2. Goal
The student will be able
to correctly utilize
service specific CPAP
devices in a respiratory
compromised patient
[img]http://hammondems.com/images/d_1976.jpg
3. Objectives
At the completion of this training, the BLS
provider will:
Describe respiratory anatomy and physiology
Verbalize understanding of respiratory
disorders / illnesses
Appreciate the benefits and limitations of
CPAP in alleviating patient symptoms
List indication and contraindications for use.
7. Exhalation
Passive process
Muscles relax;
size of chest
decreases
Positive pressure
created; air
pushed out
continued
8. Negative Pressure
Respiration driven by process of negative
intrathoracic pressures
Negative pressure
Initiates inhalation and acquires O2
Assists to increase intrathoracic blood flow
Equalization of pressures
initiates exhalation and elimination of CO2
9. Bronchi / Bronchioles
Cartilage structures give
way to smooth muscle
May divide up to 25
times before reaching
terminal bronchioles
http//medicalpicturesinfo.com/bronchial-tree/
10. Alveoli
Expand and contract with breathing
Contact with pulmonary capillary beds for gas
exchange
Inside surface coated with surfactant
Prevents aveoli from sticking together
Keeps alveoli open
Atelectasis
12. Functional Residual Capacity
Lung volume at end of
normal exhalation
Muscles of
respiration are
completely
relaxed
http://www.lakesidepress.com/pulmonary/htm
14. Oxygenation
Process of getting oxygen to end organs and
tissues
Inhaled through lungs
Picked up from alveoli on RBCs
Off-loaded in exchange for CO2
Measured by pulse oximetry (SpO2)
94%-100%
15. Ventilation
Process to eliminate carbon dioxide (waste
product of energy production)
Carried back through venous blood
Eliminated through exhalation
Measured by capnography
18. Respiratory Distress
Subjective indication of some degree of
difficulty breathing
Causes
Upper or lower airway obstruction
Inadequate ventilation
Impaired respiratory muscle function
Impaired nervous system
Trauma
Bronchitis, pneumonia, cancer
19. Respiratory Failure
Clinical state of inadequate oxygenation, ventilation
or both.
Often end-stage of respiratory distress
Signs:
Tachypnea (early)
Bradypnea or apnea (late)
Increased, decreased, or no respiratory effort
Tachycardia (early)
Bradycardia (late)
Cyanosis
Altered Mental Status
20. Mechanism of Heart Failure
Frequently a chronic, yet manageable
condition
Left ventricle fails to work as effective pump
(Left-Sided CHF)
Blood volume backs up into pulmonary
circulation
Most often caused by:
Volume overload
Pressure overload
Loss of myocardial tissue
21. Pulmonary Edema
Cardiac and respiratory system impairment
Acute and critical emergency
Filling of lungs with fluid
Washes away surfactant
Lipids & Proteins
Prevents collapse of alveolus at low lung
volume
Creates pink froth in sputum
Prevents alveoli from expanding
Significantly reduces or eliminates ability for gas
exchange to occur
22. Asthma
Reactive airway disorder
Exacerbation precipitated by extrinsic or
intrinsic factors
Characterized by reversible bronchial smooth
muscle contraction, increased mucus
production and inflammatory airway changes
Persistent signs and symptoms can indicate a
tenfold increase in the work of breathing
23. Asthma
Evolution of asthma attack
Mucus thickens and
accumulates plugging
airways
Mucosal edema
develops
Muscle spasms constrict
small airways
Breathing becomes
labored
http://asthma-ppt.com/asthma-pictures.html
24. Caution
Asthma Anaphylaxis
Causes Smoke, dander, dust,
pollen, cold air, mold,
cleaning products,
perfume, exercise
Nuts, shellfish, milk, eggs, soy,
wheat, insect stings,
medications, latex
Symptoms Wheezing
Coughing
Shortness of breath
Difficulty breathing
Chest tightness
Face - itchiness, redness,
swelling of face & tongue
Airway – trouble breathing,
swallowing or speaking
Stomach – abdominal pain,
vomiting, diarrhea
Total hives, rash, itchiness,
swelling, weakness, pallor,
sense of doom, loss of
consciousness
25. Chronic Obstructive
Pulmonary Disease
Obstructive lung disease
Triad of distinct diseases that often coexist
Asthma
Chronic bronchitis
Emphysema
Traditionally refers to patients with
combination of chronic bronchitis and
emphysema
26. Chronic Bronchitis
Bronchi become filled with excessive mucus
Alveoli are not affected
Diffusion of gas remains relatively normal
Patients develop low oxygen pressures (PO2)
and hypoventilation
Hypoventilation leads to high levels of CO2
and low levels of O2
27. Emphysema
Results from
pathological changes in
the lung
Permanent abnormal
enlargement of air
spaces beyond
terminal bronchioles
Collapse of the
bronchioles
Destruction of the
alveoli
http://health.allrefer.com/health/chronic-obstructive-
pulmonary-disease-emphysema.html
28. Emphysema
Patients have some
resistance to airflow,
primarily on exhalation
Hyper-expansion
caused by air trapped
in the alveoli
Breathing becomes an
active process
Sanders, M.J. (2005) Paramedic Textbook (3rd
ed.) St.
