NUR 421 Final Blueprint 2023 PDF

Tetralogy of fallot (1 question): 4 structural defects: decreased pulmonary blood flow Right ventricular hypertrophy Aortic displacement (overriding aorta) Pulmonary stenosis Septal defect (ventricular septal defect) Signs: Cyanosis, SOB, i...

Tetralogy of fallot (1 question): 4 structural defects: decreased pulmonary blood flow Right ventricular hypertrophy Aortic displacement (overriding aorta) Pulmonary stenosis Septal defect (ventricular septal defect) Signs: Cyanosis, SOB, increased RR during activities (feedings, crying) Activity intolerance - low oxygen levels Harsh systolic murmur and thrill Poor feeding/FTT - decreased in meeting milestones Treatment: KNEES TO CHEST FOR INFANTS ○ Squatting for toddlers ○ Used for cyanotic episodes ○ Increases SVR to increase pulmonary blood flow Oxygenation Calm them down IV fluids to decrease right to left shunt Meds to increase preload Surgery if needed Heart failure (1 question): signs/symptoms: Acquired heart disease Could be a consequence of a congenital heart defect, or acquired through another disorder (i.e., myocardial dysfunction following surgical intervention for CHD, hypertension, fluid volume overload, anemia, cardiomyopathy, etc). Symptoms: failure to gain weight or rapid weight gain (fluid retention), failure to thrive, difficulty feeding/sucking and then tiring quickly, SOB, syncope, decreased number of wet diapers Left-sided HF will present with fluid in the lungs, right-sided HF will present with edema in the extremities Treatment: Promote oxygenation: position the infant or child in a semi-upright position to decrease work of breathing, suction as needed, administer oxygen as ordered Support cardiac function Provide adequate nutrition: infant may require as much as 150 calories/kg/day, older children will also require higher caloric intake, offer small and frequent meals/feedings Promote rest: ensure adequate time for sleep and attempt to limit disturbing interventions, provide age-appropriate activities that can be performed quietly or in bed (e.g., books,  coloring, video games, board games) Cluster care Administer medications (diuretics, digoxin, ACE inhibitors) Medications: Rheumatic fever/heart disease - assessment/treatment (1 question): 5 major manifestations: Carditis Migratory polyarthritis Subcutaneous nodules Erythema marginatum Sydenham chorea Treatment: Focus on ensuring compliance with acute course of antibiotics and prophylaxis following initial recovery Offer support with abnormal movements Educate child on sudden jerky movements - will disappear Med math (1 question): Max safe dose: ○ What is the maximum safe dose of tylenol for an infant who weighs 10 kg? The recommended safe dose range for tylenol is 10-15 mg/kg/dose q4-6 hours. ○ The max dose is 15 mg/kg/dose. Simply multiply. ○ 10kg x 15 mg= 150 mg/dose ○ If it is dose, do NOT divide extra ○ If it is day, DIVIDE by how many times the child gets the dose Urine output: ○ mL/kg/hr ○ 200ml/10kg/12hr =1.7 ml/kg/hr ○ 1.7 Fluid maintenance: ○ 100 mL/kg x 0-10 kg= ○ 50 mL/kg x 10.1-20 kg= ○ 20 mL/kg x >20.1= ○ Total = 24 hour total fluid required to maintain hydration ○ Divide by 24 to get the 24 hour fluid maintenance rate ○ Example: What is the hourly fluid maintenance for a patient who weighs 27.84 kg? (100ml x 10kg) + (50ml x 10kg) + (20ml x 7.84) = 1,656.8/24= 69 ml/hr Coarctation of the aorta (1 question): Obstructive defect (narrowing of the aorta) Most often near the area near the ductus arteriosus  Narrowing can be preductal (between subclavian artery and ductus arteriosus) or post ductal (after ductus arteriosus) Blood flow is impeded causing pressure to increase in the area proximal to the defect and decrease in the area distal to it BP is increased in the heart and the upper portions of the body BP is decreased in the lower extremities of the body At risk for aortic rupture, aortic aneurysm, and CVA due to elevation in BP Assessment: 4 point BP - can see the difference between upper and lower extremities by 20 mmHg Echocardiogram: may disclose the extent of the narrowing and evidence of collateral circulation Chest radiography: may reveal left sided cardiac enlargement Rib notching indicative of collateral arterial enlargement CT/MRI: may be done to provide additional evidence about extent of coarctation and subsequent effects Treatment: Pharmacology - digoxin (1 question): Increases contractility of the heart Therapeutic range is 0.8-2.0 DO NOT GIVE SECOND DOSE BEFORE 12 HOURS - even if they spit it out Hypokalemia increases risk for toxicity Signs of toxicity: n/v, vision changes, dysrhythmias HOLD WHEN: HR less than 90 for infants, less than 70 for older children, and less than 50 for adults General congenital heart defect assessment, interventions, teaching (2 questions): Assessment/Interventions:  Cyanotic episodes: ○ knees to chest or squatting, oxygen as ordered For tetralogy of flow Sats may be lower at baseline due to mixing of oxygenated and deoxygenated blood Poor feeding: ○ fast flow or cross cut nipple, I/O, daily weight, do not feed longer than 20 min, up to 150 calories/kg/day Feeding baby longer than 20 min can cause them to burn more calories Can be breastfed, but needs to be hemodynamically stable growth/development/family coping: age appropriate explanations, time for questions, promote family bonding, positivity, and encouragement infection/dental care: hand washing, preventing gum disease, prophylactic antibiotics Surgery: post op dressings, PICU, possible feeding tube, increased caloric need, breast feeding if stable ○ Mother may need to pump ○ May have to fortify breast milk ○ Dont necessarily need formula Education: defect/treatments, surgery and post op care, medications, infection Teachings: DVT & PE (4 questions each