Final Exam Packet 252 cholecystitis

3 ● Significant concern with this dysrhythmia is cardiac output, with this rapid rate the ventricular filling time is reduced (less time to fill ventricles) ● Tx for stable pt.: if they are stable let them vagal, adenosine, CCB, beta blockers. ● Tx for unstable pt.: cardioversion Atrial Fibrillation with a Tachy Ventricular Rate ● Rhythm- irregular ● Rate- ventricular rate >100 ● P waves- fibrillatory waves present. ● PR interval- not measurable ● ORS- <0.12 ● Important to know if new onset or old/chronic. ● Ectopic area in atria sending chaotic electrical impulses at a rate of 350-600 per min, this electrical impulse is so high the atria cannot contract but can only quiver. ● No atrial contraction per says and w/out atrial contraction there is a reduction in cardiac output (20-30%) that would be sent from atria to ventricles. ● With this quivering- pooling of blood inside curvature of atria, predisposing individual to clot formation. ● AV node cannot receive this high rate of impulses, the AV node looks up and says “I can't get all of these through at one time” so it sporadically selects some of the impulses and sends them through the ventricles. ■ This is what makes the ventricle rate irregular when A-fib is underlying rhythm. New Onset A Fib: Converting cardiac rhythm back to a normal sinus rhythm. This can be done by different chemicals, drugs, (Cardizem drips aka diltiazem which is a CCB), synchronized cardioversion. For more difficult to treat A Fib amiodarone can be used. Beta blockers (metoprolol) may also be used in a A-Fib to slow ventricular response. ● Commonly in conversion situations a TEE (transesophageal echocardiogram) will be performed to determine if there is any pooling w/ clot formation in the atria, because with that first atrial contraction we do not want to shower the body with clots. Old Onset A Fib: Care centers on drugs for ventricular rate control. Do NOT want to convert old fib d/t risk of showering the body with clots. If ventricular rate can be managed traditionally (>60 but <100) then we can maximize the available CO, considering that the underlying a fib rhythm will still reduce by 20-30% Anticoagulants are used with A-Fib. ● With new onset the pt. will most likely be on a heparin drip until conversion to a NSR has been achieved if poss. ● With chronic or old A-Fib the pt. will be on blood thinners ranging from aspirin to warfarin due to risk associated with clot formation in the atria such as: strokes, PE, and Mis. Ventricular Tachycardia with a pulse criterion ● Rhythm- relatively regular ● Rate- >150 ● P waves- absent ● PR interval- not measurable ● QRS- greater than or equal to 0.12 ● Somewhere in ventricles an ectopic area decided to set a rate of >150. ● The SA node went on “coffee break” allowing the ectopic area to set the pace therefore there is no P wave. ● The QRS is going to take on a wide, bizarre looking characteristic. ● With an increase in the HR there is decreased filling time and with the depolarization across the ventricles there is decreased efficiency with the contractions resulting in reduced CO ● VTach can lead to VFib. ■ In some patients VTach causes cardiac arrest. Assess pts circulation and airway, breathing, LOC, and O2 level ■ For stable patient w/ sustained VTach, admin O2, and confirm rhythm via 12-lead EKG. Amiodarone, lidocaine, or mag sulfate may be given. Synchronized Cardioversion ● Cardiac monitor defibrillator is set up in sync mode so that there is a recognition of the QRS complex. R wave recognition means it is on ● When the electrical charge, the joules, go through it occurs at a specific time in relation to the occurrence of the R waves.

6 Hepatitis E - Acute infection only ● Fecal/oral transmission ● Typical symptoms and pain in abdomen and joins. ● Supportive care and rest ● Handwashing and caution traveling especially with meat and water (think fruit washed with water and ice) Alcoholic Hepatitis ● Early: asymptomatic ● Later: hand tremors, jaundice, decreased appetite, increased bilirubin, varices, edema in legs, decreased platelets and WBCs, pruritus, enlarged spleen, ascites, renal failure ● Very vitamin deficient- banana bag Cirrhosis Extensive, irreversible scarring of liver usually caused by a chronic reaction to hepatic inflammation and necrosis. Develops slowly. Progressive, prolonged, destructive course resulting in end stage liver disease. Common causes: chronic alcoholism, chronic viral hepatitis, NASH, bile duct disease. Portal HTN ● Results from increased resistance to or obstruction (blockage) of the flow of blood through the portal vein and its branches. ● Blood backs into the spleen causing splenomegaly. ● Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated. ● Can result in ascites, esophageal varices, prominent abdominal veins, and hemorrhoids. Ascites and Gastroesophageal Varices ● Ascites is a collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal HTN- a form of third spacing. ● Hypovolemia and edema can happen at the same time. ● Esophageal varices occur when fragile, thin-walled esophageal veins become distended and tortuous from increased pressure. ○ Bleeding esophageal varices are a medical emergency. Severe blood loss may occur before any observed bleeding. Variceal bleeding can occur with no precipitating factors. Any activity that increases abdominal pressure may increase the likelihood of a variceal bleed (so maybe put them on stool softeners) ○ Beta Blocker (propranolol) usually prescribed to prevent bleeding by decreased HR and hepatic venous pressure gradient. ○ If bleeding occurs- vasoactive drugs with endoscopic therapies such as vasopressin and Octreotide acetate- reduce blood flow through vasoconstriction to decrease portal pressure ○ Octreotide also suppresses secretion of gastrin, serotonin, intestinal peptides, which decrease GI blood flow to help with pressure within varices. ● To help prevent hemorrhage: PPIs twice a day, Vit. K IV or subQ (IM would cause bleeding) ● Portal Hypertensive gastropathy can occur with/without esophageal varices. Slow gastric mucosal bleeding occurs which may result in chronic slow blood loss, occult- positive stools and anemia. Splenomegaly- enlarged spleen. ● Results from backup of blood into spleen. The enlarged spleen destroys platelets causing thrombocytopenia- may be first clinical sign of liver dysfunction. Jaundice ● Pts with jaundice often report pruritus (itching)- cool water baths and use minimal soap. Hepatic Encephalopathy ● Complex cognitive syndrome that results from liver failure and cirrhosis ● Early: pts report sleeps disturbances, mood disturbance, mental status changes, and speech problems ● Factors that may lead to hepatic encephalopathy. ○ Increased protein diet ○ Infection ○ Hypovolemia ○ Hypokalemia ○ Constipation ○ GI bleeding

9 Pancreatitis: Acute or Chronic Acute Pancreatitis: ● Serious, occasionally life-threatening inflammation of pancreas ● Autodigestion and fibrosis of pancreas ● break down of pancreatic fat cells via lipase causes fatty acids that are released to bind with ionized calcium, hypocalcemia. ● Two main causes; gallstones and alcoholism ● Necrosis of blood vessels- bleeding (minor to hemorrhage) ○ Blood may escape into retroperitoneal tissues- shock, death. ● Complications of acute pancreatitis: ○ Jaundice ○ Intermittent hyperglycemia ○ Pancreatic infection (causes septic shock) ○ Hemorrhage (NHP) ○ AKI ○ Paralytic ileus- from peritoneal irritation and seepage of pancreatic enzymes into abdominal cavity ○ hypovolemic shock ○ pleural effusion ○ ARDS ○ Atelectasis ○ Pneumonia ○ Multiorgan system failure ○ DIC ○ type 2 diabetes. ○ coagulation defects-major potential complication= release of necrotic tissue and enzymes into bloodstream- altered coagulation ■ DIC involves hypercoagulation of blood with consumption of clotting factors and development of microthrombi. ● Assessment: ○ Abd pain with drinking? After eating a high fat meal. ○ biliary tract disease? ○ Family hx? ○ ERCP? ○ Pt typically presents w/ severe abdominal pain in the mid-epigastric area or left upper quadrant. Intense boring pain, worse in supine position. Can radiate to back, left flank, left shoulder, wt. loss, N/V. Relief by assuming fetal position or by sitting upright and leaning forward. ○ Inspect for generalized jaundice. ○ Cullen's sign: gray blue discoloration of abd and periumbilical area ○ Turner's sign: gray blue discoloration of the flanks ○ Observe for shock/observe for respiratory distress. ■ Hypotension and tachycardia may result from pancreatic hemorrhage, excessive fluid volume shifting or the toxic effects of abd sepsis from enzyme damage. ■ Monitor for crackles, dyspnea, wt. gain, fluid overload. ■ Observe for changes in behavior and LOC that may be related to alcohol withdrawal, hypoxia, or impending sepsis with shock. ● Nursing interventions: ○ NPO during acute period to let pancreas rest. ○ Isotonic IV fluid ○ IV replacement of calcium and Mag ○ for pain, morphine, or hydromorphone (dilaudid) best

12 ● call RRT ● keep HOB flat d/t possible shock. Diagnostic ● rule out other diseases. ● increased: WBC, AST, ALP, LDH, Bilirubin ● Ultrasound of right upper quadrant best initial diagnostic tool for cholecystitis ● Hepatobiliary scan (HIDA) determines patency of biliary system. ■ NPO before procedure Diet ● Low fat, high fiber, small frequent meals Pain ● Dilaudid Nursing interventions ● NPO until recovered. ● nasogastric tube w/ GI decompression ● advance nutrition per orders (clear, full, soft band) ● low fat, no spicy, no oily/greasy ● admin IV fluids per order Cholecystostomy tube- “C-Tube”- External catheter ● Placed through abdominal wall and into gallbladder. ● for some patients who cannot immediately have surgery to remove gallbladder ● Drains fluid from gallbladder. ● keep drainage bag lower than insertion site (at or below waist level) ● empty bag regularly, note color (yellow, brownish, greenish) and amount. ● May need to flush tubing per MD order. ● change dressing and keep skin dry/clean. T-Tube ● Works as drain and for testing w/ dye and x-ray to assess biliary tree for any stones. ● keep tubing and drainage bag below insertion site (at/below waist) ● Pt in semi-fowlers ● May have to flush or clamp tubing but need order. ● Empty/measure drainage ● Note color/amount (no greater than 500mL/day) (bloodish ting at first then green/brown) ● monitor for skin breakdown. ● IF have order to clamp may be required to clamp 1 hr. before meals and after meals, so bile can go to small intestine. ○ N/V, abd pain when clamped =BAD ○ Unclamp tube if N/V occurs Cholecystectomy ● Removal of gallbladder ● monitor for infection. ● shoulder pain with laparoscopic ○ side lying with knees bent, analgesics may help. ● Ambulation, incentive spirometer, t-tube care

