Basic Concepts

Respiratory Disorders
Nancy Stone PhD ANP ACNP

Compliance: Ability of the lungs to stretch Tidal Volume: Volume of gas inspired & expired in one normal breath Ventilation: Movement of air in one minute with one breath Respiration: Exchange of gases Perfusion: Circulation of blood thru the lungs with normal Hemoglobin level
Respiration

Basic Concepts
Va/Q Ratio: The relationship between alveolar ventilation & perfusion. The normal is 0.8 & alterations lead to hypoxemia. For example, COPD, areas of the lung where destruction of alveoli with loss of capillary beds equal high Va/Q ratio; which equals to normal ventilation but reduced perfusion Or, pt. with severe Emphysema, airways always obstructed by mucus = Low Va/Q ratio
Shunting: When a portion of the cardiac output is shunted thru the pulmonary capillary bed without becoming oxygenated Therefore, nonoxygenated blood is deposited in the arterial circulation Blood perfuses the area but no ventilation occurs.. hypoxemia COPD: During acute infection, induced exacerbation as a result of excessive amounts of pulmonary secretions that totally occlude segments of alveoli

Health Promotion
Tobacco Smoke & Air Pollution Continual bronchial irritation & inflammation Chronic Bronchitis; bronchial edema, hyper secretion mucus, chronic productive cough, bronchospasm

Health Promotion
Tobacco Smoke & Air Pollution Breakdown of elastin in connective tissue of lungs May be secondary to Alpha-1-antitrysin deficiency Emphysema: destruction of alveolar spaces; airway instability

Health Promotion
ALL will lead to: Airway obstruction, Air trapping, dyspnea & frequent infections Which THEN leads to: Abnormal ventilation/ perfusion ratio, hypoxemia, hypoventilation, & left sided heart failure

Ventilation & Perfusion Balance

Normal ventilation & perfusion: The normal function of the lungs to move oxygen from the air to the blood & CO2 from the blood to the air. Even in normal lungs, there are regional differences in ventilation, perfusion & gas exchange. These difference are due to gravity, to variations in pleural pressures & complexity of normal anatomy

Ventilation & Perfusion Balance

In the normal lung, BOTH ventilation & perfusion are greatest @ the base of the lung & decrease toward the apices HOWEVER, the gradient for perfusion from the bottom to the top of the lung is greater than the gradient for ventilation. END RESULT: In an normal, upright patient: Upper segments are relatively hypoperfused; (V/Q is high)

Ventilation & Perfusion Balance

Lower segments are relatively hypo ventilated (V/Q is low) Thus, V/Q values show marked variations in different lung units, even though V/Q may be normal for the overall lung !

Ventilation & Perfusion Balance

Three Common Causes of Hypoxemia: Hypoventilation, V/Q Mismatch, & Shunt Shunt represents the extreme end of a continuum of V/Q mismatch

Hypoxemia due to Hypoventilation

Pathophysiology: Hypoxemia always accompanied by hypercarbia Etiology: In normal lungs; damage to brains resp center (trauma, strokes CNS depressant drugs) & Neuro muscular defects (myasthenia gravis or Guillian-Barre Syndrome) In abnormal lungs; bronchitis & emphysema, or kyphosis Diagnosis: ABGs Hypoxemia with a inc PCO2 & normal DaO Therapy: Improve oxygenation by increasing alveolar ventilation; treat specific etiology

Hypoxemia due to Diffusion Abnormalities

Pathophysiology: 1.Increased diffusion pathway (prevents equilibrium between alveolar oxygen & pulmonary capillary blood so that blood exiting out the capillary is hypoxemic) .or, 2.Decreased diffusion area (destruction of membrane surface available for diffusion % loss of pulmonary capillary bed

Hypoxemia due to Diffusion Abnormalities

Etiology: 1. Accumulation of fluid (CHF) or accumulation of collagen in pulmonary interstitium (Sacoidosis).2. Pulmonary resection or destructive lung Dz (Emphysema) Diagnosis: H&P, Lab findings (PFTs & CXR) Treatment: Oxygen administration

