NUR 425 Exam 2.docx

NUR 425: Complex Care Exam 2 Blue Print Exam Two will focus on the course content of Shock, ABG, Respiratory, ARDS, Vent, and ICP Questions include multiple choice, select all that apply, and two Next Gen. NCLEX-style questions for a total of 50 questions Know the normal value ranges for ABG Values...

NUR 425: Complex Care Exam 2 Blue Print Exam Two will focus on the course content of Shock, ABG, Respiratory, ARDS, Vent, and ICP Questions include multiple choice, select all that apply, and two Next Gen. NCLEX-style questions for a total of 50 questions Know the normal value ranges for ABG Values PaO2 :80 - 100 mmHg PaCO2 :35-45 mmHg HCO3 : 22-26 mEq/L pH :7.35-7.45 MAP for Adults ICP & CPP PaO2/FiO2 ratio (what is normal; then mild - severe ARDS) SaO2 ABG Values Identify and describe the following breathing patterns Apnea Ataxic breathing Cheyne Stokes Kussmaul (CNS hyperventilation) Medications Focus Points Indications Side Effects Nursing Considerations Sodium Bicarbonate (effect on ABGs) Corticosteroids (ARDS/Respiratory Failure) Norepinephrine Mannitol 3% NaCl Medication Math (examples) Focus Points Norepinephrine: Order given in mcg/min Propofol: Order given in mcg/kg/min Double-checking your pump. How many mL/hr is correct for the dose? Norepinephrine Infusion 4 mg/ 250 mL (16 mcg/ mL) Propofol Infusion 100 mg/ 100mL Shock and CRRT Focus Points Teaching points and scenarios Categories: cardiogenic, hypovolemic, obstructive, & distributive Define shock and differentiate categories Stages: Initial →Compensatory→Progressive→Irreversible Potential causes of each category of shock Define CRRT & basic nursing care CRRT Identify pathophysiological effects & clinical manifestations→septic shock Arterial Blood Gasses Focus Points ABGs & their interventions Interpret ABGs Know clinical manifestations, causes, & treatments: Respiratory: acidosis & alkalosis Metabolic: acidosis & alkalosis Relate pathophysiology of acid-base imbalances NUR 425: Complex Care Exam 2 Blue Print (continued) Exam One will focus on the course content of Shock, ABG, Respiratory, ARDS, Vent, and ICP Questions include multiple choice, select all that apply, and two Next Gen. NCLEX-style questions for a total of 50 questions Respiratory Failure & ARDS Focus Points Early & late stages of respiratory failure Examples of VQ mismatch Compare VQ mismatch: shunt, diffusion, limitation, & hypoventilation Pathophysiology & clinical manifestations of respiratory failure Pathophysiology & clinical manifestation of ARDS Prioritize nursing & collaborative strategies for ARDS Mechanical Ventilation Focus Points Modes: CPAP, PS, AC, & SIMV Indications for mechanical ventilation Collaborative & nursing management for care of intubated patient Describe the ventilation modes & relevant nursing care Risks associated with intubation & mechanical ventilation Successful & unsuccessful weaning Knowledge of mechanical ventilation & respiratory physiology to ABGs Intracranial Pressure Monitoring Focus Points Early & late stages of high ICP Define ICP and high ICP Calculate CPP Basic nursing care & collaborative care for patient with EVD Purpose of an EVD Interventions for high ICP Interventions for low CPP Distribution of Questions by Module and Learning Outcome (LO) Shock and CRRT: approx  7 questions LO 1&3 (1 questions), LO 2,3,4 (1 question), LO 2,3,4,5 (1 question), LO 4,5,6 (1 question), LO 6 ( 1 question) LO 7 (2 questions), LO 8&9 (1 question) Associated Learning Outcomes (LO’s) Define Shock Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Describe the progression of shock from the initial stage, to the compensatory stage, to the progressive stage, to the irreversible stage Stage 1: Initial Hypoperfusion caused by decrease delivery of oxygen to tissues Stage 2: Compensatory Sustained hypoperfusion → neural endocrine, and chemical compensatory mechanisms Hypotension SNS activation Requires MORE oxygen! Stage 3: Progressive Compensatory mechanisms failing Altered level of consciousness Capillary