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Mechanical ventilation
- 1. Mechanical ventilation Hosam m Atef ; MD SUEZ CANAL UNIVERSITY
- 2. Introduction • Indications • Basic anatomy and physiology • Modes of ventilation • Selection of mode and settings • Common problems • Complications • Weaning and extubation
- 3. Indications • Respiratory Failure – Apnea / Respiratory Arrest – inadequate ventilation (acute vs. chronic) – inadequate oxygenation – chronic respiratory insufficiency with FTT
- 4. Indications • Cardiac Insufficiency – eliminate work of breathing – reduce oxygen consumption • Neurologic dysfunction – central hypoventilation/ frequent apnea – patient comatose, GCS < 8 – inability to protect airway
- 5. Basic Anatomy • Upper Airway – humidifies inhaled gases – site of most resistance to airflow • Lower Airway – conducting airways (anatomic dead space) – respiratory bronchioles and alveoli (gas exchange)
- 6. Basic Physiology • Negative pressure circuit – Gradient between mouth and pleural space is the driving pressure – need to overcome resistance – maintain alveolus open • overcome elastic recoil forces – Balance between elastic recoil of chest wall and the lung
- 8. Normal pressure-volume relationship in the lung http://physioweb.med.uvm.edu/pulmonary_physiology
- 9. Ventilation • Carbon Dioxide PaCO2= k * metabolic production alveolar minute ventilation Alveolar MV = resp. rate * effective tidal vol. Effective TV = TV - dead space Dead Space = anatomic + physiologic
- 10. Oxygenation • Oxygen: – Minute ventilation is the amount of fresh gas delivered to the alveolus – Partial pressure of oxygen in alveolus (PAO2) is the driving pressure for gas exchange across the alveolar-capillary barrier – PAO2 = ({Atmospheric pressure - water vapor}*FiO2) - PaCO2 / RQ – Match perfusion to alveoli that are well ventilated – Hemoglobin is fully saturated 1/3 of the way thru the capillary
- 12. CO2 vs. Oxygen
- 13. Abnormal Gas Exchange • Hypoxemia can be due to: – hypoventilation – V/Q mismatch – shunt – diffusion impairments • Hypercarbia can be due to: – hypoventilation – V/Q mismatch Due to differences between oxygen and CO2 in their solubility and respective disassociation curves, shunt and diffusion impairments do not result in hypercarbia
- 14. Gas Exchange • Hypoventilation and V/Q mismatch are the most common causes of abnormal gas exchange in the PICU • Can correct hypoventilation by increasing minute ventilation • Can correct V/Q mismatch by increasing amount of lung that is ventilated or by improving perfusion to those areas that are ventilated
- 15. Mechanical Ventilation • What we can manipulate…… – Minute Ventilation (increase respiratory rate, tidal volume) – Pressure Gradient = A-a equation (increase atmospheric pressure, FiO2,increase ventilation, change RQ) – Surface Area = volume of lungs available for ventilation (increase volume by increasing airway pressure, i.e., mean airway pressure) – Solubility = ?perflurocarbons?
- 16. Mechanical Ventilation Ventilators deliver gas to the lungs using positive pressure at a certain rate. The amount of gas delivered can be limited by time, pressure or volume. The duration can be cycled by time, pressure or flow.
- 17. Nomenclature • Airway Pressures – Peak Inspiratory Pressure (PIP) – Positive End Expiratory Pressure (PEEP) – Pressure above PEEP (PAP or ΔP) – Mean airway pressure (MAP) – Continuous Positive Airway Pressure (CPAP) • Inspiratory Time or I:E ratio • Tidal Volume: amount of gas delivered with each breath
- 18. Modes • Control Modes: – every breath is fully supported by the ventilator – in classic control modes, patients were unable to breathe except at the controlled set rate – in newer control modes, machines may act in assist-control, with a minimum set rate and all triggered breaths above that rate also fully supported.
