment of cellular metabolism and tissue function ▪Tissue perfusion is defined as the adequacy of blood flow through the small vessels of the extremities to maintain tissue function  Impairment of Oxygen Use ▪Cell is not receiving adequate amount of oxygen or is unable to use oxygen ▪Sodium moves into the cell, water follows→ drawn out of the intravascular space→ decreasing circulatory volume and cellular edema ▪Low ATP stores cause metabolic acidosis to occur causing cardiac and skeletal muscles to use lactic acid as a fuel source  Impairment of Glucose Use ▪Caused by either impaired glucose delivery to the cells or uptake by the cells ▪Cells to glycogenolysis, gluconeogenesis, and lipolysis to generate fuel for survival ▪Depletion of protein due to the gluconeogenesis ▪Muscle wasting caused by protein breakdown weakens skeletal and cardiac muscle  Process of Shock ▪Life-threatening condition ▪Inadequate tissue perfusion leading to anaerobic metabolism ▪If left untreated will result in cell death ▪Can lead to irreversible Multi-Organ Dysfunction Syndrome (MODS) Fig 24-41, p. 625, Power-Kean et al., (2023) Findings Compensatory Progressive Irreversible Blood Pressure Stages of Shock Normal Systolic100 bpm >150 bpm Erratic or asystolic Respiratory Status >20 breaths/min Rapid, shallow Requires resps with crackles intubation Skin Cold, clammy Mottled, Jaundiced Petechiae Urinary Output Decreased 0.5ml/kg/hr Aneuric, requires dialysis Mentation Confusion Lethargy Unconscious Acid-Base balance Respiratory Metabolic acidosis Profound Acidosis alkalosis Hypovolemic shock  Types of Shock: Hypovolemia Insufficient volume within the vascular space Decreased perfusion to tissues leading to hypoxia Etiology: ▪Loss of whole blood ▪Plasma ▪Fluid ▪Interstitial fluid  Decreased blood volume Decreased venous return Pathophysiology of Hypovolemic Shock Decreased stroke volume Decreased cardiac output Decreased tissue perfusion  Types of Shock: Hypovolemia Compensatory Mechanisms ▪Increase in HR and Afterload ▪Decrease in capillary hydrostatic pressure ▪Liver and spleen add blood ▪In the kidney, renin is activated, aldosterone released, retention of sodium and anti-diuretic hormone increases water retention ▪Potent vasoconstriction Fig 24-43, p. 627, Power-Kean et al., (2023)  Types of Shock: Hypovolemia Clinical Manifestations: ▪High afterload (SVR) ▪Poor skin turgor ▪Thirst ▪Oliguria ▪Low systemic and pulmonary preloads ▪High Heart Rate ▪Low Blood Pressure Cardiogenic Shock  Types of Shock: Cardiogenic ▪Inability of the heart to pump enough blood to tissues and end organs ▪Persistent hypotension and tissue hypo-perfusion ▪Reduced contractility ▪Impaired diastolic filling Types of Shock: Cardiogenic Etiology for Decreased Etiology for Pump Failure: Contractility: ▪Impaired diastolic filling ▪AMI arrhythmias ▪Cardiomyopathy ▪Obstruction: ▪Sepsis ▪PE ▪Myocarditis ▪Cardiac tamponade ▪Valvular disorders ▪Dysrhythmias ▪Wall rupture or defects ▪Metabolic abnormalities ▪Papillary muscle rupture Cardiogenic Pathophysiology Pulmonary Congestion Decreased Decreased Deceased Stroke Cardiac Systemic Tissue Volume Contractility Perfusion Decreased Coronary Artery Perfusion Fig 24-42, p. 626, Power-Kean et al., (2023)  Types of Shock: Cardiogenic Clinical Manifestations: Subjective Classic Objective: Additional Signs: ▪Chest pain ▪Tachycardia ▪Cyanosis ▪Dyspnea ▪Tachypnea ▪Skin mottling ▪Feeling faint ▪Hypotension ▪Rapid, faint or irregular pulses ▪Feelings of ▪JVD ▪Low U/O impending ▪Dysrhythmia ▪Peripheral edema doom ▪Low CO ▪Symptoms of end organ failure Distributive Shock  Vasodilation Maldistribution of Blood Volume Pathophysiology of Distributive Shock Decreased Venous Return Decreased Stroke Volume Decreased Cardiac Output Decreased Tissue Perfusion DISTRIBUTIVE Septic Shock How It All Begins ▪Begins with an infection that is hard to locate ▪Bacteria enters the blood stream either directly or through toxic substances released by the bacteria ▪Toxic substances act as triggering molecules in the septic syndrome ▪This