15 ● life threatening organ dysfunction resulting from a dysregulated host response. ● Widespread vasodilation and blood pooling, allowing stasis. ● Mild hypotension, low urine output, increased RR, mild-high fever ● Inappropriate clotting with microthrombi forming- DIC. ● Event with appropriate intervention, death rate among pts in this stage of sepsis is very high. ● Vasodilation and capillary leak continue from vascular endothelial cell disruption. ● At risk: reduced immunity and central lines ● Signs and symptoms: ○ Shivering, fever, very cold (reduce temp w/ antipyretic) ○ Extreme pain or general discomfort ○ pale or discolored skin ○ sleepy, difficult to wake, confused. ○ Feel like they will die. ○ short of breath ● NI Order: ○ Ox sat. ○ IV fluids ○ Vasopressors ○ Cultures (2 diff sites) ○ Antibiotics ● Lab: ○ Increased lactate level (redraw 2 hrs. later) ○ Normal-low WBC and decreasing segmented neutrophil level, rising band neutrophil level (left shift) ○ Presence of bacteria in blood supports diagnosis. ● Medications: ○ Fluid resuscitation ○ Vasopressors ○ Abx ○ IV hydrocortisone and oral fludrocortisone (florinef)- stress of severe sepsis can cause adrenal insufficiency. ○ Elevated blood glucose- insulin ○ Clots- Heparin Neurogenic Shock: BP decreased, HR decreased, skin temp increased, skin color increased, CO increased then decreased. ● No sympathetic tone ● occurs most commonly in clients with injuries above T6 and usually is experienced soon after injury. Massive vasodilation occurs, leading to pooling of blood in blood vessels, tissue hypoperfusion, and impaired cellular metabolism. ● Assessment: ○ Hypotension ○ Bradycardia ○ low temp ○ cold body ○ warm/dry extremities ○ anxiety/restlessness ● Interventions ○ Get ABGs. ○ elevate HOB 20-30 degrees. ○ maintain immobility of spinal column. ○ assess bowel sounds. ○ monitor for bowel and urinary retention. ● Medications ○ Dextran, a plasma expander, may be used to increase capillary blood flow within the spinal cord and prevent or treat hypotension. ○ IV fluids (be careful, FVO- monitor for crackles)

18 ○ To try and reduce some of the SNS stimulation, DO NOT cluster activities. ○ Maintain a calm environment. ● Medications ○ Mannitol- can be given on prn basis like Q6hrs. ■ Osmotic diuretic ■ Expected outcome: increased urine output, if ICP monitor in the ICP number should reduce. ○ Loop diuretic- furosemide, to facilitate removal of fluid through kidneys. ■ it is okay to draw fluid out w/ mannitol into vasculature but must make sure the kidneys can handle it. ■ Furosemide puts a kick in the kidney. ○ Decadron/Dexamethasone- more of a scheduled drug ■ Steroid- works to decrease swelling. ■ Does not need to be weaned off. ○ D5 & water - straight D5 in water as IV fluid through peripheral or central line at continuous infusion ■ QUESTION THIS! ● Not recommended in the world of neuro ● D5W originally considered isotonic but because the brain is a glucose hog, the sugar is metabolized and it makes remaining solution hypotonic, which causes fluid shift into cells of brain tissue-> worse cerebral edema. ● Drains ○ After sx (evacuation of hematoma, burr holes, etc.) they will have a drain, JP or hemovac (MD preference) ○ Ventricular drain: they can monitor actual ICP suing waveform and at the same time that set up allows to drain off CSF in order to adjust and bring down the ICP. ■ Pop-off ex. if ICP goes higher than 18 the way the equipment is set up it will pop off and allow CSF to exit into a sterile system until the ICP comes back down to 18. ○ VP shunts: ■ Shunting excess CSF out of that area and shunting it to another part of the body so that it can be absorbed and expelled. Head Trauma/TBI Statistics: ● Falls and MVAs. ● acts of violence and sports related injuries. ● Males: females 3:1- but looks at population, older women w/ osteoporosis have higher tendency for falls ● Most common age 14-24 ● Severity and prognosis depend on amount of neurological damage. Pathophysiology: ● Primary brain injuries: open/closed head injuries ● Secondary brain injuries: any processes that occur after initial injury and worsens or negatively impacts the pt. outcome- vascular/biochemical/cellular i.e., HTN, Hypoxia. Basilar skull fracture - CSF can leak out and if there is a place for CSF to leak out, organisms can travel in, therefore, meningitis is a risk. Pay close attention to clear drainage. ● Racoon eyes- periorbital edema and ecchymosis ● Rhinorrhea ● Postauricular ecchymosis ● Otorrhea ● Prepare pt./family for how pt. will look- it can be difficult for them. Coup Countercoup Injury ● Type of head injury where the injury occurred relative to point of impact. ● A coup injury occurs on brain directly under the point of impact. ● A counter coup injury occurs on the opposite side of the brain from where the impact occurred. ● Type of force and the motion of the brain’s movement in the cranial vault influences where these duo insults occur. Cerebral Hemorrhage - space occupying lesions, accumulation of blood is occupying space- also causing edema. ● Subdural hematoma

21 ● Obtain follow-up CT scan after tx before starting antiplatelet or anticoagulant therapy. Endovascular Interventions ● Intra Arterial thrombolysis has advantage of delivering fibrinolytic agent directly into thrombus within 6 hours of stroke. ● Carotid artery angioplasty w/ stenting: common to prevent or in some cases help manage acute ischemic stroke. IR procedure. Moderate sedation. Ongoing Drug Therapy ● Initial dose of 325 mg of aspirin is recommended within 24-48 hours after stroke onset. ● Stool softeners ● Analgesics for pain ● CCB that crosses blood-brain barrier such as Nimodipine may be given to treat or prevent cerebral vasospasm after subarachnoid hemorrhage. Mobility ● Position arm on pillow while pt. is sitting to prevent it from hanging freely which would cause shoulder subluxation. ● VTE prophylaxis for immobile pts ● Have pt. dress affected side first. ● Teach pt. to turn head from side to side to expand visual field. Seizures and Epilepsy Epilepsy ● Brain disorder ● 2 or more unprovoked seizures ● Abnormal/excessive firing of neurons ● Strange reactions ranging from sensations or emotions to convulsions. ● Rule out other causes for seizures (increased temp, alc withdraw) ○ Gaba: Inhibitory neurotransmitter ○ Glutamate: Excitatory neurotransmitter ○ Need a balance between the two. ● Low serum sodium-> cerebral edema-> seizures ● High serum sodium-> increased excitability of neurons-> seizures Partial VS Generalized ● Neurons that become hyper excitable initiate a high frequency discharge called a focus. The focus initiates a seizure. ● Partial: ○ 1 Hemisphere of brain/defined to distinct areas of cerebral cortex. ○ Usually localized to specific area in that hemisphere ○ Complex partial: most common form of partial seizures ■ Appears awake but no contact with environment- may remain still. ■ Automatism behaviors (repetitive) (chewing/lip smacking/repeating words/aimlessly walking) ■ Mild-mod confusion following event/unaware event took place. ■ Lasts 1-2 mins. ■ Sometimes sleep after ○ Simple partial: has an aura beforehand. ● Generalized ○ Both hemispheres simultaneously ○ Subtypes: absence, myoclonic, atonic, generalized tonic clonic ○ Absence ■ Remain conscious but no contact/connection w/ environment. ■ No confusion following event; unaware event took place. ■ Lasts 5-10 seconds, can occur hundreds of times/days. ○ Myoclonic ■ Sudden brief muscle contractions, usually involving arms/feet. ○ Atonic

