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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.


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


Non-cardiogenic Pulm edema

usually recover 24-48 hours. tx as ARDS

Obstructive Lung 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


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.


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).