Masks and O2 Delivery Devices PDF

Masks and O2 delivery devices Khaled M. Gaballah Assistant professor of Anesthesiology and Intensive Care  Fast Facts about O2 Makes up 20.9% of air by volume and 23% of air by weight....

Masks and O2 delivery devices Khaled M. Gaballah Assistant professor of Anesthesiology and Intensive Care  Fast Facts about O2 Makes up 20.9% of air by volume and 23% of air by weight. O2 should be Can combine with all other elements except other inert gases to form oxides. regarded as a Is a non-flammable gas. drug Accelerates combustion. At -182.9 C (-300 F) oxygen is a pale blue, tasteless, odorless liquid. Its critical T◦ is -118.4 C (above this critical T◦, O2 can only exist as a gas regardless of the pressure). An O2 enriched environment is considered to have 23% O2 in the air & is a fire hazard.  02 is administered to achieve target saturation.  It will be administered at normal or ↑ pressure & at conc > RA  There is no evidence to support the use of supplemental O2 to ↓ dyspnea in non-hypoxemic COPD pts”.  O2 therapy should be used for the least possible duration then gradually weaned.  O2 is a treatment for “hypoxemia, not breathlessness”.  O2 has not been shown to have any effect on the sensation of breathlessness in non-hypoxemic patients. ?!!!  Oxygen therapy is the administration of oxygen at concentrations greater than ambient air with the intent of treating or preventing the symptoms and manifestations of hypoxia.  Indications for Oxygen Therapy O2 –when administered correctly- may be life saving NEVER deprive any pt from O2 if it is indicated Documented hypoxemia: (inadequate DO2 to meet the tissues metabolic demands)↓ PaO2 in the blood below normal range. PaO2 of < 60 mmHg or SaO2 of < 90% on RA (PaO2 of < 50 mmHg or SaO2 of < 88% on RA in neonates) , or with PaO2 and/or SaO2 below desirable range for specific clinical situation. An acute situation in which hypoxemia is suspected e.g, AMI, postanesthesia. Substantiation of hypoxemia is required within an appropriate period of time following initiation of therapy. Severe trauma, burns, infections. Short-term therapy (e.g., carbon monoxide poisoning) or surgical intervention (e.g., post-anesthesia recovery). Pneumothorax absorption (O2 accelerates resolution of spontaneous pneumothorax) Cardiac and/or respiratory arrest. Hypotension, low CO, metabolic acidosis.. Resp distress (RR>24/min)  There is no evidence to support the use of supplemental O2 to ↓ dyspnea in non-hypoxemic COPD pts”.  O2 therapy should be used for the least possible duration then gradually weaned.  O2 is a treatment for “hypoxemia, not breathlessness”.  O2 has not been shown to have any effect on the sensation of breathlessness in non-hypoxemic patients. 3 basic ways to determine the need for O2 therapy: Lab measurements e.g, ABG testing, Presence of a specific clinical problem e.g,during CPR Clinical assessment e.g, tachypnea, cyanosis.  General roles In acutely ill pt, O2 delivery depends on presence of patent airway. Firstly, ensure patent airway. O2 can be given empirically in cases of cardiac or respiratory arrest, respiratory distress or hypotension. ABG should be analyzed as soon as possible to assess the degree of hypoxemia, PaCO2 and acid-base status. Give FiO2 of 1 (100%) in case of cardiac or respiratory arrest Give FiO2 of 0.4-0.6 (40-60%) in case of hypoxemia with PaCO2 < 40 mmHg. Give FiO2 of 0.24 (24%) in case of hypoxemia with PaCO2 > 40 mmHg. In case of CO poisoning, high FiO2 is essential despite normal PaO2 as O2 competyes with CO for Hb binding sites & ↓CoHb half life from 320 to 80 minutes Chronic lung disease pts develop subjective relief of dyspnea with CONTROLLED O2 therapy even in absence of arterial hypoxemia. ?!!! In many acute condotitions e.g, asthma, PE, even short periods of FiO2 of 0.6-1 may preserve life unill the specific treatment is administered  Treat hypoxia Goals of O2 Therapy ↓ WOB ↓ myoc work “Oxygen Therapy is usually defined as the administration of oxygen at concentrations greater than those found in ambient air”. The main goal of oxygen therapy is: “To treat or prevent hypoxemia thereby preventing tissue hypoxia which may result in tissue injury or even cell death”. Hypoxia Def: the amount of O2 available to the cells is not adequate to meet metabolic need. Hypoxia can exist even though hypoxemia has been corrected with O2 therapy? For example: At the cellular level where the cells are unable to access or use the O2 delivered At the tissue level when O2 may not reach the cells due to a blocked artery Causes of hypoxia: Hypoxemia (e.g., at high altitudes). Anemic hypoxemia (e.g., reduced hematocrit or carbon monoxide poisoning). Stagnant hypoxemia (e.g., shock, ischemia). Histotoxic hypoxia/dysoxia (e.g., cyanide poisoning).  