topic): Medications to prevent & treat; associated labs Anticoagulants: reduces the formation of other clots and prevents other clots from getting bigger Factor Xa Inhibitor: prevents conversion of prothrombin to thrombin ○ No reversal agent ○ Requires lab monitoring Warfarin: ○ Avoid food with vitamin K (dark, leafy greens)  ○ Monitor PT/INR ○ Antidote: vitamin K Thrombolytics: ○ Break up and dissolves existing clots ○ Used when pt are hemodynamically unstable ○ Monitor bleeding Heparin (unfractionated or low molecular weight/lovenox) ○ Monitor APTT ○ Antidote: protamine sulfate Patient education: Disease process/lifestyle changes Medication side effects Bleeding precautions: encourage to use electric razors, soft toothbrushes, no flossing) Diet: what to avoid when on warfarin s/s of recurrent PE/DVT: ○ Unilateral extremity edema and pain ○ Redness and warmth ○ Pleuritic chest pain and difficulty breathing Clinical manifestations: Dyspnea Pleuritic chest pain Tachypnea due to decreased cardiac output Tachycardia due to hypoxemia Pulmonary htn (blood can’t move past the obstruction) Hemoptysis Crackles Interventions: surgical and nursing -IVC filter vs. embolectomy vs. thrombolytics (when to use each) Elevate HOB: IV fluids: decreases the viscosity of the blood, watch for fluid overload Bleeding precautions Be prepared for intubation and resuscitation Surgical interventions Embolectomy: physical removal of the clot ○ Catheter is used to destroy the clot and aspirate ○ More common - requires CABG IVC filter: done if pt cannot be on anticoagulation therapy and/or has active bleeding or if another PE could be fatal ○ Filter traps emboli  Thrombolytics: can be used when pt are hemodynamically stable ○ Breaks up and dissolves existing clots Balloon angioplasty: Stent placement: Prevention: Ambulation if tolerated Venous thromboembolism prophylaxis Low molecular weight heparin (lovenox) Warfarin Fondaparinux Mechanical VTE prophylaxis: ○ SCD → min 18 hours ○ Foot pumps ○ Ted hose/compression socks OR Complications (5 questions): Anesthesia complications (MAC, local- adverse reactions) MAC: decreased LOC but maintains patent airway ○ Pt is able to respond to verbal commands and physical stimulation ○ Pt can hear what is going on - be mindful of conversations Local: can range from mild (hives/itching) to severe (anaphylactic reactions, facial swelling, trouble breathing, GI upset) ○ Usually due to overdosages, rapid absorption, or hypersensitivity ○ Mild: hives/itching ○ Severe: acute anaphylactic rx - wheezing, trouble breathing, facial swelling, GI upset General: reversal unconscious state ○ Can cause hypoxia → always monitor O2 saturation ○ Can cause malignant hyperthermia ○ htn/hypotension ○ fluid/electrolyte imbalances ○ Residual muscle paralysis ○ Neurological problems Universal Time out procedure/verification: Verify correct: patient, procedure, surgeon, position, equipment, imaging studies Presence of implants is confirmed Administration of antibiotics is necessary Correct surgical site is marked on patient Include every person in the room on the chart Malignant hyperthermia (clinical manifestations, treatment)  Complications: Triggering agent (volatile gas with exception of nitrous oxide/succinylcholine) increase intracellular calcium → sustained muscular contraction Hereditary disorder of skeletal muscle - pt who lack genes of calcium regulation results in increase in intracellular calcium Most significant sign: muscle rigidity - but first sign is unexplained tachycardia Treatment is dantrolene “Sustained muscular contractions r/t an increase in intracellular calcium ion concentration” Muscle rigidity/spasms → MOST SPECIFIC SIGN Tachycardia that is unresponsive Hyperthermia (late sign of condition) Dark urine Acidosis Cardiac dysrhythmias Rapid rise in end tidal CO2: normal range is 35-45 Htn Hypoxia treatment: DISCONTINUE THE ANESTHETIC THAT IS CAUSING THE CONDITION AND SWITCH IT OUT Dantrolene: muscle relaxant - prevents further release of calcium into the skeletal muscle Ensure O2 stays about 95% Cold IV fluids, ice packs, cooling blankets Retained surgical instrument risk factors: Pt with high BMI Emergent procedure or unexpected change during procedure Multiple surgical procedures done at once Staff turnover during procedure Lack of communication Advanced Cardiac dysrhythmias (6 questions): Identify lethal dysrhythmias & nursing/med interventions (Vfib, V tach, Asystole) Ventricular Fibrillation: Identifying characteristics:  ○ multiple chaotic impulses that are rapidly firing ○ Stops cardiac output and causes death ○ No P waves or QRS complexes Treatment: ○ Defibrillation ○ Chest compressions ○ ALCS ○ IV access for medications ○ Maintain airway Rhythm identification: shaky or quivering line that can be coarse Ventricular Tachycardia: Identifying characteristics: 3 or more PVCs in a row Treatment with a pulse: ○ Amiodarone (antiarrhythmic medication) ○ Electrolyte replacement ○ Cardioversion Treatment without a pulse: ○ CPR ○ Defibrillation ○ ACLS - maintain airway and administer rescue medications Asystole: Identifying characteristics: NO MEASURABLE ELECTRICAL ACTIVITY Treatment: CPR - no defibrillation since it can kill any small electrical impulse the patient could have ○ Make sure to confirm that this is asystole and it is not just the lead off the pt ○ Start CPR, ACLS ○ Determine the cause ○ Medication: epinephrine Rhythm identification: flat line Heart blocks: rhythm identification Caused by delay or blockage of electrical conduction at the AV node If right coronary artery becomes partially or completely blocked, AV node is deprived of oxygen and becomes ischemic - electrical impulses in atria will have difficulty traveling AV node to the ventricles along usual path Causes: primary cause for most AV blocks is