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NR-341 Exam 1 Study Guide primary ALL ANSWERS SOLVED LATEST 2022 /100% CORRECT GUARANTEED GRADE A+

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• Diagnostic Tests Acute respiratory failure o ABGs, Chest x-rays, CT, pulmonary function tests, end tidal CO2 monitoring, bronchoscopy. • Assessments o Lung sounds, work of breathing, use of accessory muscles, chest expansion, nasal flaring, respiratory rate, pulse ox • Interventions o Ineffective airway clearance  reposition patient o ARF ▪ Causes: pulmonary edema, atelectasis, pneumonia, COPD, asthma, ARDS, thoracic, spinal or head injuries, drug overdose, neuromuscular disorders ▪ Type 1 - hypoxemic or oxygenation failure • PAO2 less th • an 60 MMHG o Normal PaO2 = 80 - 100 • Hypoventilation o Hyperventilation causes further issues when trying to correct this • Intrapulmonary shunting o Blood did not get oxygenated and dispersed to rest of body system o Blood that is shunted from the right side of the heart to the left without oxygenation. o Based on rate ventilation and perfusion: Rate of ventilation= rate of perfusion; ratio of VQ = 1 o Based on amount of ventilation and perfusion: ▪ Normal ventilation (V) IS 4 L/MIN ▪ Normal perfusion (Q) IS 5L/Min ▪ Normal V/Q Ratio IS 4/5 or 0.8 ▪ VQ scan patient must lie for 30 minutes o Tissue hypoxia  anaerobic metabolism and lactic acidosis o Normal Cardiac output ▪ 600 – 1000 ML/MIN of O2 ▪ Low cardiac output  decrease O2 blood to tissues  anaerobic metabolism  production of lactic acid  metabolic acidosis ▪ Type 2 - hypercapnic or ventilator failure • PACO2 50 MM HG • Increase in PaCO2 (hypercapnia) due to decrease O2 in body and CO2 can be blown off • Increase in ventilation  excess CO2 blown off (hypocapnia) • VQ mismatch  not 1:1 ▪ Assessment of respirator failure: most common  hypoxemia  restlessness ▪ Medical management: O2, bronchodilators, corticosteroids, ventilators, transfusion, nutritional support, hemodynamic monitoring ▪ HGB 12- 16 • Anemic is less than 8 HGB o Respiratory failure causes ▪ Failure to ventilate ▪ Failure to oxygenate ▪ Failure to protect airway Acute Respiratory Distress Syndrome (ARDS) • Noncardiogenic pulmonary edema- pulmonary edema not caused by a cardiac problem. • Diagnostic criteria o 1. PaO2/FiO2(decimal) ratio of less than 200 – PaO2 divided by Fi02 … 100 divided 21 = ▪ Optimal Ratio 476.19 ▪ ***Decreasing PA02 levels despite increased FIO2 administration o 2. Bilateral infiltrates not explained by something else. (Normally air should be black, you will see white puffy stuff all over if you have this) • Risk Factors. 4 Factors o Sepsis #1*** o Pneumonia o Trauma o Aspiration of Gastric contents • Pathophysiology o Basic underlying patho: damage to type II pneumocyte, which produces surfactant o 4 steps ▪ 1. Injury to the lung that stimulates the inflammatory response (either direct or indirect) with stimulates inflammatory response. Inflammatory cells and their mediators damage the alveolocapillary membrane. ▪ 2. Onset of pulmonary edema (blood cell, cell debris, stuff) ▪ 3. Alveoli start to collapse. Production of surfactant stop and alveoli collapse. Lungs become less compliant. ▪ 4.Lungs become stiff and noncompliant. Lung becomes fibrotic. Severe gas exchange impairment. • Diagnostic Tests o Chest x-ray • Symptoms or ARDS: o Dyspnea and tachypnea and hypoxemia, that does not improve with supplemental oxygen therapy. o Elevated PACO2 50 MM of HG o Decreased PAO2 60 MM of HG o V/Q mismatch o O2 Satureation 90% o Hyperventilation with normal breath sounds o Respiratory alkalosis o Increased temperature and pulse o Worsening chest x-rays that progress to “white out” o Increased PIP on ventilation o Eventual severe hypoxemia not improved with O2 therapy o Late stages - Eventually will hypoventilate - respiratory acidosis • Treatment of ARDS o Treat the cause, more supportive care o Oxygenation and ventilation**KEY to treating ARDS ▪ Positive end-expiratory pressure (PEEP) – high amounts of PEEP 10-15cm of peep. ▪ Possible non-traditional modes of ventilation – oscillator or nvrp ▪ Decrease Oxygen consumption o Comfort ▪ Sedation ▪ Pain relief ▪ Neuromuscular blockade o Positioning ▪ Prone positioning • Better profusion to posterior part of the lung. Takes weight of heart off of the lungs • Protect airway! Face down.. In regular bed patient will be with head on side. • Skin integrity – different pressure points (hips, knees) ▪ Continuous lateral rotation therapy ▪ Complications: DIC, long term pulmonary affect, organ failure, death o Fluid and electrolyte balance o Adequate nutrition o Psychosocial support – more for family o Prevention of complications ▪ Thrombus or embolus formation, DIC, death, Organ failure, pulmonary affects • Acute Respiratory Failure as a result of Underlying Disease o Several conditions both acute and chronic can result in Acute Respiratory Failure ▪ COPD ▪ Asthma Exacerbation ▪ Pneumonia - All types ▪ Pulmonary Embolism  pulmonary angiogram is a definitive diagnosis o Treatment of ARF in Chronic Diseases (not really going to study this) ▪ Treat the underlying cause • COPD - Bronchodilators, corticosteroids, antibiotics (infection) • Asthma - IV corticosteroids, bronchodilators • Pneumonia - Antibiotics, fluids • Pulmonary Embolism - DVT prophylaxis, thrombolytics, heparin, vena cava filter Maintain Oxygenation - Administer oxygen, ventilate if needed, minimize demands Ventilation • Indications for ventilation: To support patient’s respiratory system until the cause of the respiratory failure has been treated. This is a temporary treatment. Patients are not meant to be on ventilator forever. • Reasons to be Ventilated: o Hypoxemia - PaO2 ≤ 60 mm Hg on FiO2 .50 o Hypercapnea - PCO2 ≥ 50 mm Hg with pH ≤ 7.25 o Norms: ▪ PAO2: 80 – 100 ▪ SaO2 90 – 100% ▪ pH 7.35 – 7.45 ▪ PaCO2 35 – 45 ▪ HCO3 – 22 - 26 o Progressive deterioration (changes in