Problem A disoriented postoperative male pt breathing RA exhibits tachypnea, tachycardia, & mild cyanosis of the mucous membranes. Using a pulse oximeter, the RT measures the pt’s oxyhemoglobin saturation as 90%. What should the RT recommend to the pt’s surgeon? Discussion This is a classic example of how monitoring data & results of bedside assessment can conflict. Both the pt’s condition & the observed clinical signs indicate hypoxemia, but the pulse oximeter indicates adequate oxygenation. In situations such as this, it is always better to recommend O2 therapy—treat the pt, not the monitor. This concept is particularly important in the use of monitoring technologies known to have limited accuracy, such as pulse oximetry  Monitoring Patient monitoring should include clinical assessment along with oxygen tension or saturation measurements. This should be done at the following times: when therapy is initiated; within 12 hours of initiation of therapy for FIO2 levels 300 mm Hg) Acute Lung Injury (Oxygen toxicity ) Oxidative stress Depression of ventilation or apnea in a select population with chronic hypercarbia (hypoxic drive) Retinopathy of prematurity (its risk in infants can be minimized by keeping the PO2 50% present a significant risk of absorption atelectasis. N2 normally is the most plentiful gas in both the alveoli & the blood. Absorption Breathing high levels of O2 quickly depletes body nitrogen levels. As blood nitrogen levels decrease, the total pressure of venous gases atelectasis rapidly decreases. Under these conditions, gases that exist at atmospheric pressure within any body cavity rapidly diffuse into the venous blood. This principle is used for removing trapped air from body cavities. Giving pts high levels of O2 can help clear trapped air from the abdominal, cerebral, or pleural spaces. This same phenomenon can cause lung collapse, especially if the alveolar region becomes obstructed. Under these conditions, O2 rapidly diffuses into the blood. With no source for repletion, the total gas pressure in the alveolus progressively decreases until the alveolus collapses. Because collapsed alveoli are perfused but not ventilated, absorption atelectasis increases the physiologic shunt & worsens blood oxygenation. The likelihood of absorption atelectasis is greatest if associated with ↓ TV uch as sedation, surgical pain, or CNS dysfunction. In these cases, poorly ventilated alveoli may become unstable when they lose O2 faster than it can be replaced. The result is a more gradual shrinking of the alveoli →complete collapse, even when the pt is not breathing supplemental O2.  Oxygen toxicity Becomes clinically important after 8 - 12 hours of exposure to a high FiO2 level. Probably results from direct exposure of the alveoli to a high FiO2 level. Healthy lungs appear to tolerate FiO2 values 0.50 can result in a toxic alveolar O2 concentration. Because most oxygen therapy is delivered at 1 atm barometric pressure, the FiO2 and the duration of exposure become the determining factors in the development of most clinically significant O2 toxicity. The mechanism of oxygen toxicity is related to the significantly ↑ production of O2 free radicals. These radicals affect cell function by inactivating protein sulfhydryl enzymes, disrupting DNA synthesis, and disrupting the cell membrane integrity by lipid peroxidation. Vitamin E, superoxide dismutase, and sulfhydryl compounds promote normal, protective free radical scavenging within the lung. During periods of lung tissue hyperoxia, these protective mechanisms are overwhelmed, and toxicity results The classic clinical manifestations of O2 toxicity include cough, substernal chest pain, dyspnea, rales, pulmonary edema, progressive arterial hypoxemia, bilateral pulmonary infiltrates, decreasing lung compliance, and atelectasis. These signs and symptoms are nonspecific, and O2 toxicity is frequently difficult to distinguish from severe underlying pulmonary disease.  The best treatment for O2 toxicity is preventing it from occurring altogether. O2 therapy should be directed at improving oxygenation with the minimum FiO2 needed to obtain SaO2 >90%. Inhalation treatments & ↑ expiratory airway pressure may be useful adjuncts in improving pulmonary toilet, decreasing V̇ /Q̇ mismatch, and improving arterial oxygenation. These therapies may be used to maintain adequate oxygenation at an FiO2 ≤ 0.50.  Hypoxemia Def: partial pressure of O2 (PaO2) is less than the level predicted for the individual’s age. Causes of hypoxemia: Low Pinsp O2 (e.g., at high altitude). Hypoventilation, V/Q mismatch (e.g., COPD). Anatomical Shunt (e.g., cardiac anomalies). Physiological Shunt (e.g., atelectasis). Diffusion deficit (e.g., interstitial lung disease). Hemoglobin deficiencies.  Hypoxia may result from a decrement of any of the determinants of DO2, including anemia, low CO, hypoxemia, or abnormal Hb affinity (e.g., CO toxicity) out of proportion to demand.  Hypoxia may also arise from a failure of O2 use at the tissue level (e.g., microvascular perfusion defect of shock) or at the cellular level (e.g., cyanide poisoning).  Pts on O2 therapy need to be regularly observed FiO2 should be titrated up or down to maintain the target SpO2 Discontinue O2 therapy when the pt remains stable on minimal O2 therapy.  Oxygen delivery ↑ FiO2 → ↑ delivery to tissues by improving Hb saturation with oxygen & ↑ dissolved O2. O2 delivery, the amount of O2 delivered to the body by the heart: DO2 = CO x CaO2 CaO2= arterial oxygen content CO = cardiac output DO2 = oxygen delivery  O2 treatment targets correcting arterial hypoxemia. In case of tissue hypoxia without arterial hypoxemia, we should target correction of the underlying cause e.g, heart failure , anemia. Inadequate O2 dose → more deaths (O2 should be given at a dose that corrects hypoxia & minimize side effects)  Oxygen Delivery Devices Low Flow (device flow 44% communication with the No PEEP health care personnel Not as effective in pts with deviated nasal septum or nasal polyposis High flows are uncomfortable The anatomic reservoir for a NC consists of nose, nasopharynx, and oropharynx, and it is about one third of the entire normal anatomic dead space (including trachea). E.g, 150 mL ÷ 3 = 50 mL; assume a NC O2 flow rate of 6 L/min (100 mL/sec), TV of 500 mL, RR of 20 breaths /minute, insp