Critical Care_ Exam 1.pdf

1Critical Care: Exam 1 Topics: ✅ ✅ Critical Care patients/emergency care/Trauma ✅ Hemodynamic Monitoring ✅ Endocrine ✅ Renal...

1Critical Care: Exam 1 Topics: ✅ ✅ Critical Care patients/emergency care/Trauma ✅ Hemodynamic Monitoring ✅ Endocrine ✅ Renal ✅ Organ Transplants ✅ Immunological Health Complex Systemic Failure Introduction to Critical Care Powerpoint —------------------------------------------------------------------------------------------------------------------ ICU vs PCU? Progressive care unit is a “step down” unit; downgrade from ICU ICU - 2:1 patients PCU - 3:1, trach vents but no ET Tubes Acuity - how much care a patient needs Triage - to sort patients by assessing for critical ailments in terms of acuity and life-threatening problems - 5 Levels on the ESI (emergency severity index) to indicate acuity - 1 = most critical - Imminent danger/dying; must assess for life-threatening condition - Unstable VS - Ex. codes, unresponsive trauma victims, drug OD or severe RD - 2 = high risk pt - Shouldn’t wait to be seen - VS stability threatened - Ex. strokes, mi, suicidal - 3, 4, 5 = less/least critical - 3: Stable, may need lots of diagnostic tests to diagnose - 4: stable, may need one diagnostic test - 5: stable, only need an exam (no insurance and just want to be checked out - ESI allows HCP to know which patients should be treated first AFTER TRIAGE → detailed assessment by emergency nursing - Systematic head → toe - TRAUMA PT’s → Primary & secondary survey - NON-TRAUMA PT’S → Primary survey & focused assessment Primary survey - If life-threatening/critical finding during ABCs assessment, address BEFORE moving to D, E, F, etc. - AKA, go from most life threatening issue to least. If they're bleeding out, address C before A&B ABCDEFG – LMNOP A - Alertness/Airway w/ cervical spine stabilization/immobilization - If the patient is unconscious, they are more likely to have trouble breathing - Jaw Thrust Maneuver - thrusting a patient’s jaw forward from the base to protect/open their airway from obstruction B - Breathing  - Bilateral auscultation of lung sounds C - Circulation/Control hemorrhage - Bruising? VS, low BP? Cap refill? Pulse ox? Carotid/Femoral pulse check because they are CENTRAL pulses that perfuse vital organs D - Disability - degree of cognition - Are they confused? Answering appropriately? Baseline? GCS? E - Exposure/environmental control - Cut off clothing to assess skin, burns cuts lesions - Keep them warm with overhead lights, warm blankets, bear hugger (plastic blanket that gets filled with warm air for hypothermic patients) F - Full set of VS/Family presence G - Get monitoring devices/give comfort LMNOP L - lab tests M - monitor EKG rate & rhythm N - NGT O - Oxygen P - pain management Secondary Survey - brief, systematic process to ID all injuries H&I - Health + History - Inspect/palpate posterior surfaces - Use LOG ROLL to protect the cervical spine & posterior Emergency - any extraordinary event that requires quick/skilled response that community resources can handle Mass Casualty Incident (MCI) - natural or manmade disaster that overwhelms community’s resources/ability to respond - Triage Tags to indicate likelihood of survival: assigned within 15 seconds - Black - dead/expected to die - Red - life threatening; immediate intervention needed (bleeding out from one orifice) - Yellow - urgent but not life-threatening (ex. Broken bone) - Green - minor injury (bring to safe area) Trauma Levels: Level 1: - Can provide care to every trauma patient 24/7  - Research & teaching faculty Level 2: - Can care for most trauma pt’s most times - Lacking in one areas either d/n offer research or d/n offer teaching Level 3: - Can care for minor trauma pt’s most of the time but will transfer major traumas to lvl 1-2 Nutrition for CC pt’s: - Enteral feeding: gastric tube - Total Parenteral Nutrition (TPN) - nutrition through a vein - Residual - volume of feeding in the stomach during