vitals, using accessory muscles) ▪ Increasing RR ▪ Decreasing VT ▪ Increase WOB • Positive pressure ventilation o Opposite of how we normally breath making it somewhat uncomfortable o Air is pushed into the lungs instead of drawn in this is positive pressure. o Movement of gases into lungs through positive pressure o Normal breathing is negative pressure. • Ventilator Settings o FiO2 ▪ Fraction of inspired O2 or amount of O2 the machine gives (how much oxygen are we breathing) ▪ Room air = 21% ▪ Ventilator can be set to 30-100% • Sp02 – pulse ox – 02 on Hgb • Pa02: ABG – oxygen in arterial system o Tidal Volume (VT) ▪ How much air will the patient get with each breath or How much volume am I taking in. ▪ Normal is 350 - 550 – Taken off height and weight. ▪ Adjusted according to peak and plateau pressure o Respiratory rate: ▪ 10 -m20 breaths initially, usually 12-14 – How many breaths am I taking in. ▪ Cheyne stokes- cyclical with apneic periods ▪ Bios – cluster breathing ▪ Kussmaul – deep, regular and rapid o I: E Ratio Inspiration: Expiration ratio; normal 1:2 ( 1 sec of inhale to 2 sec of exhale). We take more time on exhalation. o Positive end-expiratory pressure (PEEP) ▪ Instills a small amount of pressure into the patients lungs at the end of expiration. ▪ Purpose: Helps to keep airway and keep alveoli open to improve gas exchange. ▪ 5-20 cm H2O ▪ Can cause reduced cardiac output if high and blocks venous return. Hyperinflation of the lungs increases thoracic pressure and compresses the heart ▪ High levels can pop alveoli and cause pneumothorax ▪ Keep alveoli to improve gas exchange o Sensitivity ▪ Amount of patient effort. How hard the pt has to work to get flow of O2 from the ventilator (how hard does the patient have to work to get oxygen from the ventilator. ▪ Goal is to avoid patient-ventilator dyssynchrony (“fighting the ventilator”) • Data to Monitor During Mechanical Ventilation o Exhaled tidal volume (EVT) – how much your patient is exhaling, how much is coming out of the patients lungs. ▪ Amount exhaled should be equal to amount going in Ex: If you are getting 250 then you want 250 out. Could be air trapping.. there is something going on. ▪ Should not be more than 50 mL different from set VT o Peak inspiratory pressure (PIP) ▪ How hard the ventilator has to work to deliver a breath. ▪ Should be less than 40 mm Hg ▪ High PIP can be caused by three main reasons. • 2. Mucous plug • 1. Noncompliant or stiff lungs due to ARDS or pulmonary fibrosis • 3. Pt is biting the tube. Usually use oral airway to prevent this used as bit block. o Total respiratory rate – What the patient is doing, we set the ventilator rate but patient can take more breaths then we set the machine at. ▪ Count total rate, which accounts for set rate and patient effort • Ventilator Modes o Volume Assist/Control (V-A/C) – 40%, 12 Rate (3) ▪ Ventilator does most of the work because the patient cannot ▪ Given to wean a patient off to SIMV  patient who codes goes straight to AC first ▪ Pt can take additional breaths but they get the same tidal volume as when ventilator initiates the breath Ex: patient who just has surgery and is still sedated, brain injuries ▪ Set a rate, set a tidal volume, Fi02, and peak ▪ Every minute 12 breaths  AC 12 • RR should be 12 or higher ▪ ▪ If patient wants to take additional breaths that is fine ▪ When the patient initiates a breath, the ventilator will assist them to get whatever the set tidal volume, The ventilator is assisting the patient with every breath. ▪ Tidal volume will be the same for both ventilator and pt. breath. ▪ *Key is that when patient initiates a breathe, the ventilator will assist them to get whatever the set tidal volume is o Synchronized intermittent mandatory ventilation (SIMV) – 40% 12 Rate ▪ Patient does most of the work ** When patient initiates breath they will get the tidal volume that they alone can take, the ventilator will not assist them. ▪ Set a rate, set a tidal volume, Fi02, and peak ▪ When ventilator takes a breath you are going to get a set volume but when patient takes a breath you are only going to get the tidal volume that they alone can take. ▪ On SIMV the ventilator will synchronize the breaths. Ex: 12 min 5- V, 10 - V P – 13, 18 - V, 23 - V. It will retime itself to how you are breathing so it doesn’t give you to many breaths. ▪ Pt can take additional breaths but they only get the volume they can take in not the amount the ventilator gives on the breaths they initiate. ▪ Ventilator then synchronizes next breath after the pt initiated breath. If rate is every 5 seconds, then the machine schedules next breath for 5 seconds after the patient takes their own breath. ▪ *Key is that when pt initiates a breath they will get the tidal volume that they alone can take, ventilator will not assist them. o Pressure Ventilation ▪ Patient has to be able to breathe on their own, initiate breath on their own ▪ Ventilator set to allow air flow until preset pressure is reached ▪ VT is variable ▪ PIP can be better controlled ▪ Only gets pressure during inspiration ▪ Risk of hypoventilation and respiratory acidosis ▪ Includes CPAP, pressure support (PSV), pressure A/C, inverse-ratio ventilation, and airway pressure release (APRV) o Pressure Support (PS) – have to be able to breathe on own, the machine will not give any breaths. Used of weaning. Will only get pressure during inspiration. 40%, Rate varies. Pressure 5-20 cm H20 on inspiration ▪ Patient’s spontaneous effort is assisted by preset amount of positive pressure • 6 to 12 cm H2O ▪ Decreases WOB with spontaneous breaths ▪ Also useful in weaning ▪ Pressure support ventilation requires the patient to trigger each breath, which is then supported by pressure on inspiration ▪ Patient may vary amount of time in inspiration, respiratory rate, and tidal volume (VT) o Advanced Modes ▪ Pt is very sick and has non-compliant lungs(lungs are very stiff) – Usually seen with

