Download Airway Management, Ventilation, Oxygen Therapy

Oxygen Therapy
Dr.Dhaher JS Al-habbo
FRCP London UK
Assistant Professor in Medicine
DEPARTMENT OF MEDICINE
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Oxygen Therapy
• Oxygen was discovered independently by the Swedish
apothecary Karl W.Scheele, in 1772, and by the
English amateur chemist Joseph Priestly,in August
1774.
• Priestley first liberated oxygen by intensely heating
'mercurius calcinatus' (mercuric oxide) placed over
liquid mercury in a closed vessel. He called this new
gas "dephlogisticated air, "oxygenated."
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Karl W.Scheele
in 1772
Joseph Priestly
in1774
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Oxygen Therapy
• Joseph Priestley and Carl Wilhelm Scheele both
independently discovered oxygen, but Priestly is usually
given credit for the discovery.
• Priestley called the gas produced in his experiments
'dephlogisticated air' and Scheele called his 'fire air'.
• The name oxygen was created by Antoine Lavoisier who
incorrectly believed that oxygen was necessary to form all
acids.
The Element Oxygen
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Atomic Number: 8
Atomic Weight: 15.9994
Melting Point: 54.36 K (-218.79°C or -361.82°F)
Boiling Point: 90.20 K (-182.95°C or -297.31°F)
Density: 0.001429 grams per cubic centimeter
Phase at Room Temperature: Gas
Element Classification: Non-metal
Period Number: 2
Group Number: 16 Group Name: Chalcoge
Oxygen is a drug
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Colorless, odorless, tasteless gas, makes up 21%
of room air .It is NOT flammable but does
support combustion.
should be regarded as a drug .
Has a Drug Identification Number (DIN)
Oxygen must be prescribed in all situations
(except for the immediate management of
critical illness).
Oxygen should be prescribed to achieve a target
saturation (Sp02), which should be written on
the drug chart .
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Basic Concepts of Oxygen
• Composition of Room Air Nitrogen 78.08% ~78%
Oxygen 20.946% ~21% Trace gases ~1%
• Normal PO2 in arterial blood (PaO2) ≥ 95mmHg:
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decrease with age.
PO2 in mitochondria ≥ 18 mmHg required to
generate high energy phosphate bonds e.x ATP
At rest the average adult male consumes about 225250 ml of O2/min.
This can increase up to 10 folds during exercise.
There’s very small O2 reserve that can be consumed
within 4-6 minutes of cessation of spontaneous
ventilation.
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Oxygen content of blood
• The theoretical maximum oxygen carrying
capacity is 1.39 ml O2/g Hb, but direct
measurement gives a capacity of 1.34 ml O2/g
Hb.1.34 is also known as Hüfner’s constant.
• The oxygen content of blood is the volume of
oxygen carried in each 100 ml blood.
It is calculated by: (O2 carried by Hb) + (O2 in
solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023
x PaO2)
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Mechanisms of Hypoxia
O2 Utilization
O2 Utilization
O2 Delivery
O2 Delivery
Shift from aerobic to anaerobic metabolism
Increase Lactic acid
Progressive Acidosis
Cell Death
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Basic Concepts of Oxygen
Oxygen Cascade:
Inspired = 150 mmHg at Sea Level
↓ Alveolar PO2= 103
↓ Arterial=100
↓ Capillary= 51
↓ Mitochondrial= 1-10
(FiO2 expressed as 0.21-1.0 or 21- 100%)
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Clinical Conditions With Increased Risk of
Hypoxia
• Myocardial infarction
• Acute pulmonary
disorders
• Sepsis
• Drug overdose
• Liver failure
• Head trauma
• CHF
• Hypovolemic shock
• Blunt chest trauma
• Acute neuromuscular
disease
• Acute abdomen
(splinting)
• Acute pancreatitis
• Spinal cord injury
Indications for Oxygen Therapy
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Tachypnea
Cyanosis
Restlessness
Disorientation
Cardiac arrhythmias
Slow bounding pulse
Tachycardia
Hypertension
• Dyspnea
• Coma
• Labored breathing (use
of accessory muscles,
nasal flaring)
• Lethargy
• Tremors/seizure activity
Oxygen Therapy
• “Generally speaking”, a patient who is
breathing less than 12 and more than 24
times a minute needs oxygen of some kind
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Oxygen therapy To ensure safe
and effective treatment
• Oxygen is required for the functioning and
survival of all body tissues and deprivation
for more than a few minutes is fatal.
• In immediately life threatening situations
oxygen should be administered.
