NUR 425 Exam 2 Blueprint PDF

NUR 425 Exam Two Study Outline To prepare for your exam, have a fully charged laptop and an updated Respondus lockdown browser. Remember to observe academic integrity practices and refer to the ASU Prelicensure Student Testing Information for details about testing procedures. Exam one will consist...

NUR 425 Exam Two Study Outline To prepare for your exam, have a fully charged laptop and an updated Respondus lockdown browser. Remember to observe academic integrity practices and refer to the ASU Prelicensure Student Testing Information for details about testing procedures. Exam one will consist of 50 questions, each worth 1 point. You will have 75 minutes to complete it. The questions may be in various formats, including multiple-choice, fill-in-the-blank, multiple-answer, and alternate-style Next Generation NCLEX questions. Module #6: Acid Base Balance-Arterial Blood Gases- 15 Questions 1. Relate the pathophysiology of acid-base imbalances to the compensatory mechanisms. Acid Base Imbalance- sx of disease, not a disease itself; DM, COPD, kidney disease + GI disturbance can lead to this Compensatory Mechanisms ○ Buffer System- fastest acting sys, change strong acids → weak acids; binds acids to neutralize their effect; can’t maintain w/o good kidney + lung funct ○ Respiratory System- 2nd fastest, temporary; CO2 Metabolic Acidosis= Hyperventilation = ↓ PaCO2 = ↑ pH Metabolic Alkalosis= Hypoventilation = ↑ PaCO2 = ↓ pH ○ Renal System- slower than lungs, but more sustainable; HCO3 + H+ Respiratory Acidosis= kidneys reabsorbHCO3 + ↑ excretion of hydrogen (in urine) = ↑ HCO3 formed in renal tubule = ↑ HCO3 retained in blood = ↑ pH Respiratory Alkalosis = kidneys excrete HCO3 (in urine) + retain H2 = ↑ urine alkaline + ↓ HCO3 in blood = ↓ pH ○ Respiratory Opposite Metabolic Equal 2. Interpret the components of an arterial blood gas and the normal values for each component. pH= 7.35-7.45; acidity/alkalinity of blood ○ Respiratory Acidic pH Causes: hypoventilation- resp drive issues (head injury), chest expansion issues (rib fx, fatigue), neuromuscular innervation (spinal cord injury), airway issues (anaphylaxis) ○ Respiratory Alkalotic pH Causes: hyperventilation (anxiety, labor, high altitude) ○ Metabolic Acidic pH Causes: acid build up/retention (renal failure, aspirin overdose, hypoperfusion → lactic acid buildup → hypovolemic shock), base loss (diarrhea) ○ Metabolic Alkalotic pH Causes: acid loss- V, NG tube suction, K-wasting/loop + thiazide diuretics, base retention- antacid overuse, citrate from blood transfusion PaCO2= 35-45 mmHg; enough or too much CO2 is blown off or is it building up? HCO3= 22-26 mEq/L; how are the kidneys working? PaO2= 80-100 mmHg; O2 in the blood SaO2= >95%; % of hemoglobin saturated w/ O2  3. Evaluate arterial blood gases results for mixed, uncompensated, partially compensated, and fully compensated acid base imbalances. Disturbance- matches pH; aka the CAUSE Compensation- does not match the pH Uncompensated- pH + other value is abnormal, other value normal (not compensating) Partially Compensated- all values abnormal; distinguish which one is the cause, which one is trying to fix the problem; pH is still abnormal Fully Compensated- pH is normal (7.4 is the reference point; 7.35-7.4: normal acid, 7.4-7.45: normal base), PaCO2 + HCO3 abnormal (cause + fix) Mixed- all values are abnormal (acidic or basic); neither sys is trying to compensate, both causing the disturbance, both resp + meta probs 4. Compare the clinical manifestations, causes, and treatments for respiratory acidosis and alkalosis, metabolic acidosis and alkalosis. Respiratory Acidosis ○ Causes: hypoventilation CNS Depression- drugs (sedatives, opioids), alcohol, brainstem injury Pulmonary Disease- COPD, PE, pneumonia, pulm edema Respiratory Muscle Weakness- paralysis, fatigue ○ Tx = breathe more (↑ RR and/or depth) Narcan/reduce sedation Intubate or change existing vent settings (↑ RR or size of each