22 ■ Sudden loss of postural muscle tone (they can fall to ground), lasting about 1-2 seconds. ■ Consciousness briefly impaired ■ No postictal confusion ○ Generalized Tonic Clonic ■ Lasts about 1-2 mins. ■ Often begin with a loud scream, become unconscious ■ Have tonic (rigid), clonic (jerking), or tonic-clonic behaviors. ■ Cyanosis d/t tonic-clonic activity with respiratory muscles ■ Deep sleep-in postictal phase, lasting mins-hrs. ● Seizures have a clear beginning, middle, and end. ● Observation important, help determine type of seizure and can help in selecting type of antiepileptic drug. ● AIRWAY AND SAFETY, OBSERVATION OF SEIZURES, STOPPING THE SEIZURE Airway and Safety- Priority ● Cushion the head/protect the airway. ● You can also turn head to side. ● Do NOT put anything in their mouth. ● May require O2 (100% non-rebreather) ● Protect but do not restrain the limbs. ● Use recovery position during postictal period. ● Room set-up for someone with seizures: O2, suction equipment, padded side rails ● If in chair, STILL cushion head/protect airway- may look like standing behind and stabilizing. ● If need to get them to the floor, slide them down your leg. ● If in a chair, keep them there, if in a recliner, recline them Observation of the seizure ● Most seizures self-limiting and do not require stopping them. ● Status Epilepticus: Seizure lasting longer than 5 min or repeated seizures over course of 30 min occurring without adequate recovery time between seizures. The longer the seizure, the higher the mortality rate ○ Drugs of choice are from the benzo category. ■ Lorazepam (Ativan) IV push- enhances the GABA. ■ Diazepam (Valium) can be used rectal, nasally, injector pen formats for out of hospital setting. Antiepileptic Drugs (AEDs) ● Selection based on type of seizure. ● Many are thought to augment the inhibitory mechanism, the GABA, or reduce excitatory, the glutamate. ● Others block synapse by altering the sodium channels, chloride, or calcium channels. ● Others interfere w/ enzymes that metabolize the principal mechanisms for neurotransmission. ● Monotherapy is goal, 3 attempts. ● Once drug is begun, it may take 6 weeks to months to determine effectiveness. ● AEDs are not stopped abruptly, they are tapered down and titrated up. ● Ataxia, dizziness, fatigue, somnolence, headache disorders, nervousness, and N/V are troublesome side effects. ● Side effects may impact compliance. ● Drug-drug interactions, warfarin, and contraceptives ● Some AEDs interfere with one's fertility ability. ● No citrus juice (grapefruit) ● Check LFTs, BUN/Creatinine Non-Pharm ● Remove seizure foci sites. ● Vagal nerve stimulation ● Ketogenic diet Education ● Stay w/ person. ● Cushion head/protect airway.

23 ● Observe and time seizure. ● Do not restrain them. ● Prevent them from injuring themselves. ● Know when to give rescue treatments. ● Know when to call 911. ● Showers rather than baths and use shower chairs. ● Go w/ buddy when swimming and with a floating device. Reasons for seizures other than epilepsy ● Hypoglycemia: Check BG, D50, if alert- Give PO glucose w/ protein, take BG again in 10-15 mins ● Alcohol withdrawal: CIWA protocol and Ativan ● Peds Febrile: 18 months-5 years is common, 102+ fever, tympanic temp, use cooling measures (everything but diaper off), acetaminophen and ibuprofen (suppository), you can use Ativan but check airway. ● Oncology ● Eclampsia ● Cerebral hemorrhage: worried about increased intracranial pressure -> seizures. Parkinson’s Disease -Degenerative disease caused by depletion of dopamine, which interferes w/ inhibition of excitatory impulses, resulting in a dysfunction of the extrapyramidal system -Slow progressive disease-> crippling disability Assessment ● Bradykinesia, abnormal slowness of movement and sluggishness of physical and mental responses ● Akinesia ● Monotonous speech ● Handwriting that becomes progressively smaller ● Tremors in hands/fingers at rest (pill rolling) ● Tremors increasing when fatigued and decreasing with purposeful activity or sleep. ● Rigidity w jerky movements ● Restlessness and pacing ● Mask like faces ● Drooling ● Difficulty swallowing and speaking. ● Loss of coordination and balance ● Shuffling steps, stooped position, and propulsive gait Interventions ● Assess neuro status. ● Assess ability to swallow/chew. ● Provide high calorie, high protein, high fiber soft diet with small frequent feedings. ● Fluid intake 2000mL/day ● Monitor for constipation. ● Promote independence along with safety measures. ● Avoid rushing pt. with activities. ● Assist with ambulation and provide assistance devices. ● Instruct pt. to rock back and forth to initiate movement. ● Instruct pt. to wear low-heeled shoes. ● Encourage pt. to lift feet when walking and to avoid prolonged sitting. ● Provide firm mattress and position pt. prone, w/out pillow, to facilitate proper posture. ● Instruct pt. to avoid foods high in Vit B6 because they block effects of antiparkinsonian meds. ● No MAOIs-> Hypertensive crisis ● ROM!! ● May not be able to handle cluster care. ● Finger foods ● Wide base walk

24 ● Face them and speak clearly. ● Support them. ● Sleep disturbances- rituals to help w/ sleep. Pharmacology ● Carbidopa/Levodopa (Sinemet) ● Carbidopa protects so it can get across the BBB. ● Not a cure, helps with symptoms. ● Usually given in morning due to side effects ● Give on empty stomach. ● Side efects: ○ Dyskinesia ○ Involuntary body movements ○ Chest pain ○ N/V ○ Constipation ○ Urinary retention ○ Sleep disturbances insomnia, or periods of sedation ○ Orthostatic hypotension and dizziness ○ Confusion ○ Mood changes, esp. depression ○ Hallucinations ○ Dry mouth ● “Sinemet Vacation” when put back on it works better. Spinal Cord Injury Who is at risk? ● MVA #1 cause ● Sports ● Violence ● Drugs/alcohol ● Tasks (using a ladder) ● Age (think about falls and older adults), 16-30 (think about risky behavior) ● Men ● Sensory tract runs up the spinal cord, motor tracts run down the spinal cord. ● Motor tracts are on the same side of the cord, the left side. ● Sensory tracts cross over, ex. pain, temp, touch is located on the right side of the spinal cord for the left side of the body. ● Cervical Nerves: Head and neck, diaphragm, deltoids, biceps, wrist extensors, triceps, hands ● Thoracic Nerves: Chest muscles and abd. muscles ● Lumbar Nerves: Leg muscles ● Sacral Nerves: Bowel, bladder, sexual function ● Level of injury/insult is considered lowest neurological segment with intact or normal moor/sensory function. ● With the initial injury, there can be edema and involvement up to two levels higher than where the actual SCI occurred. ○ Knowing location drives nursing interventions and expected outcomes How the respiratory function is impacted. ● Anything C3 or above requires mechanical ventilation w/ advanced airway. ● C5 and above involves diaphragm (diaphragm does most work in breathing) ● C1-C7 is neck/shoulder/accessory muscles. ● T1-T11 are intercostals (intercostals for deep breathing/coughing) ● T9-T12 are abdominal muscles (abd muscles for coughing)

25 ● Quad Cough: ○ Place one hand on top of the other and place the heel of your hand midway between the pts umbilicus and the lower rib cage, your hand should be in the center beneath ribcage, have the pt. take 3 breaths and then cough when they exhale on 3rd one at which time you gently press inward and upward into the abdominal cavity; this produces an increased intra-abdominal pressure-> increased intrathoracic pressure and shifts air upwards and out of the respiratory system, thus producing more forceful cough ● T1-T8 tends to have poor trunk control as a result of lack of abd control. In comparison, T9-T12 do allow good trunk control and therefore they can use traditional wheelchairs. Complete VS Incomplete: ● Complete injury means no function below the level if the injury, no sensation, and no voluntary movement, both sides of the body are equally affected. ● Incomplete injury means that there is some functioning below primary level of the injury, a person an incomplete injury may be able to move one limb more than the other, may be able to feel parts of the body that cannot be moved or may have more functioning on one side of the body than the other. Upper Motor Neurons VS Lower Motor Neurons: ● Upper motor neurons lie within the spinal cord, carry messages back and forth from the brain. ● Lower motor neurons branch out from spinal cord to other parts of the body. ○ Reflex arcs are a component of the lower motor neurons. Spinal Shock ● Immediately after injury-> 48 hours ● Produces flaccid paralysis and loss of reflex activity below level of injury/insult. ● During this time, reflex arcs do not work. ● Once resolved, there is muscle spasticity or muscle spasms, but it is still a paralysis. ○ Concern is that these spasms can be misinterpreted by pt. and family as movement returning. ● Bowel and bladder can give you clues. ○ During flaccid paralysis phase there is bowel and bladder retention ○ During spastic paralysis phase there is bowel and bladder incontinence Neurogenic Shock ● Occurs within 24 hours of injury. ● SCI T6 and above ● Bradycardia ● Hypotension ● Vasodilation- Loss of vascular tone and dysfunctional SNS- HUGE tank (distributive shock) ● Body can regulate BP and HR in the first 1-1.5 hours ● Aggressive fluid replacement with isotonic fluids will be needed and vasopressors may be needed. ○ Never use vasopressors w/out first filling your tank- if you need to, contact the HCP to get fluids. ● For perfusing spinal cord during acute phase of an SCI, the goal is MAP >85. ● Solumedrol drip implemented within first 4 hours for reducing edema by altering that secondary cascade of events with the inflammatory-immune process. Autonomic Dysreflexia ● Noxious stimulus is the cause (distended bladder, bowels, pain) ● SCI T6 and above ● Bradycardia ● Severe HTN ● Severe HA ● Flushing above level if injury ● Cool below level of injury. ● Uninhibited SNS response to stimulus

26 Nursing Interventions for AD: ● Sit upright and get vital signs. ● Medications (buy you time) ○ Nitroglycerin ointment (can be wiped off after noxious stimulus found) ○ Hydralazine IV push ○ Sometimes not effective and only alleviating noxious stimulus will decrease BP. ○ Once noxious stimulus alleviated, WATCH BP! Might drop too low. ● Alleviate noxious stimulus (when Dr. D repositioned the pt., he emptied his bowel and bladder) ○ If wound debridement, think pain. ○ If the noxious stimulus is pain, no need to bladder scan. ● Recap: ○ Sit up, get vitals. ○ Meds ○ Alleviate noxious stimulus. ○ Monitor BP. TX and management of SCI ● ABCDs and added twist of immobilization. Immobilization: ● Goal is to prevent further injury. ● Do not move pt. until appropriate help is available. ● Position in proper alignment ● Log roll to turn. ● Halo Vest ● Gardner-wells or Crutchfield tongs ● Gardner-wells tongs and halo fixation device maintains proper alignment while also immobilizing spinal cord to prevent further injury. ○ Keep weights hanging freely. ○ Check placement of tongs. ○ Provide pin care w/ either saline or hydrogen peroxide. ○ Halo vest not only aligns but also immobilizes cervical collar. ■ Check screws for tightness. ■ Provide pin care. ■ Check skin at edges of jacket. ■ Vest/jacket NOT to be removed (unless they need to get CPR) ■ Dry well under the vest after bath. ● Kinetic bed may be used (useful for repositioning and shifting pressure points on body by using rotating type bed) How will you open the airway of someone with head/neck injuries? ● Cannot use typical chin/head tilt. ● Use “jaw thrust” method. ABCDs- Airway, Breathing, Circulation, Disability/functional ability Airway/Breathing ● Airway management priority in cervical spinal cord injuries ● T6 and above pts are at risk for respiratory complications d/t impaired functioning of intercostal muscles, ineffective cough, and decreased mobility. ● When brought to ED assess breathing patterns and ability to cough (unless it is like L5 and breathing will not be affected Circulation ● SBP needs to be treated if <90mmHg.