feeding - Return residual to pt - No greater than 200mL in stomach at a given time (too much residual = not absorbing tube feed) Hospice vs. Palliative Care 1. Hospice: last phase of terminal disease expected to die in 6 months or less - No possibility of curing disease, no more tx to try to fix them - Focus on comfort care and easing distress in final moments - End of Life - final phase of illness w/ death imminent, still unknown when the patient will die - Dignified death/Comfort/Emotional support to family - Signs of death: - Apnea - temporary cessation (stopping) of breathing for at least 10 seconds - Cheyne-Stokes Respiration - alternate apnea & deep, rapid breaths - Death Rattle - Grunting, gurgling, or noisy congested breathing 2. Palliative care: focus on reducing sx severity in conjunction with curative treatment a. Still receives care to prolong life Advance Directive (or living will) - written document by patient with what they do/don’t want done POLST - Physician’s order for life-sustaining treatment (legal version of advanced directive put in by doc) Code Status - Full Code or DNR/DNI/DNH (do not hospitalize) Power of Attorney - person in charge of decision making if patient is unable to Rapid Response Team - Critical Care Unit - Progressive Care Unit - Brain Death Criteria - not on exam..?  - Pt must be observed for adequate period of time - cause of brain death must be known and irreversible After these standards are met..: - Brain stem reflex test - gag, cough reflexes tested and there is no reaction to painful stimuli - Spontaneous Breathing - pt is removed from ventilator for 8-10 minutes to observe if they can breathe on their own; then, blood is drawn to assess CO2 levels and ventilator is reconnected - CO2 increase to a level that would stimulate breathing but none was observed = brain death likely - Cerebral Angiography - photographic study to assess blood flow to brain - Can also use ultrasound/nuclear scan - EEG to assess brain function - flat EEG = no brain activity Hemodynamic Monitoring —------------------------------------------------------------------------------------------------------------------ Invasive ways to measure pressure: 1. Arterial Blood Pressure 2. Central Venous Pressure (CVP) - end-diastolic pressure of RV 3. Pulmonary Artery Wedge Pressure (PAWP) - end-diastolic pressure of LV Vocab: Preload - volume of blood left in ventricle at the end of diastole Afterload - forces opposing ventricular ejection CO - amount of blood pumped by the heart in one minute Cardiac Index - CO adjusted for body surface area Stroke Volume - volume ejected with each heartbeat (about 70mL) Stroke Volume Index - adjusted for body surface area SVR - systemic vascular resistance - When added to arterial pressure = LV afterload PVR - pulmonary vascular resistance - When added to pulmonary arterial pressure = RV afterload Arterial blood pressure monitoring (A-line) - Invasive, must go into an artery to measure (usually radial, femoral) - Placed by HCP + sutured in place, site must be immobilized - Indications: any reason BP may need to be monitored Examples: Shock, Hypotensive/hypertensive crisis, Large surgery, Multiple ABGs, Neuro injury, Titratable drugs Starting an A-line: 1. Place 500mL NS bag into Pump bag and inflate to 300 mmHg - delivers 1-3 mL of saline/hr. Maintains patency of line and prevents thrombus a. Pressure bag also ensures blood flow will not back up into tubing; otherwise, high pressure from heart will cause blood to pump into tubing/bag (pt is BLEEDING) 2. Monitor hooked to transducer, leave transducer at phlebostatic axis a. Phlebostatic axis - 4th intercostal space (AKA level of atria/heart) b. Referencing - placing transducer so zero-reference point is at phlebostatic access c. Zero Balanced - confirms that system is reading correctly by closing stopcock to patient → should flatline bc no pressure is being put against tubing from artery i. Perform zeroing with initial setup and periodically