Respiratory Talk

Essentials of Respiratory Care Paul Barraza RRT, RCP Education Coordinator, Santa Clara Valley Medical Center Adjunct Faculty, Department of Biological Sciences, Foothill College

Contents
Anatomy and Physiology of the Respiratory System
Function of Respiratory System
Upper vs. Lower Airway
Cellular Properties of the Alveolus
Ventilation / Respiration
Diffusion / Perfusion
Basics of Acid-Base Imbalances
Arterial Blood Gas Interpretation

Contents
Mechanical Ventilation
Indications
Goals
Monitoring
Basics of ventilation
Sedatives, Analgesics, and Paralytics
Disease Specific Management
Pneumonia
Pulmonary Embolus
Chest Trauma
ARDS

Anatomy and Physiology

Function
Primary function of the respiratory system is the continuous absorption of O 2 and the excretion of CO 2
External Respiration
The exchange of gas from the atmosphere and the blood
Internal Respiration
The exchange of gases between blood and the tissues

Upper vs. Lower Respiratory Tract
Upper Respiratory Tract
All structures starting at the mouth or nose and extending down to the trachea
Nose
Vestibule (hairs act as gross filter)
Concha (turbinates increase surface area of nose to aid in filtration and humidification)
Oral Cavity
Soft palate and uvula (control flow of air, fluid and food during eating, drinking, sneezing and coughing)

Upper Respiratory Tract Cont.
Pharynx
Subdivided into:
Nasopharynx
Oropharynx
Hypopharynx
Larynopharynx
Primary function is to aid in filtration and in speech

Upper Respiratory Tract Cont.
Larynx
Formed by cartilage and muscle
Thyroid
Cricoid
Epiglottis
Vocal Cords
Primary function
Protect the respiratory tract during eating and drinking
Phonation

Lower Respiratory Tract
Conducting Airways
Trachea
Right & Left Main Bronchi
Lobar
Segmental
Subsegmental
Bronchi
Terminal bronchi
Bronchioles (No cartilage)
Terminal Bronchioles (No cartilage)
Primary Function
Airway conduction

Lower Respiratory Tract
Respiratory Airways
Respiratory Bronchioles
Terminal Respiratory Bronchioles
Alveolar Ducts/Sacs
Alveoli
Primary Function
Gas exchange

Estimates range from 270 to 790 million
Average 480 million
Number increase with height of subject
Average 0.2mm in diameter when at FRC
Larger in apecies than in bases due to organ weight
Alveoli

Type I pneumocytes (extremely flat squamous epithelia)
Covers 93% of alveolar surface
Create patchwork like surface over the alveolar capillaries forming the gas exchange surface of the alveolus
Type II pneumocytes (cuboidal epithelia)
Cover 7% of the alveolar surface
Manufacture surfactant and secretes it onto the alveolar surface
Alveoli

Macrophages
Defensive cell that patrol alveolar region and phagocytize foreign particles and cells (bacteria)
Canals of Lambert
Small openings that connect the alveoli to the respiratory bronchioles
Pores of Kohn
Small openings in the alveolar septa that allow gas to flow from one alveolus to another
Alveoli

Alveolar Capillary Membrane
Surfactant Layer (outermost layer)
Type I cell
Interstitial Space
Basement membranes
Matrix material connective tissue fibers
Alveolar capillary
Plasma
Erythrocytes

Ventilation vs. Respiration
Ventilation
The process of moving gas into and out of the lungs
Respiration
The process of getting oxygen into the body for tissue utilization and removal of carbon dioxide into the atmosphere

Diffusion/Perfusion
The process whereby molecules move from areas of high concentration to areas of low concentration
Driven by kinetic energy
Gases have high kinetic energy
Lighter gases diffuse more rapidly than heavy gases
Increasing kinetic energy will increase diffusion
Heat
Mechanical agitation

Diffusion/Perfusion
O 2 & CO 2 move between the lungs and the tissue via diffusion
Oxygen
PO 2 ~ 159mmHg in atmosphere
PO 2 ~ 40mmHg in capillaries
Carbon Dioxide
PCO 2 ~ 60mmHg in the cells
PCO 2 ~ 1mmHg in room air

Barriers to Diffusion/Perfusion
Alveolar epithelium
Interstitial space
Capillary endothelium
Erythrocyte Membrane