27 ● MAP goal is >85. ● Steroids (methylprednisolone continuous drip) initiated within first 4 hours of injury helps limit secondary cascade. Disability/Functional Ability ● Mobility skills: ROM tones muscles, stimulates blood supply to muscles and promotes flexibility of joints. Turning has more outcomes at preventing complications. ROM is HUGE. ● Bowel/Bladder ○ Upper motor neuron injury the bowel/bladder function results in incontinence-> condom Cath ○ Lower motor neuron injury the bowel/bladder function results in retention -> straight Cath ■ Valsalva might help empty. ■ Know when to decrease or increase time interval between straight Cath to prevent renal/kidney issues. ● With upper motor neuron injuries most can have reflex erections but cannot ejaculate ● With lower motor neuron injuries most cannot have an erection ANA code of ethics 2.1- Primacy of patient’s interest ● Involve them in their plan of care, educate them in their plan of care, and respect their decision regarding participation in the plan if care. Spina Bifida ● Central nervous system defect, results from failure of the neural tube to close during embryonic development. ● Placement in prone position ● Latex precautions Burns Thermal burns ● Dry heat (open flame- house fire, explosion) ● Moist heat (involves water- hot liquid, steam) Electrical- electrical wiring or lightening ● Direct damage to nerves, blood vessels, causing tissue anoxia and death. ● Wound/burn not visible on skin, maybe just entry/exit wound. ● At risk for dysrhythmias d/t electrical current and severe metabolic acidosis (d/t tissue destruction) ● Iceberg effect ● Electrical burn -> muscle damage ->increased myoglobin -> AKI Contact- hot metal (iron, space heater, grease) Chemical- acid/alkaline/organic compound/meth ● Affect respiratory, kidneys, liver, and eyes. ● If you put water on Drain-O burn, it makes it worse. NEVER put water on chemical burns Radiation- more serious in industrial settings Inhalation- Can occur w/ thermo or chemical burns. ● W/ thermal burns, look for risk (Are there burns on the face? Soot in the nose/mouth? Lip edema? Eyebrow/nasal hair singed?) ● Meth chemical vapors can cause inhalation burns. Rule of 9’s ● Tool to determine total body surface area. ● Arm 9% each ● Head 9% ● Leg 18% each ● Trunk front 18% ● Trunk back 18%

28 ● Groin ~1% Parkland-Baxter Formula ● Fluid resuscitation formula ● Based on % burn and pts weight in kg ● Time sensitive- when did the burn occur? What fluids have been given? ● Half volume given in the first 8 hours. ● Remainder of volume given over the next 16 hours. ● Close monitoring of I/Os, VS, LOC, urine specific gravity ● 4mL x wt.(kg) x %TBSA ○ Divide by 2 (first half-first 8 hrs., second half-remaining 160 ○ Subtract any amount already received by pt. from the first half. ○ Subtract any time elapsed since injury happened. Classification of burns Location of burns ● Face, neck, or chest= increased risk of respiratory compromise ● Hands, feet, joints, eyes affect pts ability to care for themselves. ● Circumferential burn= circulatory compromise -> compartment syndrome ○ Ex. entire arm burned -> swelling goes all around and compresses internal vessels so area will not have blood flow -> must have sx to relieve the pressure. ● Risk factors for healing/complications ○ Older adults ○ Pre-existing conditions: Cardiovascular, respiratory, renal diseases ○ DM= poor healing and risk of gangrene ○ Alcohol/drug abuse/poor nutrition ● Superficial (ex-sunburn) ○ Color: pink red ○ Edema: mild ○ Pain: yes ○ Blisters: no ○ Eschar: no ○ Healing time: 3-6 days ● Superficial partial thickness burn (scald burns, hot brink) ○ Color: pink-red, moist, does blanch ○ Edema: mild mod ○ Pain: yes ○ Blisters: yes ○ Eschar: no ○ Healing time: 2 weeks ● Deep partial thickness burn (may need skin graft) ○ Color: red, white, may or may not blanch ○ Edema: moderate ○ Pain: yes ○ Blisters: rare ○ Eschar: yes, soft, and dry ○ Healing time: 2-6 weeks ● Full thickness burn (skin grafts) ○ Color: black, brown, yellow, white, red ○ Edema: severe ○ Pain: yes and no (depends on nerve damage) ○ Blisters: no ○ Eschar: yes, hard, and inelastic

29 ○ Healing time: wks.-months ● Deep full thickness burns (skin grafts) ○ Color: black ○ Edema: absent ○ Pain: no ○ Blisters: no ○ Eschar: yes, hard, and inelastic ○ Healing time: wks.-months ○ May require amputation. Phases of burn care: resuscitation/emergent phase, acute phase, rehab phase Resuscitation ● First phase lasting 24-48 hours. ● Priorities: ○ Secure airway ○ Support circulation and organ perfusion by fluid replacement ○ Pain management ○ Prevent infection. ○ Maintain body temperature. ● Problems during this phase: ○ Fluid imbalance ○ Edema ○ Respiratory ○ Decreased circulation. ○ Cardiac output will remain low 18-36 hours after burn. ○ Hypovolemic shock is a common cause of death in this phase. ● Order of Activities ○ Airway status ○ 2 IVs and fluid ○ Determine % with rule of nine. ○ Sterile saline dressing ○ Morphine IV ● WBCs go to area of burn. ● Need two large bore IVs now. ● Monitor pulses if extremities are involved in the burn. ● Limit severity of burn (remove clothing with a chemical burn) ● Airway management ○ Intubation? Trach? Humidified O2 100% NRB? ○ Portable CXR ○ Pulse ox ○ ABGs ○ Soot on face? Hair singed? ○ Bronchoscopy to determine burn in lungs. ○ Carbon monoxide poisoning- cherry red skin color, decreased LOC, seizures, nausea. ○ Look for sign and symptoms of hypovolemic shock. ○ Look at extremities due to risk of compartment syndrome. Renal/Urinary ● Monitoring UO during fluid resuscitation, goal= 30-50mL/hr. or 5mL/kg/hr. ● We do want to protect skin and protect wounds but only after patent airway, adequate circulation, and fluid replacement have occurred. Meds ● Pain management given IV, antianxiety, antibiotics, tetanus vaccine.

30 Nutrition ● Early and aggressive nutrition optimizes wound healing. ● Burn pts are in a hypermetabolic state= cardiac needs are 5000kcal/day ● Early enteral feedings promote healing. ● Supplemental iron and vit D ● High protein (promotes healing) Labs ● Hgb and Hct will be elevated due to fluid volume loss, so blood is more concentrated. ● Glucose elevated due to stress response. ● Sodium levels decrease due to sodium trapped in edema and lost through plasma levels. ● K+ increased d/t tissues destruction and RBC hemolysis ● pH low d/t metabolic acidosis ● PaO2 low d/t increased demand and decreased supply ● PaCO2 increased d/t lung injury ● Protein decreased d/t protein loss through wounds. GI ● Risk of ileus may have NG tube to relieve air and pressure. ● Early enteral feedings help promote GI motility. Thermoregulation ● Monitor temp (keep room warm, 85+) ● Warm fluids, warm room, warm blanket AMS ● Sign of hypoxia Acute phase of burn injury ● Longest phase- beings 36-48 hours after injury and lasts until wound closure is complete. ● Priorities: ○ Continued assessment (priority cardiovascular and respiratory) ○ Burn wound care. ○ Pain control ○ Psychosocial interventions ● Weigh pt. daily- if 10% wt. loss present, interventions are required. ○ High cal, high protein feedings ● Infection is a massive risk -> sepsis. ● Maintain AROM and PROM as able ● Debridement may be done either w/ water, hydrotherapy, or medications like enzymatic ointments or can even be done surgically. ○ Standard wound care is gauze w. topical antimicrobial agents (silver sulfadiazine, bacitracin) ○ Maintain aseptic technique and wear PPE (gown, surgical mask, sterile gloves, head cover) ● DVT and peptic ulcer prophylaxis are crucial. No SCDs if legs are burned, use anticoagulants with caution because pt. is already at risk for bleeding. ● Curling ulcer is a risk for all burn pts -> acute gastric duodenal ulcer that occurs w/ stress of severe injuries, can develop within 24 hrs. after burn injury d/t decreased GI blood flow and any necrosis damage from the Rehab phase of burn ● Can take years. ● Begins with wound closure and ends when the pt. achieves the highest level of functioning. ● Priorities: ○ Psychosocial adjustment ○ Prevention of scars and contractures ○ Resumption of pre-burn activities Potassium: ● Resuscitation phase: Increased