leads to a pro inflammatory response of septic mediators  Inflammatory Response ▪Vasodilation- nutrient delivery, cellular access ▪Increased Microvascular Permeability- nutrient transport, cellular access ▪Cellular Activation- phagocytosis, host protection, wound healing, further mediator stimulation(Histamines, Kinins, and Prostaglandins) ▪Coagulation- prevent blood loss, wall off injury  SIRS Systemic Inflammatory Response Syndrome (SIRS) *Meet more than one of the following: ▪ Temp 38oC ▪ HR >90 bpm (beats per minute) ▪ RR >20 bpm or PaCO210% bands Patient Symptoms of SIRS ▪General non-specific symptoms ▪Fever ▪Malaise ▪Loss of appetite ▪Aching ▪Weakness  Septic Shock “Septic shock is seen in patients with sepsis who develop underlying circulatory and metabolic abnormalities resulting in hypotension that require vasopressors to maintain a MAP of > 65 mmHg and having a serum lactate level of > 2 mmol/L despite adequate volume resuscitation, resulting in a higher risk of mortality” Singer et al. (2016)  The Sepsis Continuum Sepsis: SIRS + infection Septic Shock: sepsis with profound hypotension and perfusion abnormalities despite resuscitation MODS (Multi-Organ Dysfunction Syndrome): multi-system organ failure that often leads to death  Global Uncontrolled Inflammatory Response Systemic Inflammation response leads to vascular leakage, decreased SVR, increased temperature, increased HR Coagulation disruption in the microvasculature leading to platelet aggregation and clot formation Impaired fibrinolysis creating an inability to dissolve clots resulting in decreased tissue perfusion THE ENTIRE BODY IS AFFECTED! Fig 24-46, p. 629 Power-Kean et al., (2023)  Common Sepsis You will Encounter in Acute Care 3 common sources for sepsis ▪Urinary Tract Infection leading to urosepsis ▪Pneumonia leading to full systemic sepsis ▪Integumentary ▪Necrotizing Fasciitis What Does the Patient with Septic Shock Look Like? Hypotension Tachycardia Febrile Decreased Systemic Vascular Resistance Depressed Myocardial Function Lactic acidosis Leukopenia or leukocytosis Thrombocytopenia Vascular leakage Pulmonary congestion Tissue necrosis Organ Failure DISTRIBUTIVE Anaphylactic shock  Distributive: Anaphylactic Shock ▪Caused by a severe allergic reaction when a patient who has already produced antibodies to a foreign substance (antigen) develops a systemic antigen- antibody reaction. ▪An antigen-antibody reaction causes mast cells to release potent vasodilators such as histamine and bradykinin, also causing increased capillary permeability Fig 24-45, p. 628, Power-Kean et al., (2023)  Insect Bites and Stings: Bees, Hornets, Yellow Jackets Skin Contact with Inhaled Allergens: Allergens: Triggers for Pollen, Dust, Mold Poison, Pollen, and Mildew Anaphylaxis Animal Dander, Latex Food Allergens: Peanuts, Tree Nuts (Walnuts, Almonds, Cashews, Hazel Nuts and Brazil Nuts) and Shellfish  Anaphylaxis: Clinical Manifestations: ▪Dyspnea ▪Headache, throbbing ears ▪Wheezing, hoarseness ▪Feeling of “lump in throat”, can’t swallow ▪Choking, drooling ▪Tingling in throat, chest ▪Sneezing , tongue, mouth, face bronchospasm, stridor ▪Increased Heart Rate, chest ▪Dizziness, nausea pain DISTRIBUTIVE Neurogenic Shock  Distributive: Neurogenic Shock ▪Vasodilation occurs as a result of a loss of sympathetic tone. ▪Can be caused by spinal cord injury, spinal anesthesia, or nervous system damage. ▪Bradycardia is a specific characteristic vs. tachycardia as seen in other shock states Fig 24-44, p. 628 Power-Kean et al., (2023)  Multiple Organ Dysfunction Syndrome ▪Progressive process that involves the ultimate failure of two or more organ systems after a severe illness of injury ▪Initiated and perpetuated by uncontrolled system inflammatory and stress responses ▪Characterized by hypermetabolic and hyperdynamic state that persists as organ dysfunction develops Fig 24-47, p. 631, Power-Kean et al., (2023)  Covid-19 Pathophysiology: ▪ SARS-CoV-2 enters the host cell by biding to the ACE2 receptor in the lung→ membrane fusion of the virus