Hypoxemia due to V/Q Mismathching

Pathophysiology: Low V/Q units with perfusion in excess of ventilation= hypoxemiablood traversing these units is not fully oxygenated..or..Low V/Q units may result from partial obstruction of airways (secretions, edema, foreign object, etc.) Etiology: Obstructive airway Dz (chronic bronchitis, emphysema, asthma); pulmonary vascular Dz; or Restrictive Dz (obesity, interstitial lung Dz) Diagnosis: H& P, ABGs (widened DaO), CXR, PFTs, V/Q Scan Treatment: Oxygen administration, identify cause

Hypoxemia due to Shunting (R to L)

Pathophysiology: Venous admixture occurs when deoxygenated, mixed venous bypasses functional alveolarcapillary units & mixes with normally oxygenated blood in circulation; shunts may be anatomic or physiologic Etiology: Anatomic shunts: normal shunts (bronchial, pleural or thebesian veins), intrapulmonary shunts (pulmonary A-V fistula), intracardiac shunts (Tetrology of Fallot, Eisenmengers syndrome) or other shunts assoc. with neoplasms.or..Physiologic shunts: Alveolar collapse (atilectasis, pneumonia, pleural effusion), alveoli filled with foreign material (ARDS, pulmonary edema)

Hypoxemia due to Shunting

Diagnosis: Hypoxemia with a normal or decreased PaCo2, & widened DaO Treatment: Oxygen administration has little effect; proper therapy depends on specific etiology

Observable signs: Changes in PO2

80-95%= normal 80-95%=Breathes with mouth open; SOB; RR 25 75-80%= Inc use facial muscles; tachycardia; speech sort with broken sentences 70%= Mild duskiness; RR 30-35 60 % and lower= Restless & Combative; RR >40; Gray & cyanotic; BP decreases; within minutes of cardiac arrest!!

Observable signs of Change in PCO2

20%= Tetany 35-45 %= Normal 53%= Headache & dizziness 76%= Dizziness, muscle twitching, unconsciousness 110%= Convulsions & Coma 200%= Deep Coma

O2 Delivery Systems
Nasal cannula: Low concentrations of O2 (up to 50% @ 6-8L/min). In a low flow system, the larger the tidal volume, the lower the FiO2; or the smaller the tidal volume the larger the FIO2. More than 6L/min does little to inc O2 concentration..because the anatomic reservoir is filled. This device beneficial in correction mild hypoxemia, ACS, COPD

O2 Delivery Systems
Simple Face Mask: Should not run @ less than 5L/minotherwise exhaled gas will accumulate in the mask reservoir might be rebreathed. Flow rates above 8L/min result in little inc inspired O2 concentration because the reservoir is filled. Useful with correction with moderate hypoxemia. DO NOT use with when precise control of O2 is needed in order to avoid excessive hypercapnia

O2 Delivery Systems
Partial Re-breathing Mask: The incoming O2 is delivered directly into the reservoir bag. As the pt. inhales, gas is drawn from the room through the exhalation ports. As the pt. exhales, the first 1/3 rd of exhaled gas goes back into the reservoir bag & is rebreathed with subsequent breathe. The L flow is adjusted so that it is in excess of the pts minute ventilation & the reservoir bag does not collapse during inspiration A flow rate 6-10 L/min= 60-90% O2.

O2 Delivery Systems
Non Rebreathing Mask: (100% O2 mask) Similar to partial rebreather with the addition of two one way valves. One valve is placed between the reservoir bag & mask, & the other one way valve acts as a check valve on the mask to prevent inhalation of ambient air These one way valves ensure 100% O2.

O2 Delivery Systems
Venti Mask (Air Entrainment Mask) : Allows O2 & air to be mixed in a precise ratio & insures a fixed FIO2 for the pt. within limits of Liter flow. Prevent CO2 buildup. Attachments deliver: 24, 28, 31, 35, & 40% FIO2. It is the O2 delivery device of choice in pts. with a ventilatory drive that is partially dependent (or totally) on hypoxemia!! Hypoxemia accompanied by an arterial PCO2 that is high .is indication for venti mask.check ABGs.