thereafter 3. Dynamic Response Test (or square wave test) - when using the fast flush feature on the A-line tubing, you will observe a square waveform on the monitor; no interventions needed a. Dynamic response test: is the a-line “Optimally dampened”? = AKA: system is working, bp is accurate 4. Ensure EKG & A-line correlate! If both flatline = emergency; if one is flatlined but not the other… issue with setup a. Dicrotic notch - closure of the aortic valve; should be observable in waveform High-low pressure alarms - select parameters of when to be notified of a concerning pressure change (ex. Alarm sounds with pressure below 90 mmHg) Risks/Complications of A-lines: - Hemorrhage - pt at risk to bleed out - Infection - Thrombus - clot may form around tip of catheter in artery → causes blood impairment to extremity → perform neurovascular check HOURLY (5 P’s, Allan’s test) distal to A-line site - 5 P’s: - Pulselessness - Paralysis - Pallor - Paresthesia - Pain - Allen’s test - occlude blood vessels to hand while having pt pump their fist; should turn pale. Let go of one side of the wrist and see if the hand is perfusing - Neurovascular impairment - Loss of limb  Central Venous Pressure Monitoring - CVP CVP - measures preload of RV (reflects fluid volume) - Normal is 2-6 Central Venous Catheters (CVCs) OR Swan Ganz Catheters (PAC, pulmonary artery catheterization) - can be used to measure CVP - Sites: Internal Jugular (most typical), Subclavian, or femoral (usually emergent situations only, dirty stick & must be removed within 72hrs) PICC - peripherally inserted central catheter to the superior vena cava Midline - large bore catheter inserted into the midline, not as close to the heart as a CVC or PICC Implanted Port - sits under the skin Indications for CVC/PICC: - Vesicants needed - Permits frequent, continuous or rapid admin of fluids/meds - TPN is ALWAYS administered through a CVC; high incidence of infection - Can monitor central venous pressure (CVP) because it goes right into the vena cava/RV Advantages of CVC: - Immediate access, not gonna blow - Reduced venipunctures (can take blood from CVC) Disadvantages: - CLABSI - central line associated bloodstream infection Pulmonary Artery (PA) Catheter - ex. Swan Ganz PA diastolic pressure and PAWP are sensitive indicators of heart function/fluid volume status PA catheter - tells us the pressure with which blood is being pumped to the lungs - HF, cardiogenic shock, issues with afterload, etc. - Measure three pressures: - PA diastolic pressure (PAD) should be between 5-16 mmHg - PA systolic,15-28 mmHg - PAWP - 16 mmHg - Allows us to know fluid volume status - How to treat high BP in PA? Vasodilators - PACs can measure every pressure because it is a long catheter with many ports - High risk for bleeding and dysrhythmias - Chest X-ray must be taken to confirm placement - Before inserting catheter: - Oxygenation - pH / acid-base balance - Electrolyte status - Coagulation status Swan-Ganz Catheter - a type of PAC - Distal lumen in PA - allows for precise manipulation of preload - inflate balloon to measure PAWP - 2 proximal lumens that can: measure CVP, inject fluid for CO, draw blood, admin meds/fluids - Temp sensor near distal tip Complications of PA catheter: Infection & sepsis - Prevention (same as A-line): change tubing, flush bag, transducer & stopcock q96hrs, Air Embolus - Prevention: monitor balloon integrity - should feel resistance when inflating balloon (can only check this when actually checking PAWP with a doc’s order) - Luer-Lok Connections - must be on with clamped access, no leur-lok cap = air embolism; alarms on Pulmonary Infarction or PA rupture: - Prevention: - d/n inflate balloon with more than 1.5mL - Monitor waveforms continuously - Blunted waveform - more flat than normal - Maintain continuous flush system - Risks: - Catheter could advance into WEDGE position → tell doc - Embolus can form on the distal end of catheter and travel - Balloon may rupture