time of 1 second, and exp time of 2 seconds. If the terminal 0.5 second of the 2-second exp time has negligible gas flow, the anatomic reservoir (50 mL) completely fills with 100% oxygen, assuming an O2 flow rate of 100 mL/sec. Using the preceding normal variables, the FiO2 is calculated for a patient with a 500-mL and a 250-mL VT The larger the TV or faster the RR,→ the lower the FiO2 & vice versa. Because of their simplicity and the ease with which patients tolerate them, nasal cannulas are the most frequently used oxygen delivery devices Check frequently that both prongs are in pts nares Never deliver >2-3 L\min to pt with chronic lung disease  Irritation of the nasal mucosa and the paranasal sinuses occurs most often when high flow rates of oxygen are used. The problem appears to be greater with nasal cannulas that use straight rather than curved prongs. With straight prongs, oxygen flow is directed toward the superior aspects of the nasal cavity, which promotes turbulent flow; with curved prongs, oxygen entering the nose is directed across the nasal turbinate, thus enhancing laminar flow as the gas flows through the nasal cavity. Problem A pt admitted to the ER with resp distress dt poneumonia, RR 20/min, TV 500 mls. The RT applied a nasal cannula @ 6 l/min. Calculate the delivered FiO2. Later, this pt deteriorated, RR increased to 40//min with same TV (500 mls). Calculated the delivered FiO2 Reservoir nasal cannula Reservoir systems incorporate a mechanism for gathering & storing O2 between pt breaths. Pts draw on this reserve supply whenever inspiratory flow exceeds O2 flow into the device. Because air dilution is reduced, reservoir devices generally provide higher FiO2 than low-flow systems. Reservoir devices can ↓ O2 use by providing FiO2 comparable with nonreservoir systems but at lower flow. At low flow, reservoir cannulas can ↓ O2 use 50% -75%. A pt at rest who needs 2 L/min through a standard cannula to achieve an arterial SaO2 greater than 90% may need only 0.5 L/min through a reservoir cannula to achieve the same blood oxygenation. Mustache reservoir cannula Pendant reservoir cannula. Nasal catheter A nasal catheter is a soft plastic tube with several small holes at the tip that is inserted by gently advancing it along the floor of either nasal passage & visualizing it just behind & above the uvula. Once in position, the catheter is taped to the bridge of the nose. If direct visualization is impossible, the catheter may be blindly inserted to a depth equal to the distance from the nose to the earlobe. If placed too deep→gagging, aspiration. Rarely used nowadays  Transtracheal catheter A transtracheal O2 catheter is a thin polytetrafluoroethylene (Teflon) catheter inserted percutaneously into the trachea between the 2nd & 3rd tracheal rings using seldinger technique and secured by a chain necklace. Because flow is so low, no humidification is needed. Because the transtracheal catheter resides directly in the trachea, O2 builds up both there & in the upper airway during expiration→ effective expansion of the anatomic reservoir &↑ the FiO2 at any given flow. Compared with a nasal cannula, a transtracheal catheter needs approximately half of the O2 flow to achieve a given PaO2. Flow 0.5 – 4 l/min. This flow bypasses the anatomical dead space allowing O2 tp pass directly to the trachea. This reduced flow can be of great economic and practical benefit to patients needing continuous long-term O2 therapy because it can greatly increase the duration of flow from portable O2 systems. However, transtracheal O2 therapy can pose serious problems & risks (e.g., collection of mucus which can obstruct the airway), invasive, and these devices are not currently in widespread use.  Transtracheal oxygen benefits 1. Decrease dead space as O2 from the catheter enters the trachea lower in the airways 2. Decrease total inspired minute ventilationdue to flow from the catheter less gas is inspired at the mouth, reducing WOB 3. Increase CO2 elimination efficiency, as fresh gas flowing from the catheter flushes the area proximal to the catheter tip during expiration reducing the amount of CO2 that returns to the alveoli with the next insp cycle. In addition, gas exiting the catheter tip at high velocity generates turbulence that enhances gas mixing distal to the catheter tip, increasing CO2 washout. As a consequence, PaCO2 remains unchanged despite a decrease in total inspired minute ventilation. Nasal mask Hybrid of nasal cannula & face mask Covers the nose, the lower edge rest on the upper lip Adv: comfortable, no air jetted Disadv: sores on long term use Variable performance masks (medium concentration; MC) (Delivers unpredictable FiO2 that vary with flow rate) Used to deliver O2-enriched air (6-10 L/min) (O2 35 – 60 %) to the pt. Air % depend on mask-face fitting For heavy mouth breathers & postop (after extubaion, in PACU). but Not for CO2 retainers. Often it is used when ↑delivery of oxygen is needed for short periods (i.e., 8 L/min do not significantly ↑ the FiO2 above 0.60 because the oxygen reservoir is filled. A minimum flow of 5 L/min is necessary to prevent CO2 accumulation and rebreathing. Humidification may be needed if high flows caused nasal dryness If FiO2 values above 0.60 are required, a partial rebreathing mask, nonrebreathing mask, or high-flow system should be employed. Mask efficiency depends on how well it fits Not tolerated by severely dyspneic pts  Mechanism of action 1. Ambient air is entrained through the holes on both sides of the mask. The holes also allow exhaled gases (CO2) to be vented out → flow ≥6 L/min to prevent rebreathing if flow > 10 L/min is needed for satisfactory oxygenation →use of a device capable of a higher FiO2 should be considered. 