acute coronary syndrome - unstable angina, acute NSTEMI, acute STEMI, electrolyte imbalances and med toxicities 421 final guide pg 18 First degree AV block: Identifying characteristics: ○ Looks similar to NRS ○ PR INTERVAL IS PROLONGED - more than 0.20 sec or 5 blocks long ○ Atrial depolarization is delayed in the AV node ○ Rhythm: regular ○ Rate: that of underlying rhythm = PRI is greater than 0.2 seconds ○ QRS: usually normal Interventions: ○ Treatment is not typically required for first degree AV block unless having symptoms (rare occurance) ○ If symptomatic, underlying causes are treated to alleviate the symptoms Second degree AV block type 1: Identifying characteristics: ○ ALSO KNOWN AS WENCKEBACH OR MOBITZ 1 ○ More P waves than QRS complexes and PR interval gets progressively longer until QRS IS DROPED ○ “Longer, longer, longer, DROP” Interventions: ○ Considered only if pt is symptomatic ○ Pt who cannot tolerate loss of CO may experience dizziness, lightheadedness, and SOB 421 final guide pg 19  ○ Treatment for symptomatic pt is atropine 0.5 mg IVP to stimulate the heart to beat faster or use temporary pacing ← this is rare Second degree AV block type 2: Identifying characteristics: ○ DROPS QRS COMPLEXES BUT PR INTERVALS ARE THE SAME EXACT LENGTH WITH EACH COMPLEX ○ Life threatening dysrhythmia since it can quickly progress to third degree AV block ○ Non conducted P waves Interventions: ○ Dependent on pt symptoms ○ If pt is symptomatic, TEMPORARY PACING IS TREATMENT OF CHOICE ○ Transcutaneous pacing (TCP) is fastest pacing option to externally pace the heart ○ If time permits, other pacemaker options could be considered, such as a temporary transvernous pacemaker or permanent pacemaker Third degree AV block: Identifying characteristics: ○ Occurs when the AV node is completely blocked and prevents any impulses from entering or exiting ○ There is no communication between atria and the ventricles ○ ECG SHOWS MORE P WAVES THAN QRS COMLEXES 421 final guide pg 20  ○ QRS COMPLEXES MARCH OUT REGULARLY AND INDEPENDENT OF THE P WAVES ○ Sometimes the P waves are hidden within QRS complex or the T wave - important to march out p waves to see where they fall ○ Atrial rate: 60-100 bpm ○ Ventricular rate: 2 mmoL/L ○ Obtain blood cultures prior to administering antibiotics ○ Administer broad spectrum antibiotic ○ Administer crystalloid if pt is hypotensive or lactate level is at least 4 mg/dL ○ Administer vasopressors if blood pressure is unresponsive during or after fluid resuscitation; maintain MAP at 65 mm Hg - restores hemodynamic stability Blood work: serum lactate, blood cultures, CBC, coagulation studies, liver function tests, arterial blood gas Antibiotics Fluid resuscitation: crystalloid like NS or LR Vasopressors: help maintain MAP ○ Norepinephrine to help maintain MAP greater than 65 - indicator that organs are properly perfused DIC patho/symptoms (1 question): Thrombotic (clotting) phase: Large amounts of thrombin released → excessive production of fibrin clots Clots lodge into microvasculature that causes ischemia and necrosis/cyanosis → typically in digits/tip of nose These pt are at risk for PE, thrombophlebitis and stroke Bleeding phase: Starts with fibrinolysis Body attempts to break down and remove clots Increase in dibrin degradation products - anticoagulants Results in decreased ability to form fibrin clots Labs: increased d-dimer, increased fibrin degradation, decreased fibrionogen, decreased platelet, prolonged PT/APTT, decreased antithrombin 3 levels MODS (2 questions): Etiology: Apoptosis is accelerated in sepsis - causing MODS Widespread damage to vascular endothelium which results in inflammation - causes increased cap permeability and vasodilation of sepsis Microvascular dysfunction that causes maldistribution of blood flow in capillary beds Enhanced coagulation leads to clots in microcirculation (obstruction blood flow) Acceleration of production of glucose is harmful - causes increased cellular oxygen demand Toxicity of mitochondrial cells limits the use of oxygen Signs of organ Injury Initial system that is affected is respiratory - look for ARDS Then renal, hepatic, and GI 3 or more systems associated with 80-9990% mortality rate 100% mortality rate if cardiovascular and neurological systems are involved Interventions Supportive Infection control Maximize oxygenation restore/maintain intravascular volume ICP (4 questions): Normal range: less than 15 mmHg Catheter pros/cons Intraventricular catheter: Located in lateral ventricles - only one that can drain excessive CSF Pros: ○ Monitor pressure AND drain CSF ○ “Gold standard” - tip of catheter is in lateral ventricle ○ Can be inserted at bedside or OR Cons: ○ Increased risk of infection ○ Measurement drifts overtime Intraparenchyma sensor/probe: in the brain Pros: ○ Accurate measurement of ICP with less mechanical drift ○ Can be inserted bedside or OR Cons: inability to drain CSF Subarachnoid Bold (SAB)  Pros: ○ Can be inserted bedside or OR ○ Lower rate of infection because it does not have fluid reservoir Cons: ○ Inability to drain CSF ○ Measurement drift Cushing’s triad: htn, bradycardia, irregular breathing pattern Treatment (medications): Osmotic diuretics - Mannitol Cause ISF to shift into the vascular space where it is filtered and eliminated by the kidneys Causes dehydration Monitor serum osmolarity High concentration sodium chloride (3%NaCl) Make sure levels are not rising too quickly Increasing too fast can cause damage to sheath covering the neurons – can cause generalized weakness on both sides of body Burns (5 questions): Complications Compartment syndrome: Any circumferential burn to extremity is at risk for this ○ Fluid leaves interstitial spaces - exerts pressure within the tissues and results in swelling in muscle compartments Affected