- 19. Modes • IMV Modes: intermittent mandatory ventilation modes - breaths “above” set rate not supported • SIMV: vent synchronizes IMV “breath” with patient’s effort • Pressure Support: vent supplies pressure support but no set rate; pressure support can be fixed or variable (volume support, volume assured support, etc)
- 20. Modes Whenever a breath is supported by the ventilator, regardless of the mode, the limit of the support is determined by a preset pressure OR volume. – Volume Limited: preset tidal volume – Pressure Limited: preset PIP or PAP
- 21. Mechanical Ventilation If volume is set, pressure varies…..if pressure is set, volume varies….. ….according to the compliance…... COMPLIANCE = ∆ Volume / ∆ Pressure
- 22. Compliance Burton SL & Hubmayr RD: Determinants of Patient-Ventilator Interactions: Bedside Waveform Analysis, in Tobin MJ (ed): Principles & Practice of Intensive Care Monitoring
- 23. Assist-control, volume Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, & Wood LDH(eds.): Principles of Critical Care
- 24. IMV, volume-limited Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, & Wood LDH(eds.): Principles of Critical Care
- 25. SIMV, volume-limited Ingento EP & Drazen J: Mechanical Ventilators, in Hall JB, Scmidt GA, & Wood LDH(eds.): Principles of Critical Care
- 26. Control vs. SIMV Control Modes • Every breath is supported regardless of “trigger” • Can’t wean by decreasing rate • Patient may hyperventilate if agitated • Patient / vent asynchrony possible and may need sedation +/- paralysis SIMV Modes • Vent tries to synchronize with pt’s effort • Patient takes “own” breaths in between (+/- PS) • Potential increased work of breathing • Can have patient / vent asynchrony
- 27. Pressure vs. Volume • Pressure Limited – Control FiO2 and MAP (oxygenation) – Still can influence ventilation somewhat (respiratory rate, PAP) – Decelerating flow pattern (lower PIP for same TV) • Volume Limited – Control minute ventilation – Still can influence oxygenation somewhat(FiO2, PEEP, I-time) – Square wave flow pattern
- 28. Pressure vs. Volume • Pressure Pitfalls – tidal volume by change suddenly as patient’s compliance changes – this can lead to hypoventilation or overexpansion of the lung – if ETT is obstructed acutely, delivered tidal volume will decrease • Volume Vitriol – no limit per se on PIP (usually vent will have upper pressure limit) – square wave(constant) flow pattern results in higher PIP for same tidal volume as compared to Pressure modes
- 29. Trigger • How does the vent know when to give a breath? - “Trigger” – patient effort – elapsed time • The patient’s effort can be “sensed” as a change in pressure or a change in flow (in the circuit)
- 30. Need a hand?? Pressure Support • “Triggering” vent requires certain amount of work by patient • Can decrease work of breathing by providing flow during inspiration for patient triggered breaths • Can be given with spontaneous breaths in IMV modes or as stand alone mode without set rate • Flow-cycled
- 31. Advanced Modes • Pressure-regulated volume control (PRVC) • Volume support • Inverse ratio (IRV) or airway-pressure release ventilation (APRV) • Bilevel • High-frequency
- 32. Advanced Modes PRVC A control mode, which delivers a set tidal volume with each breath at the lowest possible peak pressure. Delivers the breath with a decelerating flow pattern that is thought to be less injurious to the lung…… “the guided hand”.
- 33. Advanced Modes Volume Support – equivalent to smart pressure support – set a “goal” tidal volume – the machine watches the delivered volumes and adjusts the pressure support to meet desired “goal” within limits set by you.
- 34. Advanced Modes Airway Pressure Release Ventilation – Can be thought of as giving a patient two different levels of CPAP – Set “high” and “low” pressures with release time – Length of time at “high” pressure generally greater than length of time at “low” pressure – By “releasing” to lower pressure, allow lung volume to decrease to FRC
- 35. Advanced Modes Inverse Ratio Ventilation – Pressure Control Mode – I:E > 1 – Can increase MAP without increasing PIP: improve oxygenation but limit barotrauma – Significant risk for air trapping – Patient will need to be deeply sedated and perhaps paralyzed as well
- 36. Advanced Modes High Frequency Oscillatory Ventilation – extremely high rates (Hz = 60/min) – tidal volumes < anatomic dead space – set & titrate Mean Airway Pressure – amplitude equivalent to tidal volume – mechanism of gas exchange unclear – traditionally “rescue” therapy – active expiration
- 37. Advanced Modes High Frequency Oscillatory Ventilation – patient must be paralyzed – cannot suction frequently as disconnecting the patient from the oscillator can result in volume loss in the lung – likewise, patient cannot be turned frequently so decubiti can be an issue – turn and suction patient 1-2x/day if they can tolerate it
- 38. Advanced Modes Non Invasive Positive Pressure Ventilation – Deliver PS and CPAP via tight fitting mask (BiPAP: bi-level positive airway pressure) – Can set “back up” rate – May still need sedation
- 39. Initial Settings • Pressure Limited – FiO2 – Rate – I-time or I:E ratio – PEEP – PIP or PAP • Volume Limited – FiO2 – Rate – I-time or I:E ratio – PEEP – Tidal Volume These choices are with time - cycled ventilators. Flow cycled vents are available but not commonly used in pediatrics.
