NSG 472 Exam 2 Study Guide PDF

lOMoARcPSD|48217341 Renal: Differentiate and know the causes of prerenal, intrarenal, ATN, Postrenal failure ○ Prerenal (55-60% AKI) Renal hypoperfusion occurs due to decreased blood flow, BP, and kidney perfusion prior to reaching the renal artery....

lOMoARcPSD|48217341 Renal: Differentiate and know the causes of prerenal, intrarenal, ATN, Postrenal failure ○ Prerenal (55-60% AKI) Renal hypoperfusion occurs due to decreased blood flow, BP, and kidney perfusion prior to reaching the renal artery. D/t low CO, hemorrhage, vasodilation,thrombosis Oliguria is a classic finding Monitor urine output closely Factors outside the kidneys reduce renal blood flow Prolonged hypotension (sepsis, vasodilation) Prolonged cardiac output (HF, cardiogenic shock) ○ Ischemia < 25 minutes, damage is usually mild, reversible ○ Ischemia > 60-90 minutes, basement membrane of tubule may be involved, permanent damage occurs Prolonged volume depletion (dehydration, hemorrhage) Renovascular thrombosis (thromboemboli) Can progress to intrarenal damage Medical Mgt Early recognition Fluid or volume replacement Caution in pts with underlying cardiac disease Treatment Correct underlying problem Restore effective arterial blood volume (fluids or vasopressors) to maintain a MAP > 70 mm Hg in order to improve renal perfusion Improve cardiac performance Control vasodilation Avoid nephrotoxic drugs “Renal perfusion” dopamine controversial Wean vasopressors when able ○ Intrarenal Conditions causing direct damage to the kidney Tubular obstruction ○ Acute Tubular Necrosis (ATN) is responsible for the majority of AKI cases ○ Prolonged renal ischemia ○ Endogenous toxins (rhabdomyolysis, tumor lysis syndrome) ○ Exogenous toxins (radiocontrast dye, nephrotoxic drugs) ○ Infection (Acute glomerulonephritis, Interstitial nephritis) ○ Vascular disease (prolonged hypotension, dec CO) Damage to the renal vasculature, glomerular capillaries, interstitium of the kidney, or the renal tubules Acute tubular necrosis (ATN) occurs when the internal filtering structures are damaged or destroyed Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Prevention Identify risk factors for development of ARF Avoid nephrotoxic agents especially in the elderly Prevent dehydration, decreased renal perfusion Close monitoring of I&O, BUN/Cr Rehydrate before use of contrast medium Medical mgt Correct the cause Hydration Renal perfusion, restore MAP ○ Vasoactive medication Monitor nephrotoxic agents Treat infection Improve cardiac performance Remove toxic agent ○ Acute Tubular Necrosis (ATN) Description Nephrotoxic or ischemic injury Damages kidney tubular epithelium In severe cases extends to basement membrane Epidemiology and etiology Damage prevents normal concentration of urine, filtration of wastes, and regulation of acid-base, electrolyte, and water balance Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Phases of ATN Onset phase ○ Time from event to signs of decreased renal perfusion/ischemia ○ Few hours to a few days ○ Signs & Symptoms of renal impairment are present ○ Identify the cause and treat ○ Potentially reversible Oliguric phase ○ Lasts 7-14 days ○ Result of ischemic insult ○ Less likely to recover renal function and higher mortality rate ○ Fluid overload, azotemia, electrolyte abnormalities, metabolic acidosis, and symptoms of uremia. ○ Goal: support renal function ○ Complications: hyperkalemia, hypoxemia, GI bleeding, infection Nonoliguric phase ○ Lasts 5-8 days ○ Usually associated with toxic injury (meds) ○ Renal concentrating defect ○ Urine output: normal to 2L/h Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 ○ Complication: hyperkalemia Diuretic phase ○ Lasts 7-14 days ○ ↑ in GFR with urine output as high as 10 L/day ○ The tubular obstruction clears, but edema and scarring are present ○ GFR returns before the ability of the tubules to function normally ○ Kidneys clear volume but not solutes ○ Monitor for volume depletion Recovery phase ○ BUN and creatinine improves slowly ○ May take 1-2 years for GFR to return to 70-80% of normal ○ 5% may require long-term hemodialysis ○ Postrenal Caused by any obstruction that hinders flow of urine from beyond the kidney Not common Sudden development of anuria should prompt nurse to check patency of Foley catheter Understanding Acute Kidney Injury (AKI Made Easy) Renal lab diagnostics, values, and treatment Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 ○ Serum Creatinine Creatinine: normal 1mg/dl +/-0.3 mg/dl An end product of phosphocreatine, a high energy substance used to form ATP to be used as energy by muscles Rises with RF &/or severe muscle breakdown Elevated CR is an excellent indicator of RF Serum CR of 2 mg/dl = 50% loss of renal function Serum CR of 8-9 mg/dl = 90% loss of renal function Less reliable indicator when malnourishment, liver failure, and heart failure are present Specific tests for ARF Creatinine clearance ○ 24-hour urine ○ Most specific ○ Normal 84 to 138 ml/min ○ Can calculate an