2. The final concentration of inspired O2 depends on:  O2 supply flow rate  the pattern of ventilation: If there is a pause between exp & insp → the mask fills with O2 and a high conc. is available at the start of inspiration  the pt’s inspiratory flow rate: During insp, O2 is diluted by the air drawn in through the holes when the insp flow rate exceeds the flow of O2 supply. During normal tidal ventilation, the peak insp flow rate is 20–30 L/min, which is higher than the O2 supplied to the pt and the O2 that is contained in the body of the mask, → some ambient air is inhaled to meet the demands thus diluting the fresh O2 supply. The PIFR ↑ further during deep insp and during hyperventilation  how tight the mask fits on the face. 5-6 L →40% 6-7 L →50% 7-8 L →60% Maximum 50% - 60% at 15 L/min flow. Monitor the pt frequently to check placement of the mask. Support the pt if claustrophobia is concern Secure physician's order to replace mask with nasal cannula during meal time  Mechanism of action 4. If there is no expiratory pause, alveolar gases may be rebreathed from the mask at the start of insp. 5. CO2 rebreathing from the body of the mask (apparatus dead space of about 100 mL) is usually of little clinical significance in adults but may be a problem in some pts who are not able to compensate by increasing their alveolar ventilation. Indicator of rebreathing: The pts may experience a sense of warmth and humidity. How to ↓rebreathing?  ↑ the fresh O2 flow.  Use the smallest sitable mask  ↑resistance to flow from the side holes is high (when the mask is a good fit).  Mechanism of action To deliver an FiO2 level of more than 60% with a low-flow system, the oxygen reservoir system must be increased)  Partial rebreathing mask For critically ill pt with high O2 requirements flow : 8 - 10 L/min (35 oxygen supplementation was given by nasal prongs (6 L/min) with an additional flowmeter along with the non-rebreathing mask. The adherence to closure of the mouth is not mandatory. Any escape of oxygen through mouth would increase the oxygen concentration of mask and thus decreases the CO2 concentration and hence rebreathing. The possible mechanisms of oxygenation improvement could be: 1. improved oxygen-air mixing in large airways, 2. increased oxygen concentration inside the non-rebreathing mask mask, 3. decrease in rebreathing of CO2 from the non-rebreathing mask mask. additional low flow nasal cannula oxygen supplementation to improve oxygenation in acute hypoxemic COVID-19 patients under a non-rebreathing mask as useful in resource limited settings instead of HFNC oxygenation 8. Some designs have an extra port attached to the body of the mask allowing it to be connected to a side-stream CO2 monitor. This allows it to sample the exhaled CO2 so monitoring the pt’s respiration during sedation. 9. Similar masks can be used in pts with tracheostomy (Trach collar or Trach shield). No direct connection, deliver O2 around tracheal opening. As with the face mask, similar factors will affect its performance. Care must be taken to humidify the inspired dry O2 as the gases delivered bypass the nose & its humidification.  Advantages: Simple, cheap, can be used for nebulisation & widely available. Easy to vary the O2 delivered Reservoir masks are the simplest means of delivering high FiO2 Disadvantages Variable performance device: the precise FiO is unknown 2 Rebreathing of exhaled CO2 from within the mask may occur. Claustrophobia , less tolerated, irritation of eyes. Need to be removed for eating & drinking Oxygen hoods It was introduced as a means of maintaining a relatively constant FIO2 to infants requiring supplemental oxygen. It is a clear plastic enclosure that is placed around the patient's head. Fixed oxygen concentrations (from an air entrainment device or an oxygen–air blender can be connected to the hood via an inlet port at the rear of the hood. The flow rate of gas entering the hood is set to ensure that the exhaled carbon dioxide is flushed out (i.e., the flow rate should be approximately 5 to 10 L/min).  The FIO2 must be measured intermittently or monitored continuously with an oxygen analyzer. Several studies have shown that in hoods, the oxygen seems to be layered, with the highest concentration near the bottom of the hood. The partial pressure of oxygen in the arteries (PaO2) should also be measured by arterial blood gas analysis at regular intervals. The noise levels inside an oxygen hood can present problems, and every effort should be made to minimize this effect  Fixed performance devices: VENTURI MASK Fixed performance (independent of the patient’s respiratory pattern) devices (also called high-air- flow O2 enrichment, or HAFOE). Uses: to deliver a specified O2 concentration regardless of RR or TV. The fixed performance allows interpretation of O2 saturations & blood gases in the context of a known inspired FiO2. Components 1. The plastic body of the mask has holes on both sides. 2. The proximal end of the mask consists of a Venturi device. The Venturi devices are colour-coded & marked with the recommended O2 flow rate to provide the desired O2 conc. 3. Alternatively, a calibrated variable Venturi device can be used to deliver the desired FiO 2.  