- 40. Initial Settings • Settings – Rate: start with a rate that is somewhat normal; i.e., 15 for adolescent/child, 20-30 for infant/small child – FiO2: 100% and wean down – PEEP: 3-5 – Control every breath (A/C) or some (SIMV) – Mode ?
- 41. Dealer’s Choice • Pressure Limited – FiO2 – Rate – I-time – PEEP – PIP • Volume Limited – FiO2 – Rate – Tidal Volume – PEEP – I time Tidal Volume ( & MV) Varies PIP ( & MAP) Varies MV MAP
- 42. Adjustments • To affect oxygenation, adjust: – FiO2 – PEEP – I time – PIP • To affect ventilation, adjust: – Respiratory Rate – Tidal Volume MAP MV
- 43. Adjustments • PEEP Can be used to help prevent alveolar collapse at end inspiration; it can also be used to recruit collapsed lung spaces or to stent open floppy airways
- 44. Except... • Is it really that simple ? – Increasing PEEP can increase dead space, decrease cardiac output, increase V/Q mismatch – Increasing the respiratory rate can lead to dynamic hyperinflation (aka auto-PEEP), resulting in worsening oxygenation and ventilation
- 45. Troubleshooting • Is it working ? –Look at the patient !! –Listen to the patient !! – Pulse Ox, ABG, EtCO2 – Chest X ray – Look at the vent (PIP; expired TV; alarms)
- 46. Troubleshooting • When in doubt, DISCONNECT THE PATIENT FROM THE VENT, and begin bag ventilation. • Ensure you are bagging with 100% O2. • This eliminates the vent circuit as the source of the problem. • Bagging by hand can also help you gauge patient’s compliance
- 47. Troubleshooting • Airway first: is the tube still in? (may need DL/EtCO2 to confirm) Is it patent? Is it in the right position? • Breathing next: is the chest rising? Breath sounds present and equal? Changes in exam? Atelectasis, bronchospasm, pneumothorax, pneumonia? (Consider needle thoracentesis) • Circulation: shock? Sepsis?
- 48. Troubleshooting • Well, it isn’t working….. – Right settings ? Right Mode ? – Does the vent need to do more work ? • Patient unable to do so • Underlying process worsening (or new problem?) – Air leaks? – Does the patient need to be more sedated ? – Does the patient need to be extubated ? – Vent is only human…..(is it working ?)
- 49. Troubleshooting • Patient - Ventilator Interaction – Vent must recognize patient’s respiratory efforts (trigger) – Vent must be able to meet patient’s demands (response) – Vent must not interfere with patient’s efforts (synchrony)
- 50. Troubleshooting • Improving Ventilation and/or Oxygenation – can increase respiratory rate (or decrease rate if air trapping is an issue) – can increase tidal volume/PAP to increase tidal volume – can increase PEEP to help recruit collapsed areas – can increase pressure support and/or decrease sedation to improve patient’s spontaneous effort
- 51. Lowered Expectations • Permissive Hypercapnia – accept higher PaCO2s in exchange for limiting peak airway pressures – can titrate pH as desired with sodium bicarbonate or other buffer • Permissive Hypoxemia – accept PaO2 of 55-65; SaO2 88-90% in exchange for limiting FiO2 (<.60) and PEEP – can maintain oxygen content by keeping hematocrit > 30%
- 52. Adjunctive Therapies • Proning – re-expand collapsed dorsal areas of the lung – chest wall has more favorable compliance curve in prone position – heart moves away from the lungs – net result is usually improved oxygenation – care of patient (suctioning, lines, decubiti) trickier but not impossible – not everyone maintains their response or even responds in the first place
- 53. Adjunctive Therapies • Inhaled Nitric Oxide – vasodilator with very short half life that can be delivered via ETT – vasodilate blood vessels that supply ventilated alveoli and thus improve V/Q – no systemic effects due to rapid inactivation by binding to hemoglobin – improves oxygenation but does not improve outcome
- 54. Complications • Ventilator Induced Lung Injury – Oxygen toxicity – Barotrauma / Volutrauma • Peak Pressure • Plateau Pressure • Shear Injury (tidal volume) • PEEP
- 55. Complications • Cardiovascular Complications – Impaired venous return to RH – Bowing of the Interventricular Septum – Decreased left sided afterload (good) – Altered right sided afterload • Sum Effect…..decreased cardiac output (usually, not always and often we don’t even notice)
- 56. Complications • Other Complications – Ventilator Associated Pneumonia – Sinusitis – Sedation – Risks from associated devices (CVLs, A- lines) – Unplanned Extubation
- 57. Extubation • Weaning – Is the cause of respiratory failure gone or getting better ? – Is the patient well oxygenated and ventilated ? – Can the heart tolerate the increased work of breathing ?
