NUR 4120Shock and Multiple Organ Dysfunction Syndrome.

Document Content and Description Below

 Medical Management of Septic Shock  Identification and elimination of source of infection (goals are to id & tx within 3 hrs to increase pt outcome)  Pan culture/Labs/Lactic acid (greater ... than 2)/ABG  Remove infected lines/catheters  then replace  Fluid replacement through aggressive fluid resuscitation is key (monitor bp, CVP, fluid responsiveness w/ passive leg raise, u/o, serum lactate levels)  Vasopressors (norepinephrine 1st line or dopamine to achieve MAP of >65; inotropic; PRBC to support O2 delivery; neuromuscular agent & sedation may be required to reduce metabolic demands & provide comfort; DVT plus SCD prophylactic, antacid [PPI])  Broad spectrum antibiotics; Change to appropriate antibiotics when cultures returned (do blood & urine culture prior; can take 24-36 hrs depend on labs)  Nutritional Therapy (within 24-48 hrs in ICU to address hypermetabolic state; if not it will further impair pt’s resistance to infection enteral feeding if GI tract have good peristalsis)  Nursing Management of Septic Shock  Respiratory support  Transfuse when Hgb < 7 g/dL  Glucose control (< 180 mg/dL)  DVT prophylaxis  GI prophylaxis (antipeptic & protonic especially bc they on steroids)  IV hydrocortisone  Advanced planning  If pt is hyperthermia: give acetaminophen or apply hypothermia blanket (avoid shivering)  Patient & Family Support  Anxiety  Support of coping  Patient, family education  Communication  End-of-life issues  Grief processes Neurogenic Shock  Pathophysiology  Vasodilatation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation o Sympathetic stimulation: vascular smooth muscle constriction (in neurogenic state the SNS is not able to respond to body stressor) o Parasympathetic stimulation: vascular smooth muscle relaxation  Parasympathetic stimulation is predominant  Relative hypovolemia with adequate volume status  Clinical Manifestations & Etiology (remember SNS is not able to function properly, so the s/s that will appear with neurogenic shock will be parasymptomatic signs)  Causes bradycardia (slow HR), hypotension (low BP) & blood pooling  Etiology o Spinal cord injury o Spinal anesthesia* o Nervous system damage o Depressant action of medications o Hypoglycemia/ lack of glc (insulin reaction) o Low bp, low HR, cyanosis, hypothermia, blank stare, Dry/warm skin  Medical Management  Restore sympathetic tone either by stabilization of a SCI or position pt properly  Proper positioning  Treat the cause! Pacemaker, atropine, vasopressor  Nursing Management  HOB up 30 degrees with epidural anesthesia  Assess for DVT  increase pooling of blood from vascular dilation (not able to feel anything if they have SCI daily check for lower extremity pain, redness, tenderness & warmth passive ROM of the immobile extremities help promote circulation early prevention includes SCD’s & antithrombotic agents [Lovenox])  Asses for signs/symptoms internal bleeding that could lead to hypovolemic shock Anaphylactic Shock  Anaphylaxis  Severe allergic reaction in patient who has already produced antibodies to an antigen  Systemic antigen-antibody reaction o IgE mediated  The antigen-antibodies reaction provokes mast cells to release potent vasoactive substance as histamine, bradykinin, inflammatory cytokines released o Widespread vasodilation and increased capillary permeability  Common triggers o Food (peanuts) o Medication (ARB, ACE-I, ASA, NSAIDS, antibiotics, beta-blockers) o Insects (bee’s) o IV dye, iodine  People who have been previous expose have worsened reaction to the 2 times, can occur in many year  Clinical Manifestations 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) 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  Shock: Definition  Life-threatening condition  Results from inadequate tissue perfusion  Prevents adequate oxygen delivery to cells  Shock: Overview  Adequate blood flow requires (need an effective pump)  Shock: General Physiologic Responses  Regardless of the initial cause of shock, physiological responses are common to all types of shock:  Pathophysiology: Cellular Responses  Cellular swelling occurs  Pathophysiology: Cellular Responses  Cellular changes that occur with shock:  BP regulation requires adequate  Pathophysiology: Coagulopathic Responses  Pathophysiology: Inflammatory Responses 1. )  How is BP regulated? MAP= CO x PVR (peripheral vascular resistance)  Blood Pressure Regulation: pressure Receptors  Blood Pressure Regulation: RAA (kidney regulator, slowest system yet safest)  3 Stages of Shock  Compensatory Stage of Shock  SNS causes vasoconstriction, increased HR/increased heart contractility  Inadequate tissue perfusion  Progressive Stage of Shock  Mechanisms that regulate BP can no longer compensate  Progressive Stage of Shock  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 [Show More]

Last updated: 1 year ago

Preview 1 out of 27 pages