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47 Cards in this Set
- Front
- Back
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ABG Interpretation
pH 7.25 PaCO2 50 PaO2 85 HCO3 22 |
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pH 7.46
PaCO2 49 PaO2 90 HCO3 35 |
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What is acute respiratory failure? (type 1 and type II)
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failure of oxygenation or respiration
type 1- hypoxemic with normocapnic respiratory failure type 2- hypoxemic with hypercapnic respiratory failure |
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What are the two types of causes of ARF?
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extrapulmonary
intrapulmonary |
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What causes the hypoxemia in ARF?
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1.) alveolar hypoventilation.
it is a ventilation/perfusion mistmatch. V/Q mismatch- ventilation and blood flow are mismatched. Alveoli are underventilated, they cannot adequately perform gas exchange. 2.) Intrapulmonary shunting- blood hits arterial system without any oxygenation |
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How to diagnose ARF?
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ABG values on room air
PaO2 under 60 (hypoxemia) PCO2 over 45 (hypercapnia) pH under 7.35 (acidosis) also: CXR, bronchoscopy, CT, PFTs |
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What is the clinical presentation of ARF?
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SOB, lung sounds, pulse ox, skin, neuro
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what is the treatment of ARF?
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**find underlying cause
-oxygenation/positive airway pressure with ventilation if necessary meds: bronchodilators, steroids, sedatives, analgesics immediate tx: -correct acidosis -prevent complications -position pt to optimize v/q matching -suction PRN -prevent desats -nutrition support -monitor for complications -comfort and pt education |
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What is Acute Lung Injury (ALI)?
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pulmonary presentatio in MODS
-it is noncardiac pulmonary edema. injury to the pulmonary vasculature or airways. The severest form of ALI is acute respiratory distress syndrome (ARDS) |
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What are the direct injury risk factors in ALI? 7
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-aspiration
-near drowning -toxic inhalation -pulmonary contusion -pneumonia -oxygen toxicity -thoracic radiation |
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What are the indirect injury causes in ALI?
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-sepsis
-cardiopulmonary bypass -severe pancreatitis -embolism -DIC -shock states |
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What are the phases of ALI?
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exudative-acute phase
fibroproliferative phase resolution phase |
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What occurs during the exudative-acute phase of ALI?
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leakage of fluid due to increased pulmonary capillary permeability. This causes interstitial/alveolar edema, which leads to intrapulmonary shunting and V/Q mismatching.
-Then, there is decreased lung compliance secondary to atelectasis with an end result of pulmonary HTN. |
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what is the clinical presentation of the exudative-acute phase of ALI?
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-tachypnic/restless
-resp. alkalosis -PaO2 normal -CXR normal -use of accessory muscles/lungs may be clear |
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What occurs during the fibroproliferative phase of ALI?
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the alveoli become enlarged and mishapen, causing scarring of the pulmonary capillary membrane. this causes further decreased compliance "stiffening" of the lungs. Therefore results in pulm HTN and further hypoxemia. also, refractory hypoxemia.
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What is the clinical presentation of the fibroproliferative phase of ALI?
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worse than before: hyperventilation (tachypnea), agitation, accessory muscle use
new problems: lactic acidosis, decreased SVO2, CXR now shows infiltrates, HR up BP down, and now the lungs start to sound shitty (cracles/rales---wetness) |
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what happesn during the resolution phase of ALI?
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recovery takes several weeks, and there is restoration of the alveoli.
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What is colaborative MGMT of ALI/ARDS?
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-O2/intubate/mechanical ventilation
(permissive hypercapnia and pressure control) -PEEP -Maximize CO -prone position -suction PRN -prevent desats -nutritional support -provide comfort Meds: bronchodilators, sedatives, analgesics, neuromuscular blocking agents -prevent complications (encephalopathy, dysrhythmias, venous thromboembolism, GI bleeding, barotrauma, volutrauma, O2 toxicity) |
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Activities that increase Oxygen consumption
-dressing change |
10%
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Activities that increase Oxygen consumption
-physical exam |
20%
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Activities that increase Oxygen consumption
-bath |
23%
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Activities that increase Oxygen consumption
-CXR |
25%
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Activities that increase Oxygen consumption
-suctioning |
27%
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Activities that increase Oxygen consumption
-increased WOB |
40%
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Activities that increase Oxygen consumption
-position change |
31%
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Activities that increase Oxygen consumption
-linen change |
22%
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Define PNA.
name the 3 types |
acute inflammation caused by infection.