- 58. Extubation • Weaning (cont.) – decrease the PEEP (4-5) – decrease the rate – decrease the PIP (as needed) • What you want to do is decrease what the vent does and see if the patient can make up the difference….
- 59. Extubation • Extubation – Control of airway reflexes – Patent upper airway (air leak around tube?) – Minimal oxygen requirement – Minimal rate – Minimize pressure support (0-10) – “Awake ” patient
Editor's Notes
- This presentation will review the basics of mechanical ventilation. First there will be a review of the indications for mechanical ventilation, followed by a brief review of basic anatomy and a more extensive discussion of the physiology of gas exchange in the lungs. Different modes and settings on the ventilator will be examined as well as some problems and potential solutions. After a section on complications related to mechanical ventilation, the process of weaning and extubation will be reviewed.
- Patients are often (ideally) intubated before they reach the point of respiratory failure. Respiratory distress can be due to inadequate ventilation, oxygenation or a combination thereof. The process can be either intrinsic to the lungs (pneumonia, for example) or to the chest wall (“pump failure”, as in muscular dystrophies). For some patients, the work of breathing may be such that they are unable to gain weight even in the face of adequate ventilation and oxygenation.
- Not every patient who is intubated has a primary pulmonary pathology. For patients in cardiogenic shock or with CHF, the demands of the respiratory system may precipitate cardiovascular collapse. Supporting the patient with mechanical ventilation can reduce the demands on the heart, allowing it to recover. Intubation can also serve to protect the airway for those who cannot do it themselves. Mechanical ventilation offers the option of hyperventilation for patients with intracranial hypertension.
- Remember that the upper airway is a significant site of resistance and this can be added to by iatrogenic devices (nasogastric tubes) or relieved by other devices (nasal trumpets). When delivering a gas to any patient, give it the way nature does - give it humidified. The lower airways can be broken down into dead space and the sites where gas exchange occurs. Anything that increases dead space (e.g., PEEP) will impact upon ventilation unless it also increases the area where gas exchange occurs.
- During inspiration the gradient becomes more negative as you approach the alveolus. This is an active process; part of the energy used for inspiration is stored in the tissues. This is used in exhalation, which is effectively a passive process. Recall that work = volume x pressure. For infants with their more compliant chest wall, they will have a proportionally greater work of breathing which helps predispose them to respiratory distress. The point at which the recoil between the alveolus and the chest wall is balanced is equivalent to functional residual capacity. I wanted to try to give some background to this slide without getting too weighed down in the physiology of breathing and respiratory failure. Besides, it always confuses me.
- http://www.biology.eku.edu/RITCHISO/301notes6.htm
- http://physioweb.med.uvm.edu/pulmonary_physiology/ Note that the compliance characteristics of the system (T) is the sum of the compliance curve for the lung (L) and of that for the chest wall (W). At FRC the total pressure in the system is zero - the outward recoil of the chest wall balances the tendency for the alveolus to collapse.
- The partial pressure of carbon dioxide in the arterial blood is directly related to metabolic production and indirectly related to minute ventilation. To be accurate, it is alveolar minute ventilation that matters. When a child is tachypneic, the minute ventilation may not change since the increase in rate is balanced by a decrease in tidal volume. However, the amount of dead space has not changed so the effective tidal volume will decrease and hence the effective minute ventilation and thus PaCO2 will increase despite the increased respiratory rate. Likewise, any process that increases dead space without changing minute ventilation will result in an increase in PaCO2 .