estimated value ○ [(140-Age in years) X (body weight KG)] / [72 X Serum creatinine (mg/dl)] *women multiply result by 0.85 Creatinine clearance Approximates GFR ○ 80-120mL/min or adjusted to BSA can range 120-125mL/min/1.73m^2 BSA ○ After age 40, decreases average of 6.5 mL/min/decade Normal ○ Male norm (97-137ml/min)> female norm (88-128ml/min) due to more muscle mass Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 ○ Blood Urea Nitrogen (BUN) BUN: normal 8-20 mg/dl End product of endogenous or exogenous (dietary) protein metabolism 75% excreted by kidney, 25% by bowel Rises with RF, increased protein breakdown (GI bleed, fever) Affected by non-renal causes BUN: CR ratio (10:1) BUN/Cr ratio Normal BUN/Cr ratio is 10:1 Prerenal causes of RF increases the BUN proportionally greater than Cr (20-40:1) i.e., hypovolemia Intrarenal causes of RF increases the BUN and Cr but maintains a more usual ratio (10-15:1) ○ Serum Osmolality Reflects the concentration or dilution of vascular fluid and measures the dissolved particles in the serum Normal is 280 to 290 mOsm/L Elevation: dehydration (DI) Decreased: volume overload (SIADH) ○ Albumin Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Slightly more than 50% of the total plasma protein is albumin Made in liver Normal is 3.5-5g/dL Maintains colloid osmotic pressure Decreased levels-kidney/liver diseases, low protein diet Increased levels-dehydration, high protein diet Assessment of hemodialysis access sites ○ From ChatGPT ○ Assessment of a hemodialysis access site is crucial to ensure proper function and to monitor for any complications. Here are the key aspects to consider during the assessment: ○ Physical Examination: Palpation: Feel for the thrill (vibration) and auscultate for the bruit (swishing sound) over the access site. A strong thrill and bruit indicate good blood flow. Inspect the Skin: Check for any signs of infection, such as redness, warmth, swelling, or discharge. Check for Bruising or Hematoma: Look for any areas of bruising or swelling that could indicate bleeding or clotting issues. Assess Temperature: Compare the temperature of the access site to surrounding areas to detect signs of infection. ○ Monitoring Blood Flow: Assess the adequacy of blood flow through the access site. This can be done by feeling the thrill and listening to the bruit. Ensure that there are no signs of stenosis (narrowing) or thrombosis (clotting) that could impair blood flow. ○ Assessment of Dialysis Adequacy: Evaluate whether the dialysis treatments are effectively removing waste and excess fluid from the bloodstream. This involves monitoring pre- and post-dialysis weights, laboratory tests (such as urea and creatinine levels), and clinical symptoms. Prevention of nephrotoxicity ○ To prevent contrast nephrotoxicity Evaluate risks, weigh risk/benefits Promote hydration 0.9NS or 0.45% NS before procedure (1 ml/kg/hr) for 8-12 hrs prior and 4 hrs or more afterwards Hydration increases renal prostaglandins → renal medullary blood flow Kidney protective drugs Acetylcysteine (Mucomyst) Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Fenoldopam (Corlopam) Third leading cause of acute renal failure in hospitalized patients Most cases are reversible I/Os Urine + insensible losses = 750 to 2400 ml/day Insensible losses (perspiration, stool, water vapor from lungs) Urine: oliguria = 60%; Toxicity with FiO2 > 60% for >24 hr ○ Continuous positive airway pressure (CPAP) Maintains positive airway throughout resp cycle Keeps alveoli open during inspiration and prevents alveolar collapse No preset rate delivered, patient does all the work of breathing Used as a vent mode for weaning process ○ Positive end-expiratory pressure (PEEP): Positive pressure exerted at the end of exhalation to keep alveoli open Improves oxygenation. Required with severe gas exchange disturbance ○ Pressure support: positive pressure on inspiration to ease breathing workload Indication for tracheostomy ○ Preferred for long-term intubation ○ If intubated with ETT (endotracheal tube) for more than 2 to 3 weeks ○ Recommendation: earlier tracheostomy at 72 hours after intubation to facilitate earlier weaning ○ Upper airway obstruction or trauma ○ Neuromuscular diseases VAP prevention ○ Ventilator-associated pneumonia; aspiration of bacteria from oropharynx or GI tract ○ Causes: contamination of lower airway, respiratory therapy devices, malnutrition, impaired immune system, NG tubes, antacids and histamine inhibitors ○ Treatment: bacteria-specific abx ○ Prevention Handwashing and standard precautions Aseptic suctioning of ETT Oral and nasal care (q 2-4 hrs, chlorhexidine) Maintain ETT cuff pressure Elevate HOB > 30 degrees Assess gastric residual volumes Turn and reposition frequently Chest tube mgmt. ○ Chest Tubes Nursing Care Management Assessment NCLEX Review Drain… ○ Maintain patency and function of chest tube system Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 ○Coil tubing loosely on bed to prevent kinks in dependent loops ○Never raise