Nursing 405 EXAM 2 REVIEW RESPIRATORY Assessment: -Pulmonary Circulation: The distance b/w pulmonary capillaries and alveoli

li is minimal so diffusion can occur rapidly -Pulmonary Capillaries: easily damaged by pressure (PHPT) and increased TV Normal PAP 20-30/10-15 -Pulmonary HTN: Pulmonary Artery Pressure PAP: 60/28 Pulmonary Capillary Wedge Pressure PCWP:10 -Inhalation: 1) air flows to 2) negative pressure in the pleural space 3)negative pressure generated by inhaling also causes increased venous return to the heart thus increasing preload (CVP) i. Negative Pressure: sucking in straw or vacuum cleaner ii. Positive Pressure: blowing out lowing bubbles or inflating a balloon -What controls breathing? 1) Brainstem and pons are the respiratory centers 2) chemicalsincreased CO2 and Decreased O2 -Brain death: determine level of brain damage: loss of reflexes (cough, gag, corneal), flaccidity, lack of resp Pulmonary Assessment: Dyspnea, SOB, Paroxysmal nocturnal dypsnea (PND) orthopnea, cough (nonproductive:not bacterial or viral), Chest Pain(stop activity, O2, assess pain-pleuritic or cardiac?), pleurisy(well localized, cutting/sharp pain) peripheral cyanosis(unreliable) thoracic configuration (tells you: 1) patient has underlying health issues 2) patient is at greater risk of developing pulmonary complications 3) be careful administering high levels of O2 to these patients COPDers, can take away their hypoxic drive), Respirations, Tachypnea(metabolic acidosis), Bradypnea(metabolic alkalosis, loss of hypoxic drive), WOB (accessory muscles?), Trachea midline, Palpation, Pain and tenderness, Crepitus, Oxygen Saturation (look at Hgb!!) Auscultation: i. Tracheal breath sounds: over trachea, loud and harsh ii. Bronchial breath sounds: over large airways they are normal; anywhere else they are not normal iii. Bronchovesicular: medium in pitch, heard over bronchioles iv. Vesicular: heard over distal airway, quiet and low pitched v. Crackles: inspiratory, fluid filled alveoli vi. Rhonchi: continuousfluid in the larger airways, often clears with cough and suctioning vii. Wheeze: inspiratory +/or expiratory indicates bronchconstriction viii. Pleural friction rub: heard best on inspiration, have patient hold breath to rule out pericardial rub ix. Diminished: shallow respirations r/t pain, obesity, ascites, etc. x. Absent: pneumothorax, atelectasis, pleural effusion -Arterial Blood Gases: ROME Respiratory Opposite, Metabolic Equal pH 7.35-7.45 HCO3 22-26 PaCO2 35-45 PaO2 80-100 -Respiratory: determined by PaCO2 levels ( normal 35-45) i. Hyperventilation: blows off CO2 thus lowering it (c/w respiratory alkalosis) ii. Hypoventilation: causes CO2 to be retained, thus increasing CO2 levels (c/w respiratory acidosis) -Metabolic: Bicarb = HCO3 = the metabolic component, normal levels 22-26 i. Too much HCO3 or too little acid, is c/w metabolic alkalosis ii. Too little HCO3 or too much acid is c/w metabolic acidosis Respiratory (pCO2) Acidosis pH <7.35 Respiratory Acidosis pCO2 45 I cant catch my breath Causes: COPD, Pulmonary Disease, Head trauma, over-sedation, anesthesia, drug OD, Guillian Barre, chest wall injury S/S: Hypoventilation, rapid shallow HCO3 22 Causes: Hypoperfusion, DKA, ASA overdose, ETOH S/S: Headache, weakness, nausea, disorientation, vomiting, hyperkalemia, Metabolic (HCO3) Metabolic Acidosis

respirations, dyspnea, headache, hyperkalemia, disorientation, CO, muscle weakness, hypoxia, hypotension, tachycardia, arrhythmias, drowsiness, coma, warm flushed skin Compensation: Kidneys will eliminate the H+ ions acidic urine; kidneys will retain HCO3 and K+, H+ ions go into the cells, kicking K+ out causing an in K+=hyperkalemia; H+ jumps onto Albumin, kicking Ca++ off= ionized calcium serum calcium Treatment: stop sedation, Narcan, pulmonary toilet, TCDB, elevate HOB, RR, suction, assess for loss of hypoxic drive in COPDers Alkalosis pH >7.45

arrhythmias, muscle twitching, hypotension, change in LOC, cold clammy skin, abdominal pain, Kussmaul Respirations (compensatory hyperventilation deep rapid RR) Compensation: RR to blow off CO2, kidneys eliminate H+ ions and hold on to K and HCO3. H+ goes into the cell, and K+ comes out of the cell = hyperkalemia, Ca++ jumps off of Albumin, H+ jumps on= ionized calcium serum calcium Treatment: Sodium Bicarb, treat the cause, improve perfusion and tissue oxygenation, correct DKA

Respiratory Alkalosis pCO2 35 Im scared and confused and dizzy! HCO3 26 Causes: fear, anxiety, pain S/S: Seizures, deep/rapid breathing, hyperventilation, confusion, dizziness, hypokalemia, numbness/tingling, light headedness, arrhythmias, tachycardia, sensitivity to digitalis, tetani, Compensation: Kidneys will conserve the H+ ions alkaline urine; kidneys will excrete HCO3 and K+, H+ ions goes out the cells, bringing K+ into the cell causing an in K+=hypokalemia; H+ jumps off of Albumin, bringing Ca++ off= ionized calcium, serum calcium Treatment: calm the patient, anti-anxiety meds, pain meds, increase sedation, decrease RR, re-breathing CO2

Metabolic Alkalosis

Causes: prolonged vomiting, gastric suctioning, over administration of antacids S/S: restlessness followed by lethargy, dysrhythmia, hypotension, decreased LOC, confusion, tetani, parasthesia, seizures, N/V, slow respirations, respiratory failure, hypokalemia Compensation: RR to retain CO2, kidneys eliminate K+ and HCO3, retain H+, H+ goes out of the cell, K+ goes into the cell= hypokalemia; H+ jumps off of albumin, Ca++ jumps on, ionized calcium serum calcium Treatment: replace K+ and Ca++, seizure precautions, vomiting tx, education

