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Page 1 Critical Care Final Study Guide Notes. ICU Environment * Open ICU: physician responsible for pt. admits the pt. to ICU & keeps formal responsibility for pt. & their tx. Intensivist is a consultant w/o primary responsibility * Closed ICU: pt.is admitted to ICU & responsibility for pt. & tx is transferred to intensivist * Sensory Overload o Noise o Bright lights © Loss of privacy- multiple caregivers, people in & out of room © Lack of nonclinical physical contact o Emotional & physical pain = Confusion = Lack of control = Sleep deprivation = Thirst = Anxiety = Pain = Depression = Difficult communication * Sensory Deprivation © Lackof visitors co White walls o. Staff stay out of room to give co Nostimulation privacy c Tv&phone $$ ° * Modification of environment © Noise reduction: soothing music, acoustical tiles/designs, private areas for communication for caregivers & family members © Adequate lighting: natural lighting, night/day synchronization © Design of new units to promote health & safety: nature in the view, bring family into experience © Reorient every time you walk inthe room! o Palliative Care * Designed to relieve sx that negatively effect the pt. orthe family + Should be implemented with all patients not just the dying + Elements: o Earlyidentification of end-of-life pts. © Pain management © Pharm &non pharm interventions to relieve: pain, anxiety, & other distressing sx = Pain = Nausea = Anxiety = Diarrhea = Hunger = Confusion = Thirst = Agitation = Dyspnea = Sleep disturbance + Nursing interventions: [Date] Page 2 © Frequentrepositioning © Peaceful environment © Good hygiene o Painrelief o Skincare ©. Spiritual needs o End of Life Care inICU Prep the family—not an event but a process Emphasizes comfort rather than cure Philosophy of care, not a place Views ding as anormal process o Terminal Weaning Let both the pt & family know what happens— may or may not pass away immediately Ensure pt. is comfortable Look right at the patient, make physical contact when explaining what is happening Pain medication (morphine) enough to decrease WOB & antianxiety med (benzos) © Titrate pain meds & sedation throughout relieves tachypnea, dyspnea, & use of accessory muscles © Ongoing assessment of response to therapy & comfort Patient specific for comfort, ask about religious preferences “Plug is pulled” by RN & RT Comfort cart for family Family may take part in post-martem care Unforeseen death, ET tube & IV left in until medical examiner is present Family has a right to refuse autopsy however cannot refuse medical examiner Up ta family to call funeral home If family wants to turn off the machine for the wrong reasons® call ethics committee—no longer need MD order oO o MOLSTForm Mutually agreed on between the provider & pt. or surrogate Clearly specifies the kind of care the pt. prefers at the end of life fe} o Ethics Committee Multidisciplinary Can say their finding contraindicates healthcare proxy’s request if itis immoral & unethical petition court Nurse’s share in the moral responsibility of their institution to ensure that the best ethical decision making pracess is in place to meet pt. needs, uphold the institution’s philosophy, & preserve the integrity of the nursing profession. o Trauma Look for mechanism of injury “ how did it happen?” , did their plane change? Height or surfaces they fell from? Prioritize tx to ABC’s If neck is not stabilized] stabilize w/ cervical collar—no backboards in NY [Date] Page 4 o Chemical Contact, inhalation of fumes, ingestion, injection Severity r/t type, volume, duration of contact, concentration of agent Tissue damage continues after agent neutralized o Systemic Effects of Chemical Acids—bathroom cleaners, swimming pool chemicals o Necrosis of skin, can bind to serum Ca if taken po Alkalies— oven cleaners, fertilizers © Loosen skin P->liquefaction necrosis & seepage into tissues. Bind to P sa hard ta stop burning process Organic compounds ~ gasoline o CNSdepression, hypotension, hypothermia, pul edema, chemical pneumonitis, hepatic & renal failure © Warfare, terrorist attacks Burns from chemicals or thermal exposure Methamphetamine labs oa Inhalation, thermal & chemical burns oO eo Electrical AC~—alternating current (commercial) Greater risk of vfib, “locks’ pt to electricity->resp muscle paralysis DC-direct current—lightning, car batteries Point of contact (entry & exit) injury depends on: Type & pathway of current, duration, environment, body tissue resistance, cross section of body involved Urine output goal 75-100 mL/hr ©. Inhalation Injury from carbon monoxide Binds to hgb better than O2->tissue hypoxia Injury above glottis Thermal- damage in pharynx& larynx, may cause airway obstruction Injury below glottis Chemical- impaired cilia, erythema, edema, hypersecretion, ulceration, increased blood flow, bronchial spasm ° o House Fires * Whencomponents of ourhomes burn © Degrades into toxic substances = Carbon monoxide « Carboxyhemoglobin (COHgb) — binding of carbon monoxide to hgb [Date] Page 5 « Hard to detect s/s « COHgb <10-15% headache, impaired vision, « PaO2 &02 sat may be WNL « COHgb 15-40% CNS s/s vary- restless, confusion, impaired dexterity, dizzy, N/V « COHgb 40-60% LOC, tachycardia, tachypnea, cherry red or cyanotic skin « COHgb >60% coma->death * Cherry lips, Cherry face o Oxygen therapy FIRST! o Remember, Carbon monoxide binds to hgb...o2 replaces it = Formaldehyde =~ Cyanide ° co CARE FORTHE BURN PATIENT: Pre-hospital Phase Emergent Phase/Resuscitative Phase Acute Phase Rehab Phase © 1. PRE-HOSPITAL PHASE —primary concerns are ABC’s (airway, breathing, circulation) Remove from the burn source Check patency of airway and for adequate ventilation Check for adequate circulation Treat as needed -—flush the skin for chemical injuries, remove clothing, 100% O2 for carbon monoxide poisoning Prevent hypothermia -— only cool for < 10 minutes co Il, EMERGENT PHASE/Resuscitative phase — main concerns are hypovolemic shock and edema Airway management: may need intubation R/T edema or swelling of the airway, 100% humidified 02 [Date] Page 7 Relieve itching Psychological support: patient may have permanent disfigurement due to scarring, assess for coping skills and family support Rehabilitation phase © PT/OT co Assessment Alteration in skin integrity o Susceptible to infection and hypothermia Edema co Burnedand unburned tissue = Increased capillary permeability o Severity Superficial (first degree burn) Partial thickness (second degree burn) Deep partial thickness Full thickness (third degree burn) Burn wounds mature or progress within the first few days May be hard to differentiate between partial & full thickness wounds o Zone of Coagulation (inner) = Site of greatest heat transfer = Irreversible skin death occurs © Zone of stasis = Salvageable area however infection and inappropriate volume resuscitation hinders this co ZoneofHyperemia (outermost) = Vasodilatation and increased blood flow = Minimal cell death = Spontaneous recovery can occur Rule of Nines © Total body surface area (%TBSA) o Used in Prehospital Setting o Bodydivided into surface areas of 9% Lund and Browder Method o Highlyaccurate © Usedin Hospital Setting Berkhow Method © Infants and Children Depth of Injury Physiological Response [Date] fo} fo} Page 8 Increased capillary membrane permeability ->shift of protein, fluid, lytes from intravascular to interstitial (third spacing) Due to loss of intravascular proteins, additional fluid is pulled into the interstitial tissue further increasing edema Nais shifted into the cells - with water -> cellular swelling -> further edema Location of burns + Face/mouth fe} oO Singed hairs of nares noticed at scene by