31 ● Acute phase: Decreased Sodium ● R: Decreased ● A: Decreased Glucose ● R: Increased ● A: Decreased pH ● R: Decreased ● A: Decreased HCT ● R: Increased ● A: Decreased ● Module 3 Acid Base Balance pH: 7.35-7.45 PaCO2: 35-45 HCO3: 22-26 PaO2: 80-100 O2 Sat: >94% ● If pH and bicarbonate are in the same direction= metabolic ● If pH and PaCO2 are in different directions= respiratory ● Respiratory system kicks in for metabolic. ● Kidneys kick in for respiratory. ● When respiratory system kicks in, it can either reduce the RR so that it can retain CO2 and increase the PaCO2 or it increases the RR so it can blow off CO2 and lower the PaCO2. ● What the kidneys will do is either excrete hydrogen ions in an effort to retain bicarbonate OR they will excrete bicarb and retain the hydrogen ions if it needs to lower the bicarbonate levels ● Kidneys kick in at over 24 hours. ● Respiratory system can kick in fast but burns out quick. ● Too much base in the body: can either slow down breathing and retain CO2 to get more acid, or can get rid of base via the kidneys, they will rid the body of bicarb and hold on to H+ ● Too much acid in the body: the first way to get rid of acid is through the respiratory system by increasing RR and blowing off CO2. The other option is holding on to the base and getting rid of H+ ● Do not correct something that is helping. AKA: if kidneys have kicked in, our focus should be on respiratory origin- kidneys will fix themselves when respiratory corrects

32 ● Hydrogen-Potassium swap ○ When acidotic: too many hydrogen ions ○ H+ is the most volatile and needs to be dealt with first. ○ Body takes the excess H+ and puts them into the cell. ○ The cell needs to be electroneutral, so potassium leaves the cell resulting in Hyperkalemia. ○ Remember: High K+ levels and low K+ levels cause dysrhythmias ○ Once the acidotic state is fixed, the H+ comes out of the cell, the K+ goes back in and this results in Hypokalemia. ● Vomiting: getting rid of acid= alkalosis ● Diarrhea: getting rid of base= acidosis Respiratory Failure ● Clinical state of inadequate oxygenation, ventilation, or both ● Crackles -> fluid in alveoli -> diuretic ● Wheezes -> air passing through narrowing airways ->bronchodilator. ● Ronchi -> mucous component -> IV fluids most important ● Beta agonist first then anticholinergic ● Pulse ox is only as reliable as hemoglobin, if hemoglobin is 12 then pulse ox is reliable, if hemoglobin is 6 then pulse ox is not reliable. ● When pts requires supplemental oxygen, they want to avoid hyperoxia because what can happen is the alveoli get damaged within the alveolar spaces, so keep O2 sat between 94-99% General indicators of increasing respiratory severity. -Breathless walking -> talking -> at rest -Talks in sentences -> phrases -> words -Resp. rate increased -> decreased -> apnea -Wheeze moderate -> loud -> very loud -> absent (does not mean it got better) -Pulse rate tachy -> brady -> cardiac arrest ● Fix O2 issue before CO2 issue. ● CO2 detectors: ○ Difficult to determine ventilation component until that respiratory pattern is too suppressed so we use CO2 detectors. ○ Whenever we put an ET tube in someone, we usually use a color-metric type device that will tell that CO2 is being exhaled especially when we bag them; also, there are devices that will produce waveforms that will give a numerical value in relationship to/correlating to what the CO2 is. Devices to support ventilation: ● Ambu bag ○ Can add oxygenation to give the pt. % O2 w/ inspiratory breath and when the pt. exhales the CO2 is removed. To remove CO2 faster, bag the pt. faster. ● Ventilator ○ Will typically have an advanced airway as well but can also use noninvasive methods. ● Continuous positive airway pressure (CPAP) machine ○ Noninvasive positive pressure ventilation ○ Cause positive airway pressure to be present so that the airway can get splinted open, so we can get oxygenation in and CO2 out. ● Positive end expiratory pressure (PEEP) ○ Positive pressure exerted during expiratory phase- this is to help prevent alveoli from collapsing, because the lungs are kept partially inflated so that there is alveolar capillary gas exchange promoted throughout ventilatory cycle. ○ Think PEEP as splinting open airway to get a better exhale. ● Bi-Pap ○ Bi level positive pressure in the airway

33 ○ Can set specific pressure to keep airway open during inspiration and a second pressure to keep the airway open during exhalation. ABG criteria for Acute Respiratory Failure ● The 50/50 rule: CO2 is >50 and PaO2 is <50. ● PaO2 <60, SpO2 <90, PaCO2 >50, occurring with acidosis. Acute Respiratory Distress Syndrome (ARDS) ● Non cardiac pulmonary edema, major trigger is a systemic inflammatory response, and the major site of injury is the alveolar capillary membrane. ● In the interstitial space- not inside alveoli yet- is where the fluid is, which is high in protein concentration (very thick) ○ The pts is having difficulty breathing, cannot get O2/CO2 exchange because of the fluid. ○ Will not hear crackles yet. ○ O2 is dropping, they are heading towards resp. failure. ○ Not until later that the fluid shift happens where the thick fluid gets into the alveoli and rales become present. ● Most important thing is too correct hypoxemia. ● Intubate, low tidal volume (400), PEEP (trying to open the collapsed alveoli) ● Prone position ● Cautious with fluids, focus on having negative fluid balance (conserve) ● Pulmonary vasodilator ● Anti-inflammatory agents- Solumedrol? ● Antibiotics ● Enteral or parenteral nutrition started as soon as possible. Advanced Airways -Breathing is different on a mechanical ventilator. Air is pushed in, it is a positive pressure that pushes the air in ● Endotracheal Tube: Down oral airway into the trachea with a cuff as the end inflated so that nothing can go down into the lung cavity. ○ Auscultate as the pt. is being bagged to see if the gas exchange is audible- first place to auscultate is the stomach because if the tube is in the esophagus, air will be heard in the stomach and the tube needs to be removed and reinserted. ○ Another confirmation is a colorimetric device. ○ Most confirming is a CXR. ○ Always have an ambu bag, wall O2 flow meter, and suction at the bedside ● Tracheostomy- The ET tube is an emergent situation, after 3-5 (per Dr. D but it is really 10-14) days the MD will put in a trach due to the risks involved with leaving an ET tube in for a long period of time. Normal Vent settings: ● TV: Tidal Volume ○ 400-500 ● Mode: ○ Breathing pattern ● Rate: ○ Think CO2, if CO2 is increased, contact MD to increase the rate. ● FiO2: ○ Think O2, if PaO2 is decreased, contact MD to increase percentage of O2. ○ Usually set at 40% -Specific modes may be used to help wean a pt. off the ventilator and strengthen their lungs -If a pt. says that they do not want a mechanical ventilator, is it the vent or the invasive airway method they do not want? -Find out and educate Nursing focus for the intubated patient

34 1. Oxygenation and ventilation a. Have ambu bag, O2 flow meter and suction. b. If on a trach, have 1 extra of the same size and one size smaller. c. Pulse ox and end tidal CO2 monitor. 2. Suctioning a. Hyper-oxygenate with 100% O2 for 2-3 min before and suction for 10 seconds or less and only apply suction on the way out (while twisting) b. Suction only as needed, not for funsies. Check Q2hrs to see if suction is needed. 3. Repositioning and increasing activity a. Good lung down theory: Position the lung that does not have infection/infiltrates down for 2 hours- improved oxygenation due to improved perfusion. b. Prone positioning with ARDS c. Mechanical ventilator does not prevent the pt. from being mobile. 4. Communication a. For pts with endotracheal tubes, the vocal cord area is blocked, and they will not be able to speak. b. Use word boards, alphabet boards, assess their ability to write. c. LEAST effective way of communicating is mouthing words. d. Gesturing can be effective. 5. Pharmacological therapy a. Propofol: Amnesic, no pain control, cannot have if allergic to eggs. b. Benzos: amnesic/anxiolytic, no pain control c. Dexmedetomidine (Precedex): anxiolytic/amnesic/sedative, inhibits release of neurotransmitters, mild analgesic property, does not produce respiratory depression, also decreases needs for opioids due to analgesic property. Pts do better on this drug d. Bronchodilators e. Steroids f. Antibiotics 6. Sedation vacation a. Purpose is to wean as early as possible. b. Assess neurological state during this time. c. Assess strength of their lungs and see if they can support their own breathing patterns. 7. Early nutrition a. Increase cals to strengthen lung muscles. b. Might increase fats or cards depending on their comorbidities. c. Increase protein. d. Enteral feeding through NG tube or PEG tube e. If cannot do enteral feedings -> central line and TPN 8. Preventing VAP a. Hand hygiene is the #1 priority. b. HOB 30 degrees or greater to prevent aspiration. c. Oral care Q2 hrs. d. CHG Q12 hrs. e. High-low ET tube has a double port is for the cuff that is inflated, and one port is a little bit of a suction device right around the epiglottic area and we hook to it about 20mmHg low wall suction and we keep that area above that cuff removed of secretions to reduce bacteria. f. Sedation vacations a part of VAP protocol. 9. Weaning from vent a. Mechanical vent is a weaning tool itself- we can adjust the modes for delivering of breaths, we can make them different assists, can use the pressures versus using a specific rate or VS a tidal volume. b. Decrease amount of supplemental O2. c. Preparing to extubate suction, ambu bag w/ 100% O2 at bedside. d. If after extubating the pt., they struggle to breath, use non-invasive mechanical ventilation with a face tent. Tracheostomy