-Arterial Lines: can be used for continuous BP monitoring and to draw lab work, including ABGs ALWAYS confirm BP at the beginning of the shift and if changes occur by taking a manual cuff BP, ALWAYS observe and prevent hemorrhaging from the site -PCXR: used to determine lung pathology and line placement, done after procedures (ie CVC insertion) to r/o pneumothorax, acutely ill patients who are intubated generally have PCXR q day -Bronchoscopy: Tumor complications: check gag reflex (aspiration), bleeding, infection, bronchial perforation, Bronchospasm (Ambu) or laryngospasm (solumedrol), pneumothorax air becomes trapped in the pleural space causing the lung to collapse -Thoracentesis: Complications: bleeding (vitals, check site) Infection, pneumothorax (Ck BBS, CXR) Disorders: -Pneumothorax: Air enters space b/w visceral and parietal pleurae, results in partial or complete lung collapse 1. Spontaneous Pneumothorax- No obvious cause, can occur with or without underlying lung disease 2. Traumatic Pneumothorax- invasive procedures and barotraumas (pressure injury of the alveoli) r/t: mechanical ventilation other causes include blunt and penetrating trauma (As pressure in the pleural space rises, the lung collapses vital capacity (TV), ventilation-perfusion mismatch (V:Q) Hypoxemia; Hypercapnia c underlying pulmonary disease, client hyperventilating to PaO2,

Sudden onset of pleuritic pain, SOB, WOB, dyspnea, O2 sat, asymmetrical expansion, distant or absent BS on affected side, hyperresonant to percussion, crepitus, tachycardia, tachypnea i. Diagnosis and Treatment: CXR and ABGs, O2, insertion of chest tube to water seal or to suction 3. Tension Pneumothorax: air enters chest wall, unable to escape; air builds in the pleural space, progressively collapses lung; with no relief, pressure moves to heart and lungs on the unaffected side (mediastinal shift); vascular collapse occurs, followed by death i.Assessment: same as pneumothorax, plus: severe pain with respiratory distress (pts on vents will be restless, JVD, cyanosis, decreased O2 saturation, tracheal deviation, shock (decreased BP, increased HR, RR) NEED to document that trachea is midline during assessments with vent patients because of barotrauma ii.Treatment: when s/sxs of tension pneumo are present in a patient on vent, do not wait for CXR 1. MD must insert CT stat or 16 or 18 gauge needle in the 2nd ICS 2. Cook chest drain valve: cook chest drain valve, connection tubing, one-way stopcock, syringe and molnar disc with pull tie intended for one-time use, 2 ICS of affected side 3. CT move with inspiration and expirationmedicate patient before taking out chest tube, hold pressure on insertion site then put occlusive dressing on confirm CXR to be sure lung hasnt collapsed again. -Pulmonary Embolism50% originate from DVT VIRCHOWs TRIAD: Venous Stasis, Hypercoagulation, Injury to vein walls Other risk factors: birth control, obesity, varicose veins, RVHF, cancer, abdominal infections, sickle cell anemia, bedrest, trauma to LE, CVC lines, age (the risk doubles with each decade of life) Venous Stasis Hypercoag Vascular Injury Variscosities Malignant Ca IV injections Prolonged BR Blood disease Trauma Obesity Dehydration Ortho/Surg procedure Surgery Oral contraceptives Contrast Media CHF Some ATB Pregnancy -S/Sx: Varies on size of emboli, where it lodges in pulmonary circulation, preexisting heart or pulmonary disease -VQ Mismatch: Alveoli are ventilated but not perfused (V>Q) -Small to moderate PE: dyspnea, SOB, pleurtic CP, cough, restlessness, increased HR, RR, T, diaphoresis, apprehension, fear, decreased BS, crackles, wheezing; leg swelling and or pain (Homans sign dorsiflexion) -Massive PE: sudden shock-like symptoms (increased HR, decreased BP), Cyanosis, syncope, Hemoptysis r/t alveolar damage in infracted area, sudden increase in PASP indicating PHPT -Saddle Emboli: occur when it lodges in bifurcation of the main pulmonary artery; this often blocks blood flow from the right side of the heart; the result is death in most cases -Pulmonary Infarction: = dead lung tissue! causes above s/s + EKG changes all leads, lg blood clots expectorated -Diagnosis: VQ scan tells extent of the occlusion, amount of perfusion lost inhale contrast media, spiral CT, pulmonary angiogram: gives definitive diagnosis; supported by CXR, ABGs, ECG, D-Dimer (blood test that indicates degraded products of pulmonary infarcts contrast media is hard on the patient (monitor BUN and Cr need to be normal if not, no contrast media or it is diluted) Spiral CT/Angiogram: NPO, Need good PIV (PICCs get blown a lot) assess allergies, renal fx(BUN & Cr) prior ABGs may not show changes if embolus is small 1. Hyperventilation = decreased PaCO2 and increased pH 2. VQ mismatch = decreased PaO2 Medical Interventions: 1. Anticoagulation: Heparin bolus and drip initially, then lovenox (dose determined by renal function) Coumadin for 3-6 months; Thrombolytics are used only for massive PE who are hemodynamically unstable and likely to bleed //SIDE NOTE: IV Heparin is the only drip we titrate for PTT 2. Bedrest, immobilize source, O2, Pain meds: morphine, dilaudid 3. Embolectomy 4. Vena Cava Umbrella (has meds in it and it releases medication to prevent clots) --takes days to weeks for thrombus to be dissolved