Types 1. A fixed FiO2 model, which requires specific inspiratory attachments that are color coded and have labeled jets that produce a known FiO2 with a given flow 2. A variable FiO2 model, which has a graded adjustment of the air entrainment port that can be set to allow variation in delivered FiO2. Mechanism of action  The Venturi mask uses the Bernoulli principle (in order to maintain a constant flow, a fluid must increase its velocity as it flows through a constriction), in delivering a predetermined and fixed O2 conc to the pt.  The size of the constriction determines the final concentration of O 2 for a given gas flow. This is achieved despite the pt’s respiratory pattern by providing a higher gas flow than the peak insp flow rate.  As the flow of O2 passes through the constriction, a negative pressure is created. This causes the ambient air to be entrained and mixed with the O2 flow. As the total energy is constant, there is a decrease in the potential energy so a negative pressure is created. This causes the ambient air to be entrained and mixed with the O2 flow. The devices must be driven by the correct O2 flow rate, calibrated for the aperture size if a predictable FiO2 is to be achieved. Because of the high FGF rate, the exhaled gases are rapidly flushed from the mask, via its holes. Therefore there is no rebreathing and no ↑ in dead space. These masks are recommended when a fixed FiO2 is desired in pts whose ventilation is dependent on the hypoxic drive. Check that air intake valves are not blocked factors affecting the amount of entrained air: 1- the jet size (smaller jet→ higher velocity→ ↑ entrainment (↓FiO2)+↑total output flow 2- the air entrainment port size (larger port→ ↑ entrainment (↓FiO2) +↑total output flow  The minimum total flow requirement should result from entrained room air added to the fresh O2 flow and equal 3 to 4 times the minute ventilation. This minimal flow is required to meet the patient’s peak inspiratory flow demands.  Venturi color FiO2 % O2 flow Total gas flow (l/min) (l/min) Blue 24 2-4 51-101 white 28 4-6 44-67 yellow 35 8-10 45-65 Red 40 10-12 41-50 green 60 12-15 24-30 Note that there is an inverse relationship between FiO2 delivered by venture and the total gas flow  The FiO2 depends on the degree of air entrainment. ↓ entrainment →↑FiO2 is delivered.  This can be achieved by using smaller entrainment apertures or bigger ‘windows’ to entrain ambient air.  The smaller the orifice is, the greater the negative pressure generated, so the more ambient air entrained, the lower the FiO2.  The O2 conc can be 24, 28, 40 or 60%.  The total energy during a fluid (gas or liquid) flow consists of the sum of kinetic and potential energy. The kinetic energy is related to the velocity of the flow whereas the potential energy is related to the pressure.  As the flow of fresh O2 passes through the constricted orifice into the larger chamber, the velocity of the gas increases distal to the orifice causing the kinetic energy to increase. A 24% oxygen Venturi mask has an air : O2 entrainment ratio of 25 : 1 This means an oxygen flow of 2 L/min delivers a total flow of 50 L/min, well above the peak inspiratory flow rate. Deliver flow of 4-12 L/min (24-60% O2). For example, a 24% O2 Venturi mask has an air : oxygen entrainment ratio of 25 : 1. This means an O2 flow of 2 L/min delivers a total flow of 50 L/min, well above the PIFR. The mask’s side holes are used to vent the exhaled gases only (as above) in comparison to the side holes in the variable performance mask where the side holes are used to entrain inspired air in addition to expel exhaled gases. Designed for both adult & paediatric use. The Venturi attachments, with a reservoir tubing, can be attached to a tracheal tube or a supraglottic airway device as part of a T-piece breathing system. This arrangement is usually used in recovery wards to deliver O2-enriched air to patients.  Problems in practice & safety features 1. These masks are recommended when a fixed O2 conc (moderate requirements) is desired in pts whose ventilation is dependent on their hypoxic drive, such as those with COPD. However, caution should be exercised as it has been shown that the average FiO2 delivered in such masks is up to 5% above the expected value. 2. The Venturi mask with its Venturi device and the O2 delivery tubing is often not well tolerated by pts because it is noisy and bulky. 3. Its ability to deliver a high flow with no particulate H2O makes it beneficial in treating asthmatics, in whom bronchospasm may be precipitated or exacerbated by aerosolized H2O administration. 4. Aerosol devices should not be used with these devices. Water droplets can occlude the oxygen injector. If humidity is needed, a vapor-type humidity adapter collar should be used. Advantages Simple & light weight. Able to deliver a specific & consistent O2 conc to the pt under most circumstances, provided that the set O2 flow is above the minimum recommended by the manufacturer. The pt’s respiratory rate & pattern do not alter the FiO2. High flows come from RA, saving O2 Disadvantages Risk of hypoxia by under-delivering O2. High flows of O2 can lead to drying of airways. Less accurate at higher inspired conc of O2. At low O2 flows & very high inspiratory flows, the device stops behaving like a fixed performance O2 delivery device & may behave like a variable performance device. Expensive, uncomfortable, can not deliver high FiO2  Air-entrainment nebulizer (jet nebulizers or large volume nebulizers) Flow : input : 10-15 L/min→ output : 60 L/min FiO2 35-100% Have most of the features of air-entrainment nebulizers (AEMs) + additional humidification & T⁰ control. Humidification is achieved through production of aerosol at the nebulizer jet. T⁰ control is provided by an optional heating element. these 2 added features allow the delivery of particulate water (aerosol) (in excess of needs for body T⁰ & pressure) to the airways. How to assess whether the flow an air-entrainment nebulizer meets the pt’s needs? 