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NR-341 Exam 1 Study Guide primary ALL ANSWERS
SOLVED LATEST 2022 /100% CORRECT GUARANTEED
GRADE A+
Acute respiratory failure
• Diagnostic Tests
o ABGs, Chest x-rays, CT, pulmonary function tests, end tidal CO2 monitoring, bronchoscopy.
• Assessments
o Lung sounds, work of breathing, use of accessory muscles, chest expansion, nasal flaring,
respiratory rate, pulse ox
• Interventions
o Ineffective airway clearance reposition patient
o ARF
▪ Causes: pulmonary edema, atelectasis, pneumonia, COPD, asthma, ARDS, thoracic,
spinal or head injuries, drug overdose, neuromuscular disorders
▪ Type 1 - hypoxemic or oxygenation failure
• PAO2 less th
• an 60 MMHG
o Normal PaO2 = 80 - 100
• Hypoventilation
o Hyperventilation causes further issues when trying to correct this
• Intrapulmonary shunting
o Blood did not get oxygenated and dispersed to rest of body system
o Blood that is shunted from the right side of the heart to the left
without oxygenation.
o Based on rate ventilation and perfusion: Rate of ventilation= rate of
perfusion; ratio of VQ = 1
o Based on amount of ventilation and perfusion:
▪ Normal ventilation (V) IS 4 L/MIN
▪ Normal perfusion (Q) IS 5L/Min
▪ Normal V/Q Ratio IS 4/5 or 0.8
▪ VQ scan patient must lie for 30 minutes
o Tissue hypoxia anaerobic metabolism and lactic acidosis
o Normal Cardiac output
▪ 600 – 1000 ML/MIN of O2
▪ Low cardiac output decrease O2 blood to tissues anaerobic
metabolism production of lactic acid metabolic acidosis
▪ Type 2 - hypercapnic or ventilator failure
• PACO2 > 50 MM HG
• Increase in PaCO2 (hypercapnia) due to decrease O2 in body and CO2 can be
blown off
• Increase in ventilation excess CO2 blown off (hypocapnia)
• VQ mismatch not 1:1
▪ Assessment of respirator failure: most common hypoxemia restlessness
▪ Medical management: O2, bronchodilators, corticosteroids, ventilators, transfusion,