- To be simplistic, oxygenation involves getting enough oxygen to an alveolus that is perfused. The more volume of gas that can be delivered for exchange, the better. The higher the driving pressure for that gas exchange, the better. Ideally, ventilation (V) and perfusion (Q) are matched so that oxygen is where the blood is (V/Q = 1). When gas exchange does take place, it is so rapid that a hemoglobin molecule passing through an alveolar capillary is fully saturated before it is one third of the way across. The rest of the capillary represents a reserve for when transit time is increased (e.g., tachycardia) or for when diffusion is slowed (e.g., pulmonary edema, fibrosis) so that hemoglobin still may be fully saturated when it exits the capillary. [I made this slide to replace the old one that listed factors that affect the rate of gas exchange. I agree that V/Q mismatch will be hard to do well but it is important. I can’t believe that I never realized it wasn’t in my original set of slides. I tell residents that saying “V/Q mismatch” in response to any respiratory question in the ICU will usually be right………What I would like to try to do is to link the physiology of normal gas exchange to abnormal gas exchange and then link that to what we do with the vent…..I.e., increase PEEP to increase area for gas exchange and improve oxygenation, etc etc. This will be tough to do without discussing V/Q mismatch. For what it is worth, here is my attempt at this….]
- http://www.biology.eku.edu/RITCHISO/301notes6.html The sigmoidal shape of the oxygen disassociation curve is of critical importance. Hemoglobin can only carry so much oxygen (1.34 ml per gram of hemoglobin) regardless of high the PaO2 may be. Furthermore, dissolved oxygen contributes very little to oxygen content (0.003 ml oxygen/dL/mmHg PaO2 ). As a result, increasing the PaO2 oxygen in oxygenated blood cannot overcome the effect of shunted blood that is deoxygenated and the patient will be desaturated to a degree proportional to the magnitude of the shunt. I am going to see if I can scan the curve for carbon dioxide and put it after this slide…..This would be the text for that slide…...
- The disassociation curve for carbon dioxide is far more linear and is steeper. As a result, there is much less of a limit on how much carbon dioxide can be carried by hemoglobin and exchanged at the alveolar-capillary barrier. Since carbon dioxide is also far more soluble than oxygen (by a factor of 20), dissolved CO2 contributes significantly -about 10% - to the amount that is exchanged at the alveolus. For these reasons, PaCO2 is not affected by shunt or diffusion barriers as is oxygen (and explains why a child with cyanotic heart disease is hypoxemic but not hypercarbic).
- As outlined in the preceding slides, hypoxemia (not hypoxia) can be the result of hypoventilation (not enough delivered) or not matching the delivery to the loading sites (V/Q mismatch). Shunt, whether intracardiac or intrapulmonary, is the ultimate form of V/Q mismatch (V/Q = ). Diffusion impairments must be significant to result in hypoxemia and are rarely of clinical relevance in pediatrics. Hypoventilation is the primary cause of hypercarbia. V/Q mismatch must be profound before hypercarbia results for the reasons discussed in the previous slide.
- Maneuvers designed to improve V/Q are beyond the scope of this introductory lecture. Suffice to say, it is hard to selectively manipulate one area of the lung without affecting the entire system. For example, inhaled bronchodilators improve ventilation by relieving bronchospasm; they can also improve perfusion by producing vasodilatation in the alveolar capillary and thereby improve V/Q mismatch. However, there can be systemic absorption of these bronchodilators; this can lead to vasodilatation of vessels that were vasoconstricted secondary to hypoxia. The result is worsening V/Q mismatch and hypoxemia. The last sentence is awkward on the slide …..as you said, V/Q will be tough to do……I would also like to try and get the topic of proning in briefly later on…the whole idea of “good lung down” or is that up? I think would be hard to do if we want to keep this at 50-60 slides…..should we just mention it but not discuss it ?
- We can manipulate the same things a patient does - increase the respiratory rate and tidal volume for each breath. We can also try to keep alveoli from collapsing (as a baby does when they grunt)with positive end expiratory pressure. Unlike patients, we can manipulate the FiO2 or even the atmospheric pressure. We can also try to open up collapsed areas by applying increased positive pressure. Remember that an alveolus that has collapsed will require a greater amount of pressure for a given change in volume than an alveolus that starts at FRC (see the section on compliance). Increasing the area available for gas exchange improves oxygenation and ventilation. Perflurocarbons are experimental drugs; they are liquids through which oxygenation and ventilation can occur; one of their advantages is that oxygen is more soluble in perflurocarbons than it is in air. A full discussion of perflurocarbons is beyond the scope of this lecture. Use this slide to bride pathophsy and vents…..