causing air embolus - Prolonged inflation causes obstructed blood flow Ventricular Dysrhythmias - Monitor during insertion/removal - bangs against the walls of the heart and causes dysrhythmias, even V-Tach - From migration of PA catheter Endocrine Disorders - —------------------------------------------------------------------------------------------------------------------ Iatrogenic - caused by a drug/procedure from a doctor Adrenal Glands - produce hormones that regulate metabolism, immune function, BP, stress response etc. LOCATED ON THE TOP OF BOTH KIDNEYS Adrenocortical Insufficiency: - Addison’s Disease - hypofunction of the adrenal cortex - Immune system attacks adrenal glands by mistake (80% of occurrence)  - Lack of Pituitary ACTH (adrenocorticotropic Hormone) secretion (secondary cause, indirect) Cushing’s Syndrome - chronic exposure of excess corticosteroids Addison’s Disease - - Predominantly autoimmune issue at 80%; most common in white females - Can be Iatrogenic via: - Adrenal hemorrhage - Chemotherapy - Ketoconazole therapy for AIDS - Bilateral Adrenalectomy Can cause Addison’s: - TB - Amyloidosis - Fungal infections - AIDS - Metastatic cancer Sx: slow onset; non-specific sx mean it may take a while to diagnose - N/D/weight loss/anorexia/fatigue/abd. pain - Progressive weakness - Orthostatic hypotension - Salt cravings HALLMARK SIGN - Headache - Joint pain - Hyperpigmentation (darkening of skin) HALLMARK SIGN Complications: - Addisonian Crisis - life threatening sudden, sharp decrease in hormones - Acute adrenal insufficiency - Various triggers - Extra stress? Need more meds; addison’s means cannot handle stress well - Manifestations of glucocorticoid & mineralocorticoid deficiencies - hypotensive/tachycardic - Dehydration - hyponatremia/glycemia, hyperkalemia - Fever, weak, confused - Severe V/D/pain - Shock → circulatory collapse Dx: - ACTH tests - pt’s with addison’s will be very high; but not go higher with an injection - CRH test -  - Hyperkalemia → ECG changes - Hypochloremia, natremia, glycemia - Anemia - Increased BUN - CT/MRI Tx: - Manage underlying cause of addison’s - Hormone therapy - Hydrocortisone (↑ during times of stress) - Fludrocortisone (florinef) - ↑ salt intake - Addisonian Crisis: - Manage Shock and BP → will probably be in ICU - High dose hydrocortisone (a steroid) - Fluids: NS & D5W (for hypoglycemia) - Daily weights, I/Os, VS/Neuro - F/E balanced? - Watch s/s of Cushing’s → caused by high doses of steroids - Steroids can mask WBC count → becomes an unreliable indicator of infection - Educate client on ways to avoid getting sick - Protect from extremes: Light, Noise, Temp - Medical hx to dx cause? Cushing’s Syndrome - Caused by: - Excess corticosteroids - ACTH-secreting pituitary adenoma - Adrenal tumors Sx: - Thin hair, skin & subcutaneous tissue - Acne - Red cheeks & moon face - Buffalo hump, supraclavicular fat pad, & pendulous abdomen with purple stretch marks - Slow wound healing - Weight gain - Increased body/facial hair Clinical manifestations: - Hyperglycemia → HALLMARK SIGN - Osteoporosis  - Muscle wasting - Delay of wound healing - Hypokalemia - HTN - Virilization in men & feminization in men (facial hair in ladies, breast development in men) Dx: - Increased cortisol level - midnight salivary cortisol level - Low Dose dexamethasone depression test - 24 hr urine cortisol test - Plasma ACTH levels → may be low or high, helps doc figure out if it’s from the pituitary or adrenal glands - Hypokalemia & alkalosis Tx: - Find the cause and treat it - Surgical removal or irradiation of pituitary adenoma - Adrenalectomy for adrenal tumors or hyperplasia - Removal of ACTH-secreting tumors - If Iatrogenic: - Gradually d/c therapy Nursing Considerations/actions: - PMH, meds - Malaise, weakness, fatigue, insomnia, poor sleep quality? - Back, joint, bone, rib pain? - Poor concentration, memory, negative feelings, anxiety, emotional lability, psychosis, mood disturbances? - Low libido, amenorrhea - Anorexia or weight gain? ID pt’s at high risk for developing cushing’s Watch VS, daily weights and GLUCOSE (increased from cortisol level) Encourage wearing med bracelet Avoid infection, stress, extreme temps Adjust meds when stressed Lifetime replacement therapy if they had surgery on adrenal gland Renal - —------------------------------------------------------------------------------------------------------------------ AKI vs CKD CKD - can be asymptomatic until 50% damage to nephrons AKI - happens quickly; can be from prerenal, intrarenal, or postrenal cause - prerenal - decreased perfusion, heart related usually - Intrarenal - damage directly to the kidney; such as harsh medications (most complex tx) - Postrenal - UTI, kidney stones, prostate issues etc. Acute tubular necrosis - poor blood flow causes tissue necrosis which causes “casts” that show up in a: UA RIFLE classification in text book..? Labs: BUN, Cr. , & GFR (below 60 = disease) Three Phases: of AKI 1. Oliguric Phase a. < 400mL/day b. Occurs within a week after injury and lasts up to 2 weeks c. UA - may have casts (which indicate acute tubular necrosis), WBC or RBCs d. F/E imbalance - watch potassium! Can be high and cause dysrhythmias e. Metabolic Acidosis - hydrogen ions cannot be excreted by kidneys 2. Diuretic Phase a. Urine output: 1-3L/day b. May reach 5L or more c. Hypo- natrmia, kalemia, dehydration 3. Recovery Phase a. May take up to 12 months to stabilize kidney function b. GFR → above 60, BUN & Cr. begin lowering to normal levels again Dx: - Renal Scan - Biopsy - CT scan - Ultrasound - UA, Cr. Contraindicated: MRI/MRA w/ contrast d/t contrast being excreted by kidneys Tx: - Hemodialysis - indications: hyperkalemia that won’t drop w/ other tx, BUN above 120 - Monitor I/Os, add 600mL for “insensible losses”; ie. like sweat that you can’t measure - Nutrition - - Restrict Phosphorus - 30-35 cal/kg/day - Needs fat; 30-40% of caloric intake; unsaturated fats like nuts, avocados, fish  - Bad appetite → TPN or enteral feeding tubes; bring dietician onboard - Protein → should consume 0.8-1 g protein/day. NO PROTEIN; MAKES KIDNEYS WORK HARDER!! Other: - VS, especially BP that will help awareness of fluid volume status - UA, casts, protein - Confusion? Urea or ammonia levels? LOC? - Oral mucosa/lung sounds/skin turgor CKD - progressive, irreversible loss of kidney function; issues mostly same as AKI - GFR < 60mL/min for greater than 3 months - Kidney damage Diabetic Neuropathy → most common cause of CKD due to poorly controlled hyperglycemia; very small blood vessels make kidneys and eyes easy target for poor vasculature in DM complications/manifestations of CKD: - Hyperkalemia - Anemia d/t low erythropoietin (stimulates production of RBCs) that is secreted by the kidneys - Metabolic acidosis - Hyponatremia Manifestations: - Tachypnic from metabolic acidosis - May need HD for cardio - Increase in urea → breath smells like urine, metal taste in mouth, itchy skin - Ammonia increased → confusion, lethargic → seizure/coma w/o management - fractures/osteoporosis from decalcification of bones - Lowered estrogen, progesterone, testosterone → infertility Dx: - UA, dipstick test for protein - Renal ultrasound/biopsy - Albumin-Cr. Ratio - GFR Tx: - Same as AKI Dialysis - an exchange of fluid with the use of dialysate to filter the blood and excrete waste products; usually over 3-4 hrs at 750 mL/hr - peritoneal dialysis - used to filter blood; dialysate is put into catheter in abdominal cavity and then drains out once filtered - Continuous ambulatory PD - happens all day long while they live  - Automated PD - done at night while sleeping; about 4 exchanges; 1-2hrs long per exchange - Exchange - cycle of PD - Inflow (fill) - fluid is infused into peritoneal cavity - Dwell (equilibration) - electrolytes/waste exchange - Drain - dialysate is drained from cavity (15-30 mins) - Complications: - Exit site infection - use aseptic technique; if dialysate is cloudy = infection present - Peritonitis - rigid, board-like abdomen; deadly - Hernias - Lower back problems - from extra pressure in abdomen cavity - Bleeding - normal for the first few days; should resolve after that - Pulmonary complications - from extra fluid; displaces the diaphragm; at risk for atelectasis/pneumonia - Protein loss - lose about 5g in each liter of dialysate → increase dietary protein that don’t include phosphorus - Hemodialysis - blood filtration via dialysis machine - Assess: - VS, temp, fluid status & weight pre/post dialysis - Complications: - Hypotension - from rapid fluid removal - Taper amount of fluids being taken off at once → Tx w/ more fluids - Muscle cramps - d/t fluid shift/hypotension - Loss of blood - high risk of bleeding during decannulation of graft/fistula → huge vein with arterial blood; DO NOT PICK THE SCAB! - Accidental separation of catheter during tx - Hepatitis - - Fistula - dialysis access that matures in 3-4 months; connects a vein & an artery for mixed venous/arterial blood - Feel for a “thrill” - a buzzing sensation - Auscultate for a bruit - a swishing sound - If present: site is working - Graft - severe PVD & cannot tolerate fistula procedure → a bridge between artery & vein, takes 2-4 wks to mature - Perma Cath - short-term, has the same placement as a CVC - Use heparin in line to prevent clotting - Wearable Artificial Kidney (WAK) - recently developed & approved, literally is what it’s called  - Connects to pt via catheter, filters blood in ESRD (end stage renal disease) - Can run continuously Case Study: 1. AKI 2. Pre-renal d/t lower CO from hypertension/DM → impaired perfusion to kidneys 3. Potassium is elevated b/c it is excreted by the kidneys which are not filtrating properly with a GFR of 28 mL/min 4. Monitor I/Os, BP/heart rhythm, treat any F/E abnormalities, take labs like U/A, GFR BUN/Cr., manage hyperkalemia → insulin, glucose, lokelma 5. Dx tests: UA w/ casts, renal biopsy, ultrasound, renal scan, CT, 6. Dietary recommendations: regular protein, 30-35 cal/kg, high unsaturated fat diet, no phos 7. Complications: altered LOC d/t increased urea & ammonia, dysrhythmias from hyperkalemia, hypotension, anemia, metabolic acidosis (low bicarb), hyponatremia, older adult may not fully recover, pulmonary edem Kidney/Organ Transplant Organ donation qualifications: over 18, no cancer or HIV, severe infection Transplant Compatibility studies - 1. HLA typing - donor & recipient tested to match antigens A, B, DR (total of 6 antigen minimum; less matches = higher rejection chance) 2. PRA: Panel of Reactive Antibodies - donor & recipient tested for lymphocyte percentage (higher percentage of reactions = more likely to reject; you want a low percentage) a. High PRA → recipient has large number of cytotoxic antibodies and is highly sensitized; high percentage = poor chance of success/finding good crossmatch negative donor b. Tx → Immune globulin (IvIg) and plasmapheresis is used to lower number of HLA antibodies 3. Crossmatch - tests donor & recipient lymphocytes to test for pre-formed antibodies that would attack donor organ a. Final crossmatch → happens right before transplant b. DO NOT WANT A POSITIVE CROSS MATCH, you want negative! Transplant Recipient Selection - Contraindications for giving someone organ: - Disseminated malignancies - metastatic cancer - refractory/untreated cardiac disease - not responsive to tx; transplant likely to fail - Chronic RF  - Extensive vascular disease - Chronic infection - Unresolved psychosocial disorders - like addiction Precursors: - Surgery may be required before transplant: - CABG or coronary angioplasty - Cholecystectomy - b/l nephrectomy New kidney → goes to iliac crest on anterior right abdomen Transplantation: - Education: - Dialysis may be needed post surgical → jump-starts kidney, gets it going - Need immunosuppressive drugs to prevent rejection; higher risk for infection → will take these drugs for the rest of their life - Balance between