, 2
nutritional support, hemodynamic monitoring

, 3

▪ HGB 12- 16
• Anemic is less than 8 HGB
o Respiratory failure causes
▪ Failure to ventilate
▪ Failure to oxygenate
▪ Failure to protect airway

Acute Respiratory Distress Syndrome (ARDS)
• Noncardiogenic pulmonary edema- pulmonary edema not caused by a cardiac problem.
• Diagnostic criteria
o 1. PaO2/FiO2(decimal) ratio of less than 200 – PaO2 divided by Fi02 … 100 divided 21 =
▪ Optimal Ratio 476.19
▪ ***Decreasing PA02 levels despite increased FIO2 administration
o 2. Bilateral infiltrates not explained by something else. (Normally air should be black, you will
see white puffy stuff all over if you have this)
• Risk Factors. 4 Factors
o Sepsis #1***
o Pneumonia
o Trauma
o Aspiration of Gastric contents
• Pathophysiology
o Basic underlying patho: damage to type II pneumocyte, which produces surfactant
o 4 steps
▪ 1. Injury to the lung that stimulates the inflammatory response (either direct or indirect)
with stimulates inflammatory response. Inflammatory cells and their mediators damage
the alveolocapillary membrane.
▪ 2. Onset of pulmonary edema (blood cell, cell debris, stuff)
▪ 3. Alveoli start to collapse. Production of surfactant stop and alveoli collapse. Lungs
become less compliant.
▪ 4.Lungs become stiff and noncompliant. Lung becomes fibrotic. Severe gas exchange
impairment.
• Diagnostic Tests
o Chest x-ray
• Symptoms or ARDS:
o Dyspnea and tachypnea and hypoxemia, that does not improve with supplemental oxygen
therapy.
o Elevated PACO2 > 50 MM of HG
o Decreased PAO2 < 60 MM of HG
o V/Q mismatch
o O2 Satureation < 90%
o Hyperventilation with normal breath sounds
o Respiratory alkalosis
o Increased temperature and pulse
o Worsening chest x-rays that progress to “white out”
o Increased PIP on ventilation
o Eventual severe hypoxemia not improved with O2 therapy
o Late stages -> Eventually will hypoventilate -> respiratory acidosis

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