Theory of O2 Administration
We give O2 to improve PO2 PO2 only; PCO@ will only be effected if hypoxia is resolved & ventilatory pattern is changed. We are actually inc the kinetic activity of the oxygen molecule by inc its partial pressure (Daltons Law= pressure of gas is = pressures of all parts of the gas) Indications: PO2< 60 mmHg (Torr); O2 Sat <90%

Theory of O2 Administration
Complications: 1. O2 induced hyperventilation 2. Atelectasis 3. Retrolental Fibroplasiaia 4. O2 Toxicity 5. ARDS

Respiratory Failure
Acute & Chronic Forms Hypoxemic & Hypercapneic failures Mechanisms of hypoxemia & hypercapnea have an effect on gas exchange

Review: Functions of Respiratory System

Respiratory control function Function of respiratory muscle Mucociliary apparatus Defense function Metabolic function

Definition
Respiratory Failure: Alteration in function & result in impairment of gas exchange Remember.goals of respiratory system is oxygenation & ventilation

Acute Respiratory Failure

Inadequate exchange of O2 & CO2 Physiologically defined condition Multiple etiologies Develop over minutes, hours, or days Setting: Previous normal lung function & preexisting disease Body is not able to meet the need for O2 @ rest

Effect on Gas Exchange

Respiratory Failure: Arterial PO2< 60 mm Hg Hypoxemic: Respiratory Failure Arterial PCO2> 50 mm Hg with pH 7.30 Hypercapneic: Respiratory Failure

Clinical Significance: Therapeutic Strategy

Hypoxemic RF Support oxygenation Monitor SaO2 Hypercapneic Support ventilation Monitor ABGs

Some pts. may present with both!

Status Clinical Correlation

Hypoxemic Failure Pulmonary embolism ARDS Pulmonary fibrosis Pneumonia Atelectasis Pulmonary infarction Circulatory collapse Right to left shunt Cardiogenic pulmonary edema Hypercapneic Failure Status Asthmaticus COPD Alveolar Hypoventilation (drug overdose, paralysis, sleep apnea, neuromuscular weakness) Pulmonary Fibrosis (end stage) Severe ARDS Pneumonia

Indications for Endotracheal Intubation

Cardiopulmonary Resuscitation Airway Protection Need for mechanical ventilation Control of copious secretions Sever upper airway obstruction

Review Hypoxemia
Arterial Hypoxemia: arterial PaO2< 80mmHG Defined as oxygen deficiency @ tissue level Effects of Hypoxemia: impaired judgment, drowsiness, anorexia, N&V, vomiting, tachycardia, hypertension, H/A, disorientation O2 Failure: Transfer of O2 from the alveolar gas to pulmonary capillary blood is affected: PAO2, diffusion across the alveolar-capillary membrane & matching of alveolar ventilation to capillary perfusion

Review Hypoxemia
Mechanisms of Hypoxemia Low inspired Oxygen Alveolar Hypoventilation Ventilation-Perfusion Mismatch Shunt Diffusion abnormality

Mechanisms of Hypercapnia
Result of Alveolar Hypoventilation Mechanism: Centraldecrease normal resp drive Neuromusculardecrease in neural or muscular, transmission or translation of drive signal Abnormalities of chest wall Abnormalities of lungs & airways

Signs & Symptoms

ACUTE RF No Compensation: in setting of lung Dz or normal function Rapid resp rate Use of accessory muscles Alteration in MS CXR: may show Dz process Labs: hypoxemia+/hypercapnia CHRONIC RF Compensation: COPD; most common Breath @ higher lung volumes Barrel chest; purse lip breathing Cyanosis RV failure; cor pulmonale CXR: Hyperinflated Labs: high bicarbonate, polycythemia

Treatment
Low flow O2.unless acutely hypercapneic Antibiotics if infection Bronchodilators Steroids: inhaled vs oral IPPB