35 ● If on a mechanical ventilator, need to have a cuffed and inflated cuffed trach to protect trachea airway. ● Need correct size suction Cath that will fit down trach tube. ● When discharged, the pt. will probably get a trach that is not cuffed. ● The pt. will also need to communicate. ○ Passy-Muir Valve sits right on top of the trach tube, it is a one-way valve so they will breathe in through the valve and exhale through their mouth and that shifts air to go past vocal cords and allows individuals to be able to speak. If this tube were cuffed, there would be no way to get air out. ○ A Passy-Muir Valve is NOT placed on a cuffed tube. Chest Trauma/Chest Tube/Chest Surgery ● Unexpected trauma: Injury (blunt force, penetrating, infection) ● Therapeutic trauma: chest surgery (lobectomy, pneumonectomy, LVRS, etc.) ● Open trauma: external source of entry that penetrates chest cavity wall and causes internal trauma (knife, gun, arrow) ● Closed trauma: injury source may originate externally or internally- no external penetration of entry (blunt external force, infection, etc.) ● Central line can be considered a form of unplanned chest trauma whether it is viewed as the closed category or the open category, in either circumstance, unequal chest expansion post central line insertion is indicative of a pneumothorax and a chest tube would be warranted. Air VS Fluid ● Air in pleural space is called a pneumothorax. ● Fluid in pleural space is dependent on what type of fluid is present for determining terminology used. ○ Pleural effusion: excess pleural fluid ○ Empyema: puss/infectious process ○ Hemothorax: blood in the pleural space Chest Tubes: ● Placing a tube into the pleural cavity ● Re-expansion of lung results in improved ventilation capability and this improved oxygenation. ● Air rises so chest tubes placed to remove air will be placed high. ● Fluid removal from pleural space: around 5th intercostal space or below is where the chest tube would most likely be located since fluid settles. What do we need for chest tube placement? Chest tube insertion tray, chest tube, CDU. Closed Chest Drainage Unit- CDU Keep the CDU device below the level of the chest. ● Collection chamber: ○ Whether air or fluid being removed, this is initial entry point between pts chest tube and the CDU device. ● Water seal chamber: ○ Specific amount of sterile water is placed in this chamber. ○ Acts as a one-way valve. ○ Allows air to come out of pleural space and move through the chambers but it will not allow air to travel backwards. ○ Intermittent bubbling is okay. ○ Continuous/excessive bubbling is not okay. ○ Once healed, the intermittent bubbling will stop. ○ If there is continuous bubbling, the integrity of the CDU may be compromised, or the chest tube might have migrated out of the insertion site allowing the eyelets of the chest tube to be exposed. ● Suction control chamber: ○ Filled with a specific amount of sterile water but this amount is ordered by the MD and is usually at the 20 sonometer mark. ○ The amount of fluid determines the amount of suction. ○ Any wall suction added only produces a small amount of additional draw. ○ If low wall suction is applied, there should be a gentle continuous bubbling. ○ Turn off the wall suction Q24hrs to assess the fluid level.

36 Pleural Vac w/ dry suction mechanism: ● Suction control chamber uses a dial to activate degree of suction. ● No bubbling with a dry suction unit Heimlich Valve ● Small device that can be placed at the end of a specific type of chest tube. ● Can be used w/ a pneumothorax. ● Air travels down the tube and enters the valve (is a one-way valve) ● Suction is not required. ● Pts w/ spontaneous pneumothorax could have this type of chest tube apparatus inserted in an IR department on an outpatient basis. ● Portable and does not interfere with activity/mobility. Pleurx drainage system ● Used more frequently with chronic conditions such a recurrent pleural effusion in lung cancer pts or empyema’s in pts with chronic infections. ● Inserted for long term use. Care of a patient with a chest tube ● Need to ensure that the connection is sound at the juncture, where the CDU tubing enters the end of the chest tube. ● Use a figure 8 method for taping, also need to apply a sterile petroleum gauze dressing around the chest tube insertion site and then cover with a sterile occlusive dressing. ● When an open chest wound, not a chest tube, most likely will be putting on a three-sided dressing so that the wound is not closed off and prevents any outflow of air. This could cause a collapsed lung. ○ W/ an open chest wound, if you put on an occlusive dressing and the pt. becomes severely dyspneic and hypotensive explore the reason why -> recognize that the way for air to escape is closed off -> release one side on the dressing. Collection chamber ● Do you expect fluid? Air? ● What is the volume of the chest tube drainage? ● Greater than 70-100 mL of fluid per hr. is when the MD needs to be notified. ● Assess the color if the drainage in the tubing of the CDU PRIOR to it reaching the collection chamber. ● Notify the MD if the drainage is bright red or the amount of fluid increases suddenly. Water seal chamber ● Do you expect bubbling? ● If there is continuous bubbling, the integrity of the CDU may be compromised, and the unit needs to be changed. ○ Dyspnea and the pts respiratory status would determine how quickly this would need to take place. ○ Disconnect the chest tube from faulty CDU device and place the end of the chest tube in a bottle of sterile water- sterile water will act as a one-way valve. Chest tube notes and emergency situations: ● Nurses cannot clamp the tube. ● If CDU is compromised, disconnect, and put the end into a bottle of sterile water. ● What if, while repositioning, the pt. inadvertently disconnects the device? ○ What if you reach for a bottle of sterile water to put the end in and there isn't one? ○ You can reconnect the current CDU since its integrity is still intact and then get a new one, set it up, and switch it out. ● What is the pt. pulls out the actual chest tube? ○ Immediately cover the open insertion site with a gloved hand until you can cover it with a dry gauze dressing. ○ If the pt. is in respiratory distress, secure the gloved hand over the insertion site while the pt. inhales, then release the pressure as the pt. exhales. GET IMMEDIATE HELP. ○ If the pt. is NOT in respiratory distress, secure a petroleum gauze 4x4 in an occlusive manner. Then assess the pts lung fields for aeration followed by vital signs and a pulse ox reading and notify the MD (it might have been time to take the tube out)

37 ● Things to keep at the bedside. ○ Bottle of sterile water ○ Petroleum gauze dressing ○ Sterile 4x4 ○ Tape Removing chest tube ● Instruct the pt. to hold their breath whether it is on end inspiration or end expiration, either is acceptable, they hold their breath, they bear down, the chest tube is pulled, and the site is immediately covered with a petroleum gauze dressing topped with a sterile 4x4 and taped as an occlusive dressing. ● If the pt. is on a mechanical ventilator, the chest tube is pulled on end expiration. Therapeutic chest trauma ● Lobectomy: Take out a specific lobe of the lung -> air leak and serous-serosanguinous drainage ● Wedge resection: Section from a lobe is removed. ● Segmentectomy: Removal of a segment ● Pneumonectomy: entire lung is removed, and bronchial stump remains on affected side -> air, serous fluid, and blood post-op ● Lung Volume Reduction Surgery (LVRS): Option for end stage COPD pts. ○ One lung at a time is deflated and abnormal hyperinflated areas are removed, remaining good lung tissue is connected and reinforced ->air leakage. Focus of nursing care: ● Control pain for a purpose ○ Look at pain, activity, and breathing together- all 3 interlace and affect each other. ● If pt. has pain due to a thoracic trauma, they are going to have shallow breathing, with this shallow breathing they will not be able to carry out activities needed. ○ These pts will not have the O2 supply for the O2 demand. ● Limiting activities interferes with strengthening the muscles. Acute Kidney Injury (AKI) -Primary functions of the kidneys ● Elimination of waste ● Maintain homeostasis. ○ Fluid balance ○ Electrolyte imbalance ○ Acid base balance ● Blood pressure regulation ● Endocrine functions ○ Erythropoietin, which stimulates the production of RBCs. ○ Vit D converting enzyme to promote calcium absorption from the gut. Definition of AKI ● Serum creatinine is increased. ● Urinary output- <0.5mL/kg/hr. for >6hrs ● Glomerular filtration rate decreased. ● Albuminuria increased. Two components of AKI ● Sudden onset ● Secondary to something else Three categories of AKI 1. Prerenal- before injury into the kidney 2. Intrarenal- within the kidney 3. Postrenal- leaving the kidney. Prerenal- the nephrons are structurally intact; it is the perfusion that is compromised.

