Shock and Multiple Organ Dysfunction Syndrome (MODS) chapter 14, Exams of Nursing

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Shock and Multiple Organ Dysfunction Syndrome (MODS) chapter 14  Shock: Definition  Life-threatening condition  Results from inadequate tissue perfusion  Prevents adequate oxygen delivery to cells  Effects all body systems  May develop rapidly or slowly→ progression is neither linear nor predictable  Rapid assessment and response by nursing is essential to patient recovery  Although all shocks are different but all have the same result  decrease perfusion  Normal EF 55%-70%: indicator of perfusion, CO, oxygenation  Know diff fluid type: hypo, hyper, iso  Shock: Overview  Adequate blood flow requires (need an effective pump) o Effective cardiac pump o Effective vasculature (circulatory system) o Adequate blood volume (assist with organ perfusion) o If pt is losing blood (H&H, O2 sat decreases)  Shock results in: o Cellular hypoxia (cell not getting enough o2, passed normal body compensation) → Cell death→ progresses to organ dysfunction→ Death  No adequate volume at least 60 mEq for kidney to perfuse  bun/cr, & K build up once kidney shut down  If you don’t have flow, pt develop shock shake  Shock: General Physiologic Responses  Regardless of the initial cause of shock, physiological responses are common to all types of shock: o Hypoperfusion of tissues o Hypermetabolism (increase demand) o Activation of inflammatory response  Prognosis o Depends on body’s ability to effectively respond  Failure of compensatory mechanisms to respond o End Organ Dysfunction o If pt losing a lot of blood tacky occur to compensate then decrease when it can no longer compensate o Also, a decrease in bp  Pathophysiology: Cellular Responses  Cellular swelling occurs  Cell membrane becomes more permeable  Fluid & electrolytes seep into the cell  Mitochondria & lysosomes are damaged  Cell death occurs  Pathophysiology: Cellular Responses  Cellular changes that occur with shock: o Inadequate blood supply therefore, cell produce energy in anaerobic (w/o O2) metabolism due to the changes cell function ceases (cell death) o Hyperglycemia occur (secondary to stress state) [doesn’t mean pt is diabetic] o Biochemical mediators (cytokines) stimulate vasoconstriction or vasodilation o Insulin resistance (not good since pts are already hyperglycemic) o Organ failure  BP regulation requires adequate 1. Blood volume (Tank) 2. Cardiac pump (Pump) 3. Vasculature (Pipes)  Pathophysiology: Coagulopathic Responses  Fibrinolysis o In healthy individual removal of fibrin o Inflammation initiates coagulation cascade o In severe sepsis , endothelial injury  production that impairs fibrinolysis  Over time & if untreated can  DIC  Pathophysiology: Inflammatory Responses  Inflammation 1. Neutrophils 2. Myocardial depressant factor 3. Cytokine release  pro-coagulation 4. Vasodilation 5. Excessive inflammation & coagulation damage endothelium dysfunction & capillary leak  fluid shift into tissue (edema)  How is BP regulated? MAP= CO x PVR (peripheral vascular resistance)  Cardiac Output o What components make up the cardiac output? HR & SV o What influences these components? SNS; preload, contractility, & afterload  Peripheral Vascular Resistance o Diameter of arterioles  Causes of increased PVR? Arteries constriction  Causes of decreased PVR? Arteries dilation  What physiologic responses change our BP? Stress, exercise, weight… o MAP< 65 mm Hg decreases oxygen and nutrients delivered to cells (must exceed 65 mm Hg for cells to receive o2 & nutrients needed to metabolize energy in amounts sufficient to sustain life)  Blood Pressure Regulation: pressure Receptors  Baroreceptors (located in carotid sinus & aortic arch; responsible for monitoring circulatory volume & regulating neural & endocrine activities) o How does the body restore BP? o Promote rest & comfort: minimize cardiac workload by reducing pt physical activity & tx pain & anxiety o Support fam members  Irreversible Stage of Shock (Refractory)  At this point, organ damage so severe that patient does not respond to treatment, cannot survive (despite tx, BP remain low, resp system d/f prevent adequate oxygenation & ventilation despite mechanical vent support) o End-organ perfusion is decreased significantly o Organ damage is severe o Progresses to multiple organ dysfunction syndrome (MODS)  Complete organ failure o Judgment that shock is irreversible only made in retrospectively on the basis of the pt’s failure to respond to tx  Medical & nursing management is same as progression