extremities should be elevated Assess pulses hourly Clinical manifestations: diminished pulse, numbness, tingling, pain with flexion or extension Requires surgical intervention to salvage limb  Treatment: elevate the limb, assess pulse, call provider stat Escharotomy: surgical incision through eschar; performed to relieve the pressure ○ Should only extend through eschar and into immediate subcutaneous fat ○ May be performed at bedside using scalpel or electrocautery device Fasciotomy: performed when burn extends into muscle and is more commonly see who have sustained electrical injury and have developed compartment syndrome ○ Incision that extends through subcutaneous fat and muscle fascia ○ Allows for expansion of muscle compartment ○ Done under sterile conditions in operating room Burn shock: Due to massive fluid shift (intravascular - interstitial space) ○ Due to increased vascular permeability Results in edema and decrease in intravascular volume ○ Leads to increases hematocrit level and increase in blood viscosity - causing shock s/s: ○ Hypotension ○ Tachycardia ○ Decreased urine output ○ Altered mental status ○ Shifts in potasium Potassium will initially be elevated - due to damage to cells and vascular space Potassium and sodium leaks into the intravascular space - causing the patient to be hypokalemic and hyponatremic Suspect inhalation injury if: Toxic effects of heat/chemical products of combustion on lungs and in the airways Respiratory epitheiulm may be damaged as result of inhaled gases and particulate matter Mucus production/impaired ciliary function may result - may lead to cell death and sloughing of respiratory tract If pt was in enclosed space - house/car fire Burns to face, neck, or chest s/s: facial burns, singed nasal/facial hairs, inability to swallow, hoarseness, crackles Calculate fluid resuscitation: Used for pt who suffered burns greater than 20% Objective is to maintain tissue perfusion and organ function while avoiding potential complication of inadequate/excessive fluid Fluid of choice: LR with 2 large bore IV Uses rules of nines:  ○ Anterior chest - 18% ○ Anterior arms - 9% each ○ Anterior legs - 18% each ○ Peri area - 1% ○ Palms - 1% each Based on age, weight in kg, TBSA, and whether the burn was electrical or not ○ TBSA should be greater than 20% ○ Give half of solution for first 8 hours and give the other half the next 16 hour ○ 4 ml - electrical burns ○ 3 ml - pediatrics ○ 2 ml - everyone else ○ Urine output - 0.5-1 mL/kg/hr UO for non-electrical burns should be 0.5 mL/kg/hr UO for electrical burns should be 1 mL/kg/hr System effects: Cardiovascular: ○ Greatest threat to pt with major burn injury - burn shock Mix between distributive and hypovolemic shock Results secondary to massive fluid shift ○ Electrolytes, water, plasma, proteins leak out of intravascular space → interstitial space because of increase in capillary permeability - results from body’s initial inflammatory protective mechanism ○ Large fluid loss within the intravascular space increases viscosity of the blood - sluggish blood flow, decreased oxygen deliver, decreased CO ○ Pt will present with elevated hematocrit ○ If fluid resuscitation is not adequate, burn pt begin to demonstrate manifestations of shock: hypotension, tachycardia, reduced urinary output, altered mental status ○ If this progresses without proper fluid resuscitation, pt will decompensate and result in multisystem organ failure ○ Burn shock slowly begins to resolve after 24-48 hours after injury - fluid gradually returns to intravascular space and urinary output continues to increase secondary to pt diuresis Fluid electrolyte: ○ Main electrolytes to worry about: sodium and potassium ○ Initially will start with hyperkalemia due to release of potassium from damaged cells into vascular space ○ As fluid shifts, potassium and sodium leak out into intravascular spaces and hypokalemia and hyponatremia result ○ Replacement therapy is warranted Renal: ○ Due to initial decrease in circulating blood volume, may be impaired secondary to  decreased renal perfusion ○ Destruction of RBC results in free hemoglobin being released into the body following a major burn injury ○ If pt has sustained muscle damage as result from burn injury, myoglobin may be present in blood stream ○ If resuscitation is inadequate, myoglobin and hemoglobin have potential to occlude renal tubules - causes acute tubular necrosis ○ Usually seen with electrical injuries Gastrointestinal: ○ Complications secondary to a decrease in both nutrient absorption and gastrointestinal motility ○ NG tube placed in pt with large burns for long-term feeding access and to relieve initial gastric distention, nausea, vomiting ○ Pt who suffer significant injury and require massive fluid resuscitation are at risk of developing abdominal compartment syndrome Metabolic: ○ Puts pt in constant hypermetabolic state ○ Double normal resting energy expenditure and greatly increase pt caloric need ○ Factors affecting metabolic rate: age, gender, infection, concomitant trauma, pain, surgery, sleep, ambient temperature ○ Without additional nutritional support for those with burn greater than 20% TBSA, wound healing will be impaired ○ If pt has open wounds, they can have impaired thermoregulatory function; keep room warm, give heating blanket, warmer Immunological: ○ High risk of infection and sepsis because of loss of protective function of skin, altered immunological defenses, and presence of open burn wounds ○ Loss of skin integrity is compounded by release of abnormal inflammatory factors - alter pt underlying metabolic profile ○ Systemic Inflammatory Response Syndrome (SIRS): occurs for pt with extensive burns - exaggerated inflammatory responses that occur in the body after injury and may precede in development of