and the host cell is activated after the binding, viral RNA is released into the cytoplasm, establishing infection ▪ ACE-2 is expressed on the type II alveolar epithelial cells, and weekly expressed on the surface of the epithelial cells, proximal tubule cells of the kidney and bladder urothelial cells, as well as the enterocytes of the small intestine, especially in the ileum ▪ RAS plays a significant role in COVID-19 infections https://theconversation.com/what-is-the-ace2-receptor-how-is-it- connected-to-coronavirus-and-why-might-it-be-key-to-treating- covid-19-the-experts-explain-136928  Covid-19 https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03120-0/figures/3  Post-COVID 19: Long Haulers ▪Occurs when people still show symptoms of COVID-19 weeks or months after recovery ▪Occurs in some people after infection when: ▪ were hospitalized or needed intensive care during recovery OR ▪ Had mild to severe infection with symptoms or even mild infection without symptoms Children ▪Fatigue ▪Anxiety and depression ▪Fatigue ▪Sleep disturbances ▪Memory problems ▪General pain and discomfort ▪Headaches ▪Stuffy or runny nose ▪Sleep disturbances ▪Difficulty thinking or concentrating ▪Weight loss ▪Difficulty thinking or concentrating ▪Shortness of breath ▪Posttraumatic stress disorder (PTSD) ▪Muscle pain  COVID-19: Pediatrics Multisystem Inflammatory Disease ▪ Increase in children with symptoms of Kawasaki disease (CV lecture) ▪ Inflammation in multiple body systems such as: heart, lungs and kidneys, brain, skin, eyes, and GI organs Clinical Manifestations: ▪ Fever ▪ Abdominal pain ▪ Vomiting ▪ Diarrhea ▪ Neck pain ▪ Rash ▪ Bloodshot eyes ▪ Feeling extra tired Multi-System Inflammatory Syndrome-C Shock and the Pediatric Patient  Shock and the Pediatric Patient ▪Physiological consequences of shock are: hypotension, tissue hypoxia and metabolic acidosis ▪Shock results in hypovolemia, altered peripheral vascular resistance, or pump failure  Clinical Manifestations of Shock COMPENSATED DECOMPENSATED ▪Apprehensiveness ▪Confusion and somnolence ▪Irritability ▪Tachypnea ▪Unexplained tachycardia ▪Moderate metabolic acidosis ▪Normal BP ▪Narrowing pulse pressure ▪Oliguria ▪Thirst ▪Cool, pale extremities ▪Pallor ▪Decreased skin turgor ▪Diminished urinary output ▪Poor capillary filling ▪Reduced perfusion of extremities  Clinical Manifestations of Shock IRREVERSIBLE ▪Thready, weak pulse * Key differentiating signs are ▪Hypotension observed in the degree of tachycardia, perfusion to ▪Periodic breathing or extremities, LOC and BP apnea ▪Anuria ▪Stupor or coma  Shock and the Pediatric Patient: Hypovolemic Shock ▪ Compensatory increase in the force and rate of the cardiac contraction and constriction of arterioles and veins to increase peripheral vascular resistance ▪ Diminished venous return to the heart, low CVP, low CO, and hypotension ▪ Low volume releases catecholamines, ADH, adrenocorticosteroids, and aldosterone to conserve blood volume reducing flow to the skin, kidneys, muscles, and viscera leaving the skin cold and clammy, poor capillary filling, and significantly reduced U/O ▪ Impaired perfusion leads to hypoxemia producing lactic acidosis ▪ Complications: cerebral edema, cortical infarction, intraventricular hemorrhage, renal ischemia with tubular or glomerular necrosis, renal vein thrombosis, ARDS, GIB and perforation associated with splanchnic ischemia and necrosis of intestinal mucosa, hypoglycemia, hypocalcemia, and other electrolyte disturbances  Shock and the Pediatric Patient: Anaphylaxis ▪Clinical manifestations: ▪ Symptoms occur within seconds of minutes of exposure ▪ Rapidity of reaction is directly related to intensity ▪ Symptoms of uneasiness, restlessness, irritability, severe anxiety, headache, dizziness, disorientation, paresthesia ▪ Cutaneous signs of flushing, urticaria are common early signs, followed by angioedema, most notable in the eye lids, lips, tongue, hands, feet, and genitalia ▪ Bronchiolar constriction causing a narrowing of the airway, pulmonary edema and hemorrhage, laryngeal