Nursing Interventions 1. Administer O2 and elevate the HOB, assure bedrest immediately 2. Calm the patient, obtain ABGs, CXR, VS, Auscultate lung sounds, assess for DVT 3. Call the MD with findings 4. Draw PT/PTT/CBC stat, daily and prn 5. Start heparin drip at ordered rate, confirm rate with another RN or pharmacy 6. Obtain order for anti-ulcer medication (risk for bleeding) 7. Protect from injury, observe for bleeding 8. Measure extremity with DVT daily and record 9. Prevent in pts that are at risk: SCDs, ROM, Prophylactic anticoagulation, early ambulation, hydration -Respiratory Failure: a sudden life threatening condition in which there is CO2 retention and inadequate oxygenation -defined as: pH <7.35, paCO2 >50, paO2 <50 (In patients with normal baseline ABGs) -Causes: intrinsic pulmonary disease (obstructive sleep apnea, bronchitis, pneumonia), disease of the pleura and chest wall (pneumothorax), cardiovascular disease (p. edema, p.embolus), neuromuscular disease (MG), peripheral nerve and spinal cord disorders, disorders of the CNS (head injury, CVA) -Hypoxia: dyspnea (classic) increased WOB, cyanosis (PaO2 <50), restlessness, confusion, anxiety, delerium, increased RR, HR, BP, dysrhythmias, increased tremors (CO2 toxic to brain) RESTLESS -Hypercapnia: dyspnea, headache, (peripheral and conjunctival hypermia -- vasodilation), increased RR, HR, BP, ALOC r/t CO2 narcosis; Papilledema (IICP) these patients are SLEEPY -Diagnosis: definitive diagnosis is made by ABGs: tests to determine cause--> CXR, PFT, VQ Scan, Lab work, ECG, Sputum C & S, Angiography, CT, bronchoscopy, Thoracentesis Medical Management: determining if pt requires intubation is first priority-- hypoxia can result in lifethreatening dysrhythmias and anoxic encephalopathy (brain goes without O2 for too long = irreversible) -For decreased PaO2: give only as much O2 as it takes to increase SaO2 >90% or higher -For increased PaCO2: consider--> Oversedation: give narcan; Bronchospasm: bronchodilators and steroids; Infection: culture and antibiotics; CHF: digoxin, lasix, NTG, dobutamine Nursing Interventions: patient is red lift the head Elevate HOB, administer O2, Slow IVF or instert IV, Obtain ABGs and CXR, Assess the system, Call the doctor! -**Decrease O2 Demands, Increase O2 Supply!!! -Acute Respiratory Distress Syndrome (ARDS): Restrictive disorder which is a combination of associated symptoms in which there is widespread: atelectasis, pulmonary edema, stiff noncompliant lungs, increased airway resistance (PIP) 1. Hallmark of ARDS: arterial O2 levels in spite of O2 administration -- REFRACTORY HYPOXEMIA 2. Causes of ARDS: secondary to some bodily insult which alters capillary permeability: shock, sepsis, hyper/hypothermia, drug OD, DIC, pulmonary infections, burns SIRS, Coronary Bypass, aspiration, pancreatitis, multiple pRBCs 3. Systemic Insults can cause SIRS: SIRS = Systemic Inflammatory Response Syndrome the lungs may be the earliest and most common system affected by SIRS, most patients with ARDS manifest the s/s of SIRS 4. SIRS ARDS MODS: SIRS leads to a cascade of continuous cycle of ARDS and MODS (multi-system Organ Dysfunction Syndrome) 5. SIRS criteria: must have 2 or more of the following: T <96.8 or > 100.4, HR > 90, RR >20 or PaCO2 <32, WBC < 4,000 or >12,000 or more than 10% bands 6. Cytokines cause symtpoms: cytokines attract neutrophils to kill bacteria x. Neutrophils are WBCs that are activated early on in the inflammatory process xi. Cytokines produced fever, tachycardia, and tachypnea also create peripheral vasodilation 7. Earliest signs of ARDS: Dyspnea, confusion, RR and HR, BBS clear, No change on CXR until 12-24 hours 8. Less than 24 hours: WOB, signs of air hunger, restlessness, agitation, O2 levels despite O2 admin, (REFRACTORY HYPOXEMIA), CP, dysrhythmias, Metabolic Acidosis (contractility to heart muscle), with respiratory muscle fatigue r. acidosis and lethargy, coarse, bilateral crackles 9. Late S/sxs: Decreased BBS related to consolidation, Decreased lung compliance = Increased PIP (Peak inspiratory Airway Pressure), Increased PIP pneumothorax// Decreased CO, Decreased BP

Diagnosis: CXR(consolidation, pulmonary edema, infiltrates wet snowstorm), ABGs: initially hypoxemia, hypocapnia, and metabolic acidosis. later: hypercapnia with respiratory acidosis, Hx: usually young with history of injury within the last 72 hours. Culture blood, sputum, wound, urine; CT to rule out abscess, Interleukin 1 and TNF (Tumor necrosis factor) levels; arterial lactate levels; PA catheter readings i. Treatment: Intubation, PEEP (to overcome non-compliant lungs but this risk of barotrauma and tension pneumo), ECMO, CONTINUOUS turning with pronator bed, Drug Therapy: Surfactant, Steroids, Ketoconazole (antifungal), antibiotics if known infection only, bronchodilators and mucolytics, sedation, paralytics, DVT prevention, antiu-ulcer medication 12. Nursing Interventions: i. Nutrition: preferably enteral feedings ii. Monitor labs, vs, hemodynamics, ABGs, PIP, I & O, daily weights and call abnormals iii. Prevent fluid overload in at risk patients iv. Sedate as necessary to prevent barotrauma v. Pulmonary Toilet 14. BEST treatment is PREVENTION TREATMENTS 1. Pulmonary Medications 1. Bronchodilators: Relieves bronchospasm, increases HR and CO, increases O2 demand, diuretic effect i. SE: nervousness, anxiety, arrhythmias, hold if HR is >150 or many PVCs ii. Effectiveness? Decreased RR, WOB, wheezing, restlessness, improved ABGs, improved BBS 2. Diuretics: Lasix edema in CHF, renal failure, pulmonary edema, preload (CVP), BP i. SE: hypoK, metabolic alkalosis, BP, polycythemia, DVT, thirst, tachy, hyperglycemia, BUN ii. Usually 10-40 mg but can be higher, administer slowly to avoid ototoxicity (10 -20 mg/min) If giving more than 40 mg, put on a mini-infuser or pump iii. Effectiveness? Decreased HR, RR, BP, CVP, PAP, PCWP, edema, JVD, crackles, SOB, WOB, no further S3, increased UOP, O2 sat, PaO2 // make sure you know how to calculate I and O, change weights to mL or L ( 1 kg = 1 L, 1 lb = approx 500 mL) if the Cr is increased, be careful administering Lasix iv. Nursing Precautions: ALWAYS obtain BP and K before giving, hold if SBP <100 (CVP <8 CALL MD PTA) Hold if K < 3.5 ( <4.0 if no K ordered) watch trends, Consider foley, give in the AM, call MD if no increase in UOP i. Oxygen (considered a drug): > 4 L/m via NC humidified. > 60% O2 over 36 hours or 100% over 24 hours can result in O2 toxicity, can result in ARDS, Give lowest O2 necessary, S/S O2 toxicity: tickling in the throat, cough, burning of the trachea/bronchus (early) DOE, n/v, h/a (late) 2. Anticoagulation Therapy: used in the treatment and prevention of pulmonary embolus d/t immobility, arrhythmias, DIC, heart surgery, stroke, MI, dialysis, and cardiopulmonary bypass pump Heparin, Lovenox (decreased risk of bleeding), Coumadin , make sure you know how to titrate and administer heparin -Nursing Precautions: Monitor coag studies prior to treatment and as needed (before invasive procedures), hemoccult stool, emesis and NGT drainage, protect from injury, anti-ulcer medications, hold pressure to all lab sticks, hold medication and call MD prior to invasive procedures 3. Morphine Sulfate: the single most effective drug in the treatment of pulmonary edema decreases anxiety, venous dilator (decreases preload), arterial dilator (decreases afterload) decreases O2 demands, bronchodilates -Nursing precautions: hold med or give with extreme caution if SBP <90 mmHg, Hold if RR <12, antidote is Narcan, evaluate effectiveness, S/E: vomiting 4. Sodium Bicarbonate: usually given for Metabolic Acidotic States, doseage determined by ABGs, 1 amp = 50 mEqs of NAHCO3, flush before and after administering 5. Digoxin (Lanoxin): increase contractility increase CO and WOH, decreased HR increased SV// therapeutic level = 0.5-2.0; monitor serum blood levels. >2.0 is toxic, increased risk of toxicity with hypokalemia; S/Sx toxicity brady-tachy syndrome, green halos, nausea and vomiting 6. Steroids: Solucortef/Solumedrol: given to reduce inflammation, increase glucose, NA and H20 retention, risk of GI bleeding; causes immunosuppression (increase WBC counts and fever are not always seen with infection) you