Diffusion/Perfusion Impairment
Interstitial lung Disease (thickening of interstitium
Pulmonary Fibrosis
Asbestosis
Sarcoidosis
Emphysema (destruction of alveoli)
Pulmonary Vascular Abnormalities
Pulmonary hypertension
Pulmonary embolus

Ventilation/Perfusion Mismatch
Dead space (physiologic)
Areas ventilated but not perfused
Anatomic dead space
The volume of the conducting airways ~ 1ml/lb
Alveolar dead space
The volume of gas ventilating unperfused alveoli
Shunt
Areas perfused but not ventilated

Ventilation/Perfusion Mismatch

Basics of Acid-Base Imbalances

Terminology
Acid : A substance that donates hydrogen ions
Base : A substance that accepts hydrogen ions
Acidemia : a condition of blood pH of less than 7.35
Alkalemia : a condition of blood pH of greater than 7.45
Acidosis : is the process of causing acidemia
Alkalosis : is the process of casing alkalemia
Correction : is the process in which the system that was not properly functioning is repaired and hereby returns the pH toward the normal range

Terminology
Compensation : is the process in which the system that is still functioning properly is responsible for returning the pH toward the normal range.
pH : power of hydrogen measures blood acidity and concentration of hydrogen ions
PaO 2 : tension of O 2 gas in the arterial blood
PaCO 2 tension of CO 2 in the arterial blood
HCO 3 - : Blood bicarbonate. The principal buffer against drastic changes in pH that would occur with changes in PaCO 2 . It is an indicator of metabolic/ kidney function.
Buffer : is a substance that resists change in H+ concentration upon addition of a strong acid or base

Normal Adult Blood Gas Values at Sea Level 0 + 2 0 + 2 B.E. 24 mEq/L + 2 24 mEq/L + 2 HCO 3 - 70-75% 95% or better SaO 2 41-51 mmHg 40 mmHg (35-45) PaCO 2 35-40 mmHg 80-100 mmHg PaO 2 7.36 (7.31-7.41) 7.40 (7.35-7.45) pH Venous Arterial

Causes of Respiratory Acidosis
With normal lungs
CNS depression--sedatives, CNS disease, obesity, hypoventilation
Neuromuscular disease
Trauma
Severe restrictive disorders
With abnormal lungs
COPD
Pneumonia
Pleural disease (pneumothorax)
Acute airway obstruction (asthma exacerbation)

Signs & Symptoms of Respiratory Acidosis
Tachypnea
Headache
Confusion
Drowsiness
Coma
Dysrhythmias

Causes of Respiratory Alkalosis
With normal lungs With abnormal lungs
Anxiety Usually a respiratory
Fever response to hypoxia
Stimulant drugs Acute asthma exacerbation
CNS lesion/trauma Pneumonia
Pain Pulmonary edema
Sepsis
High altitude

Signs & Symptoms of Respiratory Alkalosis
Dizziness
Numbness & Tingling
Muscular weakness
Twitching
Irregular heart rhythm

Causes of Metabolic Acidosis
Lactic acidosis (hypoxia)
Keto acidosis (diabetes)
Ingestion of base depleting drugs
Aspirin
Alcohol
Renal failure
Diarrhea

Causes of Metabolic Alkalosis
Excessive administration of steroids
(K+depletion---incr. HCO3- reabsorption)
Gastric suctioning/vomiting
Hypochloremia (usually from vomiting)
Hypokalemia
Several days of IV therapy w/o adequate replacement of K+, diuretic therapy, diarrhea)
Excessive administration /ingestion of HCO 3 - (licorice)

Acid-Base Disorders and Parameter Changes     N chronic N N N   acute Respiratory Alkalemia (alveolar hyperventilation)  N    N chronic N N N   acute Respiratory Acidemia (ventilatory failure) Cl - K + HCO 3 - PCO 2 pH

Acid-Base Disorders and Parameter Changes    N  acute      partially compensated N N   N compensated Metabolic Acidemia N N   N compensated      partially compensated    N  acute Metabolic Alkalemia Cl - K + HCO 3 - PCO 2 pH

Acid-Base Disorders and Parameter Changes Cl - K + HCO 3 - PCO 2 pH      Combined Respiratory and Metabolic Alkalemia      Combined Respiratory and Metabolic Acidemia