Louis: Mosby-Elsevier
29. Emphysema
Risk of pneumothorax
Interior airway pressure
CO2 Retention
Potential worsening with CPAP
31. The use of CPAP prehospitally
reduces the need for intubation
by 30% and reduces mortality
by 20%
Annals of Emergency Medicine, September 2008
32. CPAP
Non-invasive ventilation
Continuous O2
delivered at a set
positive pressure
throughout the
respiratory cycle
www.ems1.com/cpap-for-ems
33. Positive Pressure
PUSHES air into the chest
Overcomes airway resistance
Bag valve mask
Demand valve
Intubation / mechanical ventilation
CPAP
34. Effects of CPAP
Increases functional residual capacity
Increases alveolar surface area available for
gas exchange
Increases oxygen diffusion across alveolar
membranes
Reduced work of breathing
35. Indications
Severe Respiratory Distress / Respiratory
Failure
Accessory muscle use?
Persistent hypoxia despite appropriate /
aggressive oxygen therapy?
Marked increased work of breathing?
Inability to speak full sentences?
Differentiate Pulmonary Edema versus other
Respiratory Disorder
36. Contraindications
Respiratory rate < 10 breaths / minute
Systolic blood pressure < 100 mmHg
Confusion
Inability to understand directions and
cooperate with application of CPAP
History of pneumothorax
History of recent tracheo-bronchial surgery
Active nausea or vomiting
Unconscious
Facial Injuries
37. How CPAP Works
Maintains constant level of airway pressure
Keeps and maintains alveoli open.
Moves fluid into vasculature (pulmonary edema)
Improves gas exchange
Buys time for medications to work
38. PEEP & Fi02
Positive End-Expiratory Pressure
The purpose of PEEP is to increase the volume of gas
remaining in the lungs at the end of expiration in order to
decrease the shunting of blood through the lungs and
improve gas exchange.
Fraction of inspired oxygen
The fraction or percentage of oxygen in the space being
measured.
Natural air includes 20.9% oxygen, which is equivalent to
FiO2 of 0.21.
Each additional liter of oxygen adds about 4% to their FiO2
Peep
39. Procedure
Prepare C-PAP Equipment
– Adjust FiO2 to 95%
– Set PEEP at 5 cm H2O
– Set O2 flow at (minimum 15 LPM)
– Ensure adequate supply of oxygen (main
and portable)
Reassess patient every 5 minutes
If patient continues to have severe
difficulty breathing after 5 minutes,
consider increasing PEEP to 10 cm
H2O
40. Limitations
CPAP is not a mechanical ventilator
Tight mask seal can create claustrophobic
response
Consider allowing patient to self-seal (hold
own mask) until initial benefits recognized
CPAP is powered by on-board oxygen supply
41. Oxygen Utilization
Cylinder
Flow
1000 PSI 1500 PSI 2000 PSI
D-15 LPM 8.5 min 13.8 min 19.2 min
D- 25 LPM 5.1 min 8.3 min 11.5 min
E- 15 LPM 14.9 min 24.3 min 33.6 min
E- 25 LPM 9 min 14.6 min 20.2 min
Cylinder
Flow
500 PSI 1000 PSI 1500 PSI
M- 15 LPM 31 min 83 min 135 min
M- 25 LPM 18 min 50 min 81 min
G- 15 LPM 48 min 129 min 209 min
G- 25 LPM 29 min 77 min 125 min
42. Summary
Pre-hospital studies have proven the
effectiveness of CPAP in treating patients
with severe respiratory distress, regardless of
disease process.
Presenter should briefly review basic function of each component of respiratory tree
Point out that while diaphragm is outside of the respiratory tree it is a functional unit of the respiratory process
Talking Points: The negative pressure that causes inhalation is created by chest expansion and contraction of the diaphragm.