sepsis ○ Factors: change in mental status, increased fluid requirements, decreased urine output, decline in respiratory function pain management IV narcotics: ○ Morphine ○ Hydromorphone ○ Fentanyl ○ Morphine ○ NSAIDs Pain meds need to be on a schedule vs PRN to effectively manage pain CO poisoning: Symptoms: Carbon monoxide binds to hemoglobin, tissue hypoxia results when carbon monoxide levels are above normal Oxygen measurement by pulse ox is useless because of determination between oxygen and carbon dioxide saturating the hemoglobin is not possible Normal carboxyhemoglobin: less than 2%, 5-10% for smokers May cause cherry red discoloration of skin in pt with carbon monoxide levels higher than 40%, often seen in half of cases Clinical manifestations: Headache, confusion, n/v, dizziness, death Interventions: 100% non-rebreather mask Hyperbaric chamber speeds up the process Older adult risk factors: Older adults are not able to tolerate aggressive fluid replacement resuscitation and may not be candidates for surgery Small burns can be fatal for older adults Trauma (5 questions): Primary survey; ABCDE Identifies life threatening conditions and institutes management of care A - airway: Priority interventions: open airway, provide oxygen, prepare for advanced airway If airway is not patent, open and clear the airway using jaw thrust ○ ALWAYS USED FOR TRAUMA PT WHEN SPINAL CORD INJURY IS SUSPECTED TO PREVENT PRIMARY OR FURTHER INJURY TO SPINAL CORD ○ Also effective with creating good seal with face mask of bag-mask device Make sure airway is patent and clear Gasping, cyanosis, vomiting, drooling, hoarseness, LOC, anxiety, shallow respirations, accessory muscle use Turn them on their side Suction if necessary Jaw thrust method: push jaw forward away from the spine ○ Opens airway and keeps spine stable ○ Use with all trauma pt to avoid spinal injury B - breathing: Priority interventions: providing oxygen, diagnosisng/treating life threatening breathing injuries All trauma pt should receive O2 via face mask and should be placed on pulse ox  Chest xrays should be done to check for injuries Lab studies: arterial blood gases Any abnormal findings should be acted on If pt is in respiratory distress, hemodynamic instability and/or decrease breath sounds on injured side, SUSPECT PNEUMOTHORAX Tension pneumothorax: caused when air entering the pleural space cannot escape on expiration, increasing the intrathoracic pressure - results in fully collapsed lung and mediastinal shift RR, depth, chest rise and fall Apply oxygen via face mask Pulse ox s/s of ineffective breathing: noisy breathing, grunting, snoring, agonal, absence of RR C - circulation: Priority interventions: IV access and fluid resuscitation Pt needs 2 large bore IV (18g or greater) If IV is difficult, pt should prepare for central line Intraosseous cath is option if peripheral blood vessels are inaccessible Surgical cutdown may be performed as last resort - surgery that exposes a vein allowing IV cath placement Fluid resucitation is dictated by pt condition Starts with infusion of warmed isotonic crystalloid If blood products are indicated if pt is excessively bleeding IV access (isotonic crystalloids - LR) - 2 large bore needle Blood products D - disability: Neuro assessment - look for decreased LOC GCS E - environment/exposure: Assess front and back to look for additional injuries Temperature control (reduce the risk of hypothermia) - use warming blankets, warming light Secondary survey Done after primary survey If anything changes, the pt goes back to primary survey Full head to toe assessment, pain assessment, vitals, labs, diagnostic tests Insertion of foley catheter, NG tube, surgical stabilization Chest trauma interventions Assess pt ABC’s Medication administration Analgesics to help with pain and maintain deep breathing - morphine Chest tube interventions:  Cloudiness can indicate infection Red drainage greater than 70 mL/hr can indicate hemorrhage Continuous bubbling indicates and air leak Water levels can fluctuate with respiratory effort Document output and color Maintain a closed system Keep collection apparatus below chest level NEVER CLAMP CHEST TUBE Apply sterile occlusive petroleum jelly dressing after removal If chest tube is accidentally removed, apply in sterile water or sterile petroleum jelly to maintain negative pressure Trauma triad Hypothermia → coagulopathy → metabolic acidosis Hypothermia: causes peripheral vasoconstriction - decreases amount of oxygen that goes to organs and tissues ○ This causes hypoperfusion (results in lactic acidosis and coagulopathy) Coagulopathy: coagulation is inhibited - results in increased bleeding that can result in metabolic acidosis Can result in serious complications or death FAST - Focused Assessment with Sonography for Trauma Ultrasound that looks for free fluids in chest and abdomen Positive test indicates blood in abdomen or chest HHS (2 questions): Clinical manifestations Usually for type 2 DM Insulin deficiency and insulin resistance Leading trigger is infection Characteristics: hyperglycemia, hyperosmolality, and dehydration without significant ketoacidosis Polyuria, polydipsia, polyphagia, weakness, blurred vision, altered mental status Labs: Plasma glucose greater than 600 Serum osmolality greater than 320 pH greater than 7.4 Bicarbonate greater than 15 low/absent ketonemia Altered LOC Nursing interventions: Fluid replacement:  Normal saline (0.9% or 0.45) → give ½ NS if sodium levels are elevated Correct electrolytes: Less than or equal to 3.3 replace prior to insulin administration When administering insulin, it drives glucose into cells, but also drives potassium back into cells In order to prevent hypokalemia, keep potassium at 4.0-5.0 Administer insulin: Administer IV insulin Monitor blood glucose