NCM 118: Care of Clients With Life-Threatening Conditions PDF

NCM 118: CARE OF CLIENTS WITH LIFE-THREATHENING CONDITIONS, ACUTELY ILL/MULTI-ORGAN PROBLEMS HIGH ACUITY AND EMERGENCY SITUATION  Attendance is mandatory and checked within the first 15 minutes of the designated class schedule. A student with accumulated 3 absences of the total clas...

NCM 118: CARE OF CLIENTS WITH LIFE-THREATHENING CONDITIONS, ACUTELY ILL/MULTI-ORGAN PROBLEMS HIGH ACUITY AND EMERGENCY SITUATION  Attendance is mandatory and checked within the first 15 minutes of the designated class schedule. A student with accumulated 3 absences of the total class meetings will be dropped from the roll. Maximum participation is expected in all classroom activities. At all instances, respect for classmates and instructors are expected. Observe proper decorum. Come in complete uniform. Use of cellphones, tablets and other gadgets for social and other purposes not related to the learning material are strictly prohibited during class. It is expected that all written outputs are submitted on time on the designated dates.  PERFORMANCE TASK: 25%  Formative (Self assessments, Individual and group projects, module exercises)  Summative (Term Papers, Case Study, Research) 20%  Participation 20% Quizzes 15% Term Exams 20% Total: 100% SHOCK OBJECTIVES 01 02 03 04 Understand the disease Review of process of shock and Differentiate the types Application of normal cellular its types, of shock. knowledge manifestations and functions. management.  SHOCK ↓ tissue perfusion Shock can best be defined as a clinical syndrome that results from - inadequate tissue perfusion, creating an imbalance between the delivery of oxygen and nutrients needed to support cellular function - - (Maier, 2015; Moore, Dyson, Singer, et al., 2015). ESA - ISA = Q cardiac Jump ① Effective V ③ Sufficient Vasculature) CS Y ③ Adequate a = tissueperfun mised  SHOCK PHYSIOLOGIC RESPONSE: oftissues ① Hypoperfusion ② Hypermetabolism inflammatory & Activation of response  NORMAL CELLULAR FUNCTION ENERGY METABOLISM Incore of 9 mate per - 2 ways : wish APP 02 * energy ① acrobio anaerobic -002- ②- ↳ lactic acid ↳ liver ↳ Glycogeny Glucose  PATHOPYSIOLOGY CELLULAR CHANGES In shock, the cells lack an- adequate blood supply and are E deprived of oxygen and nutrients; therefore, they must produce - A low energy energy through anaerobic metabolism - ↳ acidotic intracellular envi ① cell swell ② all nembrane men permeable = cell dramage = cell death  PATHOPYSIOLOGY CELLULAR CHANGES Glucose is the primary substrate required for the production of cellular energy in the form of ATP. glucagms , (norepinepi) cortisol contamines , insulin resistance cytokines = hyperglycemia ① Gluconeogenesis - proteins a fats cose - ⑧ GLYCOGenOLYSIS glycogeO - - z bind glasse  PATHOPYSIOLOGY CELLULAR CHANGES - The clotting cascade, also associated with the inflammatory Obecomes activated, which compounds this pathologic process, cycle. clotting cascade - cell injury > - Shock D operproductive ↳ small clots ↳ hamper cel Inlar perfusion hypergazin  PATHOPYSIOLOGY VASCULAR RESPONSES - - u - - - mediate cell/immure cells) Biochemical ↓ an action triggers site waso anstriction vasodilations  PATHOPYSIOLOGY BLOOD PRESSURE ESA REGULATION oo Three major components of the circulatory system—blood volume, the