Knowledge Application: Have students describe the pressures of breathing. Discuss the role of both positive and negative pressure in moving air.
Regular contraction and relaxation of diaphragm and intercostal muscles results in negative pressure causing air to be drawn in to lungs
Hemodynamic Effects
Contraction of diaphragm and external intercostal muscles produces negative intrathoracic pressure
Negative pressure engorges vena cava increasing cardiac preload
Relaxation of diaphragm and contraction of intercostal and abdominal muscles produces positive pressure
Positive pressure loads blood into the right atrium increasing Left Ventricular filling and cardiac output
Process of inhalation stops when stretch receptors send signal via vagus nerve that pressure has equalized
In adults the trachea is about 2.5 cm (1 inch) in diameter and the smallest bronchioles are less than 0.5 mm (19 / 1,000th inch) in diameter
Smooth muscle can constrict decreasing the internal diameter of bronchiole (bronchoconstriction)
Bronchoconstriction can be protective against inhalation of potentially harmful substances but can become life threatening when airflow significantly decreased as in asthma
Adults have 300 to 600 million aveoli
Adult lungs have between 50 to 100 square meters of alveoli surface area for gas exchange to occur
Surfactant – phospholipids in a near-saline solution
Phospholipids reduce surface tension of the saline making it easier for the lungs to expand and decreases work of breathing
Atelectasis – decrease in amount of surfactant which allows for alveoli collapse
Inspiration (inhalation) is an active process where the intercostal muscles and diaphragm contract, expanding the size of the chest cavity and causing air to flow into the lungs
Inspiration stops when stretch receptors in the lungs send a signal to the respiratory centers in the brain via the vagus nerve.
Expiration (exhalation) is a passive process in which the intercostal muscles and diaphragm relax, causing the chest cavity to decrease in size and forcing air out of the lungs
At FRC ONLY the tendency of the lungs to collapse is exactly balanced by the tendency of the chest wall to expand
In total, the lungs of an average sized adult hold about 5 - 6 L of air (Tidal volume of 500 ml x 10 – 12 breathes per minute)
The volume of air moved in one inspiratory / expiratory cycle of breathing is called tidal volume.
Multiply the tidal volume by the respiratory rate to determine minute volume, the amount of air that goes in and out of the lungs in 1 minute
Minute volume can be effected by either tidal volume or rate, or both.
Remember – not all of the minute volume air reaches the alveoli. Approximately 150 ml (in an average adult) occupies the space between the mouth and the alveoli but doesn’t reach the are of gas exchange.
This is referred to as dead space volume
Alveolar ventilation only occurs with air that actually reaches the alveoli
Principle of gas exchange within lungs
Each alveolus is continually ventilated with fresh air
Respiratory membrane is composed of alveolar wall (fluid coating, epithelial cells, and basement membrane), interstitial fluid, and the wall of a pulmonary capillary (basement membrane and endothelial cells).
Gases (oxygen and carbon dioxide) diffuse across the respiratory membrane.
Pulse oximetry measures percentage of hemoglobin molecules that are bound in arterial blood
provides an indirect indication of oxygenation in the blood
Reliable down to approximately 85%
Accuracy of reading effected by adequate amounts of hemoglobin in blood, and total blood volume
Pulse oximetry does NOT measure partial pressure of oxygen or carbon dioxide in plasma
Unlike respiratory failure, patients in respiratory distress are able to maintain near-normal blood gas levels and oxygenation
Occurs anytime that the body’s need for oxygen exceeds its ability to deliver oxygen
Most patients in respiratory distress have dyspnea.
CC – I can’t catch my breath or shortness of breath
VS – changes in rate, regularity, depth and / or effort of breathing
Effect approximately 5 million Americans and is responsible for 7,000 to 10,000 hospital admission each year
Blood volume is delivered to but not fully ejected left ventricle
Increase in end-diastolic blood volume increases left ventricular end-diastolic pressure. Pressure is transferred to left atrium and then to pulmonary capillaries and veins
As pulmonary capillary pressure increases, plasma portion of blood is forced into alveoli
Can have rapid onset or be a by-product of untreated or poorly treated heart failure
Filling of lungs with fluid – pulmonary edema occurs because of the accumulation of extravascular fluid in the lungs and alveoli
Cardiac pulmonary edema — also known as congestive heart failure — occurs when the diseased or overworked left ventricle isn&apos;t able to pump out enough of the blood it receives from your lungs. As a result, pressure increases inside the left atrium and then in the veins and capillaries in your lungs, causing fluid to be pushed through the capillary walls into the air sacs.