- Most ventilators used in pediatrics are time cycled and operate either in a pressure limited or volume limited mode. Flow cycled ventilators are available but not commonly used. As almost all of my experience is with servo’s I do not know of any time-limited vents….what would be the difference between a flow-limited and time-cycled vent and a time-limited flow cycled vent? Should we clean up this slide and just say you can limit by pressure or volume and cycle by flow or time?
- These are some of the basic terms used with ventilators. CPAP is equivalent to PEEP except the term is usually used when referring to patients who are not intubated (i.e., on nasal CPAP).
- In a control mode, the ventilator will guarantee that the patient receives the set tidal volume or PAP with every breath. The patient can breathe “above” the set rate but will receive full support regardless of their effort.
- IMV modes support breaths only at the set rate and interval. If the set rate is 10, then every six seconds the patient will receive a machine triggered breath (synchronized to their own effort if the mode is SIMV). In between those 10 breaths, the patient is free to breathe but those breaths are not supported. These breaths can be supported with pressure support (see more below). Lastly, the vent may not give any breaths at all but support the patient’s spontaneous efforts - this is pressure support/CPAP. Newer machines allow for the pressure support to be fixed (e.g., 10 mmHg) or variable (enough support so that the patient receives a tidal volume of 200cc).
- As stated before, the limit of support can be volume or pressure.
- If one parameter is set, then the other will vary as dictated by the patient’s compliance. The parameter that varies can be followed as an index of the patient’s compliance.
- Ref: Burton SL and Hubmayr RD: Determinants of Patient-Ventilator Interactions: Bedside Waveform Analysis,s in Tobin MJ (ed): Principles and Practice of Intensive Care Monitoring. New York, McGraw-Hill, Inc, 1998, p. 656. Note that the FRC rests on a favorable part of the compliance curve. Small changes in pressure result in large changes in volume. If a patient’s compliance is on this part of the curve, then a given tidal volume will result in low peak pressures. If the compliance worsens (i.e., moves to the left or far right) then the pressure needed to deliver that same tidal volume will increase and the PIP will increase. The same is true if a set pressure is delivered - as compliance improves, the tidal volume will increase. If compliance worsens then a smaller tidal volume will result for the same PAP. Ideally, you want the alveolus to be at the bottom inflection point (FRC) at the beginning of each breath (end of each breath).
- Ref: Ingento EP and Drazen J: Mechanical ventilators, in Hall JB, Scmidt GA, and Wood LDH(eds.): Principles of Critical Care. New York, McGraw-Hill, Inc., 1992, p.144. In assist control modes (pressure control, volume control), the machine will deliver a full breath whether it is triggered by patient effort (note the negative deflection in the uppermost graph indicating patient effort) or triggered by the machine (the machine will act if a set amount of time (T) elapses without discernible patient effort).
- Ref: Ingento EP and Drazen J: Mechanical ventilators, in Hall JB, Scmidt GA, and Wood LDH(eds.): Principles of Critical Care. New York, McGraw-Hill, Inc., 1992, p.145. “Positive pressure, volume-cycled breaths are delivered at a preset rate similar to control mode ventilation, except that between breaths, the inspiratory valve to the patient is open, allowing for spontaneous breathing.”
- Ref: Ingento EP and Drazen J: Mechanical ventilators, in Hall JB, Scmidt GA, and Wood LDH(eds.): Principles of Critical Care. New York, McGraw-Hill, Inc., 1992, p.146. (Would we also want to put slides with pressure mode graphs as well to show the different flow characteristics ??) During SIMV, the ventilator divides time by the set rate to determine cycle-length. During the early part of this cycle, the patient may breath spontaneously without support. During the terminal phase of this cycle (% varies by manufacturer) the ventilator will synchronize a full breath with detected effort by the patient.