edema with severe acute upper airway obstruction ▪ Vasodilation, capillary permeability and loss of intravascular fluid ▪ Sudden hypotension and impaired CO with poor perfusion are seen  Shock and the Pediatric Patient: Septic Shock ▪Please review the Table: Age Specific VS and Laboratory Variables in Septic Shock [Table 47.7, pg. 1276, Keenan-Lindsay et al. (2023)] ▪Early sepsis: chills, fever, and vasodilation with increased CO that results in a hyperdynamic phase * ▪Second Stage, normodynamic, cool or hyperdynamic- decompensated stage (lasts only a few hours), skin is cool, but pulses and BP are still normal, U/O diminishes and mental state becomes depressed ▪Late sepsis: DIC, signs of circulatory collapse, hypodynamic, hypothermia, cold extremities, weak pulses, hypotension, and oliguria or anuria, severely lethargic or comatose  Shock Summary Hypovolemic Shock ▪Blood VOLUME problem Cardiogenic Problem ▪Blood PUMP problem Distributive Shock ▪Blood VESSEL problem Acid/ Base Imbalance  Homeostasis Maintain balance in the body ▪Temperature ▪Oxygen ▪Carbon Dioxide ▪pH  Relationships between pH/Hydrogen/Buffer Systems Hydrogen ions necessary to maintain membrane integrity and speed of enzymatic reactions When balance disturbed, may be a severe reaction H+ ions pH (the more acidic) Lungs, kidneys and bones are most important in acid/base balance Relationships between pH/Hydrogen/Buffer Systems Body Acids come in two forms : ▪Volatile Acid → Respiratory Acid CO2 ▪Non-volatile→ Metabolic Acids which are eliminated by kidneys or metabolized by liver Buffers react to changes in acid-base status ▪Located in ICF and ECF compartments ▪Carbonic acid (H2CO2), hemoglobin and bicarbonate are common buffers  Finding Balance pH= Base = Renal Regulation Acid Pulmonary Regulation Respiratory compensates for changes in pH by increasing or decreasing ventilation Renal system compensates by producing more acidic or more alkaline urine  Acid- Base Imbalance Normal Values: ▪pH 7.35-7.45 ▪CO2 35-45 mmHg (Respiratory) ▪HCO3- 22-26 mmol/L (Kidneys) Acidosis pH< 7.35- 7.45 > Alkalosis https://courses.lumenlearning.com/suny-ap2/chapter/disorders-of-acid-base- balance/  Metabolic Acidosis pH < 7.35 and HCO3- 7.45 and HCO3- >26 mmol/L ▪Occurs when bicarbonate increases or there is a loss of metabolic acids ▪Kidneys attempt to hold onto hydrogen acids and reduce urine output ▪Respiratory system attempts to hypoventilate https://www.pinterest.ca/pin/11470174023738607/ Respiratory Acidosis pH < 7.35 and CO2>45 mmHg Caused by hypoventilation CO2 is retained increasing hydrogen ions Caused by: ▪Respiratory depression ▪Respiratory muscle paralysis ▪Disorders of the chest wall ▪Disorders of the lung parenchyma https://fmss12ucheme.wordpress.com/2013/05/06/the-dangers-of-alkalosis- and-acidosis/ Respiratory Alkalosis pH > 7.45 and CO2 45 mmHg What is the HCO3-? (Kidneys) ▪< 22 mmol/L or > 26 mmol/L Is the condition uncompensated, partially compensated, or fully compensated?  By the End of this Lecture You Will: Critically reflect upon the body as a whole where alterations of shock and instability can lead to significant changes systemically Explain pathophysiology and effects on the body related to: Types of Shock for adult and pediatric clients ▪ Hypovolemic, Cardiogenic, Distributive (sepsis, anaphylaxis and neurogenic) Acid Base Analysis Begin to prioritize patient conditions related to nursing assessment and clinical manifestations for multi system failures  Key Points to Remember ▪Can you perform a full head to toe assessment with knowledge of physiological landmarks and anatomy and physiology related to Neuro, CV, Resp, GI and GU assessment? ▪Explain the “why” associated with head to toe assessment and connections to other systems ▪Identify and apply concepts of lab values related to mult-system failure ▪ Do you understand the pathophysiology, clinical manifestations and nursing assessment related to : Types of Shock ▪ Hypovolemic, Cardiogenic, Distributive (sepsis, anaphylaxis and neurogenic) Acid Base Analysis