1- simple visual inspection : With this approach (generally used only with a T tube), the RT sets up the device to deliver the highest possible flow at the prescribed FiO2 & observes the mist output at the expiratory side of the T tube. As long as mist can be seen escaping throughout inspiration, flow is adequate & the delivered FiO2 is ensured. 2- to compare it with the pt’s peak inspiratory flow. A pt’s peak inspiratory flow during tidal breathing is at least 3 times MV. As long as the nebulizer flow exceeds this value, the delivered FiO2 is ensured. If the pt’s peak flow exceeds that provided by the nebulizer, the device functions as a low flow system with variable FiO2. Advantages: provide humidification Disadvantages: ↑ infection risk, variable FiO2  The maximum gas flow through the nebulizer is 14 - 16 L/min. As with the Venturi masks, less room air is entrained with higher FiO2 values → total flow at high FiO2 values is decreased. To meet ventilatory demands, 2 nebulizers may feed a single mask to ↑ the total flow, and a short length of corrugated tubing may be added to the aerosol mask side ports to ↑ the reservoir capacity If the aerosol mist exiting the mask side ports disappears during insp, RA is probably being entrained, and flow should be increased. Circuit resistance can ↑as a result of water accumulation or kinking of the aerosol tubing. The ↑ pressure at the Venturi device →↓ RA entrainment, ↑ the FiO2 level, and ↓ total gas flow. If a predictable FiO2 level >0.40 is desired, an air-oxygen blender should be used. Air-oxygen blenders can deliver consistent and accurate FiO2 values from 0.21 to 1.0 and flows of up to 100 L/min with humidification. The higher flows tend to produce excessive noise through the large-bore tubing. Air-oxygen blenders are recommended for patients with increased minute ventilation who require a high FiO2 level and in whom bronchospasm may be precipitated or worsened by a nebulized H2O aerosol. With an artificial airway, a 15- to 20-inch reservoir tube should be added to the Briggs T-piece to prevent the potential of entraining air into the system. Single-unit and double unit mechanical aerosol systems Problem Your physician orders 40% O2 through an air-entrainment nebulizer to a pt with a tidal volume of 0.6 L & a RR of 33 breaths/min. If maximum nebulizer input flow is 12 L/min, will the pt receive 40% O2? If not, what total flow is needed to meet this patient’s needs? Solution 1. Estimate the patient’s inspiratory flow: Peak inspiratory flow=MV×3= 0.6×33×3=59.4 L/min 2. Compute the total flow of the nebulizer: Sum of ratio parts (3:1) × In put flow (12 L/min) = 48 L/min 3. Compare value 1 with value 2 (patient with nebulizer): 59.4 L/min (patient) > 48 L/min (nebulizer) Under these conditions, the pt does not receive 40% O2 To deliver a stable 40% O2 concentration, the total flow would have to be at least 59.4 L/min  In patients breathing at high inspiratory flow, conventional O2 sources result in additional air entraining around the mask, thereby diluting the O2 and lowering the FiO2. In addition, conventional delivery devices have other drawbacks that reduce their efficacy and tolerance such as insufficient humidification and warming of the inspired gas at high flows that cause patient discomfort.  Humidified high-flow nasal oxygenation A special type of nasal cannula that delivers warm & humidified high inspiratory flow of accurate O2 concentrations (better pt compliance). It acts as a fixed performance device. Its use in ICU, HDU, ORs and A&E has ↑ recently in attempts to ↓ incidence of tracheal intubation & mech vent, & as part of a controlled ventilation weaning strategy. Longer apneic oxygenation in cases of difficult intubation Components 1. Flow generator 2. Air/oxygen blender to adjust FiO2. 2. An active humidifier. 3. A single heated circuit of corrugated tubing. 4. A nasal cannula.  Indications 1. Acute hypoxemic resp failure 2. Acute hypercanic resp failure 3. Postop resp failure (in cardiothoracic, HFNC= NIV in preventing PPC) (hypoxemia occurs in 10-50% after major abdominal surgery dt derecruitment and basal atelectasis) 4. Acute heart failure, pul edema 5. Preintubation & postextubation oxygenation 6. Obstructive sleep apnea 7. Donot intubate pts (immunocompromised pts) 8. Viral bronchioloitits in children 9. Pulmonary fibrosia 10. Sepsis 11. Chest trauma 12. Astha, mild COPD with exacerbation  Clinical applications 1. acute hypoxemic resp failure (↓ dyspnea, ↑oxygenation, ↓invasive ventilation needs) 2. Immunocompromised pt with resp failure (↓ dyspnea, ↑oxygenation, ↓ intubation rates , may ↓ mortality) 3. Cardiogenic pul edema (↑oxygenation, ↓ cardiac afterload) 4. COPD exacerbation (↑ gas exchange, ↓ PaCO2) 5. Postextubation (↑ gas exchange, ↓ reintubation rates) (extubation in ICU is followed by reintubation in 12-14% of cases within 72 hours. NIV is recoomended. HFNC can be an alternative) 6. Resp procedures (↑oxygenation during endoscopic procedures) 7. Difficult intubation : transnasal humidified rapid insufflation ventilatory exchange (THRIVE) (extends safe apnea time to 17 minutes with PaCO2 ≈60-75 mmHg) 8. Weaning from mechanical ventilation (prevent post-extubation resp failure & ↓reintubation compared