-community acquired pneumonia (CAP) -hospital associated pneumonia (HAP) -ventilated-associated pneumonia (VAP) |
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Risk Factors for community acquired pneumonia (CAP)
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-ETOH abuse
-COPD -comorbidities -impaired swallowing -altered MS |
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Risk factors or HAP/VAP.
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-age
-ETOH abuse -smoking -decreased LOC -thoracic abdominal surgery -ETT/mechanical ventilation -enteral feedings -cross contamination -H2blockers/antacids -antibiotic therapy |
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What is the patients clinical presentation in pneumonia?
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-dyspnea, fever, cough
-course crackles -dullness to percussion |
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What are the diagnostics of pneumonia?
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-infiltrates on CXR
-Gram stain -bronchoscopy -CBC with diff -blood cultures -chem panel -ABGs |
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What is the collaborative MGMT of pneumonia?
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-O2 therapy/independent lung ventilation
-antibiotics -bronchodilators -positioning -suction PRN -provide adequate rest and recovery -monitor for complications- ARF -comfort and support |
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What is aspiration pneumonitis?
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-injury to the lung from aspiration
-80% of HAPs |
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What are the risk factors of aspiration pneumonitis?
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-decreased LOC
-supine position -NGT -vomiting -tracheal intubation -mechanical ventilation -subglottic secretion -cuff deflation with trachs -gastric feedings -bolus feedings -poor oral health -age -hyperglycemia |
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what is the clinical presentation of aspiration pneumonitis?
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presents with acute respiratory distress symptoms
-SOB -wheezing -cyanosis -crackles -copious amounts of sputum -CXR VS: hypoxemia, tachycardia, tachypnea, fever |
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what is the collaborative MGMT of aspiration pneumonitis?
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-O2
-witnessed- secure the airway!! -position pt -immediate suctioning of upper airway -may require bronchoscopy -correct hypoxemia- may need intubation -fluid replacement- fluid shifts into the lungs, intravascularly dry -monitor for PNA/ARF/ALI -antibiotics- if s/s persist or infection is noted |
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what are nursing measures in addition to collaborative MGMT of aspiration pneumonitis?
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oxygenate and ventilate- positioning (good lung where?), preventing desats, suction PRN
-prevent further aspiration |
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what is a pulmonary embolism? what are the two types?
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a clot which occludes an area in a pulmonary arterial bed.
-Thrombotic Emboli (DVTs, UEs, right ventricle) -Nonthrombotic emboli (fat tumor, amniotic fluid, air, foreign bodies) |
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What ar ethe causes of a thrombotic emboli?
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DVT, UE
The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart leads to the symptoms and signs of PE |
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What are the causes of a nonthrombotic emboli?
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fat, tumors, amniotic fluid, air, foreign bodies
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What patients are at risk for a PE?
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DVTs/venous stasis/immobility
-Afib -injury to the endothelium (infection/atherosclerosis) -hypercoagulability -surgery -cancers -trauma -pregnancy |
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What are the two main forms of side effects with a PE?
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pulmonary and hemodynamic
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What are the pulmonary effects of a PE?
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dead space
bronchoconstriction shunting-hypoxemia |
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What are the hemodynamic effects of a PE?
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pulmonary HTN
right ventricular failure- leads to a decrease in L ventricular preload, CO, BP, and shock |
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what is the clinicla presentation of a PE?
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tachycardia
tachypnea dyspnea/SOB fever rales/crackles pleuritic chest pain cough DVT hemoptysis |
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How do you diagnose a PE?
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ABG (what do you expect to see)
d-dimer ECG CXR Echo VQ scan pulmonary angiogram DVT studies |
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What is the treatment of a PE?
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PREVENTION!!!!
O2 (intubate? mech vent?) thrombolytics? anticoagulants bronchodilators inotropic agents sedatives/analgesics fluids positioning watch for bleeding greenfield filter |