paramedics or first responders = Intubate at scene Due to chance of edema occurring over time in transit to hospital and will be unable to intubate or make it difficult Assess lung sounds first upon arrival Assess lung sounds again to see if they will need to be intubated — any signs of adventitious lung sounds Protect airway —look to intubate if there is any compromise or threat to airway at all + Extremities fe} fo} Single area burns = Topical treatment Circumferential = Distal pulses « Make sure circulation has not been compromised «Inform providerIMMEDIATELY if decrease in pulses « Passible fasciatomy * Hands/feet fo} fo} fo) Goal = Must preserve movement/function of the hands/feet = Dorange of motion even when healing = Ifyou don’t use it you lose it Look for the normal and the abnormal findings Nutrition + Increased need for calories due to increase metabolism of healing fo} Negative nitrogen balance Treatment + Fluid Resuscitation fo} Massive fluid resuscitation = Effect is monitored based on urine output of 30-50mL/hr o Complications of burns [Date] Page 10 * Increase room temperature to create a warm environment for patient during wound care * Open method—open to warm dry air with fluidized bed to prevent pressure wounds and facilitate removal of * Occlusive method -sealed on all sides * Semi open method —changed every other day + Autograft © Only permanent measure of grafting for burn oO Tiny water blisters 2-6 weeks after wound closure—heal within 3-5 days, keep clean co Mildskin cream for 6-8 weeks (Bacitracin) © Pruritis © Benadryl and moisturizing creams co Hypertrophic Scarring © Tubular support bandages 5-7 days after grafting is completed © Worn for 6 months to 1 year after grafting ° * Assessment and nursing care of burns of different parts of the body Rehabilitation phase oO o Endocrine o Hyperglycemia * Results from increased gluconeogenesis & decreased peripheral use of glucose * Ptsare high risk for hyperglycemia due to: © Stress of illness © Hormone response to illness o CCUenvironment + Hyperglycemia causes harm in critical illness: o Decreased WBC production © Osmoticdiuresis © Poor wound healing o Decreased erythropoiesis o Increased hemolysis © Increased thrombosis © Vasoconstriction o Neurondamage o Decreased resp muscle function © Impaired gastric motility + FarALL pts, glycemic level is a priority © No longer using “Tight glycemic control” © Keep BS between 110-180m¢/dl o Hospitals have Glycemic Protocols o Hypoglycemia * Tube feeding are reduced or d/c without adjusting insulin dose [Date] Prior dx of DM Sepsis Use/change in vasoactive support, corticosteroids, inotropic drugs Hypoglycemia is preventable ° o Pancreatic Endocrine Emergencies ¢ Carbohydrate metabolism © Increases glucose transport acrass cell o Promotes storage glucose in liver & muscle * Fatmetabolism o Increases triglycerides o Stimulates fatty acid synthesis © Increases fat in adipose tissue + Protein metabolism o Increases amino acid transport across cell o Helps P synthesis & stops P breakdown * Counter regulatary hormones - released in response to stress & decreased glucose levels o Glucagon © Somatostatin o Catecholamines 2 Growth hormone o Cortisol ¢ Reduction of effective action of circulating insulin PLUS elevation of counter regulatory hormones ¢ Thereis increased hepatic & renal glucose production but glucose can not be utilized by the peripheral tissues * Endocrine emergency ° o DKA * Diabetic ketoacidosis + Usually Type 1 diabetics « Surgery, trauma, illness, cardiac, psychogenic «Maybe first time patient is informed of diagnosis « Ex. Insulin pump fails o Battery fails © Noinsulin infused © Patho ¢ Highextracellular glucose->osmotic gradient ¢ Fluid moves out of cells (osmotic diuresis) « Glycosuria occurs when renal threshold of glucose is met (approx BS 300) Page 11 [Date] Page 13 © Caused by