Compensatory Mechanisms for Acid - Base Imbalances
Respiratory Acidosis
Kidneys restore pH by reabsorbing HCO 3 - into the blood
Respiratory Alkalosis
Kidneys restore pH by urinary elimination of HCO 3 -

Metabolic Acidosis
The lungs restore the pH by eliminating CO2
Metabolic Alkalosis
The lungs restore the pH by retaining CO2

Lungs compensate quickly for metabolic acid-base abnormalities because ventilation can change the CO 2 within seconds
Kidneys require more time to retain or excrete HCO 3 - therefore compensation is much slower

PaO 2
Varies with age
Normal PaO 2 = 104 - (0.3 x age)

Hypoxemia
Normal PaO 2 80 - 100 mmHg
Mild hypoxemia PaO 2 60-79 mmHg
Moderate hypoxemia PaO 2 40-59 mmHg
Severe hypoxemia PaO 2 <40 mmHg

Arterial Blood Gas Interpretation

Steps for Interpretation
Step 1: Acidemic or Alkalemic
Step 2: Is the primary disturbance respiratory or metabolic
Step 3: Assess for compensation

pH indicates the status of the body
pH > 7.45 is alkaline
pH < 7.35 is acid
The pH of the arterial blood gas measurement identifies the disorder as alkalemic or acidemic.

Categorize pH
Determine whether it is:
Acid Base Normal
7.25
Acid_____ Base_____ Normal___
X

Step 2: Primarily Respiratory or Metabolic
A respiratory disturbance alters the arterial PaCO 2 (normal value 40, range 35-45)
If PaCO 2 < 35 respiratory acidosis is present
If PaCO 2 > 45, respiratory alkalosis is present
A metabolic disturbance alters the serum HCO 3 - (normal value 24, range 22-26)
If HCO 3 - < 22, metabolic acidosis is present.
If HCO 3 - > 26, metabolic alkalosis is present

PH 7.25 Acid__ Base__ Normal__
PaCO 2 37 mmHg Acid__ Base__ Normal__
HCO 3 - 17 mEq/l Acid__ Base__ Normal__
When either (or both) the lung or kidneys agree with the body it is the cause of the body’s condition
Step 2: Primarily Respiratory or Metabolic X X X

What if both PaCO2 & HCO3 are abnormal?
Example: pH = 7.27 (low) PaCO 2 = 27 mm Hg (low) HCO 3 - = 10 mEq/L (low) One represents the primary disorder; the other represents compensation. Which is which? The value that is moving in the right abnormal relationship is the primary problem.

Step 3: Assess for Compensation
Whenever resp & metabolic conditions are in opposite directions compensation is presumed.
When either the lungs or kidneys disagree with the body it is a compensatory mechanism.
Compensation is complete when the pH is within normal limits.
Compensation is partial when the pH remains out of range (but closer to normal than if there was no compensation.
The body will never fully compensate.

Example 1
pH = 7.29 (low) PaCO 2 = 31 mm Hg (low) HCO 3 - = 12 mEq/L (low)
Partially Compensated Metabolic Acidosis

Example 2
pH = 7.36 (Normal) PaCO 2 = 25 mm Hg (low) HCO 3 - = 12 mEq/L (low)
Compensated Metabolic Acidosis

Example 3
pH = 7.37 (Normal) PaCO 2 = 60 mm Hg (high) HCO 3 - = 30 mEq/L (high)
Compensated Respiratory Acidosis

Blood Gas Interpretation Practice
Practice 1
pH = 7.25
PaCO 2 = 65 mmHg
PaO 2 = 55 mmHg
HCO 3 - = 28 mEq/L
Respiratory Acidosis with moderate hypoxemia

Practice 2
pH = 7.10 PaCO 2 = 99 mmHg
PaO 2 = 22 mmHg
HCO 3 - = 30 mEq/L
Partially compensated respiratory acidosis
with severe hypoxemia

Practice 3
pH = 7.55 PaCO 2 = 38 mmHg
PaO 2 = 155 mmHg
HCO 3 - = 32 mEq/L
Uncompensated metabolic alkalosis
with hyperoxia

The Base Excess
The amount of acid (in mmol) required to restore 1 litre of blood to its normal pH, at a PCO 2 of 40mmHg.
During the calculation any change in pH due to the PCO 2 of the sample is eliminated, therefore, the base excess reflects only the metabolic component of any disturbance of acid base balance.