stage  General Management Strategies for Shock  Early identification  Timely treatment  Sequence of events for different types of shock will vary o Management & care of patient will vary o Intubation right away if pt is in shock  Support of respiratory system w/ O2 & mechanical vent to provide oxygenation  Fluid replacement to restore intravascular volume  Vasoactive medications to restore vasomotor tone & improve cardiac function  Nutritional support to address metabolic requirement that are often dramatically increase in shock  It doesn’t matter if you give med to increase bp there’s nothing to constrict  Labs  ABGs  Lactic acid  Glucose  Electrolytes  H/H  Cultures (shock pt can be infected, must do culture before antibiotic) urine simple (if pt can’t urine, straight cath)  Coagulation studies  Cardiac enzymes (troponin, CK/MB, C-reactive, myoglobin)  LFT’s  Diagnostics  A line (for ABG & core bp)  PA catheter (for pressure & volume monitoring CVP and hemodynamic monitoring)  ECG monitoring  Echo  CT  Cardiac Catheterization (why in presence of shock state to address circulatory function)  CXR  Measuring Tissue Perfusion  ALOC (confuse, not orientated to self is earliest signs)  Vital signs (O2 sat, BP)  Urine output  Skin color/temperature (cold & clammy, normal temp in compensatory stage)  Continuous central venous oximetry : evaluates mixed venous blood oxygen and indicates severity of Hypoperfusion states (normal 70%) o Intervention focuses on decreasing tissue oxygen requirements  Fluid Replacement  Crystalloids o Electrolyte solutions that move freely between intravascular and interstitial spaces o More volume needed o Isotonic contain same concentration as extracellular fluid (0.9% NaCl, LR)  LR contain lactate ion which should not be confuse for lactic acid  lactate ion will buffer overall acidosis that occur in shock o Monitor for pulmonary edema (pink frothy sputum) o Hypertonic (3% NaCl): Large osmotic force pulls fluid from intracellular to extracellular space (treatment for severe symptomatic hyponatremia, do not give wide open)  Colloids (large molecule IV solution & blood component [PRBC, FFP, & plt] o Similar to plasma proteins o Expand intravascular volume by exerting oncotic pressure o Pulls fluid into intravascular space  Albumin (high cost) [volume extender; monitor for anaphylactic reactions]  Hetastarch (synthetic)  Complications of Fluid Administration  Cardiovascular Overload (CVP 2-6, for fluid administration & monitoring) o Balance  Fluid Volume Overload  pulmonary edema-ARDS, compartment syndrome, MODS  Fluid Volume Deficit  higher morbidity o CVP of 14 or 20  pt volume is hypervolemic o CVP of 1  pt is hypovolemic  Abdominal compartment syndrome ACS (collection of fluid leak into the abd creating pressure in diaphragm which compromise breathing, & venous return to the heart)  Pulmonary dysfunction/edema  Must understand shock state! Hypovolemic Decreased intravascular volume Cardiogenic Impaired myocardial contractility Circulatory (Distributive) Intravascular pooling of blood in vessels 3 type of shock: Septic (self limiting), neurogenetic (can't occur unless pt experienced a spinal shock that has been resolved) & anaphylactic shock  General Management Strategies: Vasoactive Medication Therapy (given when fluid alone can’t maintain adequate MAP)  Alpha adrenergic o Blood vessels constrict in the cardioresp & GI system, skin, & kidneys  Beta adrenergic o Beta 1  HR & myocardial contractility increase o Beta 2  Vasodilation in the heart & skeletal muscles, & bronchioles relax  These meds help increase strength of myocardial contractility, regulate HR, reduce myocardial resistance & initiate vasoconstriction  Monitor vs frequently (Q15min until stable); given via central venous line otherwise tissues necrosis or sloughing may occur  Dosage are to be tapered & not stop abruptly  Management Strategies: GI Response to Shock States GI responsible for good and bad bac & immune system GI system respond to shock state: ischemia, impairment of layers ulcers that lead to bleeding leading to translocation of bac due to perforation (bacteria leak in ulcers & out of the bowel), irritated bowel lining  General Management Strategies: Nutritional Support  Increased metabolic rates during shock increase requirement & therefore caloric requirement (require more than 3000 Cal daily)  Catabolic process  Enteral nutrition preferredpromoting GI function through direct exposure to nutrient & limiting infection complication assoc w/ parenteral feeding  Stress ulcer prevention antacids, H2 blockers (famotidine) & PPI (lansoprazole, esomeprazole mag) inhibit gastric acid secretion or increase gastric pH  Tx pt via oral or enteral (ng tube or PEG tube for pt who are in shock)  Feeding protect the mucosa lining from ulcer & to prevent bacteria translocation  Classifications of Shock  Hypovolemic  Cardiogenic  Correction of underlying causes (O2 supply to heart muscle so that it can contract properly)  Initiation of first-line treatment o Oxygenation (NC 2-6 L, monitor ABG, pulse ox, work of breathing all determine whether pt need more aggressive method of O2) o Pain control (since pt have angina [morphine is not for anxiety] give IV morphine for pain relief, it’s also dilated blood vessels) o Hemodynamic monitoring assess pt respond to tx o Laboratory marker monitoring (ABG’S, troponin, CK-MB, myoglobin, C- reaction protein, mag, CA [8.5-10.5], chest X-ray, ECG, CVP reading [2-6], PCWP [4-12, anything >18 problem], echocardiography done at bedside shows EF & contractility) o Fluid therapy: fluid bolus should never give rapidly bc rapid fluid administration in pt w/ cardiac failure may result in acute P. edema o Mechanical assistive devices  IABP balloon pump takes over the work of the heart beat and the cardiac system  Mechanical assist device  Pharmacologic Management ***bc improve contractility & decrease cardiac workload are opposing actions both inotropic & vasodilators are given o Dobutamine o Dopamine o Nitroglycerin (low dose dilates vein & high dose dilate arteries) o Other vasoactive medications (norepi, epi, milrinone, vasopressin, & phenylephrine; diuretics [furosemide] to reduce workload of heart by reducing fluid accumulation) o Antiarrhythmic medications (if they are arrhythmic) ***metabolic acidosis must be corrected to ensure max effectiveness of vasoactive meds  Cardiogenic Shock: Intra-aortic Balloon Pump o Goals (increase CO)  Improve stroke volume  Improve coronary artery perfusion  Decrease preload  Decrease cardiac workload  Decrease myocardial oxygen demand o Look similar to condom that go over a suction catheter for trach o LVAD (left ventricular assist device) is consider a bridge for highest severity of HF on the transplant list it will decrease the workload of the heart  Nursing Management  Preventing cardiogenic shock (maintain CO & perfusion; prevent MI [provide O2 to address pain and perfusion])  Monitoring hemodynamic status (A lines & ECG monitoring, report abnormality)  Administering medications, intravenous fluids (know what you monitoring the pt for ex: if you give morphine or nitro: monitor decrease in bp; assess A line or All must be given IV Protect the gut via enteral feeding it protects the lining Circulatory Shock has 3 types Septic Shock Neurogenic Shock Anaphylactic Shock venous puncture for bleeding, remember all vasoactive drug must give thru central lines, monitor U/O, serum electrolyte, BUN/cr to detect renal function)  Maintaining intra-aortic balloon counter pulsation  Ensuring safety, comfort (enhance comfort & reduce anxiety)  Circulatory (Distributive) Shock  Etiology  Occurs when blood volume is abnormally displaced in the vasculature  Blood volume pools in peripheral blood vessels  Causes a “relative hypovolemia”  Caused by o Loss of sympathetic tone o Biochemical mediators from cells that causes vasodilation  Blood is displacing, it’s there but in the wrong location (Not necessarily hypovolemic but not where it’s supposed to be)  Circulatory Shock (Change in the vascular)  Leads to: o Massive arterial and venous dilation allows for venous pooling o Reduction in systemic venous resistance o Decreased cardiac output o Decreased BP o Decreased perfusion Septic Shock  Septic Shock  Most common type of circulatory shock  Caused by widespread infection or sepsis  Leading cause of death in non-coronary ICU patients  18 million cases/year (1,400 deaths/day worldwide)  Etiology  Health care-associated infections: o Intra-abdominal infections o Bacteremia associated with intravascular catheters (blood) o Indwelling urinary catheters (urosepsis) o Pneumonia (Ventilator associated pneumonia) o Wound infections (do blood culture at suspicion)  Immunocompromised: ETOH, malignancy, AIDS  Chronic illness (DM, hepatitis, CKD)  Invasive procedures  Indwelling medical devices  Increased number of antibiotic resistance microorganisms  Malnourishment Pathophysiolog y  Older population  Early Recognition= Early Goal Directed Therapy (EGDT)  Lactic acidosis  Oliguria  Altered level of consciousness  Thrombocytopenia/coagulation disorders  Altered hepatic function  Clinical Manifestations  No predictable