Acute Respiratory Distress Syndrome

Acute Respiratory Failure & bilateral infiltrates on CXR Also known as: adult hyaline membrane disease, Adult Resp. Distress Syndrome, non-cardiogenic pulmonary edema, shock lung

ARDS: Lung injury

Capillaries & alveoli are damaged & necrotic Fluid & protein leak into alveoli to give the appearance of pulmonary edema Reduction in surfactant Hyaline membrane forms Late phase of ARDS: fibrosis, emboli, loss of pulmonary capillaries

ARDS: Etiologies
Shock, septic shock (50%) Infection Trauma Aspiration, pH<2.5 (40%) Drugs Gas inhalation Misc medical & surgical

ARDS: Causes
Infection: outpatients, viral infectioninpatients/NH gram-negative infections Drugs: : Heroin, Methadone, Propoxyphene, Barbituates, Salicylates, Thiazides, Chlordiazepoxide, Cholchicine & Dextran-40 Inhalation Injuries: O2, smoke, nitrous oxide Miscellaneous: Outpatient; pancreatitis, eclampsia, bowel infarction, high altitudes, neurogenicInpatient; transfusions, IV contrast, air emboli, post-bypass, uremia, DKA, amniotic fluid emboli

ARDS: Diagnostic Criteria

Identifiable cause or associated condition Dyspnes Hypoxemia (refractory to O2) Bilateral infiltrates Reduced lung compliance No cardiac factors

What happens to ARDS survivors

If high oxygen requirements for more than 24 hours then there will likely be @ least some evidence of lung dysfunction @ one yr Severity of ARDS score predicts survival & lung function @ one year

ARDS Mortality
There is a 40% mortality from ARDS alone without any other organ failure This is better than 60-70% mortality seen 20 yrs ago Gram neg shock + ARDS= 90% mortality Lung fibrosis from ARDS is unpredictable but clearly carries a higher mortality due to prolonged ICU stay

Complications of ARDS
Pulmonary fibrosis, emboli, barotrauma, pneumonia GI hemorrhage, perforation Cardiac Renal Failure Iatrogenic, central lines, ETT Malnutrition Sepsis, Multiple Organ System Failure

Management of ARDS
Mechanical Ventilation Extracorporeal Resp. Support Patient Positioningprone pos. Fluids Oxygen transport Pharmacology

???Drugs that treat ARDS

Surfactant, although incredibly useful in RDS of newborns, has not been effective Steroids should not be used before 72 hrs (late phase). The use of high dose steroids after 72 hrs is under study Nitric Oxide..yes to maybe Prostaglandins.no Vasoactive.no

Why Mortality is Decreasing in ARDS

Corticosteroids for late phase (> 72 hrs) Fluid management Hemodynamic support Nutrition Antibiotics for nosocomial infections Ventilator support

???Best method for mechanical ventilation in ARDS

Mechanical ventilation can damage the lungs as a result of high pressures or high volumes In theory, this is due to overdistension & shear injury to lung alveoli Mechanical ventilation strategies: conventional, least PEEP, open lung

Least PEEP for oxygenation

Because high pressures may be required to deliver ventilator volumes, PEEP@ levels up to 15-20 cm H2O add significantly to total MAP Least PEEP is an attempt to use the minimal PEEP required for adequate arterial oxygenation with less than 60% inspired oxygen

Open Lung Strategy

Goal of this approach is to recruit as many alveoli for best possible oxygenation Higher PEEP is often used

Does Barotrauma lead to poor outcome in ARDS ??

Pneumothorax & air leaks in first 4 days does not inc 30 day mortality. No reason to limit airway pressure Lung protective ventilation improved survival @ 28 days Limited pressure ventilation did not reduce mortality & inc complications

Unconventional Ventilation
High frequency Ventilation ECMO Intravascular membrane oxygenation Extracorporeal CO2 removal Apneic oxygenation

Summary
ARDS is the end result of multiple types of lung injury Aspiration, sepsis (Gram negative) likely causes Attention to patient support in the ICU appears to improve mortality Mechanical ventilation to limit barotrauma

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