38 ● Conditions that result from decreased blood flow to the kidneys ● Decreased renal blood flow -> decreased GFR -> decreased oxygen to the nephrons. ● MAP of >65 is required for adequate renal perfusion. ● Most common causes of AKI fall in the prerenal category and it is volume depletion. ● Other causes: HF, burns, shock, ACEs/ARBs ● Early intervention and risk recognition is the biggest factor for prerenal. ○ Intervene early with fluids, possible blood products and vasopressors. Intrarenal- damage to glomeruli, interstitial tissue, or tubules ● Direct damage to the kidneys ● Causes: toxins, glomerulonephritis, acute tubular necrosis, infections, nephrotic drugs (aminoglycosides, many antibiotics, NSAIDs, various chemo agents) ● Ex. elderly individual falls and is laying on the floor for a prolonged period of time, muscle begins to breakdown due to immobility, myoglobin’s bring released from muscles (rhabdomyolysis). These myoglobin’s travel through the system and reach the kidneys and clogs up the kidneys. This results in intrarenal pressure exceeding glomerular pressure- GFR reduced- and ultimately stops. Tx would be to flush out the myoglobin’s using IV fluids. ● Knowing the cause drives interventions and treatments ● Certain antibiotics are nephrotoxic- use peak and trough and monitor BUN/creatinine at least every 48 hrs. (called “pharmacy dosing protocols”) Postrenal- come from outside the kidney, leaving the kidney. ● Cause is from obstruction of urine flow outside the kidneys. ● Obstruction of urine flow causes backflow into the kidneys. ● Urine backs up into the kidneys and increases the pressure -> decreases GFR -> nephron/tubular damage. ● Causes: BPH, urethral strictures, kidney stones, cancers, or tumors ● Goal: alleviate blockage and facilitate the forward movement of urine ● Done with medications for BPH, surgical procedures to remove tumors of urinary tract, ureteral stent placements to open ureters and kidney lithotripsy for kidney stones. Labs: ● BUN: ○ Gives insights to volume depletion and protein breakdown. ○ Measures effectiveness of kidneys exception of nitrogen- the liver metabolizes protein with a byproduct of urea-nitrogen, the kidneys filter this and excretes it in the urine. ○ Urea lyses RBCs, so as the BUN elevates for whatever reason, pay attention to your RBCs. ● Serum Creatinine: ○ Freely filtered at glomerulus when GFR is normal because the kidneys do not metabolize or reabsorb serum creatinine, the serum CR level reflects both CR clearance and GFR. ○ CR levels do not increase until at least 50% of the kidney function has been affected or lost. ● BUN and CR together is a 10-20:1 ratio. If BUN rises faster than CR, the cause is most likely due to protein breakdown or volume depletion. If BUN and CR rise together, it is indicative of kidney dysfunction. Metabolic acidosis ● Kidneys cants retain bicarbonate (HCO3) ● Kidneys cants excrete H+ ● Results in decreased HCO3 and ph. ● Kussmaul breathing (rapid, deep breathing) to balance (decreasing PCO2) Phases of AKI ● Initial phase ● Oliguric phase ● Diuretic phase ● Recovery phase

39 Initial- time between injury and the reduction in kidney function ● Recognition is paramount. ● Monitor urine output. Oliguric phase - fluid overload, hyponatremia, hyperkalemia (holding fluid at this point) ● Indicator for oliguric phase is reduction in urinary output <400mL/24hr period. ● Overload is focus for volume (so question fluid orders) ● Balance is focus for E+ and acid base. ● The pt. is retaining fluid during this phase and issues with fluid overload are of concern. ● Hyponatremia due to delusional effect is prevalent in this phase and there is also impaired renal reabsorption of sodium (SEIZURE PRECAUTIONS!) ● Hyperkalemia as a result of decreased urinary output so kidneys cannot excrete potassium Acid base imbalance of metabolic acidosis also predisposes to further elevation in the K+ level due to the H+ and K+ swap (think cardiac dysrhythmias!) ○ Methods for reducing K+ include. ■ D50 IV in conjunction with regular insulin IV ■ Sodium bicarb IV ■ Kayexalate PO or edema format ● Treatment focuses on fluid replacement with normal saline IV fluids due to Na+ levels and with diuretics for the overload stage. This fluid/diuretic strategy maintains renal hemodynamics, CO, BP, and decreases pulmonary congestion. ● Continuous renal replacement therapy is an option for this phase in the event hypervolemia, hyperkalemia, and/or metabolic acidosis cannot be managed effectively with other alternatives. ● Fluid restrictions not uncommon in this phase- total intake for the next 24 hrs. would be determined on output of the last 24 hrs. plus 500-700 mL. Diuretic phase- hyponatremia, hypokalemia, hypovolemia, and hypotension ● UOP can be as night as 5 L/day. ● “dumping” phase: all is low (except UOP) ● Risk of constipation so give docusate sodium. ● Replacement is the focus for volume. ● Balance is the focus for E+ and acid base. ● Kidneys are dumping fluid but not filtering. ● Monitor fluid status, E+ status and acid base status. Recovery phase- some pts never make it to this phase -> CKD. ● Takes several weeks to a year. ● BUN and creatinine return to baseline. ● Goal: education to protect the kidneys ● Pt needs to make sure their PCP and any other consulting HCP are aware w/ their event of AKI: certain meds such as NSAIDs and certain diagnostic studies such as those using contrast could put them at risk for further nephron damage. Nutrition ● BUN levels give insight into protein metabolism whereas the albumin levels provide insight into protein needs. Will not be doing high increases in protein but should be monitoring albumin levels to determine amount of protein needed for the diet. ○ If albumin level is high, then control protein intake w/ a lower amount. ○ If albumin level is low, then increase the intake of protein. ● Use high quality proteins: animal protein. ● Need more calories for repairing - cals can come predominantly from fats and carbohydrates- do not want to break down protein for calorie needs. ● When looking at Na+ and K+, be aware of what stage you are in ○ In oliguric phase- limit K+ intake ○ In diuretic phase- replenish K+ ○ In oliguric phase- be cautious with Na+ intake since this is due to a delusional effect and the sodium requirement may shift as the volume status shifts ○ In diuretic phase- Na+ intake would not need to be limited

40 ○ Oliguric phase= fluid restriction ○ Diuretic phase = aggressive fluid replacement Chronic kidney disease (CKD) ● 90-95% of nephrons destroyed in CKD. ● Top 3 causes: DM, HTN, Glomerulonephritis ● HTN has duo effect: HTN leads to CKD and CKD causes HTN. Five stages of CKD 1-3: focus on controlling risk factors (such as HTN or DM) and maximizing the remaining GFR. 4: renal replacement therapies are an option. 5: End stage kidney disease (ESKD), renal replacement therapies are a must for survival. ● GFR is accurately reflective of kidney function. ● GFR and albuminuria have been used together since before 2002 as a means for classifying CKD. ● Proteinuria -> ACEs usually help; but careful. What would you expect? ● GFR- expect a reduction, we do not have the number of nephrons to carry out workload of kidneys. ● BUN/CR- if our kidneys are not able to eliminate waste then the CR and BUN levels will be elevated. ● We would expect baseline CR level for CKD pts to be elevated- therefore treatments and therapies are focused on returning the CR level back into their elevated baseline. ● Albumin- Would not usually expect to see albumin in the urine so when albuminuria is present, that is an indicator of kidney damage. Electrolytes ● Na+ ○ In the early stages of CKD, hyponatremia will be seen due to fewer nephrons to reabsorb sodium. In the late stages of CKD, sodium levels rise because kidneys cannot excrete sodium anymore because of the reduced urine output and hypernatremia becomes the issue. ● K+ ○ Potassium is excreted mainly in kidneys, so with reduction in kidneys ability to excrete potassium, hyperkalemia becomes the issue. Also, the acid base imbalance and H+ and K+ swap further increases K+. Think cardiac dysrhythmias. ● Calcium and Phosphorus ○ Kidneys produce vit D converting enzyme which activates vit D for adsorption of Ca+ from gut, if kidneys are not able to carry out this function, then calcium levels are affected. ■ Ex. The body says, “I need more calcium” and the parathyroid hormone tells the bones to release more calcium, but I still will not have that vit D because I do not have that converting enzyme like I would with a normal functioning kidney. So, the calcium gets depleted from the bones, but the calcium does not get used because I do not have the vit D converting enzyme to activate the vit D needed for calcium absorption. ■ As for phosphorus, it has a reciprocal effect with calcium and so phosphorus levels will increase and usable calcium levels will decrease- bones will become fragile and brittle and fractures become a high risk. ● Metabolic Acidosis ○ Kidneys cannot reabsorb bicarb and the kidneys cannot excrete hydrogen ions -> low bicarb, low pH= metabolic acidosis. ○ Kussmaul breathing can ensue as a compensatory mechanism -> oxygenation issues. ○ Sometimes a daily maintenance dose of sodium bicarbonate PO is required for those w/ CKD that have this issue on a recurring basis. ● RBCs

41 ○ Erythropoietin is a hormone produced by the kidneys which stimulates bone marrow to produce RBCs. In CKD, there is a reduction or absence of the kidneys ability to produce the erythropoietin, resulting in a lower RBC level. ○ Also, urea lyses RBCs, therefore the elevated BUN w/ CKD results in reduced RBC levels. ○ With fewer RBCs, HGB and HCT drop ○ Anemia is associated with CKD. Focus of nursing care. 1. Homeostasis a. Fluid b. Electrolyte c. Acid-base 2. Safety 3. Risk for injury 4. Nutrition 5. Coping and education Homeostasis ● Stages 1-3, we look at urinary output to help us determine fluid status, but by stage 4-5, RRTs may influence the fluid status and I&O may be difficult to determine or interpret. By stage 4-5, the individual may have little to no urine output. ● Daily weights have the greatest value. ● Bodyweight should not increase more than 3 lbs. between hemodialysis treatments. ● Daily weight gain in those using dialysis is usually indicative of fluid retention rather than true body weight gain. ● Daily weight gain of 2lbs or more overnight or 5lbs or more weekly should be reported to the healthcare provider. ● 2.2lbs= 1kg = 1L of fluid ● Pulmonary edema due to left sided heart failure because of fluid overload from the CKD but can also be due to injury of blood vessels in the lungs because of inflammation and capillary leakage into the lung tissue and alveoli cause by uremia from the CKD- assess for signs and symptoms of pulmonary edema. Safety ● Seizure precautions for Na+ abnormalities ● Cardiac monitor for pts with K+ abnormalities Risk for injury ● Low calcium levels predispose pts to fragile and brittle bones and puts them at risk for fractures. ● Fall precautions. ● Use lift sheets to reposition in bed. ● Low calcium levels along with low RBCs lead to weakness and fatigue. ● Mobility of joints and strength of the muscles can be the focus when advancing activities. ● ROM, slowly positioning to upright positions, use of assistive devices, involvement of OT and PT. ● Balance activity and rest ● Safety with meds ○ Pts are at risk for digoxin toxicity due to issues with calcium and potassium associated with CKD. Nutrition ● Foods high in Ca+ are also high in phosphorus- when the diet involves increasing foods rich in calcium but at the same time reducing phosphorus intake, there can be difficulty with that. Coping/Education ● Lifelong management