to conventional oxygen in low-risk pts)  Special populations Immunocompromised pts with ARF Acute hypoxemic resp failure is one of the most frequent reasons for ICU admission in immunocompromised pts. It is important to avoid intubation in these pts to limit the infectious complications related to invasive mechanical ventilation. Bundles to limit the risks of ventilator-induced lung injury and infectious complications reduced the mortality of invasively ventilated immunocompromised pts. However, ≈ 50% of intubated pts may die in hospital. Then, the role of noninvasive oxygenation strategies remains an important matter of debate in this setting. Compared to standard oxygen, NIV was not associated with better outcome in immunocompromised pts. HFNO in comparison to standard oxygen, nearly similar mortality rates but lower intubation rates. Most recent evidence indicates that therapeutic protocols for respiratory support in immunocompromised pts should not be different from those applied to non-immunocompromised pts with acute hypoxemic respiratory failure. In fact, thanks to the improvement in the prevention of infectious complications related to invasive mechanical ventilation and contrarily to what was previously thought, immunocompromised pts do not benefit from an approach aimed at avoiding endotracheal intubation and invasive ventilation at any cost.  Special populations Tracheostomised pts HFO can be delivered through a tracheostomy through a dedicated interface with an open circuit. Tracheal HFO at the highest flow rates (50–60 L/min) provides small degree of positive airway pressure, slightly improves oxygenation, and ↓ RR. These effects are, however, significantly milder than those of HFNO at similar flow rates. In tracheostomised pts, HFO delivered through a dedicated interface can → beneficial physiological effects and can ↓ the time to successful decannulation. Contraindications 1. Need for immediate mechanical ventilation 2. Low level of consciousness (GCS≤8) (can be used to facilitate intubation without desat) 3. Abnormalities or surgery in the face, nose or airway that preclude fitting of the nasal cannula 4. Post CPR or resp arrest  37 °C , 44 mg/L 100% RH Benefits Optimal Humidity High Flow Mucociliary Accurate O2 Washout of Low level Comfort Anatomical Dead PEEP Clearance delivery Space -Improves secretion Quality - ↓ re-breathing of exp In comparison to CO2 conventional facemask, – Create a reservoir of – Maintains mobility of HFNC improves fresh gas in the upper secretions for transport dyspnea, mouth airway, ready for the next out of the airway inspiration dryness, and overall comfort – Allow for better – ↓risk of resp ventilation &oxygenation infection ACCURATE O2 DELIVERY FACE MASK HFNC Conventional O2 therapy devices → Provide much lesser flows than insp flow rates Higher flows are not tolerated by the pts. Inconsistent FiO2s Masks & reservoirs increase the dead space Warm humid gas is associated with better conductance & pulmonary compliance compared to dry, cooler gas  Low level PEEP (1 mmHg for every 10 L/ min flow) ↓ cardiac preload Recruitment Hazards of poor humidification Dryness of secretions ↓ ciliary function Poor mucous flow Mucous plugging Airway obstruction Atelectasis Desaturation Washout of dead space Clear expired air from upper airway → ↓ rebreathing  HFNC clinical use algorithm Acute hypoxemic resp failure Check for criteria for immediate intubation (shock, hemodynamic instability) NO YES HFNC initiation Intubation & MV FiO2 1, flow 60 l/min, T◦ 37◦ C HFNC helps in perintubation oxygenation Monitoring within 1-2 hrs RR>25 bpm, SpO2 45 mmHg, pH 20 l/min on NRM @ 15 l/min, you may not be helping the pt as much as you think.  Bag valve mask (Resuscitation device) (should be available in every room) By Ambu, therefore Ambu bags. The primary benefit is the self-inflating bag→ can be used without a pressurized gas supply. Components : 1. Inflating bag 2. O2 inlet nipple & tube 3. Air intake valve 4. O2 reservoir 5. Non rebreathing (exp) valve 6. Standard 15 mm adapter for mask, ETT 7. PEEP valve 8. Down pop off valve (releases @ 60 cmH2O)  Uses: emergency ventilation (manual IPPV), with or without a pressurized gas supply. May also be used to ventilate via an ETT or LMA. Made of clear silicone & returns to its original shape when squeezed. Between the bag and the mask is a one-way ‘non-rebreathing’ valve which vents expired gases. Most valve designs permit both spontaneous & controlled ventilation. May be used with room air, or with supplementary O2 (@ 15 l/min). Most have an O2 reservoir to maximize the conc of insp O2. Portable, used during resuscitation, transport and short-term ventilation. A pediatric version exists with a smaller inflating bag & a pressure relief valve. Sniffing position + 2 hands (C&E maneuver + bag compression )…. ↑ inflating pressure → Gastric distension ↑ vent rates → ↑ intrathoracic pressure ≈12 breath /min , 6-7 ml/kg (≈500 ml) (1/4 of the bag volume) over 1-2 sec Most adult bags hold 2 litre. In hypoxic pts, ↑ FiO2 or add PEEP Tightly fit the mask Oro or nasopharyngeal airway are very helpful.  To achieve the highest possible FiO2 with a bag-mask device, the following always should be done: 1. Use an O2 reservoir of adequate size. 2. Set the O2 input flow at 10-15 L/min. 3. Deliver appropriate VT for a 1-second period (when using a mask). 