rejection/infection - Donor: - Monitor renal function, hematocrit, pain - Recipient: - Maintain F/E balance as TOP priority - Large volumes of urine may be produced post surgery d/t: - new kidney’s ability to filter BUN working overtime - Abundance of fluids during operation - Initial renal tubular dysfunction - AVOID DEHYDRATION → replace all fluids lost in first 24 hrs! Can be 1L/hr - Assess hyponatremia/hypokalemia - ATN can occur → dialysis required; can last weeks(1-2) - Maintain catheter patency Complications of Transplants: - Rejection - Hyperacute - occurs minutes-hours post transplant d/t blood vessels being rapidly destroyed - Organ must be removed for tx - Acute rejection - most common, days-months post transplant - Tx needed → give more immunosuppressants - Chronic Rejection - process occurs over months-years and is irreversible - Unknown reason or from repetitive acute rejection - Infection - most common in first month - Pneumonia - Wound infections - IV line & drain infections  - UTI - Cardiovascular disease - Increased incidence of artherosclerotic vascular disease - Immunosuppressants → worsen HTN & HLD → take ur meds! - Malignancies - at risk for developing cancer - Primary cause: immunosuppressants - Get screened regularly - Recurring kidney disease - Glomerulonephritis - IGA nephropathy - Diabetic nephropathy - Focal segmental sclerosis Heart Transplants: Transplant matching: - body/heart size - Immune assessment Post-op concerns: - Infection - Rejection → can go into HF - Orthostatic hypotension → heart not at 100% and can’t adjust to change in position - Immunosuppressive therapy: d/n focus on names; just know they’ll be on a few drugs - Corticosteroids - Calcineurin inhibitors - Cytotoxic drugs - Monoclonal antibodies - Polyclonal antibody - other Complications: - Corticosteroids: - Aseptic necrosis of hips, knees, joints - PUD - Glucose intolerance/DM - Dyslipidemia - Cataracts - Infection - Malignancies Shock, SIRS, MODS and Vasopressors - —------------------------------------------------------------------------------------------------------------------ Systemic inflammatory Response Syndrome - SIRS Caused/triggered by: - Injury → crush, burn, trauma - Ischemia or necrotic tissue - Infection → bacteria, virus, fungus, parasite - Infarction → resuscitation or shock - Crush injury, burns Criteria to indicate SIRS: two or more of the following - Fever of more than 100.4 or less than 96.8 - HR >90 bpm - RR >20 breaths/min OR PaCO2 of less than 32 - Abnormal WBC (>12,000 or 10% band forms) Multiple Organ Dysfunction Syndrome - MODS Failure of two or more organs A result of SIRS Inflammatory response → releases mediators that leak into interstitial space WBCS are activated Decreased perfusion 1st system to show s/s of MODS: Respiratory system Shock → SIRS → MODS MODS: Cardiovascular system: - MASS vasodilation - BP → drops into hypotension - HR → increases to compensate Neuro: - Results out of impaired perfusion - Sx: - Confusion - lethargic/combative/irritable Renal: - AKI d/t low perfusion and mediators - Affects waters reabsorption via activating angiotensin response-sodium GI:  - Ischemia - GI bleed - Liver - affects clotting, fluid shift - Metabolic changes - metabolic acidosis, hypokalemia, hyperglycemia & insulin resistance Prognosis → very poor How to treat: - Prevent & tx infection - Maintain oxygenation of tissues → sedated & resting, control pain and put on mechanical ventilation - Nutritional support - Watch liver, use enteral route when possible; prevents infection and maintain GI motility - Insulin therapy as needed - Tx for each organ that is failing - DIC → blood products - ARDS → O2 & mechanical ventilation - Renal Failure → CRRT Shock: - Syndrome defined by decreased tissue perfusion - Impaired cellular metabolism - Imbalance between supply and demand for oxygen at the cellular level - Demand exceed supply which causes → ischemia of the organs Types of Shock: - Cardiogenic - systolic