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46 Cards in this Set
- Front
- Back
Vital Capacity 60-70 ml/kg so 70kg patient |
4700 cc |
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Inspiratory reserve volume IRV (70kg) |
3000 CC |
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Expiratory Reserve Volume ERV (70kg) |
1200 CC |
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Residual Volume 70 kg |
1200 cc |
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FRC - functional residual capacity RV+ERV |
2400 cc |
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Risk factors for Post-op pulmonary complications |
older than 65, 40 pack yr smoking hx, COPD/Asthma, thoracic/abd surg, Productive cough, exercise intolerance, GA>3hrs. |
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Respiratory Failure |
Lungs cannot maintain adequate arterial oxygenation. - co2 elimination can be normal or abnormal. |
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Type 1 Resp Fx for Type 2 Resp Fx |
Type 1 - Hypoxemic - PaO2- less than 60 w/ FiO2>50- PNA, Pulm edema, Pulm injury Type 2- Hypercapnic-Hypoxemia - PaCO2> 50; pH depends on metabolic compensation. - Chronic Lung problems. OD, NM weakness, Polycythemia, Cor Pulmonale. |
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Determine chronic vs acute resp failure |
Look at pH if normal - chronic if pH low - Acute |
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Acute Resp Fx what to look at to determine Hypoventilation or VQ mismatch |
Look at shunt- A-a Gradient normal then hypoventilation A-a Gradient greater than 5 than think shunting. |
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Pulmonary Edema Cardiogenic |
Increase in Hydrostatic or decrease in capillary oncotic pressure. LV failure, severe mitral stenosis, LA obstruction, Aortic valve disorder GOAL: DECREASE PULMONARY CAPILLARY PRESSURE by increase LV function (inotropes) or decrease pulmonary blood flow (vasodilators), Diuretics (correct hypovolemia |
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Pulmonary Edema Non-Cardiogenic |
Fluids moves to pulmonary capillaires to interstitial space then to alveoli Albumin Leak |
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**How to know difference between Cardiogenic and Non-Cardiogenic Pulmonary Edema |
Pulmonary Artery Occlusion Pressure (PAOP) if less than 18mmHg= likely increase hydrostatic pressure (cardiogenic) Protein - decrease protein = cardiogenic increase in protein= non-cardiogenic less than 18 PAOP and Protein= Non-cardiogenic Over 18 and no protein = Cardiogenic |
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Post-Obstructive Pulmonary Edema type 1 |
Type 1 - follows sudden sever upper airway obstruction (post ex laryngospasm, croup, epiglottis) due to vigorous ins. effort - highly neg intrathoracic pressure, increased venous return, decrease CO, and fluid transudation into alveolar space |
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Post-obstructive pulmonary edema type 2 |
Develops after surgical relief of chronic upper airway obstruction - tonsillectomy or removal of upper airway tumor sudden relief of longstanding PEEP. Lung/volumes and pressure return to normal but permeability and interstitial funds does not resolve as quickly. |
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Pulm edema stages |
1- interstitial pulm edema and decreased compliance 2. intersitium overwhelmed and fluid enter alveoli 3.alveoli mostly fluid and pulm shunting 4.alveolis overwhelmed and Froth |
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Pulm edema and healthy lungs |
PPC must exceed 25 mm Hg before lymphatic reserve exhausted. -- rarely acute fall in oncontic usually hydrostatic pressure. |
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Direct vs Indirect Lung injury |
Direct - PNA, gastric fluid aspiration, Pulm contusion, fat emboli, near-drowning, inhalational injury, O2 toxicity Indirect- SEPSIS, trauma w/shock, transfusion, CPB, overdose, pancreatitis |
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ARDS and first 24 hours |
ARDS develop in first 24 hours after trauma good prognosis |
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Mendelsons syndrome |
Gastric volume >25ml Gastric pH < 2.5 Epithelial injury Tx suction and PEEP |
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ARDS and trauma risk** |
Fat embolus usually appear 1-3 days after trauma and a long bone fracture or pelvic fracture
see Petachiae, mental confusion, thrombocytopenia, and resp fx |
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Acute lung injury vs Acute resp distress syndrome diagnosing ***8 |
Identifiable cause - know why it happen Acute onset PaO2/FiO2 ratio< 300 in ALI PaO2/FiO2 ratio< 200 in ARDS Diffuse bilateral opacities on x-ray PaOP less than18 or no evidence of LA HTN |
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Usually cause of death with ARDS |
Multi-Organ System Fx |
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ARDS and Pulm fibrosis |
Patients who need prolonged ventilatory support and FiO2> 50% can develop pulmonary fibrosis- leading to decreased surfactant and increased epithelial cells. typically delayed onset |
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ARDS signs and symptoms |