4. Ensure the longest possible bag refill time. BVM devices provide 100% FIO2 during active PPV in pts with apnea. For spontaneously breathing pts, BVMs may provide an FIO2 >90% as long as a robust mask seal is maintained and room air admixture is minimal. If the mask seal is compromised, the pt will draw in room air around the mask during inspiration and significantly lower the FIO2. These bags can deliver an FiO2 >0.90 & TV values up to 800 mL when O2 flows to the bag are 10-15 mL/min. PEEP valves should be used for patients who require more than 5 cm H2O of PEEP. In spontaneously breathing pts, preoxygenation with a BVM and a good mask seal is better than a NRM at standard flow rates. Gastric inflation is a common hazard encountered when using a bag-valve device with a face mask. Gastric inflation can be minimized by providing low to moderate inspiratory flows (1 atm. Pressures during HBO therapy usually are expressed in multiples of atmospheric pressure absolute (ATA): 1 ATA = 1 bar = 760 mmHg = 760 torr = 100 kPa = 1030 cmH2O = 14.7 psi. Most HBO therapy is conducted at pressures 2-3 ATA, although other pressures may be used. These effects are mainly dt either high pressure or high O2 tension in body fluids & tissues.  High pressure: in conditions such as air embolism & decompression sickness, high pressure exerts a physical effect on air or N2 bubbles trapped in the blood or tissues → their size, & minimizing potential harm. Because pressure is crucial in these cases, HBO may be conducted at ≥6 ATA. Hyperoxia. When a pt is breathing RA, only a small amount of O2 dissolves in the plasma (≈ 0.3 mL/dl). However, At 3 ATA, it contains ≈ 7 mL/dl, a level (> average resting tissue uptake). O2 supply to the tissues affects the immune system, wound healing, & vascular tone. A tissue PO2 of at least 30 mm Hg is necessary for normal cellular function. Damaged & infected tissues often have a lower PO2. ↑ O2 supply to these tissues can help restore both WBC function & anti-microbial activity. Hyperoxia affects the CVS. HBO therapy causes generalized VC & a small ↓ in CO Although these changes may ↓ blood flow to a region, this effect is more than offset by the ↑O2 content. In conditions e.g, burns, cerebral edema, & crush injuries, VC may be helpful because it ↓ edema & tissue swelling whilemaintaining tissue oxygenation.  Hyperoxia also helps form new capillary beds (neovascularization). Although the exact mechanism is unknown, neovascularization is an essential component of tissue repair, especially in radiation-induced injuries. HBO may be useful in many other conditions, including the management of stroke, wound healing & treating stubborn soft tissue infections. Methods of Administration HBO is administered in either a multiplace or a monoplace chamber. A multiplace chamber is a large tank capable of holding a dozen or more people. Because pts are directly cared for by medical staff inside the tank, multiplace chambers have air locks that allow entry & exit without altering the pressure. The multiplace chamber is generally filled with air. If indicated, only the pt breathes supplemental O2 (through a mask or another device). Because they can achieve pressures ≥ 6 ATA , multiplace chambers are ideal for the management of decompression sickness & air embolism. A typical monoplace chamber consists of a transparent Plexiglas cylinder large enough only for a single pt. During therapy, the cylinder O2 conc is kept at 100%. The pt need not wear a mask. Because of the high O2 conc, most electronic equipment cannot be used in a monoplace chamber. In addition, many ventilators do not function properly under the high atmospheric pressures. However, monitoring systems & ventilators can be adapted to allow ttt of a critically ill pt with hyperbaric pressure. In addition, artificial airways suited to function properly under hyperbaric conditions should be used Air Embolism A complication thatcan occurwith certain CVS procedures, lung biopsy, hemodialysis, and central line placement. HBO can ↓ the size of air bubbles which may otherwise reach the cerebral or cardiac circulation & can cause symptoms or sudden death. Typical therapy involves immediate pressurization in air to 6 ATA for 15 – 30 minutes. This step is followed by decompression to 2.8 ATA with prolonged O2 ttt. Carbon Monoxide Poisoning The condition of a pt with CO poisoning improve quickly with HBO ttt because this ttt is the fastest way to remove CO from the blood. If a pt breathes air, it takes > 5 hrs to remove only ½ of the carboxyHb in the blood. Breathing 100% O2 ↓ this “half-life” to 80 minutes. The half-life of carboxyHb under HBO at 3 ATA is only 23 min. Contraindications for Hyperbaric O2 Therapy Congenital spherocytosis High fevers Hypercapnia (>60 mm Hg) Obstructive airway disease Optic neuritis Pneumothorax Seizure disorders Sinusitis Upper respiratory infections Viral infections Nitric oxide (NO) Mode of Action NO gas is a colorless, odorless, highly diffusible, & lipid-soluble free radical that oxidizes quickly to nitrogen dioxide (NO2) in the presence of O2. NO is normally produced in small amounts within the human body & activates guanylate cyclase, which catalyzes the production of cyclic guanosine 3′,5′- monophosphate (cGMP). The end result is increased cGMP levels that cause vascular smooth muscle relaxation. The therapeutic benefit of inhaled NO (iNO) stems from improved blood flow to ventilated alveoli. →↓ intrapulmonary shunting, improvement in arterial oxygenation, & ↓ PVR & PAP  Dosing For term & near-term neonates with hypoxic respiratory failure, the recommended dose is 20 ppm. Ttt should be continued until underlying oxygenation desaturation has resolved. For many pts, dosages often can be ↓ to