hourly Switch to SQ insulin when blood glucose is more under control Give dextrose if pt blood glucose is 200 or less to prevent hypoglycemia DKA (5 questions): Labs to confirm Blood glucose greater than 250 mg/dL Ketonuria (ketones in urine) and ketonemia (ketones in bloodstream) Arterial pH is less than 7.3 Serum bicarbonate is less than 18 Anion gap increases (greater than 12) Insulin mechanism of action Inadequate insulin for cells to obtain adequate glucose for normal metabolism Without enough insulin, body breaks down fat storage for energy → releasing fatty acids from adipose tissue ○ Liver converts fatty acids into ketone bodies (energy source) ○ Results in metabolic acidosis because ketones have a low pH ○ Glucagon and cortisol are released - leads to gluconeogenesis and glycogenolysis - results in severe hyperglycemia, hyperosmolality, and osmotic diuresis Nursing interventions IV fluids: Isotonic (normal saline) Not hypertonic because the blood already have too many solids - will worsen it If Na level is elevated, give ½ NS Dextrose: for blood sugar less than 200 - prevents hypoglycemia Insulin: Lowers blood glucose Inhibit acid production (when insulin is provided, preventing lipolysis) Intravenous - regular insulin Monitor BG hourly on IV insulin therapy Transitioning to SQ will need to have basal insulin at least 2 hours prior to d/c IV insulin to prevent rebound hyperglycemia, ketogenesis, metabolic acidosis Bicarbonate: Not routine Only recommended if pt arterial pressure is less than 6.9  Potassium: If less than 3.3 REPLACE PRIOR TO INSULIN ADMINISTRATION When insulin is administered, it drives glucose into cells, but also drives potassium back into cells (decreasing amount of potassium in blood) Goal: 4-5 mEq/L s/s: muscle weakness, cramping Spinal Cord Injury (5 questions): Clinical manifestations: Depends on the level of injury Inability to breathe (usually results from cervical injuries) Paraplegia will result from thoracic injuries Loss of bowel, bladder, sexual function Chronic pain Hypotension Impaired temperature control Neurogenic shock symptoms & treatment: Distributive shock occurs in pt with brain, upper thoracic, and cervical injuries Caused by sudden loss of autonomic nervous system signals to smooth muscle in vessel walls Results in loss of vasomotor tone and sympathetic innervation of the heart Cardiac output decreases bc the vessels lose tone - allows blood to pool Sympathetic pathways to the heart are blocked which cause bradycardia Clinical manifestations: vasodilation, bradycardia, body temp instability, hypotension, warm/flushed skin, increased lactate level due to oxygen not being perfused to organs, AMS due to lack of perfusion to brain Treatment: IV fluids, vasopressors, atropine for symptomatic bradycardia ○ If bradycardia is sustained, may need transcutaneous pacing or midodrine AD: symptoms and interventions Auto dysreflexia: syndrome of massive imbalance reflex sympathetic discharge occurring in 80% of pt with SCI above T5-T6 Clinical manifestations: htn, bradycardia, tachycardia, diaphoresis, SEVERE HEADACHE, flushing above and pallor below injury level Most frequent cause is full bladder, second is full bowel Evokes widespread vasoconstriction causing peripheral arterial htn Condition will resolve once stimulus is identified and removed Spinal shock: Occurs immediately after injury and applies to all phenomena surrounding spinal cord transection Results in complete but temporary loss of depression of all or most spinal reflexes Hypotensive due to sympathetic tone loss Usually caused by trauma in origin, can be caused by others Brain is unable to transmit signals to muscles - loss of sensation Clinical manifestations: flaccid paralysis of all skeletal muscles, absence of deep tendon reflexes, impaired proprioception, decreased visceral/somatic sensations, paralytic ileus, anhidrosis Can lasts for 24 hours or 1-6 weeks: return of reflex activity below the injury indicates end of spinal shock Halo traction device: Spinal immobilization to prevent further loss of function Device used to maintain cervical immobilization for specific types of cervical fractures Complications: Pin infections, skin breakdown, loosening/movement of pins, swallowing problems, possible dural tears Pressure injuries can develop under vest portion of the halo brace often result from improper vest size, poor vest application or insufficient padding Need to have meticulous skin care and assessment of early signs of skin irritation Reposition every 2 hours Assess the site for warmth, drainage - sign of infection Diabetes Insipidus (4 questions): Treatment & signs of improvement Diagnostics: Urine specific gravity of less than 1.005 and urine osmolality less than 200 mOsm/kg are key indicators Increases in sodium, serum osmolality, and hematocrit develop secondary to hemoconcentration Treatment: Mainly fluid management and medications In emergency, IV fluid administration is indicated with dextrose in water Monitor for hyperglycemia, volume overload, and correction of hypernatremia for IV administration of dextrose fluid  Desmopressin is drug of choice - synthetic analog of ADH Need to have frequent monitoring of fluid status, serum electrolytes and urine output Clinical manifestations: Dependent on significance of water loss Polyuria, polydipsia, nocturia are primary clinical manifestations Excessive loss of water leads to hemoconcentration - observed with elevations in serum sodium and hematocrit Pt may present with hypotension, tachycardia secondary to hypovolemia Patient education: Pt who are awake and alert with intake thirst mechanism need to maintain fluid volume by drinking adequate fluids Importance of taking medications (ADH replacement) as ordered: taking the meds (vasopressin/pitressin) at the same