- Control modes are used when complete control over the patient’s ventilation and/or oxygenation is desired. This is usually because the patient’s lung disease is significant enough that you that you wish to give maximal support. Another scenario may be one in which you want to precisely control the PaCO2, as in hyperventilation for increased intracranial pressure. Patients placed on control modes are often deeply sedated and may be given neuromuscular blockers. SIMV modes are chosen when you want the patient to do as much work as they can tolerate and try to minimize the support from the ventilator. SIMV modes are used to wean patients; as you decrease the set rate, the patient will need to do more on their own to maintain normal blood gases. In control modes, if you decrease the rate, the patient’s spontaneous efforts will be fully supported so you will not know how much of that particular tidal volume they are generating on their own. Note that for the paralyzed patient there is no significant difference between assist control and SIMV.
- PRESSURE-LIMITED I would not say that I have limited ability to affect ventilation in PC, though I may choose to increase the PAP recognizing that I accept the potential for increased baro/volutrauma at the same time I also accept that I may suffer a decrease in ventilation with changes in compliance. VOLUME-LIMITED Accept that changes in compliance may lead to increases in peak airway pressures and associated baro/volutrauma.
- Whichever mode one chooses, one needs to be aware of the limitations of that mode. In pressure modes, the tidal volume can drop resulting in hypoventilation or it can increase, leading to overdistention. With volume modes, the peak pressure can increase, resulting in barotrauma if the pulmonary compliance worsens. Regardless of the parameter that is controlled, the other must be monitored as it is a reflection of the compliance and hence the patient’s pulmonary function. Increasing peak pressures on volume mode (or decreasing tidal volumes in pressure modes) can also be a sign that the ETT is obstructed or of another problem with the ventilator circuit.
- Ventilators deliver breaths when they are told to do so. This occurs when a certain amount of time has elapsed (e.g., 5 seconds if the rate is 12 [60 sec/12 b/m = 5 sec]) or when the patient makes an effort. A patient’s effort may be sensed as a change in pressure in the circuit (negative deflection) or as a change in flow (also a negative deflection). Flow sensors tend to have a more rapid response time. The amount of support delivered with a patient triggered breath will depend on the mode (assist control vs. IMV vs. SIMV) and the amount of pressure support that is set.
- A patient needs to generate a certain amount of work in order to trigger it. Additionally, a patient has to breathe through an ETT that is almost always narrower than their own airway and ventilate the increased dead space imposed by the vent circuit. A patient may not be able to generate adequate tidal volumes for these reasons. To compensate for this increase in the work of breathing, pressure support is given. The ventilator generates pressure support by adding flow to the circuit during patient-triggered breaths in IMV or SIMV modes. This does not make it easier for the patient to trigger the ventilator but it does help the patient generate larger tidal volumes. Pressure support usually terminates when the flow in the circuit is 25% of the peak flow.
- As ventilator technology has advanced, newer modes have been developed. Some are variations of volume or pressure modes and some are completely unrelated to conventional mechanical ventilation. It is important to recognize that none of these modes have been shown to be better than another or to reduce mortality for any disease.
- This mode combines the benefit of a volume mode (guaranteed minute ventilation) with the benefits of a pressure mode (decelerating flow pattern and a lower PIP for the same tidal volume as compared to volume control).
- This mode is designed for spontaneously breathing patients. The machine adjusts the pressure support given with each breath so that a minimal tidal volume and minute ventilation will be achieved. As the patient improves, the amount of pressure support given will decrease. If the patient worsens, pressure support will be increased - smart pressure support. Other modes are available in which the amount of pressure support given is adjusted to the patient’s effort as compared to the actual tidal volume generated. Overall, the principle is the same - the amount of support varies in relation to the patient’s efforts.
- I am not sure how clear this is and if we should even include a discussion of it…as far as I know it is only available with the Drager and I have never used it (have contemplated its use)….. A somewhat complex mode. Two different levels of CPAP are given. The patient can breathe spontaneously at either level and at their own rate. The CPAP is “released” to a lower pressure at set intervals to avoid hyperinflation of the lungs.
- By increasing I-time, the MAP will move closer to the PIP although the PIP has not changed. This is one way to increase MAP (and thereby oxygenation) without increasing the PIP (and thereby limiting barotrauma).
- I call it a “rescue” therapy but I am not sure if this is accurate…..could we use a second slide on this ?…. A mode completely unrelated to conventional mechanical ventilation. Breaths are delivered at a rate of 3-10 Hz (180-600 breaths/min) with tidal volumes that are less than anatomic dead space. For reasons that remain unclear, it is believed that there is less barotrauma with this mode. Proposed mechanisms of gas exchange include bulk flow, molecular diffusion and pendelluft effect (lung units that fill rapidly empty into lung units that fill slowly and vice versa).