or diastolic dysfunction = compromised CO - Basically, the shock is the heart’s fault → increase the blood supply to the heart so that it can retore blood supply to the rest of the body - SD - inability to pump blood forward - DD - decreased filling of the heart = decreased stroke volume - Sx: - Early manifestations - Tachy - Hypotension - Narrowed pulse pressure Hallmark sign - Increased myocardial O2 consumption - Increased PAWP - Crackles (from backup of fluid to the lungs) - Decreased renal perfusion & urinary output - LATE manifestations  - Cyanosis, pallor - Diaphoresis - Cool & clammy skin - Weak peripheral pulses - Anuria - Tx: restore blood flow by restoring O2 supply/demand - Drugs: - Nitrates that dilate the Coronary arteries - Diuretics to reduce preload - Vasodilators to reduce afterload - Beta blockers to reduce HR - Hypovolemic - loss of blood volume greater than 30% that requires treatment via volume replacement - Fluid replacement calculated as 3:1 → 3mL or isotonic crystalloid for every 1mL of blood loss - Acute Hypovolemia - hemorrhage - Relative Hypovolemia - results from fluid movement into the extravascular space - Manifestations: - Anxiety - Tachycardia/tachypnea - Lowered CO, Stroke Volume, PAWP, urinary output - - Distributive - Neurogenic - when blood vessels become excessively dilated - Causes: 30 mins after spinal cord injury at T5 OR spinal anesthesia - Leads to: - MASSIVE vasodilation leading to pooling of blood in vessels, hypoperfusion - Can last up to 6 weeks - Manifestations: - Hypotension & bradycardia - Inability to regulate temp (heat loss) - Dry skin - Poikilothermia - taking on temp of the environment HALLMARK - tX: - Infuse fluids CAUTIOUSLY → hypotensions unrelated to fluid loss - Monitor for hypothermia - Spinal stability  - Treat BP issues via vasopressors & atropine - Anaphylactic - allergic reaction - Give Epinephrine, diphenhydramine, ranitidine - Maintain a patent airway - Aggressive fluid replacement - Septic - - Obstructive → blood obstructs the CO ex. Compartment syndrome, cardiac tamponade, etc Pulse pressure - 40-60 (the difference between sys & dias pressure) Septic shock - bacteria enters the bloodstream Wbc activates → Vessels dilate and become leaky → fluid shifts into interstitial space (3rd spacing) → body starts to bleed through increased capillary permeability → reduced clotting factors available and INCREASE in chance of DVT/stroke/mi → Manifestations: Hypotension Hypoxia Third spacing Respiratory alkalosis r/t tachypnea & hyperventilation (happens to 85% of patients) GI dysfunction, bleeds, & paralytic ileus Internally bleeding through capillaries → clotting occurs everywhere in the body which uses up all of our clotting factors → we are at a huge bleeding risk with a high PTT → higher risk for DVTs r/t all the clotting occuring internally Tx: - Fluid replacement therapy & vasopressors - Antibiotics must be administered within the first hour - AFTER obtaining cultures - Give broad-spectrum first - More specific ATBs after organism ID’d - Keep glucose less than 180 Stages of shock: Initial: - Compensatory: if addressed at this stage, pt is likely to recover - Progressive Refractory Dopamine - increases the HR & is a vasoconstrictor Norepinephrine - potent vasoconstrictor Side effects of tachyarrhythmias, peripheral ischemia, clubbing with prolonged use, possibly necessary to amputate digits r/t poor perfusion and subsequent necrosis Phenylephrine - for neurogenic shock; vasopressor Vasopressin (antidiuretic hormone) - used with norepi to perfuse kidneys - Not titratable Epinephrine - raises the BP & HR, CO & vasopressor - Cardiac arrest → first line drug - Added when norepinephrine fails to raise BP - SE: tachy, pulm. Edema, dysrhythmias, ischemia of organs Dobutamine - increase CO, not a pressor Nitroglycerine - vasodilates the coronary arteries Assessment: - ABCs - Focused assessment of tissue perfusion - VS - Peripheral pulses - LOC - Cap refill - Skin - I/Os