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need to look for other s/s of infection -- must be weaned to prevent adrenal insufficiency; causes bone loss, must have food before taking med PO; available in different strengths -- monitor glucose, hemoccult stools/gastric secretions, daily weights, observe for s/s infection, anti-ulcer medication Vasodilator therapy: nitro or nipride IV drips -- NTG preload > afterload> work of heart Tx: ACS and CHF -Nipride decreases afterload > preload increases CO decreasing pulmonary congestion and LVHF, Tx: pulmonary edema, HPT crisis -Nursing Precautions: infuse via pump only, titrate drip up and down slowly, monitor BP q 5 when starting therapy, then q 15-30, observe cyanide toxicity with nipride Cyanide Toxicity -early s/sx: metabolic acidosis, tinnitus, blurred vision, delirium, dyspnea, h/a, vomiting, need to increase drug doseage to maintain the same effect on BP (Refractory HTN) -late s/sx: coma, widely dilated pupils, distant heart sounds -Monitor labs (thicyanate levels and methemoglobin) Antibiotics: often give broad-spectrum ATB until organism is identified or ruled out -at risk for infection d/t: mechanical ventilation, steroids, decreased immune response, debilitated health and cross contamination from health care providers -obtain cultures first if possible, note allergies, monitor serum drug levels if appropriate (call md if < or > than therapeutic PTA) -Sensitivity/S= that bacteria is sensitive to that drug MRSA is sensitive to Vancomycin Sedation: the use of sedation has been found to reduce ventilator and ICU length of stay by half -Proprofol/Diprivan decrease BP and increase triglycerides, precedex--> sedative; ativan IVP or dip, versed -opiate, benzodiazepines (versed and Ativan), haldol, propofol (diprivan) IVP or drip -given to reduce anxiety associated with intubation -Opiates and benzodiazepines must be weaned off if given for 2 or more weeks, HALDOL for withdrawal i. Propofol: rapid acting and short half life, need to stop once a shift/day to assess neuro status (daily interruption), will increase serum lipid levels and lower BP (consider another med if pt has hyperlipidemia) monitor lipid levels, use short term only, rare but fatal propofol syndrome= metabolic acidosis and vascular collapse// given in mcg/kilo/min increase if tachypneic, restless, agitated, respiratory alkalosis// decrease if bradypneic, respiratory acidosis comatose does not produce analgesia, it is a hypnotic Paralytics: Neuromuscular Blocking Agents -- used when there is WOB and hemodynamic instability after intubation and maximum sedation -- used to oxygenation and prevent barotrauma (alveolar rupture) // these drugs do not provide sedation or analgesia, they DO chemically paralyze the patient 1) SEDATE then 2) paralyze -Nursing precautions: patient must ALWAYS be monitored and never left unattended, stop daily to assess neuro system, frequent peripheral nerve stimulation must be performed to assess the level of neuromuscular blockade -- i.e. Nimbex: titrate by Train of Four Pulmonary Toilet: TCDB, vibro-percussion, postural drainage, suction, incentive spirometry Rotoprone beds 1. Kinetic Therapy: turns the patient side to side continuously 2. Prone: automates the rotation to place the pt in a prone position 3. Rotoprone: places the pt prone while rotating side to side 4. Benefits: facilitates drainage of pulmonary secretions, decreases pleural pressures in the dependent portions of the lungs, eliminates compression of the lungs by the heart, improves ventilation and perfusion mismatching 5. SPECIAL CARE FOR PRONATION: Keep patient in reverse trendelenburg, avoid direct pressure on the eye, apply ointment (lacrilube) to the eyes, remove face mask and apply cold packs when supine to reduce edema, feed with post-pyoric dobhoff tube and start slow, keep ETT midline since there can be swelling of lips and tongue, replace face pack foams q 72 hours, know where the CPR button is!!! Oxygen Therapy: Nasal cannula (NC), venimask (VM), Partial Nonrebreather (PNRB), Nonrebreather (NRB), BiPAP and CPAP, Endotracheal Tube (ETT), Tracheostomy tube (Trach), Trach collar (TC) Noninvasive Positive Pressure Ventilation: can use nasal or full face, improves alveolar ventilation, decreases WOB, preserves the ability to swallow speak and cough normally

17. BiPAP vs. CPAP: Bi-level positive airway pressure delivers a higher pressure on inspiration than exhalation. can be used to ventilate patient// Continuous positive airway pressure delivers the same pressure during inspiration and expiration which helps re-expand and stabilize the alveoli. The pt must have spontaneous respirations 18. Airway Maintenance 1. Oral Airway: use in conscious patients only: use tongue blade to depress tongue and insert directly into mouth, position curved end toward the roof of the mouth and rotate 180 degrees i. Tracheostomy: used when ETT cannot be inserted or is contraindicated or when prolonged mechanical ventilation is required, usually done in the OR but can be done at the bedside -obtain PT/PTT, Ck with MD to hold anticoagulants, watch for bleeding after insertion, do not change ties or manipulate trach without MD order, give humidified O2 to prevent dehydration; hyper-oxygenate before suctioning -- sterile procedure, trach care q shift, keep cuff inflated when eating, keep additional trach at the bedside for emergencies ii. Mechanical Ventilation: the process in which a positive force is generated in the airway to inflate the lungs with humidified oxygenated air iii. Indications of Intubation: apnea, decreased RR, hypoxemia/hypoxia, aspiration, severe cardiopulmonary disease, smoke inhalation, thoracic trauma/surgery iv. Alarms: low pressure -- there is a leak in the system, check all connections; high pressure -something is obstructing air flow (decreased compliance, mucous plug, secretions). Suction patient. may require sedation, make sure they are not lying on the tubing, ambu, bronchoscopy v. What if you cant figure out the cause? first priority is the patient! ambu bag with 100%O2, have someone else check the machine -- alarms must be on ALWAYS (delay can be set for suctioning) vi. Nursing care with patient on MV: Check ETT placement (lipline) q shift and prn, check CXR. ABGs after insertion and QD, auscultate BBS q 4 hours and prn, suction only when necessary (sterile) Respiratory Acidosis: MD will increase RR, nurse should decrease sedation, implement pulmonary toilet; Respiratory Alkalosis: assess for cause, sedate, treat pain, fever, etc; high O2 levels: nurse can decrease FiO2 if MD ordered titrate O2 levels vii. Suctioning: Hyper-oxygenate with 100% O2 for 2 to prevent hypoxia, insert catheter as far as possible without applying suction-- apply intermittent suction while withdrawing and rotating catheter over less than 10 seconds-- ALWAYS observe heart monitor when suctioning for: arrhythmias: PVCs (hypoxia), Bradycardia (vagal stimulation), decreased saturation -- stop suctioning and give 100% O2, if prolonged then treat with DOC viii. VAP: leading cause of death in ICU, pneumonia that occurs 48 hours or more s/p intubation C cuff, should be inflated at 20 cm H20 H HOB elevated 30-45 degrees at all times unless contraindicated O oral care, brush teeth at least 2x daily O order enteral feedings (should be ordered w/in 48 hrs, preserve the GI mucosa, decreases translocation of bacteria) S suction subglottic secretions E ETT with dorsal lumen allows continuous drainage of tracheal secretions N no saline lavage which may dislodge bacteria in the ETT or catheter O orotracheal intubation is preferred V ventilator circuits, change only when needed, empty condensation A ambu bag, disposable on all patients P please wash hands i. Weaning: describes the process of allowing the patient to breathe with less assistance from the ventilator, by decreasing RR, TV and or FiO2 the patient develops greater strength for extubation, also demonstrates patients ability to tolerate extubation, greater success with weaning if well nourished and has normal Po4 levels (nl= 2.54.5) Should begin in early hours of the day, explain the procedure to the patient, sit them up in bed, monitor patient closely for signs of intolerance to weaning 1. Readiness criteria: hemodynamically stable (the absence of active myocardial ischemia and the absence of clinically important hypotension) --patients receiving low dose vasopressors or none at all may be considered for weaning SaO2 >92% on 40% FiO2 or less, PEEP < or equal to 5 cm H20, CXR, ABGs, lytes WNL for patient, Hematocrit >25%