cardiac O G pump, and the vasculature—must respond effectively to complex neural, - chemical, and hormonal feedback systems to maintain an adequate blood - as Ri s e - Peripura pressure (BP) and perfuse body tissues. Cardiac output x Mean arterial B4 = # SVXHR multy MAD = (CBP) + SBP Q :< 65 3 Bp : 120 (2)(8) + 120 ① = - - 3 50 98 so (((90) + 130 3 manby BP : 130 = = 109mmity = 89 T0 3  PATHOPYSIOLOGY SNS (EF) PBP BLOOD PRESSURE # constriction catecholamiAR nes& - Val REGULATION #BP - ↑ C 1. BARORECEPTORS (pressure receptors) = ↓ BP brain - cardio y respi 2. CHEMORECEPTORS a * 3. KIDNEYS PRR  PATHOPYSIOLOGY BLOOD PRESSURE REGULATION RAAS angiotension) Potenti↓ o constrictor) - Kidneys > - renin -- aldosterone ↓ retension Nab HeO Chyperlatremia) ↓ ADI ↓ kidney earned -P BV = PBP COMPENSATORY MECHANISM IN SHOCK O O O - SNS (FIF) O - - - - - - - O - - - Oc STAGES OF SHOCK 01 02 03 COMPENSATORY PROGRESSIVE IRREVERSIBLE  STAGES OF SHOCK 1. COMPENSATORY STAGE In the compensatory stage of shock, the BP remains within - normal limits. - Vasoconstriction, increased heart rate, and increased contractility of the - heart contribute to maintaining adequate cardiac output catecholamines FF ↑CO = - SNS (Brain · 21 Skin Vital organs Heart, kidmys - , Blood shunting : Lungs) , , ↓ · ↳ ↳ AUD hypractive cool/pale bowel skin sounds clammy  COMPENSATORY STAGE CLINICAL MANEFESTATION METABOLIC ACIDOSIS acid) Cplactic INCREASE RR (RESPIRATORY ALKALOSIS) (O2 (acid) - expel = PRR = - ANXIOUS CONFUSED BP (NORMAL) INCREASE HR J SNS COLD, CLAMMY & blood shunting DECREASE UO  MANAGEMENT NURSING AND MEDICAL MANAGEMENT -SYSTEMICALLYC ASSESS THE PATIENT -IDENTIFY THE6CAUSE -ADMINISTERC C IV FLUIDS AND OXYGEN -LABORATORY RESULTS ↳ metabolic levels, infection  MANAGEMENT MONITORING TISSUE PERFUSION ASSESS THA PATIENT FOR SUBTLE CHANGES IN LOC, VS, UO, SKIN, RR, AND LAB --- - VALUES - - - MONITOR SERUM SODIUM AND BLOOD GLUCOSE ↑ ① RR>22 bpmtial - - IF (+) INFECTION, BLOOD CULTURES IS A MUST E Mont ② altered renta00mmity] - systolic BP El - ⑬ MD ! - MONITOR HEMODYNAMIC STATUS REPORT SYSTOLIC BP < 90 mutty , 40mmHg , < 65 mmHg (MAP) MONITOR PULSE PRESSURE - narrow/ N : 30-40 mmHg CONTINOUS CENTRAL VENOUS OXIMETRY MONITORING (SCV 02) - CENTRAL CATHETER no SVC Or sat of blinds ue he on - go  MANAGEMENT MONITORING TISSUE PERFUSION INTERVENTIONS FOCUS ON DECREASING TISSUE OXYGEN REQUIREMENTS - AND ICREASING TISSUE PERFUSION: - -SEDATING PATIENTS cmclose) & cardiac workload = O2 reg - - -IV OPIODS FOR PAIN - -IV FLUIDS, MEDS SUPPORT, AND TRANSFUSION OF PRBC - - -  MANAGEMENT REDUCING ANXIETY EDUCATE THE PATIENT AND FAMILY MEMBERS CALM VOICE, GENTLE TOUCH CLOSE MONITORING - PREVENT FALLS - FREQUENT REORIENTATION -  STAGES OF SHOCK 2. PROGRESSIVE STAGE In the second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. - - · Hypotensive wenta) status · declining of  STAGES OF SHOCK 2. PROGRESSIVE STAGE s ischemic ①-OVERWORKED HEART - dysfunctional -o O Poz reg ② capillary permeability -AUTOREGULATORY FUNCTION FAILS ↑ ↳ Obisamical mediators =  PROGRESSIVE STAGE CLINICAL MANEFESTATION RESPIRATORY EFFECTS: RAPID AND SHALLOW, CRACKLES, DECREASE - PULMONARY BLOOD FLOW CARDIO EFEFCTS: DYSRYTHMIAS AND ISCHEMIA, CHEST PAIN -- NEUROLOGIC EFFECTS: IMPAIRED, MENTAL STATUS DETERIORATES KIDNEY EFFECTS: AKI - - - HEPATIC EFFECTS: INCREASE LIVER ENZYME, BILIRUBIN, AND JAUNDICE - - - GASTROINTESTINAL EFFECTS: ULCERS - HEMATOLOGIC EFFECTS: HYPOTENSION, SLUGGISH BLOOD FLOW, - - COAGOLATION SYSTEM IMBALNCE, HYPOXEMIA - -  PROGRESSIVE STAGE MEDICAL MANAGEMENT -cause IDENTIFY THE CUASE critically patient IV FLUIDS Songldh) untrol (a ; - membranes ↳ too large -> capilling expand concotic pressure) N crystalloids · ~ Longer duration than VASOACTIVE MEDICATION THERAPY cardio respi Gl , skin 4 kidneys -BV instrict , , ① alphadenergic receptors , receptors Betaachragic HR cardial contraction & h ↑ B2 my skeletal bronchicles - · - variditatio > - heart , ,  GENERAL MANAGEMENT NUTRITIONAL SUPPORT requirements. - - s Increased metabolic rates during shock increase energy requirements and therefore caloric 0 >3000 cal/day parenteral enteral nutrition ·  SUMMARY - - - G S - - - - - - - - - - - - O - - - - - - - HYPOVOLEMIC SHOCK  ① Intra cenimal 2/3 HYPOVOLEMIC SHOCK ② EXTRACeCURAR Intravascular · & d InFRSTIMAL 3 - 4X · : Hypovolemic shock, the most common type of shock, is characterized ↓ 15 % to 30 % - by decreased intravascular volume. + 1500 mL of blood 758 70kg 0-0-  ↓ venous returne -o A ventricular fillings ↓ IV > ↳ ↓ Su ↳ ↓ Co  MANAGEMENT 3 1 rule : loss ImL blad e FLUID AND BLOOD REPLACEMENT D LRS 3m2 : frendelenburg modified opfal - i REDISTRIBUTION - OF FLUID · trendelenburg - ↳ zerebrat conges t VASOACTIVE MEDICATIONS e ACQUIRE BLOOD SPECIMENS MONITOR PATIENT FOR POSSIBLE WOF : Cardiac Overload COMPLICATIONS - · Hypotterm19 OXYGENATION - CARDIOGENIC SHOCK - CARDIOGENIC SHOCK Cardiogenic shock occurs when the heart’s ability to contract and to pump blood isO impaired and the supply of oxygen isE inadequate for the - heart and the tissues. - - scardium ran nicular my Coronary--M1 - left ② non coronary · severe hypoxem E acidosis · valvular damage  ↓SV ↓ fissue perfusion ↓ cardiacIntractility - ↓ artery ↓ corrray perfusion = pain /anging dyssing thr as = MANAGEMENT NC O CORRECTION OF UNDERLYING CAUSE % De sat OXYGENATION 2-6 LPm => 95 dilatation of BV PAIN CONTROL IV morphine ; HEMODYNAMIC MONITORING LABORATORY MARKER MONITORING FLUID THERAPY - PHARMACOLOGIC THERAPY -  INSTROPIC = ↑ cardiac contractility CHRONOTROPIC = PAR PHARMACOLOGIC THERAPY DOBUTAMINE imtropic effect Pc6 = = vasodilator = ↓ preload Imdises ; venous NITROGLYCERIN = IV in DOPAMINE ↳ pathmetic = PHR I, contracticises mimic surpa inotropic chronotropic · N ug(kg/min 2 = , * : = load > 89/k91min = vaso constrictio = ↑ after workload I cardiac - = DISTRIBUTIVE SHOCK DISTRIBUTIVE SHOCK Distributive shock occurs when intravascular - volume pools in peripheral blood - - vessels. This abnormal displacement of intravascular volume causes a relative & - hypovolemia because not enough blood returns to the heart, which leads to - inadequate tissue perfusion. - DISTRIBUTIVE SHOCK events-o vasodilation - astile of inflammatory response precipitating ↓ O o Ju maldistributi ↓ x venous return i ↓ ↓ CO = H fissure perfusion SEPSIS AND SEPTIC SHOCK  SEPTIC SHOCK Septic shock, the most common type of distributive shock, is caused by = widespread infection or sepsis. A sepsis is “life-threatening organ dysfunction caused by a - dysregulated host response to - - - infection and septic shock is “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality (Third - International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) Task Force, 2016). in ① Immunosuppress ② CHRONIC ILLneSS ③ Invasive Procedure ⑭ Bacteremia , Pneumonia UROjePsIS , SEPTIC SHOCK cytokines mediators activation biochemical microorganism -- immune respons - ↓ events cascade of physiologic ⑪RS ↳ to tissue perfusial 738 % ① %. ② Pr ⑨ PRR ④ WBC > 12 , 000 wells/mm3 MANEFESTATIONS - - - - - - - - -  MANAGEMENT -CORRECTION OF UNDERLYING CAUSES S crystalloids par 30 min -FLUID REPLACEMENT THERAPY ↳ zomL/kg antibiotic - -PHARMACOLOGIC - THERAPY broad spectrum , -NUTRITIONAL THEPRAHY nep ! doparive - ↳ 24 to 48 hours NURSING MANAGEMENT underness 6 redress , Invasive procedures must be carried out with aseptic technique power -. IV lines, arterial and venous puncture sites, surgical incisions, traumatic A C wounds, and urinary catheters must be monitored for signs of infection - or applying a Reduce the temperature by administering acetaminophen hypothermia blanket - Administers prescribed IV -- fluids and medications, including & antibiotic agents and vasoactive medications - Monitor blood levels (serum levels of antibiotic agents, procalcitonin, - - CRP, BUN, creatinine, WBC count, hemoglobin, hematocrit, platelet levels, coagulation studies) NEUROGENIC SHOCK NEUROGENIC SHOCK In neurogenic shock,co vasodilation occurs as a result of a loss - of balance between↳ - = parasympathetic and sympathetic stimulation. Intury - D Spinal CORD are stitsia ② spinal Damage ③ nervous system meds action ① depressant of NEUROGENIC SHOCK poRI$ FIF Insury - imbalance Para & Sympa Spinal corp ⑪ ↑ dominant parasymphotenc ↳ AR, # hypotential sin - · dry warm , - vasodilation  MANAGEMENT who will receiv : spiral/epidural ↑ pet's p elevateal go" Low fowler's -Proper Positioning : HO should be - Spinal and injury : smborize -Check the patient daily for any lower extremity pain, redness, - tenderness, and warmth. VTE - - ↳ ( Heman's sign E CH) calf · Pneumaticcompu stich devices · antithrombotic agents ↳ low-morecular-reight reparin ANAPHYLACTIC SHOCK ANAPHYLACTIC SHOCK - Anaphylactic shock is caused by a severe allergic reaction when patients who have already produced antibodies to a foreign substance (antigen) develop a systemic -- antigen–antibody - reaction; specifically, an immunoglobulin E (IgE)- mediated response. # & HV medication sensitivity Anaphylaxis most ceils Transfusio reaction & O : ↓ /stings bradykinin cytokines & acuie onsent infect bites histamine ; , ② of SymprOnS ① food allergies symp and ↓ sensitivity & vasodilatio capillary permeability zw mre distress ① Latex Respi , * &D , G) , tissue skin/mucosal irritative & cardiovascular empromise MANEFESTATION headache lightheadedness nausea, vomiting, acute abdominal pain or discomfort G pruritus and feeling of impending doom. diffuse②erythema and generalized flushing - difficulty breathing - (laryngeal - edema) bronchospasm - cardiac dysrhythmias - hypotension - MANAGEMENT - - - - NURSING MANAGEMENT Assess patient forOallergies Advise the patient toOwear or carry identification - When giving meds always observe for possible =allergic reactions  SUMMARY HYPOVOLEMIC SHOCK (BLOOD) - CARDOGENIC SHOCK (HEART) - DISTRIBUTIVE SHOCK (BLOOD - VESSELS): - ⚬ SEPTIC SHOCK ⚬ NEUROGENIC SHOCK ⚬ ANAPHYLACTIC SHOCK Thank you for Listening! #YourTuRN