time daily mimics normal release and supports water reabsorption in kidneys Weigh daily at the same time on the same scale: weight is directly associated with water loss or gain, and changes of more than 2 lb per day should be reported Clinical manifestations: pt must understand patho and importance of fluid volume balance Overcorrection with DDAVP or pitressin may lead to fluid overload Resp (6 questions - includes ARDS): Signs of barotrauma: Stiffening of lungs and loss of compliance Increase the pressure and create a pneumothorax Overdistention of the alveoli can lead to an excessive amount of air entering into the pleural space, causing a tension pneumothorax This can be a life-threatening situation for the patient, and the nurse should notify the HCP immediately and prepare for chest tube insertion to allow removal of trapped air in the pleural space Assess for asymmetrical chest rise and decreased breath sounds over pneumothorax site; high-pressure alarm will alert Associated with high tidal volumes Avoid by using pressure control instead of volume control VAP prevention: Regular mouth care q 2 hours Brush teeth q 12 hours with CHG Suctioning of ETT routinely  Oropharyngeal suctioning Ventilator circuit should be changed per protocol Elevated HOB to 30 degrees to prevent gastric aspiration 421 final guide pg 43 ABG interpretation: Fully compensated: if pH is normal Partially compensated: if all 3 values are abnormal Uncompensated: if PaCO2 or HCO3 is normal and the other is abnormal If pH under the normal column, determine whether the value is leaning towards ACIDOSIS or ALKALOSIS and interpret accordingly 7.29/51/29 PaO2:87 SpO2: 98 ○ Partially compensated respiratory acidosis ○ Increase RR by having respiratory increase on vent settings, encourage deep breathing if they can ○ Can occur when weaning off the vent 7.45/30/20 PaO2:92 SpO2:100 ○ Compensated respiratory alkalosis ○ Decrease RR ○ May see when pt is crying/hyperventilating/too awake on vent ○ “Breathe into this brown bag” 7.49/30/24 PaO2:61 SpO2:88 ○ Uncompensated respiratory alkalosis ○ Pt needs oxygen due to O2 sats ○ Decrease RR ○ Increase FiO2 6.90/60/26 PaO2:50 SpO2 78 ○ Uncompensated respiratory acidosis ○ Consider giving bicarbonate ○ Increase RR to get CO2 down ○ Prone the pt since it can look like ARDS based off ABG If pH is under the same column as PaCO2, it is RESPIRATORY: ○ Respiratory ACIDOSIS: Possible treatment: bronchodilators to open constricted airways, supplemental oxygen, meds to treat hyperkalemia, antibiotics to treat infection, chest PT to remove secretions from lungs, removal of foreign body from airway, chest tube insertion to increase lung expansion, intubation to allow mechanical ventilation Interventions: maintain pt airway, monitor ABG/vital signs, administration of supplemental oxygen, assisting with intubation, monitoring potassium levels, administration of sedatives Complications: prolonged increased CO2 levels can lead to paralysis and  coma from cerebral vasodilation ○ Respiratory ALKALOSIS: Possible treatment: discontinuation/removal of causative agent, steps to reduce fever, elimination of source of sepsis, oxygen therapy to treat acute hypoxemia, diuretics to treat PE Interventions: assisting in achieving goal of reducing ventilation rate by encouraging slow, deep breathing; monitoring VS, providing emotional support Complications: seizures related to decreased oxygen-carrying capacity to cerebral cells and chest pain from cardiac/noncardiac causes related to anxiety and hyperventilation If pH is under the same column as HCO3, it is metabolic: ○ Metabolic ACIDOSIS: Possible treatment: treatment is to treat the underlying condition - sodium bicarbonate replacement neuralizes blood acidity with pH lower than 7.1 Parenteral fluid replacement to maintain fluid balance Rapid-acting insulin maybe needed to reverse DKA and drive potassium back into cells Antidiarrheals to treat diarrhea-induced bicarbonate loss Dialysis may be needed for pt with renal failure or cause by toxic reaction to med Interventions: specific to the underlying cause - include monitoring hemodynamic status through BP, pulse, RR, and cardiac rhythm Complications: if pH falls below 7.0, cardiac dysrhythmia may occur Happens as result of changes in cardiac conduction which occur in direct response in pH If caused by chronic renal failure, complications can include renal osteodystrophy ○ Metabolic ALKALOSIS: Possible treatment: depends on underlying cause Discontinue potassium wasting diuretics and nasogastric suctioning May be need to be administered antiemetic to treat underlying nausea and vomiting To increase renal excretion of bicarbonate, acetazolamide needs to be administered Interventions: specific to underlying cause but monitor hemodynamic status through RR, pulse rate, and cardiac rhythm Can administer IV fluid (0.9%NS) and electrolyte supplements Complications: dysrhythmias and coma may result from alterations in depolarization of neuronal and cardiac muscle cells  Acute Respiratory Distress Syndrome: Signs and symptoms First indication: increased work of breathing → dyspnea, tachypnea, and accessory muscle use Causes: sepsis, pneumonia, severe trauma, aspiration, massive transfusions, cigarette smoking, CABG, PE, drug/alcohol overdose Diminished or absent breath sounds (due to fibrotic lung changes and atelectasis) Anxiety and agitation (due to hypoxemia) SpO2 decreases causing FiO2 in increase Respiratory alkalosis due to hyperventilation - later that develops into respiratory acidosis Post intubation assessment Verify placement using end tidal CO2 device ○ Should be positive - will be negative if in esophagus ○ Can verify placement by assessing for symmetrical chest rise and fall with ventilation Ensure ETT cuff is inflated to about 20-25 