2. Stop the weaning if: RR > 35, Hr > 20% or higher than baseline, SBP > 180 or <90, SaO2 <90% (<92% if anemic), TV <5 ml/kg, S/S distress: labored breathing, anxiety, restlessness, diaphoresis, arrhythmias 3. Extubation Criteria: alert and follows commands, good cough and gag reflex, able to move air around the ETT when cuff is deflated and nd of tube is occluded 4. Extubation: patient is oropharyngeal suctioned, cuff is deflated and ETT removed while patient coughs and suctioned per ETT, immediately place pt on O2 mask with humidification, observe for stridor, intolerance, prepare to reintubate, steroids for stridor) 5. Complications of MV: aspiration, self extubation, bronchospasm, ventilatior malfunction, tracheal stenosis and Malacia, VAP, pneumothorax, GI bleed 6. CM Tension Pneumo on vent: increasing Peak Airway Pressure (PAP), HR, RR, decreased O2 Saturation and BP, tracheal deviation, restlessness TRAUMA -Goal of Trauma nursing care is to DECREASE MORTALITY. Improve hospital care in the Golden Hour. -REMEMBER THE ABCs during triage: treat the most life-threatened first (with MCIs treat middle third) -ER TRIAGE Level 1 (trauma) Level 2 (Cardiopulmonary Arrest) Level 3 (Abdominal Pain) Level 4 (minor fractures/sprains) Level 5 (Rash) -On the scene: Establish airway, control external hemorrhage, IV therapy, immobilize spine/extremities, neuro A Airway remove obstructions, blood, vom, secretions, maintain patent airway. Anyone with a Glasgow coma scale score of <8 needs ETT (lowest is 3). Clear airway WITHOUT stim of gag reflex Intubation: NOT with oro-nasal traumaif pt is alert get them to a position of max breathing capabilities B Breathing spontaneous? Rate, depth, skin color, pattern. With ineffective breathing administer O2, assist with ambu, ETT, tx before moving on to circulation. R/T: tension/pneumo/hemo, contusion, flail chest C Circulation PULSES -find central pulse (carotid/femoral), rate, look for external bleeding. If ineffective: tachy, distant heart sounds, ALOC, uncontrolled bleeding, JVD, pale/cool skin. Control bleeding with pressure, tourniquets, elevation of extremity -HYPOVOLEMIC shock is most common type of shock for trauma pts. (trauma, dehydration, sepsis, burns) R/T loss of whole blood, third spacing. -Classes of shock: Class 1 = minimal Class 4 = Worst Circulation interventions: Start IV, infuse ISOTONIC, warm fluids, use blood tubing/rapid infusion device, give 2L NS IV bolus, if BP is still low, give blood. Consider pneumatic anti-shock garment, obtain samples (T/C, H/H, ETOH) IF CIRCULATION IS ABSENT: Start CPR, ACLS, Administer blood. Tx life-threatening conditions such as bleeding, shock, cardiac tamponade, direct cardiac injury Cardiac Tamponade: LOOK FOR BECKs TRIAD: Hypotension, JVD, Muffled heart sounds ABC (D) Disability : Brief neuro assessment AVPU (alert, verbal stim, painful stim, unresponsive) Look at pupils, LOC, talking?, monitor ABCs, if suspected IICP hyperventilate ***SECONDARY ASSESSMENT: E Exposure/Environmental control (cut clothing, PREVENT HEAT LOSS, warmers, warm IVF, etc.) F Full set of vitals/FIVE intervevntions/Facilitate Family presence (if trauma? BPs in both arms) FIVE: 1. Attach leads, monitor rhythm, rate 2. Attach pulse ox 3. Insert foley catheter NOT if bloody, prostate displaced, blood in scrotum, suspected pelvic fracture 4. Insert gastric tube pass carefully to prevent trauma/gag, have suction ready, test contents for blood 5. Draw blood (H/H, T/C, ETOH) type/cross ASAP! (priority) G Give comfort measures H History/ Head-to-toe assessment Trauma Death: 3 Phases Immediate Within minutes Early Within hours (usually r/t CNS injury of hemorrhage) Late days to weeks following the injury (usually r/t sepsis, MODS) *Death risks increase with prolonged extrication, hypothermia, CParrest, massive fluid resuscitation/blood transf.