breath) Bronchodilators Pneumonia/pneumothorax Respiratory Alkalosis ○ Causes: hyperventilation- anxiety, pain, mech vent causing it ○ Tx = breathe less (↓ RR and/or depth) CNS Stim, analgesia, anxiolytics, antipyretics, stop/reverse drugs Change existing vent settings (↓ RR or size of each breath) Metabolic Acidosis ○ Causes: Acid Build up/Retention- renal failure (↑ uric acid ), shock (↑ lactic acid), DKA (↑ ketones), intoxication (aspirin overdose) Base Loss- diarrhea ○ Tx = excrete acid/retain bicarb (monitor for hypoklaemia as acidosis is corrected) Administer NaHCO3 Encourage Kussmaul respirations (natural comp) Dialysis, insulin, antidiarrheal Metabolic Alkalosis ○ Causes: Acid Loss- V, NG tube suction, K-wasting/loop + thiazide diuretics (hypokalemia) Base Retention- antacid overuse/OD, citrate from blood, over administration of NaHCO3 ○ Tx = excrete bicarb/retain acids D/c drugs causing imbalance, NGT suction Antiemetics, acetazolamide (Diamox)- diuretic Module #7: Oxygenation, Perfusion, RF, ARDS- 15 Questions 1. Ventilation vs Perfusion vs Oxygenation Ventilation- movement of air into alveoli; WOB, effort  ○ Poor Vent = ↑ PaCO2 (asthma, bronchitis, head injury, opioid overdose, fatigue spinal cord injury, rib fx, kyphosis) Perfusion- getting blood to alveoli ○ Poor Perfusion = ↓ PaCo2 (anemia, hypovolemia, PE, AMI, cardiogenic shock) Oxygenation- movement of O2 from alveoli to blood ○ Poor Oxygenation = vent, perfusion, diffusion probs (all of above) 2. Compare the pathophysiological mechanisms of VQ mismatch including shunt, diffusion limitation, and hypoventilation V/Q Mismatch- when ventilation and perfusion levels are unevenly distributed ○ Anatomical- apex of lungs has more ventilation than perfusion (V>Q) ○ Pathological- perfusion issues (V>Q) HF/PE; vent issues (V 50, pH < 7.35 ○ Airway patency issues, ↓ resp drive, chest expansion issues (strength, neuromuscular innervation, ability to expand) Can be both Clinical Manifestations- dependent on extent of PaO2 or PaCO2 changes (acute, chronic, ability to compensate) ○ Early Signs: changes in mental status, fatigue, restlessness, confusion, agitation, anxiety (SNS response): tachycardia, tachypnea, mild HTN, morning HA (CO2 removal issue) ○ General: tachycardia, bounding pulse, HTN, skin: cool, clammy, diaphoresis, rapid shallow breathing/SOB, retractions, use of accessory muscles, tripod, nasal flaring, pursed-lip breathing, fatigue, muscle weakness, unable to speak in full sentences ○ Late Signs: paradoxical breathing, coma, hypotension, dysrhythmias, seizures, cyanosis ○ Breath Sounds: crackles (pulmonary edema), absent/dim breath sounds (atelectasis, pleural effusion), bronchial breath sounds over lung periphery (lung consolidation seen w/ pneumonia), pleural friction rub (pneumonia involving the pleura) 4. Describe appropriate nursing and collaborative interventions for the patient with respiratory failure Nursing Care: correct hypoxemia, maintain patent airway, optimize O2 delivery, ↓ O2 demand, treat cause, prevent complications  Collaborative Care: frequent + early assessment, CXR, ABGs, CBC, ECG, serum electrolytes, CT, VQ scan, O2 delivery + vent support, ETCO2 monitoring Drug Therapy: ○ Bronchospasm = bronchodilators (Albuterol) ○ Airway inflammation = (corticosteroids, methylprednisolone) ○ ↓ Pulm Congestion = diuretics, nitrates if HF ○ Pulm Infections = IV abx ○ ↓ Severe Anxiety, Pain, Agitation = benzos, dexmedetomidine, opioids 5. Identify the basic pathophysiology and clinical manifestations of Acute Respiratory Distress Syndrome (ARDS) ARDS- sudden progressive form of acute resp failure; PaO2/FiO2 ratio of < 200 mmHg ○ Timing- within 1 week of onset of new/worsening resp sx ○ Chest Imaging- bilateral opacities ○ Origin of Edema (non cardiac pulmonary edema)- not cardiac or fluid overload ○ Oxygenation- mild p/f ratio: 200-300, mod: 100-200, severe: < 100 Patho ○ Injury/Exudative Phase- damage to alveolar cap membrane → ↑ cap permeability allows