inadequate insulin secretion © Undiagnosed or untreated diabetes o Hyperalimentation o Administration of hypertonic IV fluids o Administration of steroids. © Elderly with no compensatory mechanisms © and major illness « Patho « Similar to DKA but lower levels of free fatty acids->no ketosis ¢ Enough insulin being released in the body to prevent ketosis, but not enough insulin to prevent hyperglycemia ¢ Higher levels of glucose & hyperosmolarity->severe dehydration + Developsinsidiously, over weeks to months ¢ Older pts, type IDM ¢ Stress and infection likely to raise glucose levels and contribute to disease acute progression ¢ Fluid Volume deficits * Potassium levels critical as normalizes « Sx/Sx * Polydipsia « Nausea, vomiting, anorexia, ¢ Polyuria abdominal pain + Polyphagia (usually with weight «Signs of dehydration loss) « Mentation ranges from lethargy to « Dyspnea coma (with HHS) ¢ Generalized malaise «Absent deep tendon reflexes o Treatment Fluid resuscitation with normal saline; F/E replacement Insulin drip When glucose comes down to about 250, then lantus 10 units sq is given co Then switch over to drip with dextrose and insulin then de © Self management program © Diabetes education co Nursing care Hourly fingersticks Bring down 100 per hour o Labs Elevated glucose greater than 800 * Hourly fingersticks with insulin drip No ketones » Regular Insulin Acidosis [Date] ¢ Diabetes Insipidus = Effects ADH co Serum sodium © Extracellular osmolality © Inadequate blood volume o Trauma o Stress © Anxiety = Inhibits ADH © Decreased plasma osmolality © Increased intravascular volume co Risk for hypovolemic shock = Patho Page 14 Exercise Pain Exposure to heat Nausea Hypoxia Nicotine and dilating effects Alcohol ingestion Pituitary surgery = There are decreased levels of ADH-> diuresis and dehydration = Primary cause: trauma to posterior pituitary or hypothalamus = head trauma = Neurosurgery = Other causes: nephrogenic, excessive water intake = Can be temporary or permanent = Clinical Presentations «Pale, dilute urine © Polyuria © Urine output varies from 2-15 L/day o Urine output greater than 200 ml/hr for 2 hr should be reported to a physician + Polydipsia + §/Shypovolemia © Hypotension © Drymucous membranes o Decreased skin turgor © Tachycardia o Weightloss co Low RAP & PAOP + Neuros/s with hyponatremia & hypovolemia = Causes = Traumato pituitary = Sx/Sx [Date] Body secretes excessive ADH Fluid retention/ Risk for Fluid overload Dilutional hyponatremia Inability to secrete a dilute urine Treatment is to withhold fluids oO o Cerebral Salt Wasting (CSW) similar but.... Volume depletion Decreased serum Na Increased urine sodium Treatment isto replenish fluids o Etiology Occasionally caused by pituitary tumor. More commonly caused by a bronchogenic (oat cell) or pancreatic carcinoma./small cell Lung cancer Head injuries Endocrine disorders (Addison’s disease) Pulmonary disease (pneumonia, lung abscess, TB) Central nervous system infections (and tumors) Drugs such astricyclics, oral hypoglycemic agents, diuretics and cytotoxic agents o Sx/Sx Fluid overload = §/S mainly neurologic = Decreasedtendon Retention and nonspecific reflexes Water retention = Seizures Hyponatremia = Headache = Coma Serum hypo- = Decreased mentation = Mayleadtodeath osmolality = Lethargy = Personality changes = Nausea/vomiting/dia rrhea/anorexia © Labs Hallmark: © hyponatremia (<135 mOsm/kg) & hypo-osmolality (<280 mOsm/kg) occurring simultaneously with inappropriate concentrated urine hyperosmolality low-volume urine (more than 900mOsm/kg) Increased urine sodium Hemodilution may decrease BUN, creatinine, albumin Serum sodium below normal o Treatment Fluid restriction equal to intake Page 16 [Date] Restrict fluid intake to prevent water intoxication Correct electrolyte imbalances Daily weights 3% hypertonic saline and lV furosemide Supplemental