• Hypoxaemia. Acute hypotension. Breathing
inadequacy. Trauma. Acute illness. CO
poisoning. Severe anaemia. During the peri14
operative period.
Oxygen therapy
• Oxygen therapy Humidification Is
recommended if more than 4 litres/min is
delivered.
• Helps prevent drying of mucous
membranes.
• Helps prevent the formation of tenacious
sputum.
• Oxygen concentrations will be affected with
all delivery systems if not fitted correctly or
tubing becomes kinked and ports
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obstructed.
The oxyhaemoglobin dissociation curve showing the
relation between partial pressure of oxygen and
haemoglobin saturation
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Methods of Oxygen Delivery
• Most common methods of oxygen delivery
include
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Nasal Cannula
Venturi Mask
100% Non-Rebreather Mask
Mechanical Ventilation
Oxygen Delivery Methods
• Nasal Cannula
• Comfortable, convenient,
mouth breathing will not
effect % of O2 delivered
• Liters/min = %
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2 l/m = 24-28%
3 l/m = 28-30%
4 l/m = 32-36%
5 l/m = 36-40%
6 l/m = 40-44%
• Cannot administer > 6
liters/minute (44%)
Nasal Cannula
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Provides limited oxygen concentration
Used when patients cannot tolerate mask
Prongs and other uses
Concentration of 24 to 44%
Flow rate set between 1 to 6 liters
For every liter per minute of flow delivered,
the oxygen concentration the patient inhales
increases by 4%
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Venturi Mask
Provides precise
FiO2 Delivery
concentrations of
Blue 24% Yellow 28%
White 31% Green 35%
oxygen
Pink 40%
Entrainment valve to
Concerns
adjust oxygen delivery
Tight seal is a must
Interferes with
Mostly used in the hospital
eating/drinking
setting for COPD
Condensation collection
patients
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Venturi Mask
Red 40% 10/L/M
Blue 24% 2/L/M Yellow 35% 8/L/M
White28% 4/L/M Green 60% 15/L/M
Orange 31% 6/L/M
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Oxygen Delivery Methods
100% Non-Rebreather
• Delivery percentages
– 6 l/min = 55 – 60 %
– 8 l/min = 60 – 80 %
– 10 l/min = 80 – 90
%
– >12 l/min = 90 + %
• Benefit: Has a one
way expiratory valve
that prevents rebreathing expired
gases
• Concern
– May lead to O2
toxicity
100% Non-Rebreather Mask
partial rebreather Mask
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Oxygen Delivery Methods
Mechanical Ventilation
• Allows administration of 100% oxygen
• Controls breathing pattern for patients who are
unable to maintain adequate ventilation
• Is a temporary support that “buys time” for
correcting the primary pathologic process
Indications for Mechanical Ventilation
• Mechanical Failure
• Ventilatory Failure
• Oxygenation Failure
• General Anesthesia
• Post-Cardiac Arrest
Mechanical Ventilation
Two categories of ventilators
– Negative pressure ventilators
• Iron lung
• Cuirass ventilator
– Positive pressure ventilators
• Two categories
– Volume-cycled (volumepreset)
– Pressure-cycled (pressurepreset)
Iron Lung
Mechanical Ventilation PEEP
• Description
– Maintains a preset positive airway pressure at the end
of expiration
– Increases PaO2 so that FiO2 can be decreased
– Increases DO2 (amt of delivered O2 to tissue)
– Maximizes pulmonary compliance
– Minimized pulmonary shunting
• Indications
– PaO2 < 60 on FiO2 > 60% by recruiting dysfunctional
alveoli
– Increases intrapulmonary pressure after cardiac surgery
to decrease intrathoracic bleeding (research does not
support this idea)
Mechanical Ventilation PEEP
• Advantages
– Improves PaO2 and SaO2 while allowing FiO2 to be
decreased
– Decreases the work of breathing
– Keeps airways from closing at end expiration (esp. in pts
with surfactant deficiency)
• Disadvantages
– Increased functional residual capacity (increases risk for
barotrauma)
– Can cause increased dead space and increased ICP
– In pts with increased ICP, must assure CO2 elimination
– Contraindicated: hypovolemia, drug induced low cardiac
output, unilateral lung disease, COPD
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Mechanical Ventilation CPAP
• Description
– Constant positive pressure is applied throughout the
respiratory cycle to keep alveoli open
• Indications
– To wean without having to remove the ventilator and
having to connect to additional equipment
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Mechanical Ventilation CPAP
• Advantages
– Takes advantage of the ventilator alarm systems
providing psychological security of the ventilator being
there
• Disadvantages
– Patient may sense resistance as he breathes through the
ventilator tubing
Mechanical Ventilation Complications
• Respiratory arrest
from disconnection
• Respiratory infection
(VAP)
• Acid-base imbalances
• Oxygen toxicity
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Pneumothorax
GI bleeding
Barotrauma
Decreased cardiac
output
Ventilator Weaning
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Vital Capacity at least 10 – 15 ml/kg
Tidal Volume > 5 ml/kg
Resting minute volume > 10 L per minute
ABG’s adequate on < 40% FiO2
Stable vital signs
Intact airway protective reflexes (strong cough)
Absence of dyspnea, neuromuscular fatigue, pain,
diaphoresis, restlessness, use of accessory muscles
Primary Acid-base Disorders:
Respiratory Alkalosis
Respiratory alkalosis - A primary disorder where the first change is
a lowering of PaCO2, resulting in an elevated pH. Compensation
(bringing the pH back down toward normal) is a secondary lowering
of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not
metabolic acidosis, since it is not a primary process.