Fluid may also leak from the capillaries in your lungs&apos; air sacs because the capillaries themselves become more permeable or leaky, even without the buildup of back pressure from your heart. In that case, the condition is known as noncardiac pulmonary edema because your heart isn&apos;t the cause of the problem
Patients present with severe dyspnea, agitation (b/o hypoxia), crackles (frequently audible w/o stethoscope), JVD, significantly increased B/P, rapid labored respirations
Emergency management directed at decreasing venous return to the heart, improving myocardial contractility, decreasing myocardial oxygen demand, improving ventilation and oxygenation and rapid transport
Prior to pre-hospital CPAP, could frequently result in endotracheal intubation
Common disorder affecting 10 to 15 million Americans (4 – 5% of total US population)
Responsible for 4,000 – 5,000 deaths per year
Most common in children and young adults; can occur in any decade of life
Childhood asthma tends to improve or resolve with age
Adult onset asthma is usually persistent disorder
Exacerbation is an aggravation or increase the severity of underlying symptoms
Extrinsic (external) factors usually involved inhaled allergen, pollen or dander which sensitizes bronchial mucosa by tissue-specific antibodies
Intrinsic (internal) factors are more related to viral infections, physical exertion, aspirin use, smoke, fumes or stress which will trigger either increased release of acetylcholine or release of chemical mediators from mast cells.
Whether extrinsic or intrinsic, the end product of these stimuli is bronchoconstriction
Anaphylaxis can frequently mimic asthma
EMTs must be able to differentiate the cause of symptoms
Regardless of the cause, airway management must be the highest priority of patient care
Affect more than 17 million Americans
Predisposing factors – smoking, environmental pollutants, industrial exposures, various pulmonary infectious disease processes
Affects about 20% of men in US
Diagnosed by presence of cough with sputum production on most days for at least 3 months of the year for 2 consecutive years
Emphysema is the end stage of a process the progresses slowly for years.
Emphysema decreases the number of alveoli for gas exchange and reduces the elasticity of remaining alveoli resulting in trapping of air within the alveoli.
Therefore, residual volume (the volume of air remaining in the lungs after a maximal exhalation) increases while vital capacity (the volume in the lungs at maximal inflation minus Residual volume) remains normal
Decreases in alveolar capillaries in the lung reduces the area for gas exchange and increases resistance to pulmonary bloodflow
Patients with emphysema find they can breathe better of exhaling against resistance. They make this resistance by pursing their lips.
Over time, the chest becomes rigid (barrel shaped) requiring use of accessory muscles of neck, chest and abdomen to move air into and out of lungs.
Full deflation of lungs becomes more and more difficult and finally impossible
Patients with emphysema often develop bullae or blebs (thin-walled cystic lesions in the lungs) from the destruction of the alveolar walls. When the blebs collapse, they increase the problems with air exchange seen in these patients. They can also lead to pneumothorax.
Pressure is evenly distributed throughout the closed (respiratory) system. If lung tissue has a weakness, or ventilatory pressures are too high, the lungs can become over pressurized. Pulmonary over pressurization can cause a pneumothorax, pneumo-mediastinum, subcutaneous emphysema or tension pneumothorax
CO2 retention is a pathophysiological process in which too little carbon dioxide is removed from the blood by the lungs. The end result is an elevated level of carbon dioxide (hypercapnia) dissolved in the bloodstream.
The principal result of the increased amount of dissolved CO2 is respiratory acidosis. CO2 retention is a problem in various respiratory diseases, particularly (COPD). Patients with COPD who receive excessive supplemental oxygen can develop CO2 retention, and subsequent hypercapnia.
The mechanism that underlies this state is a matter of controversy. Some authorities point to a reduction in the hypoxic &quot;drive&quot;, a condition called carbon dioxide narcosis. When carbon dioxide levels are chronically elevated, the respiratory center becomes less sensitive to CO2 as a stimulant of the respiratory drive, and the PaO2 provides the primary stimulus for respirations. Administering excess supplemental oxygen can potentially suppress the respiratory center. However, it is unclear whether such a hypoxic drive exists in the first place.
An alternative explanation is that, in patients with COPD, the administration of oxygen leads to an increase in the degree to which diseased alveoli are perfused with blood relative to other, less-diseased alveoli. As a result, a larger fraction of blood passes through parts of the lung that are poorly-ventilated, with a resulting increase in the CO2 concentration of the blood leaving the lungs.