potassium Demeclocycline and lithium carbonate interfere with the normal ADH oO © Nursing Assess neuro status for subtle signs: Fatigue Weakness Headache Changes in LOC Seizure precautions esp if Na<120mEq/L Fluid limitation may be set at 800- 1000mI/day Oral intake should be equal to the urine output until normalization of the serum sodium Give hypertonic saline fluids slowly (no greater than 4mL/kg day) Monitor for HF Accurate 1&O Oral care, mouth rinsing without swallowing, hard candy, chilled beverages Fluid restriction but encourage to choose fluids high in Na Beef boullion, tomato juice, milk Early s/s to report: o Wtgain © Lethargy o Weakness o Nausea co Mentalstatus changes © Significance of adherence to fluid restriction © Meds; dose, action, side effects © Importance of daily weights Over correction of sodium can cause central pontine syndrome Shock, Sepsis, MODS All types of shock- Distributive, cardiogenic, hypovolemic, obstructive Shock Distributive Septic, neurogenic, anaphylactic Decrease perfusion Cardiogenic Cardiomyopathic Arrhythmic Mechanical Page 17 [Date] Page 19 © Levophed-increases systemic vascular resistance and improves tissue perfusion — used when fluid resuscitation fails. co Nitroglycerine— vasodilator, not given in inferior wall mi due to chance of subsequent arrest © Dobutamine ec Sodium Nitroprusside (nipride) + Side effectstotreatment o Ifyou gave fluids = Fluid overload = MODS = Progressive failure of two or more organs = High mortality rates and the most leading cause of later mortality in trauma patients. 0 The more organs that fail the higher the mortality rate. = Most common cause — sepsis & septic shack = Populations at risk oO Trauma ao Burns o Hypovolemic shock oO Sepsis a Pancreatitis = Primary 5 Direct injury 5 Impaired perfusion = Secondary 50 Widespread systemic infection involving organs not involved in original insult 5 Excessive biochemical mediators causing organ damage = Vasodilation causes uneven distribution of blood to organs = Increased capillary permeability 0 Third spacing = There is sequential failure of organs o ARDSusually develops first 5 Hematologic dysfunction = Petechiae, bleeding, thrombocytopenia, DIC 0 Hepaticdysfunction = Hypoglycemia, jaundice, increased liver enzymes, decreased albumin «Cardiovascular 5 Renal dysfunction 5. Cerebral dysfunction—cerebral ischemia, infarction = Prevention—eliminate the source of infection! = Earlydetection—remove potential source of infection 0 Abscess, necrotic tissue, reduce number of invasive procedures a Antibiotics [Date] Page 20 Maintaining tissue oxygenation — maintain Po2 at 88-92%, intubate if necessary Restore intravascular volume—isotonic saline Dialysis if renal failure Nutritional support —enteral feedings Causes Immunocompromised o Chemo, leukemia, lymphoma © 1x-—private room, decrease exposure, reduce infection/sepsis risk = Avoid central line use—infection risk = Check for neutropenia—avoid processed foods, raw, under cooked Treatment Fluid bolus of normal saline o 30mL/kg—may repeat if doesn’t work then o Levophed = Bolusis initial treatment due to need to treat low systemic vascular resistance associated with septic shock. © Blood cultures prior to antibiotic therapy © Then broad spectrum antibiotic therapy until C&S refines choice of antibiotics which the organism is susceptible to © Medsto support BP suchas dopamine, Dobutamine for contractility Hematology B-12 Deficiency Anemia Patho Decr. Gastric production of HCI & intrinsic factor= B 12 absorption Nursing Implications Lifetime tx Ongoing patient teaching HF prevention Special oral hygiene Monitor for persistent neurological deficits Clinical Presentation Inhibited growth of all cells: anemia, leukopenia, thrombocytopenia Demyelination of peripheral nerves to spinal cord Triad: weakness, sore tongue, paresthesias Dx Schilling Test: [Date] 