HEMATOLOGICAL DISORDERS HIT Heparin Induced Thrombocytopenia DIC Disseminated Intravascular Coagulation HIT AKA(White Clot Syndrome) -Decreased platelets related to platelet aggregation and thrombi formation -Causes clot formation limb/organ ischemia and death TYPE 1: asymptomatic (can occur 24 hrs after starting heparin), decreased platelets r/t aggregation, resolves when Heparin is d/cd, NON IMMUNOLOGICAL TYPE 2: IMMUNOLOGICAL, IgG and IgM bind to complexes.platelets are activated =arterial AND venous clots -Mortality: 25-37% -Amputation: Required by 20% - usually limb through which Heparin is infusing -Diagnosed when Platelet count drops: <100,000 (or 50% less than baseline) SEROTONIN RELEASE TEST confirms diagnosis (exclude other causes, DIC, meds, etc.) CM of HIT: A. FIRST complaint is PAIN AT IV SITE of Heparin infusion B. Cyanosis of fingers/toes C. S/Sxs pulmonary infarction, MI, ARF, CNS, CVA Prevention: Use Low-Molecular Weight Heparin Lovenox! Treatment: STOP HEPARIN Lepirudin: inhibits free and clot bound thrombin so clots dont form Agratoban: synthetic thrombin inhibitor Nursing Interventions: 1. Assure pt gets NO hidden heparin (IVF with other meds?) 2. Circulation checks Q1-2 hours 3. Notify MD immediately if s/sxs of ischemia occur 4. Manage pain 5. Prevent vasoconstriction DIC Syndrome of DIFFUSE CLOTTING and hemorrhage -Can cause severe organ damage and deathALWAYS a complication of another condition, major insult to body (shock, vasculitis, liver ds, heat stroke, blood replacement, brain injury, fluid emboli, OBGYN, trauma, surgery, etc.) - 20% of cases due to Gram Neg bacteriemia. Sepsis, cancer exposed endothelium -PATHO: triggers (INSULT) pro-inflammatory cytokines clotting cascade activated microclots in capillaries obstructed capillaries tissue/organ hypoperfusion ischemia/necrosis depletion of clotting factors clots unable to form in areas of injury hemorrhaging -For testing purposes, just know there are 2 pathways by which this occurs: intrinsic and extrinsic -Plasmin is generated (fibrin degradation products FDP) SUPER high D-Dimer levels. Interferes with platelet function and clot formation = bleeding. CM of DIC: A. No predictable pattern! B. s/sxs depend on severity of bleeding AND extent of organ damage C. BLEEDING!! Abrupt, becomes severe, oozing puncture sites, FRANK incision bleeding/OBGYN, can result in hemorrhagic shock. D. Thrombosis less obvious to detect, acrocyanosis, ARF, PE, abdominal pain, confusion/seizures/focal deficits Diagnosis: No lab test confirms, just know which labs are elevated and which labs are decreased INCREASED: PT, PTT, INR, FDP, D-Dimer DECREASED: Platelets, fibrinogen, Factor V Assay, Antithrombin III -Also increases in RBC morphology: Schistocytes abnormal size and shape RBC r/t moving thru occluded vessels, around clots -D-Dimer: =fibrinolysis, tells you clots are being lysed. Higher the number, the more clot dissolution is occurring -FDP: released when clots break down. Contain anti-coagulant properties that worsen bleeding when released

**KNOW THIS TABLE::: PT/INR PTT Platelets Fibrinogen FDP D-Dimer

LAB VALUE

SUGGESTIVE OF DIC ANY elevation ANY elevation <50,000 <100 >40 >250

ACUTE DIC: Inappropriate clotting (cyanosis, ALOC, PE, ARF, gangrene, bowel ischemia/infarct) then bleeding! Medical Interventions: PREVENTION! Eliminate the cause, atb, anti-fungals, anti-neoplastics, rehydrate, O2 Blood Transfusions: -consent, type/screen vs. type/cross, 2 RNs must confirm, start SLOW, <4hrs hanging, lasix b/w units, watch CHF PRBCs given for Hgb <8 or rapid blood loss FFP given for increased PT, PTT Platelets if < 10,000 with clinical bleeding Cryo Fibrinogen <100 Medical interventions: FFP, Cryo, PLT Vasopressors controversial use with extreme care (extremities already shutting down, BP is low) Lovenox/Heparin (not with trauma, surgery) use to tx cycle of clotting Epsilon inhibits fibrinolysis Protein C restores normal anticoagulation pathway Xygris Slows uncontrolled clotting in early sepsis only (STRINGENT CRITERIA) Eliminate all drugs that will enhance bleeding (except lovenox/heparin) Repeat all labs Q4 or as ordered (arterial lines, CVCs important here) Nursing Interventions: ABCs, warm blood products/IVF, watch hyper/hypovolemia, check all systems for complications NO: lab sticks, manual/auto BPs Hold pressure on puncture sites 15-30mins Topical hemostats PRN (fibrin, glue, thrombin gel, etc.) Suction LOW, good/gentle skin and oral care, MANAGE PAIN (BP with meds), stay calm Pulmonary: O2, ABGs, TCDB, IS, suction Cardio: circulation, LOC, UOP, vitals, CVP/PAP/PCWP/CO/SVR, lactic acid levels (infarct) Hematologic: PT, PTT, CBC, FDP, Fibrinogen, bleeding, weigh dressings, ct pads, measure fluids F/E: daily weights, I/O, monitor IVF/lytes, daily labs, CVP, watch EKG for lyte imbalances Safety: pad siderails, no sharp objects, assist OOB, watch bruising/bleding Pain: assess ischemia/infarction, warm compresses, analgesics, keep room/pt. warm HYPOVOLEMIC SHOCK :: DKA :: HHNKS Diabetic Ketoacidosis:: DKA Etiologies: Infection PNEUMONIA and UTI, diabetes (more type II than I, related to secretory defects of insulin, omitted/inadequate dosages of insulin, physical or emotional stress DKA is a syndrome of: 1) Hyperglycemia 2) Ketosis 3) Acidosis KNOW THIS: Glucose parameters according to the ADA: Fasting glucose 90-130 Post-Prandial glucose < 180 HgbA1c < 7% DKA Patho: secondary to lack of insulin increase in stress hormones liver converts glycogen to glucose fat burning for energy results in abnormal CHO, protein, fat metabolism. -Under-utilization of insulin for normal metabolism adipose tissue breakdown into fatty acids, glycerol ketone production decreased Bicarb. DKA is hyperglycemia anywhere between 250-800 mg/dl - 3 Ps Polyuria, Polydipsia, Polyphagia