permeability → anasarca (severe edema) Organ failure Stage 4: Irreversible/Refractory Profound hypotension and hypoxemia, multi-organ failure Recovery is unlikely Compensatory mechanisms are overwhelmed Differentiate between the four categories of shock Hypovolemic: Low intravascular volume Absolute: ex; hemorrhage, vomiting, diarrhea Cardiogenic: Hypoperfusion cause by poor cardiac output; aka bad pump 60% mortality rate Distributive: Hypoperfusion caused by massive vasodilation Neurogenic: Hypoperfusion caused by loss of SNS tone Anaphylaxis: Hypoperfusion caused by exposure to a sensitive substance and release of vasoactive mediators Septic: Hypoperfusion caused by systemic response to an infection Obstructive: Hypoperfusion caused by an obstruction in blood flow/reduced diastolic filling Identify expected hemodynamic measurements related to cardiogenic, hypovolemic, obstructive, and all types of distributive shock Hypovolemic: ↓: BP, PCWP, CVP, CO/CI ↑: HR, SVR/I Cardiogenic:↓: BP, CO/CI ↑: HR, PCWP, CVP, SVR Anaphylactic: ↓: BP, PCWP, CVP, CO/CI, SVR ↑: HR Neurogenic: : ↓ BP, HR, PCWP, CVP, CO/CI, SVR ↑: None Septic: ↓: BP, PCWP, CVP, SVR, CO/CI ↑: HR, CO/CI Obstructive: ↓: BP, HR, PCWP, CVP, CO/CI, SVR ↑: HR Identify potential causes for cardiogenic, hypovolemic, obstructive, and distributive shocks Hypovolemic: Volume is inadequate to fill vascular space Absolute: Hemorrhage, vomiting, diarrhea Relative: Third spacing, burns Cardiogenic: Systolic or diastolic dysfunction resulting in decreased CO/CI MI is most common cause Muscle is damaged Neurogenic: Different from spinal shock Occurs within 30 minutes of spinal cord injury at T5 and above Anaphylactic: Allergic reaction to previously sensitized antigen Septic: Exaggerated inflammatory response Sepsis: systemic inflammatory response due to suspected infection Septic shock: sepsis + hypotension despite fluid resuscitation Most common cause is gram negative and gram positive bacteria Obstructive: Pressure impeding diastolic filling Pericardial tamponade, abdominal compartment syndrome, tension pneumothorax Identify the pathophysiological effects and related clinical manifestations of septic shock Early Shock: Hyperventilation, respiratory alkalosis, warm and flushed, agitated, confused Late Shock: Hypoventilation, respiratory and metabolic acidosis, cool and clammy skin, decreased LOC Respiratory failure is common (ARDS) Describe the collaborative and nursing care necessary for a patient in shock Anaphylactic Shock: Maintain airway Epinephrine Diphenhydramine: block histamine response Colloids: bring fluid back into vessels Corticosteroids: decrease inflammation and capillary permeability Obstructive Shock: Volume resuscitation “Fluid challenges”, CVP monitoring, balance O2 consumption and delivery Initiate antibiotics, pan cultures before antibiotics May consider corticosteroids, dobutamine, norepinephrine Cardiogenic Shock: Restore blood flow to the myocardium Nitroglycerin Reduce heart workload, reduce preload, afterload, HR, contractility Balloon pump (reduces afterload & goes through the atrium), avoid aggressive IVF or colloids Dopamine and Dobutamine (inotropes to increase CO - use with caution) Hypovolemic Shock: Need intravascular fluid volume replacement Fluid resuscitation with close monitoring Neurogenic Shock: Promote spinal stability May need surgical intervention Vasopressors, atropine (bradycardia), monitor for hypothermia Define Continuous Renal Replacement Therapy (CRRT) A type of dialysis to treat an acute kidney injury Slow, continuous, best option for hemodynamically unstable patients (shock) Identify basic nursing care of the patient receiving CRRT One to one ratio Continue CRRT for up to 30-40 days Close monitoring of VS, I&O, serum chemistries, weight Monitor filter (can clot off, change q 24-48 hours), drainage/waste “ultrafiltrate”, assess device (monitor for infection/bleeding) Arterial Blood Gasses:  approx 8 questions* *Knowledge of ABGs will also be incorporated into questions