mmHg ○ Any more can cause ischemia, pressure necrosis and tracheal bleeding ○ Any less can cause aspiration of secretions, inability to deliver effective ventilations and unwanted early extubation Centimeter markings on the tube indicate where the tubing reaches the lips/teeth ○ Teeth are more commonly used (the lips tend to be less accurate) ○ Can indicate if the tubing has moved Patient positioning techniques Prone position: improves oxygenation through increased recruitment of collapsed posterior alveolar units and reduction in V/Q mismatch Good lung down Elevate head of bed: allows for better lung expansion and reduces risk of aspiration Frequent position changes: frequent changes of position (as tolerated) help prevent skin breakdown ROM excercises: Range-of-motion exercises are necessary in the sedated or medically paralyzed bed-bound patient to preserve limb functioning and decrease contracture (severe joint stiffness) Acute respiratory failure parameters Hypoxemic respiratory failure - perfusion failure: ○ PaO2 less than 60 mmHg ○ Low oxygen level ○ Initial period of respiratory alkalosis Hypercapnic respiratory failure - ventilation failure:  ○ PaCO2 greater than 50 mmHg ○ pH less than 7.30 ○ Not breathing either quickly enough or effectively enough ○ Retaining CO2 → causing acidosis Transplants (5 questions): Clinical diagnosis of brain death (brain stem reflexes): Clinical exam/cerebral blood perfusion studies: ○ Two physicians must confirm brain death on pt ○ One of the two must be a neuro or critical care physician ○ No reflexes ○ There is an apnea test - disconnect pt from ventilator for 10 min and observe any signs of vent effort ○ In normal pt, CO2 will build up and hypercapnia will trigger a respiratory effort ○ In brain dead pt, doesnt matter how much CO2 is in their system, the brain is not responding to hypercapnia ○ Pt will have glasgow coma scale of 3 - lowest you can get on that scale ○ MRI, CTA, EEG and cerebral angiographies - cerebral blood perfusion studies Core temp normal: ○ Before diagnosis, make sure pt is at normal temp Greater than 90 degrees fahrenheit or 30 degrees celsius If they are cold, that can mimic effects of brain death No drugs/poisoning: Make sure there is no drugs or poisoning that can mimic these signs - tox screen Donor management- thermoregulation, goals: Family care: ○ Do not mention organ donation to pt family (premature notification has been shown to reduce family trust in hospital and caregivers Wait to mention this until LifeNet has addressed the family themselves ○ identify family’s native/nurturing language ○ Notify LifeNet Health of any visits by family members ○ Responsibility: calling LifeNet within 60 mins of cardiac death Make sure to keep everything in normal ranges to make sure that the pt is being perfused to the maximize function for the benefit of the recipient Maintain vital signs; include BP, HR, normal temperature Maintain pulmonary care as if the pt were expected to recover (pO2 >100) even if DNR or brain death Once removed from donor, organ packed in preservative solution and sterile triple bagged Placed on ice and transported to recipient’s hospital ○ Cooling slows down metabolism and minimizes cell death  Cold ischemic time: each organ window of time in which it can safely remain outside body Obtain required necessary organ-specific labs Ensure adequate urine output and fluid resuscitation Notify LifeNet Health of any changes in the pt status Donor management goals: ○ SBP> 100 mmHg ○ HR 100/min ○ PaO2> 100 ○ UO = 1-3 mL/kg/hr ○ Core temp: 97-100 degrees fahrenheit Monitor labs: ○ Potassium, sodium, calcium, phosphate, H/H, pH ○ Might need to transfuse some blood products - esp if some sort of liver issue that is causing coagulopathy Post Transplant complication: graft rejection Risk of rejection even if immunosuppressive therapy is used Common complications: bleeding, blood clots, leaking at the anastomosis where new organ is placed into recipient ○ Due to antibodies from recipient attacking donor organ Hyperacute rejections: occurs within mins to hours after graft ○ Results in graft failure and necessitate graft removal Acute rejection: most common and treatable form - occurs during first 3 months of transplant ○ Clinical manifestations: fever, swelling, tenderness over graft site, decreased urine output, rise in serum creatinine ○ Increased doses of immunosuppressive meds are used to manage these episodes Chronic rejection: anytime - even years post transplant ○ Clinical manifestations: progressive azotemia, proteinuria, htn - evidence of progressive renal failure Other complications associated with renal transplantation: htn as result of rejection, renal artery stenosis, renal valve vasoconstriction Long-term immunosuppression is associated with complications such as viral/bacterial/fungal infections of blood, lungs, CNS due to immunosuppression GI disorders such as ulcer formation and cataract formation Corticosteroid use may lead to bone problems Tumor malignancies due to suppressing immune system New onset diabetes due to steroids increasing blood sugars Immunosuppressant related complications: Calcineurin inhibitors: ○ Inhibit cytotoxic T-cell production  ○ Ex: cyclosporine, tacrolimus (prograft) ○ Be aware if pt is on tacrolimus, provider want drug level (TAC level) Glucocorticoids: ○ Steroid hormones ○ Adjunct therapy ○ Teach about side effects Take in morning to prevent insomnia Monitor fluid intake and weight - increases sodium retention Keep eye on blood sugars ○ Ex: prednisone Cytotoxic agents: ○ Destroy target cells ○ If pt is on this, use chemo precautions Chemo gloves Dispose of wrappers in yellow bins If on IV, pharm will mix and will be in special packaging If pregnant, use buddy system ROM EXERCISE- PATIENT POSITION TECHNIQUE