Primary Event
HCO3↑ pH ~ ------↓ PaCO2
Compensatory Event
↓HCO3-
↑ pH ~ -------↓ PaCO2
Primary Acid-base Disorders:
Respiratory Acidosis
Respiratory acidosis - A primary disorder where the first change is
an elevation of PaCO2, resulting in decreased pH. Compensation
(bringing pH back up toward normal) is a secondary retention of
bicarbonate by the kidneys; this elevation of HCO3- is not metabolic
alkalosis since it is not a primary process.
Primary Event
HCO3↓ pH ~ --------↑PaCO2
Compensatory Event
↑ HCO3-
↓ pH ~ --------↑ PaCO2
Primary Acid-base Disorders:
Metabolic Acidosis
Metabolic acidosis - A primary acid-base disorder where the first
change is a lowering of HCO3-, resulting in decreased pH.
Compensation (bringing pH back up toward normal) is a secondary
hyperventilation; this lowering of PaCO2 is not respiratory alkalosis
since it is not a primary process.
Primary Event
↓ HCO3↓ pH ~ -----------PaCO2
Compensatory Event
↓HCO3↓ pH ~ -----------↓ PaCO2
Primary Acid-base Disorders:
Metabolic Alkalosis
Metabolic alkalosis - A primary acid-base disorder where the first change
is an elevation of HCO3-, resulting in increased pH. Compensation is a
secondary hypoventilation (increased PaCO2), which is not respiratory
acidosis since it is not a primary process. Compensation for metabolic
alkalosis (attempting to bring pH back down toward normal) is less
predictable than for the other three acid-base disorders.
↑ pH ~
Primary Event
Compensatory Event
↑ HCO3------------
↑HCO3↑ pH ~ ---------
PaCO2
PaCO2
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Metabolic Acid-base Disorders:
Some Clinical Causes
METABOLIC ACIDOSIS
↓HCO3- & ↓ pH
- Increased anion gap
• lactic acidosis; ketoacidosis; drug poisonings (e.g., aspirin, ethylene
glycol, methanol)
- Normal anion gap
• diarrhea; some kidney problems (e.g., renal tubular acidosis,
interstitial nephritis)
METABOLIC ALKALOSIS
↑ HCO3- & ↑ pH
Chloride responsive (responds to NaCl or KCl therapy): contraction alkalosis,
diuretics, corticosteroids, gastric suctioning, vomiting
Chloride resistant: any hyperaldosterone state (e.g., Cushing’s syndrome,
Bartter’s syndrome, severe K+ depletion)
Respiratory Acid-base Disorders:
Some Clinical Causes
RESPIRATORY ACIDOSIS
↑PaCO2 & ↓ pH
Central nervous system depression (e.g., drug overdose)
Chest bellows dysfunction (e.g., Guillain-Barré syndrome,
myasthenia
gravis)
Disease of lungs and/or upper airway (e.g., chronic obstructive lung
disease, severe asthma attack, severe pulmonary edema)
RESPIRATORY ALKALOSIS
↓PaCO2 & ↑ pH
Hypoxemia (includes altitude)
Anxiety
Sepsis
Any acute pulmonary insult (e.g., pneumonia, mild asthma attack, early
pulmonary edema, pulmonary embolism)
Production of the hemoglobin-hyerpolymers from pig blood
Haemoglobin
Haemoglobin
Multimeres
Polymerisation
PEGylated
Multimeres
Monomeres
Oligomeres
Surface
Modification
Separation
One-vessel- reaction
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Hyperpolymeres
Tamaulipas 10-2007