from other modules LO 1 (2 questions), LO 2&3 (3 questions), LO 2,3,&4 (1 questions), LO 3 (1 question) Associated Learning Outcomes (LO’s) Relate the pathophysiology of acid-base imbalances to the compensatory mechanisms. Buffer System: proteins, ions absorb and release H+ Fastest acting but low threshold Respiratory System: Changes in CO2 Moderate acting, max effect in 24 hours, not long-term Renal System: Changes in H+ and HCO3- Slowest acting, takes hours to days but more sustainable Interpret the components of an arterial blood gas and the normal values for each component. pH: 7.35 - 7.45 ; the acidity and alkalinity of the blood PaO2: 80 - 100mmHg ; how much oxygen is in the blood SaO2 : >94-95% usually ; what percent of hemoglobin is saturated with oxygen PaCO2: 35 - 45mmHg ; how much CO2 is in the blood; lungs HCO3: 22 - 26 mEq/L ; how much bicarbonate is in the blood; kidneys Evaluate arterial blood gasses results for mixed, uncompensated, partially compensated, and fully compensated acid base imbalances. Primary Uncompensated: One system is doing nothing/not compensating Mixed Acid Base: Patient has a metabolic AND respiratory problem (causing both acidosis/alkalosis) Partially Compensated: All numbers are abnormal, determined by which imbalance matches the pH Fully Compensated: pH is normal but both PaCO2 and HCO3 are abnormal, which side of the spectrum does pH fall? Compare the clinical manifestations, causes, and treatments for respiratory acidosis and alkalosis, metabolic acidosis and alkalosis. Respiratory Acidosis: Clinical Manifestations: SOB, rapid breathing, confusion, increase HR, decreased BP Causes: CO2 is being retained in the lungs Hypoventilation (breathing too slow and shallow) CNS depression (Drugs), alcohol, brainstem injury Pulmonary disease (COPD, PE) Respiratory Muscle Weakness (Paralysis, fatigue) Treatment: Need to breathe more (increase RR & depth) Narcan/reduce sedation Intubate or change existing ventilator settings Suction bronchodilators Treat pneumonia/pneumothorax Respiratory Alkalosis: Clinical Manifestations: Hyperventilating, lightheaded, confusion, numbness Causes: Anxiety, pain Hyperventilation (breathing too deep, too fast) High altitude Treatment: Need to breathe less (decrease RR & depth) CNS stimulation? Give analgesia, anxiolytics, antipyretics to decrease anxiety/pain Retain CO2 by breathing into paper bag Change existing ventilator setting to decrease RR and size of each breath Metabolic Acidosis: Clinical Manifestations: Kussmaul respirations, weakness, headache, confusion, N/V, hyperventilating, hyperkalemia Causes: Build up of acid (due to poor perfusion, organ failure, altered metabolism) Shock-lactic acid build up Renal failure-accumulation of ketoacids Intoxication (ASA overdose) Bicarb deficit/loss (diarrhea) Treatment: Need to excrete acid and retain bicarbonate Administer Sodium Bicarbonate Encourage Kussmaul respirations for natural compensation Antidiarrheal (for diarrhea) Dialysis (renal failure) Insulin (DKA) Metabolic Alkalosis: Clinical Manifestations: Hypoventilation, confusion, muscle weakness, tremors, N/V, arrhythmias, hypokalemia Causes: Loss of acid Stomach acid (NGT) Drugs causing hypokalemia → cause body to release aldosterone → triggers excretion of Ka+ and H+ ions → acid los Bicarbonate Excess Antacid overdose Over-administration of NaHCO3 (Sodium bicarb) Treatment: Need to excrete bicarbonate and retain acids D/C drugs causing imbalances (antacids, thiazide diuretics) D/C NGT suction Antimetics Acetazolamide (Diamox) Carbonic inhibitor Respiratory Failure, ARDS  approx 9 questions* LO 1 (2 questions), LO 1&2 (1 question), LO 2 (1 question), LO 3 (2 questions), LO4 (1 question), LO 5 (1 question), LO 4&5 (1 question) *Knowledge of respiratory failure will also be incorporated into questions from other modules Associated Learning Outcomes (LO’s) Compare the pathophysiological mechanisms of VQ mismatch including shunt, diffusion limitation, and hypoventilation In VQ mismatch there's an imbalance