-Ketonuria, weak acids, decreased pH, weight loss, metabolic acidosis, HCO3 <15, increased appetite -Poor tissue perfusion is what causes lactic acid levels to rise. -Pts may have offsetting alkalosis r/t vomiting or diuretics. Severe acidosis can turn into alkalosis DKA Hypovolemia dehydration = increased thirst/appetite, hyperglycemia leads to osmotic dieresis after renal threshold of sugars at 180 is exceeded. Body will try to pee off the extra sugar, urine loss-large amts of Na, Cl, K** -Electrolyte imbalances thru osmotic dieresis because fluid shifts from intracellular to extracellular LOW: Cl, Mag, Phosphate HIGH: H/H, BUN, Creatinine, especially K(often elevated, acidosis exchange H for K) DKA Patient Symptomology: Leukocytosis: Increased WBC, r/t hemoconcentration, ketosis, infection, MI, pancreatitis Amylase: elevation (hypertonicity or hypoperfusion) with persistent belly pain must r/o other causes Lipase: elevation may be indicative of pancreatitis Urinalysis: r/o UTI, look for ketones, glucose -Insulin dosages/taken, Hx, fatigue, dehydration, -Shocky sxs (tachy, hypotension, anuria, dry mucous membranes, poor skin turgor), abnormal CHO metabolism, osmotic dieresis = dehydration -N/V, abdominal pain, belly pain (not perfusing gut), acidosis/decreased mesenteric perfusion, must r/o other abdominal pathos (liver congestion, ileus), may require NGT -Kussmalls breathing (deep, sighing respirations) pt is attempting to blow off ketones, correct metabolic acidosis, OR may have tachypnea -Normo/Hyperthermia- usually fever, but body may not have enough energy to generate fever in infected state -FRUITY BREATH blowing off acetone from fat breakdown -ALOC, check sources of infection, GI bleed must r/o all other causes of the DKA Treatments: -IV Fluid Goals: insulin administration, electrolyte replacement -tissue perfusion (especially renal), loss of glucose in urine (IVF/hydration alone may correct glucose by 23%) -Pts usually need around 6 Liters of replacement (5-8) -WATCH so we dont overhydrate at risk populations! (Renal, Cardiac hx, CHF, FVO) -Most popularly used treatment plan: 1-2 L 0.9 over 1-2 hours for hydration 500 ml/hr of 0.9 NS until hemodynamically stable 250 ml/hr of plain 0.45 NaCl (to replace free water deficit, more 0.9 would be hypernatremia) ADD Dextrose to IV when glucose <250 (generally 5% solution, D5/.45 May hang D10-20 if sugars remain <100 -Insulin Therapy: DO NOT start insulin until BP is stable!! (can cause vascular collapse d/t rapid fluid shifts into intracellular spaces) Insulin drives K INTO the cell Do not start until K >3.3 (pt. could also be hyperkalemic d/t H and K shifts!) PROTOCOL: Run first 25cc through tubing @ time of new bag/tubing. Insulin adheres to tube walls GOAL: Dec sugars by 50-75/hrany faster can cause cerebral edema r/t rapid fluid shifts in the brain. ***LOW SUGARS KILL BEFORE HIGH SUGARS*** -If pt. is shocky, dont give them SQ or IM injections. Once vasculature opens up, theyll get too much -Start SQ insulin once ketosis has resolved/pt is eating again. 2 hrs post 1st dose, can d/c insulin drip -FIRST DKA insulin dose is divided into IV Bolus, and SQ or IM -Know your oral and SQ agents!! 3 types work differently (stimulate pancreatic insulin secretion, sensitize body to insulin, OR slow absorption of glucose) -Hypoglycemia Treatment: -6 oz milk, orange juice (apple juice for renal pts), 2-4 crackers, recheck sugar in 15 mins -With sugars <60 watch LOC changes, call MD stat, Need IV access!!, start D5/.45, recheck glucose -Hyperglycemia Treatment: (>400) -After capillary glucose, obtain STAT serum glucose, notify MD -DKA Potassium Replacement Therapy: LOW (r/t osmotic dieresis, emesis), HIGH (r/t acidosis, H and K shifts) -Body cant decide which to treat first, the K or the acidosis. Doesnt like either. -Start replacement when K <5.5 or 5.0 (Remember insulin drives K INTO the cell!)

-If K is 5.5 3.5 20 mEq/L -If K is < 3.5 40 mEq/L (Possibly K riders too) -DKA HCO3 Treatment: May ONLY be used for pH < 7.0. (Doesnt help much, not supported by literature) -WHEN IS DKA RESOLVED??? (studies show that insulin drip be continued for 7 hrs AFTER glucose is WNL) - Sugars <200 -HCO3 is 18+ -Venous pH > 7.3 Hyperosmolar Hyperglycemic Nonketotic Acidosis:: Most s/sxs similar to DKA, Treatment also similar (insulin and fluids) -Life threatening endocrine d/o MOSTLY new (undiagnosed) Type II. Mortality 10-35%, sicker, more dehydrated -NON KETOTIC and NON ACIDOTIC!**** Since its non-insulin dependent, insulin levels are still high enough to prevent lipolysis and ketone formation. -Causes: same as DKA, Infection, pneumonia, UTI, sepsis -Etiologies: Type II Diabetics, poorly controlled, increased insulin resistance, excecssive CHO intake Meds: beta-blockers, thiazides, loop diuretics(insulin secretion), corticosteroids ( insulin resistance) Also, parenteral nutrition has glucose and is hyperosmolar Elderly, co-morbidities, diuretic users, masked by infection or inability to treat thirst -Pathophysiology: DIURESIS = fluid deficit, underlying renal ds, H20/Na loss, GFR, with fluid loss, blood becomes thick and sticky = risk for thromboemboli (workload of heart, MI, RF, blood flow to brain, CVA) -Symptoms: weakness, N/V, dehydration, electrolyte shifts (more than with DKA), neuro sxs develop, lethargy, confusion, seizures, hemiparesis (missed dx as CVA). Poor turgor, cool extremities, thread pulses, hypotension, abd distention, Hypovolemic shock, infection, gastroparesis -Diagnosis: GLUCOSE >800-2000 Serum Osmo >320, pH >7.3 (no ketones, not fat-burning problem), profound osmotic dieresis, GFR because vasculature is dry -Treatment: 5 Steps1. Vigorous IV fluid treatment (8-10L, in first 18-24 hrs, rest in next 24 hrs. Start 0.9 then .45) 2. Electrolyte replacement (replace K <3.3) 3. IV insulin (do not decrease glucose by more than 50-75mg/dl)..fluids BEFORE insulin 4. Diagnosis of underlying causes 5. Prevention COMPARE/CONTRAST DKA and HHNKS: KNOW THIS! DKA Type I Diabetics Acidosis and Ketosis Sugars 250-800 Occurs over 1-2 days Non-hyperosmolar Lower mortality

HHNKS Type II Diabetics and older people Non-Acidotic and Non-Ketotic Sugars > 800-2000 Occurs 1-2 days to 2 weeks Hyperosmolar (thicker) blood/ALOC Higher mortality/sicker patients

ACUTE RENAL FAILURE -Sudden loss of renal function -Two hallmarks: DECREASED GFR and INCREASED BUN (azotemia, nitrogenous waste) -Any change in BP will also affect GFR/kidney perfusion. BP = GFR and vice versa -3 types: pre-renal, intra-renal, and post-renal PRE-RENAL kidney HYPOPERFUSION, most common, Pump failure (AMI, CHF, shock), RBF Also due to ACEI and NSAIDS (these drugs RBF) NSAIDS: pre-renal failure decreased GFR damages kidney. Causes decreased blood volume in pts with diuretics, dehydration, severe CHF, liver failure/ascites. and electrolytes: affects aldosterone so retains Na, K, H20 so BP and worse CHF. Hyperkalemia!