pattern o Variable cardiac output o Systemic vasodilatation o Hyperthermia/Hypothermia o Warm/flushed skin or cool/clammy/pale/cyanosis o Tachycardia/bradycardia (ominous) o GI hypoperfusion (N/V/D) o Altered mental status o Anuria/oliguria  Compensatory mechanisms may begin to fail  Sepsis Continuum SIRS screeningRequire 2 or more of the following: Temp >38C (100.4 F) or <36 c (96.8 F) HR > 90 RR >20 or PaCO2 <32 WBC >12,000 or <4,000 or 10% bands (immature WBC, increase bands mean infection) It’s all about early recognition & early tx (look at your pt and s/s they presenting with, if you suspecting they have some type of infection then you start thinking about SIRS criteria ex: pt present cough with green sputum [may indicate pneumonia])  Early stage of septic shock: Bp may be WNL, or pt may be hypotensive yet respond to fluids; HR increase, hyperthermia & fever w/ warm, flushed skin & bounding pulses, RR is increase, U/O may be WNL or decrease, n/v/d or decrease gastric motility; rising bilirubin & worsen coagulopathies (decrease plt), hypermetabolism increase serum glc & insulin resistance, confusion or agitation, lactate level is elevated bc of maldistribution of blood  As sepsis shock progresses: tissues become less perfused and acidotic, compensation begins to fail, & pt begins to show signs or organ d/f, bp does not respond to fluid resuscitation & vasoactive agent 1. Acute onset of symptoms 2. Presence of two or more symptoms (resp compromise, reduce BP, GI distress & skin or mucosal tissues irritation) 3. Cardiovascular compromise from min (2-30 min) to hrs after exposure to antigen  Headache, lightheaded  N/V, acute abdominal pain or discomfort  Pruritus, erythema, flushing & feeling of impending doom  Laryngeal edema, bronchospasm  Hypotension (due to trying to compensate)  Cardiac dysrhythmia/arrest  Characteristics of severe anaphylaxis usually include rapid onset of hypotension, neurologic compromise, resp distress & cardiac arrest  Medical Management  Remove the causative agent (such as d/c an antibiotic agent)  Administering medications that restore vascular tone o IM Epinephrine (along with 50 mg IV of Benadryl to reverse histamine) o Albuterol (Proventil) may be given to reverse histamine-induced bronchospasm  Emergency support  Fluid management is critical, as massive fluid shifts can occur within min due to increase vascular permeability  Medications (Reduce histamine) o Nebulizer treatments o Benadryl o Steroids  Nursing Management  Assess all patients for allergies or previous reactions to antigens (meds, blood product, food, contrast agent, latex) o Communicate existence of allergy to other team members (allergies to iodine or fish, previous contrast agent reaction)  Prevent further exposure (bracelet)  Observe for reactions while administering new medications (IV)  Assess for reactions  Be prepared for cardiac arrestperform CPR  Multiple Organ Dysfunction Syndrome  Altered organ function in acutely ill patients  Requires medical intervention to support continued organ function  Not always possible to predict  Associated mortality rate as high as 75% ***High level antibiotic can increase BUN & Cr in pt w/o adequate fluid balance (whatever system pt have effected, know what doctor is on the case) EpiPen must give IM to help with tissue absorption  better than IV 1-1000 0.3 mg Q1-5 Labs for liver issue: AST, ALT, albumin (s/s: jaundice, AMS, ascites) ***MODS mat be a complication of all form of shock but common in in pt w/ sepsis & result of inadequate tissues perfusion ***Organs failure usually begins in the lung & cardiovascular instability then liver, GI, renal, immunologic, & CNS follows  Clinical Manifestations  Hypotension  Respiratory compromise (ALI or ARDS) requiring intubation & mechanical vent  Hypermetabolic state o Hyperglycemia  Lactic Acidosis o Hyper-lactic acidemia (excess lactic acid in the blood)  Hepatic dysfunction elevated bilirubin & liver function test  Renal dysfunction elevated cr & anuria  Hematologic dysfunction: DIC, PT/INR, PTT  Immunocompromise worsens  Unstable cardiac system  Neurologic compromised (unresponsive/coma)  Systemic fulminant edema  swelling everywhere  electrolyte imbalance: d/r  Medical & Nursing Management (Everything about MODS is about preventing it)  Control the initiating event  Promote adequate organ perfusion  Provide nutritional support  Nursing: supportive caremay be supportive end of life care  Effective communication between nurse-patient and nurse-family Pathophysiology Pay attention to middle section MODS is the end result of all SHOCK