above the chest ○Check drainage, suction, and water seal levels frequently ○Assess for air leaks ○Secure connections with tape ○Position semi-Fowler’s; turn every 2 hrs to enhance air and fluid evacuation ○Complications Clamping of chest tubes is recommended in only two situations: To locate the source of an air leak if bubbling occurs in water seal chamber (clamping is only momentary) To replace chest tube drainage unit (clamping is only momentary) If tube must be clamped, padded hemostats are used to avoid lacerating the vinyl chest tube Continuous monitoring while transporting the patient Bronchoscopy prep ○ Lab work, CXR, fast 6-12 hrs prior, sedation Shock: Define shock ○ Acute, widespread impaired tissue perfusion ○ Results in cellular, metabolic, and hemodynamic alterations ○ Imbalance between cellular oxygen supply and cellular oxygen demand ○ Often results in multiple organ dysfunction syndrome (MODS) Systems affected by shock Cardiovascular - ventricular failure and microvascular thrombosis Neurologic- SNS dysfunction; cardiac and resp. Depression; thermoregulatory failure; coma Pulmonary- acute resp. Failure; acute lung injury (ALI) Renal- acute tubular necrosis (ATN) Hematologic- disseminated intravascular coagulation (DIC) Gastrointestinal- GI tract failure; hepatic failure; pancreatic failure Cardiogenic shock cause and diagnosis ○ Cardiogenic Shock Nursing Management, Pathophysiology, Interventions … Failure of heart to pump blood effectively aka “pump failure” Extreme CHF Etiology Primary ventricular ischemia Structural problems Dysrhythmias Risk factors: increased age, left EF ventricular assist device, extracorporeal membrane oxygenation Anaphylactic shock mechanism and treatment ○ Anaphylactic Shock (Anaphylaxis) Treatment, Nursing Interventions, Sym… antigen -antibody reaction IgE-mediated or non-IgE mediated Basophils and mast cells release histamines, prostaglandins, leukotrienes Mechanism Massive vasodilation Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Increased capillary permeability Bronchoconstriction Coronary vasoconstriction Urticaria (Hives) Myocardial depression Excessive mucus secretion Peripheral vasodilation Clinical manifestations Cutaneous, CNS, respiratory and upper airway, GI and genitourinary, Cardiovascular Treatment Early recognition Remove offending antigen Mild symptoms: oxygen, IV, diphenhydramine Life threatening: epinephrine, fluids, steroids, bronchodilators, vasopressors Airway management, VS, and hemodynamic status Enhance volume replacement Promote comfort and emotional support Maintain surveillance for complications Pt education regarding prevention Neurogenic shock-risk and cause ○ Neurogenic Shock Nursing NCLEX (Distributive) Treatment, Interventions… Loss or suppression of sympathetic tone Rarest form of shock Risk factors Spinal cord injury above level T6 Spinal anesthesia Emotional stress Pain drugs Assessment Manifestation Bradycardia, hypotension and hyperthermia due to peripheral heat loss. Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Management Remove cause of neurogenic shock Prevent cardiovascular instability. Maintain MAP and HR. Restore tissue oxygenation and perfusion Fluid resuscitation and treat hypovolemia Administer vasopressors Maintain normothermia Monitor for dysrhythmias Prevent DVT’s Septic shock-expected hemodynamics, pathologic mechanisms, medical mgmt. ○ Septic Shock Nursing (Sepsis) Treatment, Pathophysiology, Symptoms Dist… Most common cause of death in critical care units Microorganisms invade the body, initiating a systemic inflammatory response syndrome (SIRS) Sepsis -> severe sepsis -> septic shock Initiated by an infection in the pulmonary system, urinary tract, or gastrointestinal system; through wounds; or through invasive devices Proinflammatory and procoagulation state Vasodilation, maldistribution of blood flow, and myocardial depression, capillary leak in the pulmonary interstitium, ARDS, DIC, severe metabolic dysfunction Early signs of septic shock include changes in mental status (confusion or agitation), increased respiratory rate as compensation for the metabolic acidosis, and either fever or hypothermia. May be caused by any type of shock or other things like massive blood transfusion, traumatic injury, brain injury, surgery, burns and pancreatitis typically precedes septic shock Local inflammatory response becomes a systemic response that results in an unregulated inflammatory response with widespread involvement of endothelial cells and a generalized activation of inflammation and coagulation Downloaded by Ava Arpino ([email protected])  lOMoARcPSD|48217341 Systemic response to inflammation may or may not be due to an infection with the presence of ≥ 2 conditions: Temp > 38°C or < 36°C HR > 90bpm RR > 20 or PaCO2 < 32mmHg WBC > 12,000/uL or < 4000/uL or > 10% immature bands Sepsis- systemic response to infection and the presence of SIRS Severe sepsis- sepsis with organ dysfunction, hypoperfusion, or hypotension (lactic acidosis, SBP