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46 Cards in this Set

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Vital Capacity 60-70 ml/kg so 70kg patient

4700 cc

Inspiratory reserve volume IRV (70kg)

3000 CC

Expiratory Reserve Volume ERV (70kg)

1200 CC

Residual Volume 70 kg

1200 cc

FRC - functional residual capacity RV+ERV

2400 cc

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.

Respiratory Failure

Lungs cannot maintain adequate arterial oxygenation. - co2 elimination can be normal or abnormal.

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.

Determine chronic vs acute resp failure

Look at pH if normal - chronic


if pH low - Acute

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.

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

Pulmonary Edema Non-Cardiogenic

Fluids moves to pulmonary capillaires to interstitial space then to alveoli


Albumin Leak

**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

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

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.

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

Pulm edema and healthy lungs

PPC must exceed 25 mm Hg before lymphatic reserve exhausted. -- rarely acute fall in oncontic usually hydrostatic pressure.

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

ARDS and first 24 hours

ARDS develop in first 24 hours after trauma good prognosis

Mendelsons syndrome

Gastric volume >25ml


Gastric pH < 2.5


Epithelial injury




Tx suction and PEEP

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


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



Usually cause of death with ARDS

Multi-Organ System Fx

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



ARDS signs and symptoms

Dyspnea, Hypoxemia, initial PaCO2 low(breathing fast), Pulm HTN, diffuse infiltrates, PaO2/FiO2 less than 200, Resp. fx.

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

Issues with PEEP

Barotrauma in increase airway pressure


decrease venous return= decrease CO

TRALI

Non-cardiogenic Pulm edema


usually recover 24-48 hours. tx as ARDS

Obstructive Lung Disease

MOST COMMON PULMONARY DISEASE


Resistance to airflow EXPIRATION = air trapping


VQ mismatch leads to decrease gas exchange


emphysema, chronic bronchitis, asthma.

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

Asthma/Obstructive PFT's

Decreased FEV1 and Low FEV1/FVC ratio




reversibility with tx 12% improvement good indicator... 200FEV1 absolute increase



Asthma is it chronic

Yes - they always have inflammation present and are hyper-reactive

When do asthma patients have wheezing

Auscultate - usually wheezing on expiration**

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

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

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.

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

Emphysema types

Centraiacinar - Central only




Panacinar - Everything look like broccoli

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.

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

Regional vs General and Obstructive Diseases

Regional considered best choice for extremity surgery,


Avoid high spinal - COPD need intercostal for resp. also cause bronchoconstriction

Restrictive Disease

ALI, ARDS, Pulm Fibrosis, Silicosis, Sarcoidosis,




Extensive endothelial and epithelial destruction, inflammatory exudates, loss of surfactant, alveolar collapse, and protein leakage.

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.

Hyperoxia

Oxygen toxicity - O2 free radicals and cytotoxic.


causes pulmonary fibrosis.

1st sign of Hyperoxia

**Coughing increase with deep inspiration and exposure.




burning chest pain, severe dyspnea, worsening cough, decrease VC

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).