fluid to fill alveoli → pulm edema; ↓ lung compliance ○ Proliferative/Reparative- fibrin matrix forms → progressive hypoxemia ○ Fibrotic Phase- lungs become fibrotic, ↓ functional residual capacity, narrowing airways Early Signs- SNS RESPONSE ○ Difficulty breathing: dyspnea, tachypnea, cough, restlessness ○ Lung sounds- normal or fine, scattered crackles ○ ABG- mild hypoxia, resp alkalosis (tachypnea) ○ CXR- normal or scattered infiltrates Cardinal Signs ○ Severe refractory hypoxemia- low PaO2 + SaO2 despite ↑ O2; stubborn ○ White out CXR- fluid in lungs ○ Abnormalities r/t Mechanical Vent: ↑ PEEP (pressure needed to keep alveoli open; setting), ↑ PIP (resistance the vent encounters when trying to delivery breaths; response) Late Signs ○ Tachycardia, diaphoresis, mental status changes, cyanosis, pallor ○ ↑ WOB ○ Lung sounds- diffuse crackles, coarse crackles 6. Prioritize appropriate nursing and collaborative management strategies for the patient with ARDS Maintain airway = ETT Optimize O2 delivery ○ ↑ PEEP ○ Prone positioning/Rot-a-prone-bed- shifts perfusion to anterior portion from posterior bases w/ improved ventilation; risks… Delayed CPR Skin breakdown can go undetected Monitor pressure points, protect corneas by lubricating + taping eyes closed, have basin/towel for secretions ○ Mech vent (low TV, pressure mode) ○ Keep PaO2 > 60 mmHg, SaO2 > 90%  ○ ECMO- takes over heart or lung funct temporarily; removes blood, infuses O2, removes CO2, return blood to pt V-A: Veno-Arterial- resp or cardiac support V-V: Veno-Venous- resp support Risks: Closely monitor drain + return lines (risks: decannulation, infection, air embolism) Systemic anticoagulation (bleeding) Must have ECMO certified specialist continually at bedside ↓ O2 Demand- ↓ metabolic demand (stress, fevers, pain) Treat cause- sputum cultures/abx, sepsis, MODS Prevent complications- VAP, hypoxia, ulcers Module #8: Mechanical Ventilation- 10 Questions 1. Discuss the indications for mechanical ventilation. Resp failure Coma ↓ O2 levels (pneumonia) ↑ CO2 levels (COPD) 2. Discuss collaborative care and nursing management of clients requiring mechanical ventilatory support High pressure alarms ○ Secretions, Coughing, Gagging: Suction patient. ○ Fighting Vent: Administer sedation or adjust vent settings. ○ Water in Tubing: Drain water from tubing. ○ Kinked/Compressed Tubing: Reposition tubing or provide bite block. ○ Increased Resistance (Bronchospasm): Administer bronchodilator. ○ Decreased Compliance (Edema, Pneumothorax): Address underlying issue (e.g., diuretics, chest tube). Low pressure alarms ○ Vent Disconnect: Reconnect tubing. ○ Loss of Airway (Extubation): Reintubate or secure airway. ○ Cuff Leak/Deflated Cuff: Inflate cuff or fix leak. Suspected equipment failure or prob = ambu bag! Medications: ○ Analgesics (morphine + fentanyl) ○ Sedatives (midazolam, propofol, dexmedetomidine) ○ Neuromuscular blocking agents (NMB)- cause chem paralysis (pancuronium, vecuronium, rocuronium); no sedative or analgesic properties associated Suction when necessary, assess O2 by SaO2, watch clock w/ intubation attempts ○ Preliminary Assessment of ETT placement: observe chest for symmetrical rise + fall, auscultate lungs + stomach, CO2 detector Secure tube + identify cm placement, inflate cuff via balloon ASSESS + MAINTAIN AIRWAY 3. Describe the modes of mechanical ventilation and related relevant nursing care: CPAP, PS, AC, SIMV Pressure Modes Continuous Positive Airway Pressure (CPAP)- pt is spontaneously breathing; no RR, Vt, support; continuous positive airway pressure ○ Via vent (invasive) or nasal pillow, mouth/nose mask, or tight seal face mask (noninvasive)  Pressure Support (PS)- can be a setting and mode (cmH2O) ○ Setting: provide help w/ spontaneous breaths (can be added on to SIMV) ○ Mode: vent only supports spontaneous breaths; no RR + Vt Benefits: more comfortable for pt, Vt similar to normal breathing, PIP better controlled Volume Modes Assist Control (AC)- preset # of breaths + tidal vol (Vt) ○ Vt of spontaneous breaths does not vary; vent supports ALL breaths w/ set Vt ○ Vent performs most of WOB ○ For normal resp drive, but weak WOB Synchronized Intermittent Mandatory Ventilation (SIMV)- preset # of breaths + tidal vol (Vt) ○ Vol of spontaneous breaths vary; spontaneous breaths NOT supported, pt does on own ○ Considered weaning mode 4. Recognize the risks associated with positive pressure mechanical ventilation. Right mainstem bronchus intubation Unplanned extubation Laryngeal /tracheal injury, damage to oral/nasal mucosa O2 toxicity Acid-base disturbances Stress, anxiety, depression Peptic ulcer disease (PUD) Hemodynamic compromise (PEEP causing ↓ CO/BP) Ventilator Associated Pneumonia- occurs 48 hrs > after intubation ○ S/sx: purulent sputum, fever, ↑ WBC, crackles/rhonchi ○ HOB 30-45° ○ Hand washing ○ Sedation vacation to assess readiness to wean ○ DVT + PUD prophylaxis ○ Meticulous oral care q2 5. Recognize the appropriate use of paralytics in the mechanically ventilated patient Train of Four (TOF)- peripheral nerve stim; used when pts are given an NMB; delivers 4 impulses of electricity → watch for response (↓ agent) ○ 0-1 twitches = completely paralyzed ○ 2 twitches = appropriately paralyzed ○ 3-4 twitches = not paralyzed enough (↑ agent) ○ Placed on ulnar, facial, plantar nerve 6. Identify indicators of readiness to wean as well as successful and unsuccessful weaning Readiness to wean  Failure to wean: 7. Apply knowledge of mechanical ventilation and respiratory physiology to acid-base balance Pts w/ Alkalosis: pt is hyperventilation (less vent support/↑ sedation) Pts w/ Acidosis: pt is hypoventilating (more vent support) 8. Recognize the appropriate use of paralytics in the mechanically ventilated patient Use when standard sedation is insufficient to manage patient ventilator dyssynchrony (mismatch between a pt’s respiratory efforts + support provided by a mechanical vent Module #9: Intracranial Regulation-Intracranial Pressure Monitoring- 10 Questions 1. Define Intracranial Pressure and Increased Intracranial Pressure ICP- consists of right cranial vault + 3 non-compressible contents: blood, brain tissue, CSF (pressure exerted by); Normal Range = 5-15 mmHg Monro Kelli Hypothesis- if the vol of one ↑, then a reciprocal ↓ in one or both of the others must occur; aka compliance… ○ CSF- displaced into subarachnoid space ○ Blood- vasodilation/construction; displaced into venous sinuses ○ Both can only be displaced so much… ○ Brain Tissue- herniation (brain shifts from ↑ to ↓ pressure) Increased ICP- ↑ pressure exerted by brain tissue, blood, and CSF against the inside of the skull; Sustained Pressure of ≥ 20 mmHg Autoregulation- process by which the brain maintains perfusion pressure over a wide range of systemic pressures; highly dependent on MAP = 70-105  ○ Goal for Pt’s with IICP: MAP between 70-90 mmHg 2. Calculate Cerebral Perfusion Pressure (CPP) Pressure required to perfuse the brain Normal Range = 60-100 mmHg MAP - ICP = CPP (most important factor in maintaining brain health) Cerebral Blood Flow- amount of blood (mL) passing through 100g of brain tissue) 3. Identify causes + clinical manifestations of increased ICP ↑ Brain Vol Causes: ○ Cerebral edema (hydrocephalus, ischemic stroke, radiation, infected scalp lacerations, infections neurological processes- meningitis, viral encephalitis, Guillain Barre syndrome) ○ Brain mass, tumor, abscess, contusions ↑ Cerebral Blood Vol Causes: ○ Intracranial hemorrhage (closed head injuries/trauma/skull fx, hemorrhagic stroke) ○ ↑ blood flow (HTN, vasodilation- hypercapnia + hypoxia, ↑ O2 demands- fever, pain, phys activity, shivering, seizures) ○ Obstruction of outflow (impaired venous return); hyperflexion, hyperextension, rotation of neck, tight trach ties, tumor/abscess compressing venous structures, ↑ intraabd or intrathoracic pressure (pushes back against venous outflow) ↑ in CSF Vol ○ Hydrocephalus due to CSF outflow blockage ○ CSF absorption due to SAH or inf ○ Excess CSF prod Clinical Manifestations ○ ICP > 15 mmHg ○ Anyone who becomes acutely unconscious should be suspected of ↑ ICP ○ Changes in LOC (fatigue, unresponsiveness), vision, reflexes, VS, pupillary response ○ ↑ persistent HA ○ Projectile vomiting ○ Altered temp reg- poikilothermia, ↑ body tem ○ GCS- ≤ 8 = coma Late Signs ○ Cushing’s Triad- systolic HTN/widened pulse pressure, bradycardia, irreg resp pattern (cheyne-stokes, CNS hyperventilation- sustained, reg, rapid, + deep breathing, ataxic- completely irreg w/ some breaths deep + some shallow; random, irreg pauses, slow rate) ○ Posturing- decorticate/decerebrate 4. Identify appropriate nursing interventions to address reduced CPP Monitor ventilation + oxygenation Keep normotensive, hydrated, + nutritionally adequate Maintain normal ICP, CBF, CPP Watch for secondary brain injury 5. Determine appropriate nursing interventions for increased ICP Positioning- HOB to facilitate outflow + promote CPP, prevent neck flexion Skincare- inf/hemorrhage prevention Pain management, ↓ anxiety Psychosocial issues, ↓ env stimuli  ↓ Causes that ↑ ICP (metabolic demand- fever, seizures, shivering, stress, suctioning- < 10 secs at a time, abd distension) Medications ○ Mannitol (Osmotic Diuretic)- ↑ osmolarity within nephron ↓ cerebral edema; pee out ○ Hypertonic Saline (3% NaCl)- pulls fluid out of interstitial space + into intravasc space; INFUSE SLOWLY THRU CENTRAL LINE Hypotonic Saline (NS)- ↑ ICP, dilute ○ Antiseizure Drugs (Phenytoin/Dilantin)- seizures ↑ metabolic demand) ○ Corticosteroids (Dexamethasone)- ↓ swelling (brain tumors, cerebral edema) 6. Identify the purpose of an external ventricular drain Pressure signal coming from within the cranium that needs to be transduced; requires device bored into pt’s skull; pressure line set up, no pressure bag needed Indications: GCS of 3-8, used to assess response to therapy or augment neuro assessment; also trends ICP waveform + drains CSF (Epidural, subdural, subarachnoid) 7. Describe basic nursing and collaborative care of the patient with an external ventricular drain Monitor s/sx of infection (insertion site + drainage) Assess brain perfusion: CPP, neuro, IICP Ventricular Drainage- physician orders: closed/intermittent/continuous, height (open at 10 cm H20), eval CSF drainage + document (color, characteristics, amount) Levelled at the Foramen of Monro (Tragus) Strict aseptic technique during dressing changes Signade or other alerts that pt has EVD Reassess level of transducer w/ any position change; position changes + transport w/ drain CLOSED Accurate ICP Signal ○ EVD should be closed 6 minutes before waveform is formed ○ Stopcock allowing signal ○ Eval for inaccurate ICP waveforms: improper level, bubbles intubation, CSF leaks, kinks, obstructions Other things to know: Normal vital signs in adults Normal MAP in adults Normal PEEP setting (usually 5cmH20- anything higher than 10cmH20 is considered "high") ICP (and be able to define increased ICP) CPP (be able to calculate CPP) PaO2/FiO2 ratio SaO2 ABG values ○ PaO2 ○ PaCO2 ○ HCO3 ○ pH Understand the significance of the following Not required to memorize actual normal ranges Tidal Volume Be able to identify/describe the following select breathing patterns and what they could signify:  Apnea Ataxic breathing- drunken breathing; sometimes fast, slow, deep, shallow, pauses ; completely irregular Cheyne stokes Kussmaul breathing (CNS Hyperventilation) The following medications could be tested on this exam. You should know the medication’s indications, side effects, and nursing considerations when administering these: Thiazide Diuretics (effect on ABGs) Sodium Bicarbonate (effect on ABGs) Corticosteroids (the general drug category & their use for respiratory and ICP issues) Norepinephrine Mannitol 3% NaCl 0.45% NaCl ("1/2 normal saline") Fentanyl Pancuronium Metoprolol (effect on MAP and CPP)- ↓ MAP Labetalol (effect on MAP and CPP)- ↓ MAP Midazolam