between ventilation (air reaching alveoli) and perfusion (blood flow reaching the alveoli) in the lungs. Shunt: blood bypasses the lungs without participating in gas exchange, causing deoxygenated blood to mix with oxygenated blood resulting in decreased arterial oxygenation despite normal ventilation. Air reaches the alveoli but blood flow does not match it, wasting ventilation Diffusion limitation: occurs when oxygen and CO2 cant diffuse effectively across the alveoli due to thickening, fibrosis, or damage to the membrane. Despite normal ventilation and blood flow, the exchange of gasses across the alveolar membrane is impaired. Causes decreased oxygenation and inefficient removal of CO2 Hypoventilation: caused by insufficient ventilation of the alveoli relative to perfusion. Results from conditions that decrease respiratory (drug overdose, CNS disorders), or a decrease ability to ventilate adequate (chest wall deformities) Decreased oxygenation and an increase in CO2 levels in the blood due to inadequate ventilation → causing respiratory acidosis Describe the pathophysiology and clinical manifestations of respiratory failure Pathophysiology: Failure to oxygenate (hypoxic PaO2 <60mmHg) VQ Mismatch Diffusion Limitation Failure to Ventilate Airway patency issues Decreased respiratory drive Chest expansion issues (strength, ability to expand) Clinical Manifestations: Early signs: Change in mental status, fatigue, restlessness, confusion, agitation Anxiety, tachycardic, tachypnea, mild HTN Morning headache due to issue with CO2 removal Late signs: Paradoxical breathing Coma Hypotension Dysrhythmias Seizures Cyanosis Describe appropriate nursing and collaborative interventions for the patient with respiratory failure Frequent and early assessment Chest X-ray, ABG’s, CBC, ECG Sputum and blood culture Serum electrolytes, CT, VQ Scan ETCO2 monitoring Ventilation mask: Maintain goal by using lowest O2 concentration possible Noninvasive: NC, simple mask, venti mask, NRM, CPAP, BiPAP Invasive:ET tube, tracheostomy Acute Respiratory Failure Medications: Bronchospasms: Albuterol Reduce airway inflammation: Corticosteroids Reduce pulmonary congestion: Diuretics, nitrates if HF present Pulmonary infections: IV antibiotics Severe anxiety, pain, and agitation: Benzoa, dexmedetomidine, opioids Identify the basic pathophysiology and clinical manifestations of Acute Respiratory Distress Syndrome (ARDS) Injury/Exudative Phase: Damage to the alveolar-capillary membrane causing an increased capillary permeability and decreased lung compliance (stiff lungs) Proliferative Phase: Fibrin matrix forms → progressive hypoxemia Fibrotic Phase Lungs become fibrotic, reduced functional residual capacity, narrowing airways Clinical Manifestations: Early Signs: Difficulty breathing Crackle in lungs (can also be normal) Mild hypoxemia, respiratory alkalosis Scattered infiltrates Late signs: Changes in mental status Tachycardia Coarse crackles lung sounds White out Chest X-ray Increased use of PEEP (“Positive End Expiratory Pressure” Pressure to keep the alveoli open) Increasing PIP levels (“Peak Inspiratory Pressure” resistance the ventilator is encountering when it delivers breaths) Sudden, progressive form of respiratory failure Pa02/Fi02 ratio of less than 200mmHg 50% mortality rate Formula: P/F = ratio of oxygen in the blood (PaO2) compared to how much oxygen is being delivered to the patient (FiO2) Prioritize appropriate nursing and collaborative management strategies for the patient with ARDS Extra Corporal Membrane Oxygenation (ECMO) For high risk mortality Removes blood from patient, infuses with oxygen, removes CO2, return blood to patient Major risk: bleeding Closely monitor drain and return like (decannulation, infection, air embolism) Maintain airway (ET tube) Optimize oxygen delivery (Higher PEEP) Low TV pressure Keep PaO2 above 60mmHg Minimize oxygen demand (stress, fevers, pain) Treat the cause (sputum cultures, sepsis, multi-organ dysfunction) Prevent complications VAP, hypoxia, decubitus