The Base Excess
If there is a metabolic alkalosis the base excess will be positive due to a gain of base or a loss of acid from non-respiratory causes
However, if there is a metabolic acidosis, the base excess is negative due to a loss of base or a gain of acid from non-respiratory causes

Mechanical Ventilation

Iron Lung

Reasons for Mechanical Ventilation
Respiratory Insufficiency/Failure
Airway Protection
Inadequate Respiratory Drive
Surgical/Procedural

Textbook Definition:
Respiratory activity is absent or is insufficient to maintain adequate oxygen uptake and carbon dioxide clearance
Insufficiency – during exertion
Failure – at rest
Clinical Definition:
Inability to maintain arterial PO 2 , PCO 2 and pH at acceptable levels
PO 2 < predicted normal for age on R/A
PCO 2 > 50mmHg and rising
pH 7.25 and below

Signs & Symptoms of Respiratory Insufficiency/Failure

Indications for mechanical ventilation
Apnea
Acute ventilatory failure
Impending acute ventilatory failure
Severe oxygenation deficit

Clinical indications for mechanical ventilation
Primarily pulmonary
ARDS
Pneumonia
Pulmonary Emboli
Mechanical ability
Ventilatory muscle fatigue
Thoracic injury / abnormalities
Pleural diseases
Neurological diseases
Nutritional deficiencies

Airway Protection
Obstruction of the airway
Secretion
Mucosal edema
Bronchoconstriction
Airway inflammation
Foreign body obstruction
Inability to avoid aspiration
HIE (Hypoxic Ischemic Encephalopathy)
Severe CNS defects

Inadequate Respiratory Drive
CNS disorders/injury
HIE
Stroke
Structural
Neuromuscular disorders
Amyotrophic lateral sclerosis (ALS)
Multiple sclerosis (MS)
Muscular dystrophy (MD)
Myasthenia gravis
Spinal muscular atrophy (SMA)
Central Hypoventilation Syndrome AKA Ondyne’s Curse

Surgical/Procedural
Paralysis
Reduced drive due to pharmacologic agents
Opiates
Cardiac or thoracic procedure involving lung manipulation

Goal of Mechanical Ventilation
To provide the most appropriate amount of support via the least harmful and most comfortable manner

Goals of Mechanical Ventilation
Gently…….
Exchange of CO 2 (ventilation) and O 2 (oxygenation)
Achieve goal pH range
Avoid baro/volutrauma
Avoid hypo/hypercarbia, hypo/hyperoxia

Ventilation – Getting CO 2 Out
Ventilation controls PaCO 2
Determined by Minute (Alveolar) Ventilation (MV) in liters/minute
MV – amount of gas in and out of the alveoli
MV = tidal volume (V t ) x rate (RR); the more gas exchange, the lower the CO 2 ; the less gas exchanged, the higher the CO 2

Ventilation - Getting CO 2 Out
Respiratory rate (RR) - directly set
Tidal volume (V t ): Goal 8-10 ml/kg
Can be directly set (volume ventilation)
Or can be determined by the pressures used to ventilate (pressure ventilation)

Oxygenation - Getting O 2 In
PaO 2 determined by :
FiO 2 – directly set
Mean airway pressure
Mean airway pressure (MAP)
An average pressure across airway
Good estimate of alveolar pressure
Determined by PEEP and PIP
Also influenced by inspiratory time (It)

Oxygenation – Getting O 2 In
Mean Airway Pressure (MAP)
In CMV majority of MAP is determined by PEEP
As rate increases, larger contribution from PIP
Too little, not enough open alveoli (and thus lung); too much, inhibit pulmonary blood flow
Inspiratory Time (I t )

Monitoring – How Are We Doing?
Physical exam
Chest rise
Color
Examination of the chest:
Breath sounds
Air exchange
Extra sounds, i.e., crackles, wheezes, rhonchi…
Radiographic studies

Monitoring – How Are We Doing?
Gasses
pH, PO 2 , PCO 2 , serum bicarbonate (calculated)
TcCO 2 monitoring
In vivo monitoring

Now Let’s Talk About Ventilation

Some Terms
Peak End Expiratory Pressure (PEEP)
Maintains open alveoli
Distending pressure across airways
Peak Inspiratory Pressure (PIP)
Highest pressure reached during breath
Provides pressure to move gas into lungs in positive pressure ventilation
∆P = PIP - PEEP
In general, determines tidal volume