ACEIs: used to tx BP/HTN, decrease afterload, cardioprotective, nephroprotective for HTN and DM Problems because angiotensin affects vasoconstriction, GFR dependent on angiotensin II to SBP ACEIs = BP but we need higher pressures to perfuse kidneys to prevent pre-renal failure ACEIs interact with NSAIDS, antacids, increased risks of Lithium and Dig toxicity. Poss hyperkalemia INTRA-RENAL affects 4 parts of kidneys. r/t uncorrected pre-renal failure/prolonged hypertension 1. Glomeruli: lupus, glomerulonephritis 2. Vessels: scleroderma 3. Interstitium: infections, lymphoma 4. Renal Tubule: ATN (acute tubular necrosis) Due to nephrotoxic drugs: must draw peaks and troughs on these!!! -drawn on 3rd dose, peaks after 1 hour infusing, troughs 30 mins prior to next dose Can also be caused by abnormal BUN, Cr, contrast dye (use mucomyst and fluids) POST-RENAL Obstructive Renal Failure blocking urine outflow, distal to kidneys (ureter, bladder, urethra) Causes: BPH, bladder spasms, neoplasms, calculi, constriction, GYN tumors, retroperitoneal fibrosis Phases of Renal Failure: A) Onset: ischemic injury to kidney, GFR, lasts hours to days, **early tx is essential B) Oliguria/Anuria: UOP <360/24hrs, renal fx requires support, MAY be reversible, tx underlying cause Just know: oliguric is worse. Oliguria(cant pee, FVO, renal damage) Anuria (pee tons, not concentrated) C) Diuretic Phase: lasts 7-14days, gradual GFR but cant concentrate urine, electrolyte abnormalities Tx: maintain hydration, prevent lyte depletion, support renal fx D) Recovery Phase: takes several months year, 45% return to normal, some pts have permanent damage Nursing Interventions: be aware of renal impact, watch vitals/labs, foley??, check patency. erythropoetin OR hemodilution = RBCs, anemia For diuretic therapy pts: know home dosages!, too much? Pt is dry, watch pushing lasix (ototoxicity) Diagnosing Renal Failure: 1.) BUN. =byproduct of protein metabolism. Lose 2/3 of renal fx before increases. Normal 10-20 Elevated (dry): impaired renal fx, diseased or damaged, kidneys cant clear urea from bloodstream OR Renal hypoperfusion pump failure, fluid volume, RBF to excrete waste. Decreased: liver failure urea synthesized in liver, failure protein not metabolized BUN Negative Nitrogen balance, protein loss in urine/depletion 2.) Creatinine. =catabolic product of creatine phosphate used in skeletal muscle contractions. Cr and creatine dependent on muscle mass, excreted completely by kidneys. Normal is 0.5-1.5. (**MOST RELIABLE INDICATOR OF RENAL FUNCTION**) Elevated: occurs with obstruction, ATN, pump failure, shock, dehydration, rhabdo, injury, muscle bd Decreased: debilitation, decreased muscle mass (dystrophy, myasthenia gravis) 3.) Creatinine Clearance. Use 24hr urine collection, most reliable indicator of GFR. Void first then start collection, jug must be iced, put up signs so urine is not discarded Elevated: exercise, preg, increased RBF, high CO syndromes (anemia, obesity, cor pulmonale) Decreased: impaired kidney fx, renal artery atherosclerosis, any condition which RBF REVIEW MEDSURG LAMINATED SHEET ON ELECTROLYTES: ***Review normal values and all info on handout card for hyper and hypo natremia, -kalemia, -mag, -calcemia CHRONIC RENAL FAILURE -Impact of Chronic Renal Failure: NI: etiology is kidneylungs try to compensate.monitor ABGs, have good IVs Calcium/Phosphorus have an inverse relationship Hematological: erythropoetin, anemic pts, capillary fragility, monitor CBC, give procrit/eopgen Immunological: granulocytes, phagocytosis, monitor vitals, WBC, infection, watch meds c dialysis Skin: discoloration, bruising, dry glands, pruritus, uremic frost, brittle nails Diagnostic Testing: KUB and Ultrasound, CT (gastrograffin 12 in 12), NOT absorbed, no renal impact, Intravenous Pyelogram (IVP) visualize renal structures size and shape. -Hold Metformin, Glucophage 24 hrs prior to, 48 hrs after IV dye

-Treat with Mucomyst and hydration -Renal Biopsy is most invasive but best diagnostic test. BEDREST after 3 PHASES: 1.) Reduced Renal Reserve: loss of 40-75% of function, asymptomatic, Cr=2x normal, glomeruli size increase 2.) Renal Insufficiency: loss of 75-90% of function, Increased BUN, Cr=8x normal, polyuria, nocturia 3.) End Stage Renal Disease (ESRD): <10% function, all fx impaired, all lyte, BUN, Cr imbalanced Renal Replacement Therapy: A.) Peritoneal Dialysis: uses diffusion/osmosis to remove waste/fluid, concentrate, from peritoneal cavity 3 steps: Indwell (2L over 5-10mins), Dwell/Equilibration (clamp 30-60mins), Drainage (10-30 mins) B.) CAPD (continuous ambulatory), less extreme lab fluctuations, lyte levels better, usually 3-6x per day C.) CCPD (continuous cyclic), hooked up to machine at night over 8-12 hrs, less risk infection, normal life Dialysate has glucose: higher the dextrose, the more fluid it pulls! Warm everything, monitor glucose, meds First few sessions may be bloody after port placement, watch s/sxs infection, turn pt side-to-side, record strict I&O, watch for respiratory distress (too high fluid pushing on diaphragm) D.) Intermittent Hemodialysis: remove urea, Cr, uric acid, excess water, restores buffer system, lyte maintain Use AV fistula, AV graft, temporary access in subclavian/neck/groin. Nursing Care: HEAR the bruit and FEEL the THRILL, dont use that arm for BP, lab draws. E.) CRRT (continuous): for those with septicemia, nonrenal etiologies, SIRS, lactic acidosis, CHF, HD instability Types: SCUF (removes fluid), CVVH (removes fluid and waste) Kidney Transplants: Younger pt donors who die of stroke, HTN. Rather get 2 lower functioning kidneys than 1 higher fx Donor kidney placed (picture of 3), and old 2 are often left unless diseased or dead Rejection is based on immunological responses and can be either acute or chronic rejection Monitor for infection!!