ulcers (prone position) Proning - Rot-a-prone bed: Manual proning: easier to perform CPR, less skin breakdown Considered if PaCO2/FiO2 ratio is below 100 Monitor pressure points, protect cornea with lubricant and tape, towel for secretion Mechanical Ventilation Introduction:  approx 8 questions LO 1 (1 question), LO 2 (1 questions), LO 2&3 (1 question), LO 3 (3 questions), LO 4 (2 question) Associated Learning Outcomes (LO’s) Discuss the indications for mechanical ventilation. Apnea or absence of breathing Acute Respiratory Failure Impending Respiratory Failure Severe hypoxemia Discuss collaborative care and nursing management of clients requiring mechanical ventilatory support (includes care of the intubated patient) Monitor ventilation with BVM, assess oxygenation by SaO2, suction when necessary Preliminary Assessment of ETT placement: observe for chest risk and fall, auscultate lung sounds, CO2 detector Yellow means YES, Purple means Problem Proper cuff inflation Chest X-ray to confirm placement Two types of Positive Pressure Ventilation Pressure: delivers a set pressure with each breath (cm H2O is measured) Pressure vary on clients airway/lung compliance Volume: delivers a set of volume with each set (TV is set) Volume amount set based upon compliance Constant monitoring is required to prevent hyperinflation and hypoventilation Tidal Volume: 8-10mL/kg for ideal body weight FiO2: 21% to 100% PEEP: Constant, keeps alveoli open Describe the modes of mechanical ventilation and related relevant nursing care: CPAP, PS, AC, SIMV AC: Preset # of breaths and tidal volume Ventilator supports all breaths with the set tidal volume Risk of hyperventilation and respiratory alkalosis Ventilator will assist with breaths by controlling the amount of volume Synchronized Intermittent Mandatory Ventilation (SIMV) Volume of spontaneous breaths varies (whatever the patient does) Considered a weaning mode Patient contributes more to work of breathing Continuous Positive Airway Pressure (CPAP) Patient receives this setting when they have spontaneous breathing Invasive: Ventilator Non-invasive: Nasal pillow, mouth/nose mask, face mask Pressure Support (PS) Is a setting added to SIMV Will receive 10cmH2O support with SIMV and PC setting Patient must be spontaneously breathing or they won't get any breaths Recognize the risks associated with intubation and positive pressure mechanical ventilation. Ventilator Associated Pneumonia Elevate HOB to 30-45 degrees Hand washing Interrupt sedation each day to assess readiness Support for DVT and PUD Mechanical Ventilation Part 2:  approx 5 questions LO1 (1 question), LO 2 (3 questions), LO 3 (1 question) Identify indicators of readiness to wean as well as successful and unsuccessful weaning Underlying cause to ventilate is resolved Hemodynamically stable, good CO Good respiratory strength PaO2 > or = 80mmHg Minimal secretions Stable VS Alert and awake, mental readiness Short duration weaning trials (30 minute - 2 hours) Change setting so patient does more work: SIMV vs AC (both can be weaning modes if the RR is lowered) CPAP (now the patient has to trigger every breath with no extra support) Pressure Support (now the patient triggers all breaths, but they get some support) T-piece trials: strengthen respiratory muscles (no pressure, humidified FiO2 and secure airway) Failure to Wean: Hyper/hypopnea Low Tidal volume Tachycardic & HTN Apply knowledge of mechanical ventilation and respiratory physiology to acid base balance Acidosis: patient is hypoventilating so additional ventilator support is needed Alkalosis: patient is hyperventilating so less ventilator support or increased sedation is needed Avoid high FiO2 (>50%) for long periods of time Recognize appropriate use of paralytics in the mechanically ventilated patient Analgesics (morphine & fentanyl) Sedatives (midazolam, propofol, dexmedetomidine) Neuromuscular blocking agents (pancuronium, vecuronium) Two twitches: indicate proper paralysis Bispectral Index Monitoring (0-100 Scale Awake - 