PEEP
PEEP 0 5 12 20

Modes of Ventilation
Assist Control (A/C, CMV)
Synchronized Intermittent Mandatory Ventilation (SIMV)

Assist Control (A/C, CMV)
The ventilator has a number of preset machine breaths, at a set tidal volume or inspiratory pressure level (Vt or I P ) each minute.
The patient is capable of initiating their own spontaneous breaths in between machine breaths
Spontaneous breaths will be equal to preset ventilator breaths

Synchronized Intermittent Mandatory Ventilation (SIMV)
The ventilator has a number of preset machine breaths, at a set tidal volume or inspiratory pressure level (Vt or I P ) each minute.
The patient is capable of initiating their own spontaneous breaths in between machine breaths
Spontaneous breath will be whatever size the patient wants to take
Used most often in conjunction with Pressure Support (PS)

Breath Delivery Types
Volume Control
Pressure Control
Pressure Regulated Volume Control
Spontaneous Breath Types
CPAP (Continuous Positive Airway Pressure)
Pressure Support
Volume Support
BiPAP (Biphasic Positive Airway Pressure)

Breath Delivery types
Volume Control
Preset Vt, Respiratory Rate and sometimes flow
Peak Pressure (PIP) is variable while the volume remains constant.

Breath Delivery Types (cont)
Pressure Control Ventilation (PCV)
Preset RR, Inspiratory Time and Inspiratory Pressure
Vt is variable while pressure remains constant

Breath Delivery Types (cont)
Pressure Regulated Volume Control (PRVC)
Preset RR, Inspiratory Time and Vt
Pressure is variable yet limited while Vt remains constant

Continuous Positive Airway Pressure (CPAP)
Preset level of pressure added to the circuit as the patient exhales.
The patient does all the work
No set RR or tidal volume
Used most often with Pressure Support
Spontaneous Breath Delivery Types

Pressure Support (PS)
Preset level of pressure added to the spontaneous breath during inspiration only
This helps augment the patients tidal volume
Pressure is constant but tidal volume varies

Volume Support (VS)
Variable pressure support added to the ventilator during inspiration only, to deliver a preset Vt
Tidal volume is constant but pressure varies

Biphasic Positive Airway Pressure (BiPAP)
Preset level of pressure added to the circuit during both inspiratory and expiratory phases.
Differing levels of inspiratory and expiratory support
The patient does all the work
No set RR or tidal volume

The Alphabet Game
Combined Modes of Ventilation
PRVC (pressure regulated volume control)
APRV (airway pressure release ventilation)
BiVent
BiLevel
VAPS (volume assured pressure support)
VS (volume support)
Automode

Determination of Ventilator Settings
Mode
Depends on patient
Breath Delivery Type
Depends on patient
Vt
6-10cc’s/kg
RR
12 – 40 bpm’s (depending on age & desired Minute Ventilation)
FiO2
Usually start at 100%
Less if patient has been on a vent for a while
PEEP
Depends on patient
PS
Depends on patient

Patient Consideration
Humidification
HME
Heated (37 ◦ C & 44mg/L Water Vapor)
Suctioning
Saline
Nutrition
Enteral (Gavage)
Parenteral (TPN)

Sedatives, Analgesics, and Paralytics

Sedatives
Benzodiazepines
Opioids
Neuroleptics

Benzodiazepines
Drugs of choice for treatment of anxiety
Relatively low cost
Muscle-relaxing
Anticonvulsant
Amnesiac effects
May cause respiratory depression if administered to COPD patients on opioids
Minimal cardiovascular effects, BP depression possible in hemodynamically unstable patients

Most common benzos in ICU
Generic Name (Trade Name) ½ life
Diazepam (Valium) 20- 120 hrs
Rapid onset
Midazolam (Versed) 3 – 11 hrs
Onset 2-3 minutes
Lorazepam (Ativan) 8 – 15 hrs
Onset 5 – 20 minutes

Opioids
Primarily used for pain relief
Secondarily used for as anxiolytic and sedation
Many serious side effects
Respiratory Depression
Nausea
Constipation
Vomiting
Cardiovascular depression
Reduced GI motility
Convulsions
High physical dependence

Opioids
Recovery period lengthened in renal/hepatic insufficiency
May cause histamine release and bronchoconstriction
Reversal medication
Naloxone Hydrochloride (Narcan)
30 minutes half life
May require IV infusion for opioid withdrawal