Dyspnea, Hypoxemia, initial PaCO2 low(breathing fast), Pulm HTN, diffuse infiltrates, PaO2/FiO2 less than 200, Resp. fx. |
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Tx ARDS |
Primary goal preserve O2 Keep FiO2<50% VT 6ml/kg and airway pressure less than 30 PEEP and CPAP(which can turn into PEEP at high flow) Add PEEP to keep PaO2>60 and FiO2<50 |
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Issues with PEEP |
Barotrauma in increase airway pressure decrease venous return= decrease CO |
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TRALI |
Non-cardiogenic Pulm edema usually recover 24-48 hours. tx as ARDS |
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Obstructive Lung Disease |
MOST COMMON PULMONARY DISEASE Resistance to airflow EXPIRATION = air trapping VQ mismatch leads to decrease gas exchange emphysema, chronic bronchitis, asthma. |
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Asthma Early vs Late phase |
Early - smooth muscle contraction and mucosal edema, usually resolves in 1 hour Late - begins 4-6 hours post exposure, more severe symptoms by eosinophils-bronchoconstriction, edema, mucus plug small bronchi most affected (2-5mm) generation 17-19 |
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Asthma/Obstructive PFT's |
Decreased FEV1 and Low FEV1/FVC ratio reversibility with tx 12% improvement good indicator... 200FEV1 absolute increase |
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Asthma is it chronic |
Yes - they always have inflammation present and are hyper-reactive |
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When do asthma patients have wheezing |
Auscultate - usually wheezing on expiration** |
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Status Asthmaticus |
Life threatening- resp fx imminent. progressing hours to days. tx b2 agonists and hydrocortisone. albuterol, terbutaline, theophylline, aminophylline, mgso4, ett, volatile agents, ECMO |
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Stages of COPD |
Stage 1 - mild copd - FEV1 >80%, - pt may not be aware Stage 2- Fev1 50-80%, dyspnea on exertion- seeks attention* Stage 3- fev1 30-50%, increase SOB, decrease exercise, repeated exacerbations impact pt lives stage 4 - fev1 <30 or Fev1< 50 plus chronic resp fx, exacerbations life threatening |
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Chronic Bronchitis vs Emphysema |
Chronic Bronchitis - Productive cough for 3 months a year for 2 consecutive years. hypertrophy of mucus glands, increase goblet cells, fibrosis in peripheral airways (blue bloaters) obstruction to expiration Emphysema - destruction of alveolar w/airspace enlargement - no significant fibrosis (pink puffers) - alveoli and parenchyma distended/destroyed. form bullae. increase dead space. |
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Chronic Bronchitis vs Emphysema |
Chronic Bronchitis - Cough w/copious secretions, increase Hct, PaCO2 elevated, increased airway resistance, and cor pulm early Emphysema - cough w/ exertion, normal PaCO2, hyperinflation on X-ray, Cor pulm late. Diffusion impairment |
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Emphysema types |
Centraiacinar - Central only Panacinar - Everything look like broccoli |
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Emphysema #1 cause |
Smoking tx quit smoking. Wheezing - early - mild or none....later- E then I&E, Late - no airflow. ... Flat diaphragm PFT's - increase FRC, RV, TLC, ERV Early FEF 25-75% first then FEV1 and FEV1/FVC ratio. |
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Smoking Cessation |
12-24 hours - decreased CO and nicotine levels 48-72 hours- COHb levels normal, ciliary function improves 1-2 wk - decrease sputum production 4-6 wk - PFTs improve 6-8 wk - immune function and metabolism normal ***8-12 weeks - decreased postoperative morbidity and mortality |
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Regional vs General and Obstructive Diseases |
Regional considered best choice for extremity surgery, Avoid high spinal - COPD need intercostal for resp. also cause bronchoconstriction |
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Restrictive Disease |
ALI, ARDS, Pulm Fibrosis, Silicosis, Sarcoidosis, Extensive endothelial and epithelial destruction, inflammatory exudates, loss of surfactant, alveolar collapse, and protein leakage. |
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Restrictive disease clinical picture |
Pulm HTN and Right Heart Fx. PFT - Expiratory flow rates are normal more inspiratory issues. Decrease FEV1 and FVC... FEV1/FVC ratio normal greater than 80. Give small TV and lots of RR VC < less than 15ml/kg - severe. |
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Hyperoxia |
Oxygen toxicity - O2 free radicals and cytotoxic. causes pulmonary fibrosis. |
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1st sign of Hyperoxia |
**Coughing increase with deep inspiration and exposure. burning chest pain, severe dyspnea, worsening cough, decrease VC |
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Limits of Exposure to oxygen |
100%= 12 hours 80% = 24 hours 60%=36 hours less than 50% = okay long term use. risk for 1st tracheobronchitis (12hrs),2nd pulm interstitial edema (few days), and 3rd pulm fibrosis (weeks). |