80-100) Intracranial Pressure Monitoring:  approx 10 questions LO 1&5 (1 question), LO 2&3 (1 question), LO 4 (1 question), LO 2&4 (1 question). LO 4&5 (3 question), LO 4,5,&7 (1 question), LO 5, 6, &7 (1 question). LO 7 (1 questions) Associated Learning Outcomes (LO’s) Define Intracranial Pressure and Increased Intracranial Pressure Intracranial Pressure Defined: CSF, blood volume, and brain tissue (Monro-Kellie Hypothesis) Increased Intracranial Pressure: the pressure exerted by brain tissue, blood, and CSF against skull Sustained pressure of >20mmHg Normal ICP: 5-15mmHg Causes: Increases in brain volume, cerebral blood volume, or CSF volume (Cerebral edema, brain mass) Intracranial hemorrhage Increased blood flow Obstruction of outflow Calculate Cerebral Perfusion Pressure (CPP) MAP - ICP = CPP Identify appropriate nursing interventions to address reduced CPP Identify clinical manifestations of increased ICP Change in LOC, vision, reflexes Headache Vomiting Elevated body temperature Late Signs: Cushing's Triad: Compression of the brainstem Systolic Hypertension with widening pulse pressure Bradycardia Irregular respirations Posturing (decorticate or decerebrate) Determine appropriate nursing interventions for increased ICP Elevate HOB and prevent neck flexion Prevent infection and hemorrhage Pain and Anxiety management Decrease environmental stimuli Decrease cause of high ICP (metabolic demand (fever, seizure, shivering), stress, suctioning, abdominal distention) Assess neuro frequently Watch for secondary brain injury DO NOT hyperventilate Assess pupillary response (Dilated pupils indicate compressed cranial nerve III) Use Glasgow Coma Scale: Eyes, Best motor response, best verbal response (Scored 3-15) Lowest score is 3 with no response = BAD Medications for Management: Osmotic Diuretics (Mannitol) 3% Sodium Chloride: Infuse slowly and through central line (30mL/hr) Antiseizure drugs (Phenytoin/Dilantin) Corticosteroids (Dexamethasone) Reduces swelling (brain tumors, cerebral edema) Identify the purpose of an external ventricular drain Trend an ICP waveform only Drain CSF and trend ICP waveform Describe basic nursing and collaborative care of the patient with an external ventricular drain Reduce risk of/monitor signs of infection Assess brain perfusion (Neuro check, CPP, increased ICP) Evaluate CSF drainage and document ICP leveled at the Foramen of Monro (tragus of the ear) Strict aseptic technique during dressing changes Reassess level of transducer with any position change Position changes and transport with drain CLOSED Cushing triad: compression on the brainstem EVD: systemic measures to determine blood flow to brain is adequete Pa02: 80-100 what does it mean Sp02: 94-95% ARDS powerpoint: looking for what the Pa02, what their Fi02 - remember percentage to calculate Looking for what level of ARDS Berlen definition Is it mild or more severe? Description of breathing patterns, be able to identify what it is The wave forms too Indications for medications, why are they getting them Levophed/norepinephrine know what it does Epi first line of medication for shock Mannitol/3 percent ICP what does mannitol does, why is it used in ICP patients, how does hypertonic work within the ICP pts Be able to know patient would look like, what things are going on patho level for shock Know what are potential causes - read whats on the slides CRRT asking to think about basic care - blood clots, line needs to be sterile General could you tell someone if their family is going on CRRT - 2 sentence explanation of what it does For septic shock: third spacing Only uncompensated ABGs Know what causes ABG imbalances and general treatment ; what is the body going to do - think about practice quiz Resp failure/ARDS: describing the VQ mismatch Difference between resp failure and being in ARDS How to tell someone is in respiratory distress - early/late signs Getting rid of secretions, what are other things we can do when ventilating What patients need assistance with ventialtion and oxygenation