As CO2 levels increase, patients exhibit a reduction in overall level of consciousness as well as respiratory effort. Severe increases in CO2 levels can lead to respiratory arrest.
Providers need to be aware that administration of CPAP with associated high concentration oxygen has the potential to create a worsening of patient condition in CO2 retainers rather than improving it.
Research has proven the benefits of utilizing CPAP in the pre-hospital setting on patient outcomes.
CPAP provides high pressure oxygen delivered via mask under continuous pressure. This wall of air creates pneumatic splinting of airways and creates a backpressure to keep small airways and alveoli open. Patients are now breathing against a threshold of resistance
At rest respiration if a function of negative pressure which pulls air into the chest
Nasal canula, non-rebreather masks and nebulizers function within a system of negative pressure inspiration.
Positive pressure simply puts more air into the lungs
By preventing atelectasis (collapse of alveoli) more alveoli are available for gas exchange
Pressure pushed the oxygen to distal airway structures
The pneumatic splint of CPAP prevents the patient from having to exert energy themselves to breathe.
While initially indicated only for patients with CHF / pulmonary edema, pre-hospital CPAP is now appropriate for use on patients with acute blunt pulmonary trauma and those with obstructive pulmonary diseases.
In a 2003 Helsinki EMS study using only patients with Acute Pulmonary edema, patients had a noted improvement after CPAP administration even though there was a high misdiagnosis rate (84/121).
Kallio, T. et al. Prehospital Emergency Care. 2003. 7(2)
If patients meet indication inclusion criteria, DO NOT worry about specifically which Respiratory disorder you are treating with CPAP
CPAP should be initiated regardless of length of transport time
Effective use of the device requires a patent airway and intact respiratory effort
If patients do not qualify for NTG because of low BP, they do not qualify for CPAP either
Positive pressure in the chest can impact filling of the heart (pre-load) and cause a subsequent drop in BP
CPAP is an active process requiring patient cooperation and participation
Increased intra-thoracic pressure increases the risk for pneumothoraces and / or tracheo-bronchial rupture in susceptible patients
Emesis in patients with severe respiratory compromise may require aggressive airway management to prevent aspiration
Unlike BiPAP which delivers two levels of pressure (high inspiratory Positive Airway Pressure and a lower Expiratory Positive Airway Pressure), CPAP delivers a predetermined high level of pressure.
CPAP overcomes constricted airway resistances and increases airflow
Fluid in the alveoli inhibits gas exchange. CPAP moves fluid back into vasculature decreasing fluid overload and work of breathing
By overcoming airway resistance CPAP keeps alveoli open and allows for improved and increased gas exchange
Nitro spray or mist, utilized prior to CPAP, produces peripheral vasodilation, decreases cardiac preload and reduces fluid overload and pulmonary edema
If equipment allows, in-line nebulized bronchodilators can be administered while patient on CPAP
CPAP works adjunctively with medications to produce desired effects
Lasix, given in conjunction with Nitroglycerine and CPAP results in elimination of excess fluid through increased urination.
Lasix is no longer used as a pre-hospital treatment in some regions of Connecticut
https://www.youtube.com/watch?v=iuUSDR4ocCY
Any patient requiring aggressive airway management and mechanical ventilation are not candidates for CPAP. Airway pressure is maintained through use of PEEP when patients are mechanically ventilated
Patients may self-exclude themselves from CPAP use because of claustrophobia.
DO NOT FORCE THE MASK SEAL ON THESE PATIENTS – ANXIETY WILL WORSEN THEIR RESPIRATORY DISTRESS
CPAP creates a huge oxygen source demand and can deplete O2 reserves during long transports
Changes in pressure dynamics create patient improvement – NOT O2
CPAP units can be run on medical air – pressure exertion creates PEEP not O2 use
If allowed by medical control, patients on CPAP should have concomitant SPO2 monitoring
As CPAP comes in to use, it becomes even more globally important to maintain oxygen resources in vehicles, especially in services with long transport times.
Stated values are averages for several different CPAP units but are not correct for all CPAP.
Individual CPAP units can have different oxygen requirements and therefore, will impact how long oxygen sources will last.
Each agency will follow medical direction protocols for individualized oxygen parameters
While CPAP should not be the first line of treatment in patients with Severe Respiratory Distress, in conjunction with pharmacology the benefits of incorporating its use cannot be disputed.