42 ● May be more beneficial to provide information in small chunks and to find out from the individual what they want to know first. ● Need to know > Nice to know. Nutrition ● Protein control ○ Calculated on actual body weight, for those on dialysis - their dry weight (post dialysis weight) ○ Serum albumin levels are used to determine the amount of dietary protein intake needed. ○ Individual on peritoneal dialysis will have a more flexible diet with regards to protein then one using hemodialysis ○ Someone with a kidney transplant will need higher levels of protein intake for healing and repair. ○ High quality proteins should be used: animal proteins. ○ Select foods rich in protein but low in phosphorus. Fluid restriction ● Fluid restriction that involves adding 500-700ml to the amount of UOP over the course of a 24hr period ● Consider using ice chips with flavoring (more satisfying) Electrolyte restriction/vitamin supplements ● Individuals using peritoneal dialysis usually do not have to restrict their potassium intake due to the 24hr filtering process. ● With hemodialysis, the individual traditionally restricts their potassium intake as well as their sodium and phosphorus. ● For those in stages 1-3 of CKD, they will be restricting their sodium, potassium, and phosphorus intake. ● They will need vit D and calcium supplements. ● Milks low in phosphorus: rice, soy, almond ● Phosphate binders are a common medication. ● Erythropoietin needed for production of RBCs, erythropoietin stimulating agents would be expected such as Epogen. ● Iron supplements, B vitamins, and folic acid ● Need to increase calories - do not break down protein for the increased cal need. Health Maintenance ● Daily weights ○ Same scale, same time, same amount of clothing ● BP <130/80 ○ Supports renal blood flow. ○ Manages HTN ○ Educate them on how to take and track their BP. ● Balance activity and rest ○ Anemia due to reduction in RBCs ○ Weakness and fatigue ○ Use erythropoietin stimulating agents, iron, Vit B, and folic acid. ● Manage other conditions - DM, HTN, HF ○ Quit smoking. ○ Avoid NSAIDs. ○ Avoid contrast medium. Medications ● Phosphate binders ○ Got too much phosphate. ○ Take them before meals, similar to PERT. ● Digoxin ○ Risk for dig toxicity due to high K+ levels. ● Meds taken for complications of CKD such as Kayexalate or D50 and IV regular insulin for hyperkalemia events. ● ACEs/ARBs taken for HTN or HF that positively impact CKD.

43 ● NSAIDs taken for a different cause but are nephrotoxic. Renal replacement therapies ● Hemodialysis ○ The extracorporeal circuit serves as an external kidney. The patients’ blood passes through an artificial membrane to perform the filtering, absorption, and excretion functions. ○ Traditionally done 3x/week in an outpatient center ○ Roughly 4 hours per treatment ○ For in home hemodialysis, there must be a specific water system treatment installed and a backup generator. ○ Must have a skilled partner for in home dialysis. ○ AV fistula/ AV graft ■ Assessment needs to include feeling of thrill and hearing a bruit over the site to determine patency of the site. Also, need to check for adequate circulation distal to the fistula or graft. ■ Pts instructed not to carry heavy objects w/ the affected arm or to sleep with their body weight on that arm. ■ No IV sticks, lab draws, or BPs on that extremity. ■ LIMB ALERT Splash of knowledge on Hemodialysis ● Element movement ○ Sodium and potassium typically move out of the plasma into the dialysate. ○ Bicarb and calcium will move from dialysate into the plasma. ● Warming dialysate ○ Warm to roughly 100 degrees F, which will increase rate of diffusion and prevent hypothermia during hemodialysis treatment. ○ Dialysate does not need to be sterile. ● Heparin usage ○ Used to prevent clots in dialyzer. ○ Be cautious for about 4-6 hours after hemodialysis tx because the pt. is at risk for bleeding. ○ Protamine sulfate is the antidote for heparin. ● Hypotension risk ○ Hemodialysis predisposes the pt. to hypotension. ○ Do not have hemodialysis pts eat a meal 2 hours before a hemodialysis tx. ● Medication administration ○ General rule of thumb is no PO, or IV meds given before the HD tx since they will most likely be removed during the dialysis tx. ○ We need to really be cautious with any antihypertensive medications because HD predisposes pts to HoTN. ○ Once HD tx is finished, the pts meds may need to be staggered throughout the day. ● Weights ○ Pre-dialysis weight and post-dialysis weight ● Nutrition ○ Restrictions on sodium, potassium, and phosphorus ○ Fluid restrictions, usually 1.5-2L ○ Protein will be controlled. ● Concerns prior to HD: fluid overload, hyperkalemia, metabolic acidosis. ● Concerns after hemodialysis: hypovolemia, hypotension, bleeding. Continuous renal replacement therapy (CRRT) ● Hour to hour method of using dialysis on pts that have unstable hemodynamics and cardiovascular instability. ● Only about ⅓ to ½ unit of blood is out of the body at any given time. ● Blood works every 4-8 hrs. ● Can use in AKI for managing fluid overload, hyperkalemia, and metabolic acidosis. ● Use in CKD and ESKD for pts that are hemodynamically unstable.

44 Peritoneal Dialysis ● Peritoneal membrane serves as the filtrate mechanism, using diffusion and osmosis, much like the nephrons would. ● Dialysate is what the fluid is called during inflow into the peritoneal cavity and peritoneal effluent is what the fluid is called during outflow from the peritoneal cavity. ● Peritoneal dialysis exchanges are done throughout a 24-hour period. ● Exchange: Fill, dwell, drain ○ Fill dialysate into peritoneal cavity. ○ During dwell time in peritoneal cavity, the peritoneal membrane serves as a mechanism for filtering. ○ When the fluid is drained from the peritoneal cavity, the elements of waste are removed- think of this as the pts urine and it should resemble urine in color and clarity. ● Procedure: drain, fill, dwell ○ Must empty to fill, then fill, then dwell ○ Drain after 4 hours of dwelling and weigh the bag of effluent, the wt. is compared to the wt. of the dialysate that was instilled 4 hours prior, not the wt. of the dialysate that is about to be instilled. Splash of knowledge on Peritoneal Dialysis ● Peritonitis ○ When doing the exchange, everyone in the room must wear a mask. ○ Contamination of the transfer set is the primary cause of peritonitis. ○ Avoid lakes, hot tubs, and other water that is not chlorinated. ○ Assess peritoneal effluent, such as emergence of a cloudy opaque characteristic in the urine output (indicative of peritonitis) ○ Pt may also experience abd. pain and tenderness, N/V, and fever (Report to HCP) ● Constipation ○ Another complication is poor outflow due to constipation, give stool softeners! ○ If there is an outflow problem during an exchange, we can reposition the pt. during the drain time to see if that helps. ● Warming dialysate ○ Decreases abdominal discomfort. ○ Facilitates faster diffusion. ○ In practice setting, K pads are used. ○ Microwaves are not to be used. ● Weights ○ “Dry weight”- when abd. cavity is empty of the dialysate- after the drain time but before the dwell time. ● Dialysate elements ○ Little bit of heparin -prevents clotting in PD catheter, not absorbed systemically -NO bleeding risk like with HD. ● Nutritional focus ○ Do not have to have restrictions on their potassium. ○ Minimal restrictions on their sodium unless they have other comorbidities. ○ Control of their protein and management of their fluid intake is not as restrictive, again, unless they have other comorbidities. Kidney transplant ● Several ways a recipient can have a donor: ○ Living donor (pt. will usually receive blood transfusion from donor before sx) ○ Non-heart beating donor. ○ Cadaveric donor ● Two things the donor must have to be qualified. ○ Viable organ ○ Consent ■ Old kidney usually not removed with a kidney transplant.

45 ■ There are several suture sites so post-op assessment of renal function with regards to flow is important - ensuring the flow is forward and not backing up causing pressure or retention on those suture sites. ■ Recipient usually requires dialysis within 24 hours of the sx, gives new kidney a bridge before picking up the functions. Splash of knowledge of Kidney transplantation ● Donor ○ Pre and post op care ○ Need psychosocial care. ● Recipient ○ Pre and post op care ○ Need psychosocial care. ○ Accurate I&Os and daily weight ○ Foley 3-5 days post-op and urine will be pink, or blood tinged to start. ○ UOP of >100mL per hour is expected and wanted. ○ Hourly urine output will be essential as oliguria or diuresis can occur. ■ With oliguria, can expect diuretics or mannitol used and need to hone out assessment skills on signs and symptoms of fluid overload, the occurrence of HTN (which can impede blood flow) and pulmonary edema. ■ With diuresis, can expect to monitor BP as this fluid loss leads to hypotension and a reduction in renal blood flow and renal oxygenation to the new kidney- threatening survival of new graft. ● Prevent rejection. ○ Immunosuppressant medications for life of kidney are used to prevent rejection, rejection is the leading cause of graft loss. ○ Infection is major cause of death. ○ Delicate balance between enhancing healing and preventing infection and preventing rejection of the graft. Normal Lab Values: Calcium: 8.5-10.5 HCT: 37-47% W 42-52% M Total Chol: 130-200 Albumin: 3.4-5.0 Phosphorus: 2.5-4.5 BUN: 10-20 Triglycerides: <150 Vasodilator: Nitrate/Nitro WBC: 5,000-10,000 Specific Gravity: 1.010-1.030 Creatinine: 0.5-1.2 Vasopressors: Epi, Norepi (Levophen) HGB: 12-16 F 14-18 m Bilirubin: <1.0 mg/dL GFR: >90 Inotropes: Dopamine, dobutamine