Most common Opioids in ICU
Generic name (Trade name)
Fentanyl Hydrochloride (Sublimaze)
Synthetic
1 - 4 hours duration with fast onset
100 – 150 times more potent than MS
Less cardiac side effects than MS
Morphine Sulfate (Duramorph)
1- 6 hours duration with slower onset
Preferred for lower cost

Neuroleptics
Used to treat extreme agitation and delirium (increased in elderly and burn patients)
Side effects
Decreased seizure threshold
Cardiac dysrhythmias
Parkinson’s-type symptoms
Muscle rigidity
Lethargy
Drowsiness

Most common Neuroleptic Drug in ICU:
Haloperidol (Haldol)
3 - 5 minute onset
5 - 24 hours half-life

Anesthetics
Used for sedative, hypnotic & amnesiac properties
NO analgesic effects
Many hemodynamic effects
Decreased SVR
Decreased BP
Bradycardia
Good for IC bleeds
Neurosurgical patients = decreases ICP
Rapid “wake-up”… no hangover
Painful on injection
Used in OR, ICU
Lipid based solution prone to contamination

Anesthetics
Diprivan (Propofol)
Onset 1 minute,
Half-life <30 minute
Expensive

Paralytics
Used to:
Facilitate mechanical ventilation
Treat extreme agitation
Facilitate intubation and other procedures
Manage tetanus
Extreme hyperventilation
Reduction of O 2 consumption & CO 2 production
Can cause
Decreased BP
Cardiac dysrhythmias
Prolonged paralysis in patients with renal/hepatic insufficiency

Paralytics
NO SEDATIVE EFFECTS
NO ANALGESIC EFFECTS
Essentially it paralyzes your patient - MUST be given WITH analgesic and sedative!!

Paralytics
Panacuronium (Pavulon)
“ Vec” Vecuronium (Norcuron)
“ Rock” Rocuronium (Zemuron)
“ Sux” Succinylcholine (Anectine)

Respiratory Diseases
Pneumonia
PE
ARDS
Chest Trauma

Pneumonia
Definition:
Inflammation process that primarily effects the gas exchange area’s of the lung
Etiology:
Bacteria, viruses, fungi, TB, etc.
Clinical Manifestation:
Initially dry cough, turning productive with blood streaked sputum, crackles, rhonchi, dyspnea, cyanosis
Treatment:
O 2 therapy, bronchial hygiene, bronchodilators, antibiotics

Pulmonary Embolism
Definition:
Complete or partial obstruction of the pulmonary artery blood flow to a distal portion of the lung by a plug brought by the blood
Etiology:
Blood clots (blood stasis, vessel wall abnormalities, abnormal blood coagulation), Fat, Tumors, Air
Asymptomatic to death, dyspnea and sharp chest pain most common,
Treatment:
O 2 therapy, anticoagulation therapy, steroids, embolectomy

ARDS
Definition:
An acute restrictive disease of ↓ing FRC and severe hypoxia due to injury to the alveolar capillary membrane resulting in ↓ed surfactant, atelectasis and ↓ing compliance
Etiology:
Shock (severe hemorrhage, trauma, MI, CVA, CABG)
Inhalation (O 2 , aspiration, near drowning, burns)
Infection (viral pneumonia, sepsis)
Over-hydration, chemical injury, blood infusion, etc.
Rapid onset, dyspnea, hypoxia, tachypnea, tachycardia, ↓ed compliance,
Treatment:
Treat underline cause, O 2 , PEEP, CPT, Sx, diuretics, ventilator

Chest Trauma
Account for ¼ of all trauma deaths
Blunt Trauma
Steering wheels
Falls
Penetrating Trauma
Knife wounds
Gunshots
Primary concern
ABC
C-Spine

Chest Trauma
Fractures/Flail chest
High or low fx, watch for concurrent injuries
Pneumothorax
Spontaneous or trauma, < or >20%, 2 nd ICS MCL or 5 th ICS MAL
Hemothorax
Mild <300cc, Moderate b/w 300-1400cc, Severe >1400cc
Drain, surgery for >200cc/hr, transfusions
Sucking chest wound
Open flap in chest wall, sucking sound, tension pneumo ?, sterile dressing over 3 sides

Questions?

Thank you

Respiratory Talk

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