- Although the oscillator is used aggressively in some institutions, it has not been conclusively shown to be more effective than conventional mechanical ventilation. In addition, the care of patient’s on the oscillator demands skill and experience. Having said that, the oscillator is thought to be less injurious to the lungs. By oscillating around the MAP, cyclic overdistention of the lungs can be avoided and lung recruitment is easier to achieve.
- Positive pressure can be delivered to a patient either through a face mask or nasal prongs, not just an ETT. Pressure modes are used; a back up rate can be set. Benefits of NIPPV include a decreased need for sedation and the ability to avoid intubation. NIPPV can be used to support patients with obstructive sleep apnea at night, as a bridge from mechanical ventilation or in patients with ARDS as a primary mode of support.
- The initial settings for both volume and pressure are similar with one exception - you set a tidal volume or a peak pressure (or PAP). A starting tidal volume is usually 10-12 cc/kg. The starting PAP is what is needed to adequately move the patient’s chest and to generate breath sounds. This number can be between 15-20 mmH2O above PEEP.
- The starting breath rate is usually one that would be physiologically appropriate for the patient. The starting number may be increased or decreased as dictated by the clinical situation. Immediately after intubation, patients are placed on an FiO2 of 100% (1.00 to be accurate). This can be weaned down as long as the oxygen saturation remains acceptable. PEEP usually is set at 5 mmH2O and then increased as needed to achieve acceptable oxygen saturation with a FiO2 &lt;0.6. In some cases (asthma, head trauma), the PEEP may be set at 3 mmH2O to start. Most patients are started off in an SIMV mode. If their clinical situation worsens, the mode may be changed to assist control to decrease their work of breathing and give the clinician more precise control over ventilatory function.
- The decision to choose volume or pressure as a mode is based on what the clinician is more interested in directly affecting. Volume modes offer a guaranteed minute ventilation while pressure modes allow one to directly manipulate the MAP. In infants less than 5-10 kgs., pressure modes are usually chosen due to the inability of the ventilator to give small volumes (&lt;50 cc) accurately.
- Clinical situations may not always allow for such a tidy paradigm. If a patient is hypoventilating as a result of sedation, oxygenation will improve if minute ventilation is increased. Needless to say, increasing the FiO2 in this scenario would also improve oxygenation. Likewise, the patient with tracheomalacia will have improved ventilation if PEEP is applied to stent open the airway.
- PEEP has many uses. It can be used to help recruit alveoli that have collapsed or prevent alveolar collapse. By maintaining lung volume (or recruiting lung volume) PEEP can improve oxygenation and ventilation. It also can stent open areas of malacia and thereby improve ventilation and oxygenation even if these areas in of themselves do not participate in gas exchange.
- No good deed ever goes unpunished. Lung function is a dynamic process; improving one thing might worsen another. PEEP can be used to prevent alveolar collapse in cases of pulmonary edema. However this same distending pressure is applied to anatomic dead space, which is then increased. Hence, ventilation may worsen. Usually it won’t because the increase in alveolar tidal volumes outweighs the increase in dead space. PEEP can also impair cardiac output (see below) and in severe cases, this can result in worsening hypoxemia. A difficult circumstance to face is the patient with asthma and respiratory failure. These patients often require long inspiratory and expiratory times for effective gas exchange. Increasing the rate when the patient is hypercarbic may in fact worsen the PaCO2. This is because at higher rates, the lung has less time to empty completely back to FRC. Air is trapped in the alveolus and the alveolus becomes overdistended. Ventilation in neighboring alveoli can become impaired and overall, ventilation worsens even though the rate has been increased. This is an example of dynamic hyperinflation. Both these scenarios are examples of how changing one parameter on the ventilator can have a number of effects, not all of which are desirable.
- Nothing ever replaces the clinical exam. Look at the patient and listen to judge for yourself how the patient is doing. Does the patient appear pink and well perfused? Has the respiratory rate of the patient decreased? Is the chest moving? Are breath sounds present and equal? Now look at the pulse oximeter; send an ABG and maybe check an end-tidal CO2. These tests are used more often than not to confirm your clinical impression. They certainly have a role when the clinical exam may be indeterminate and they can be more sensitive in detecting small changes. A chest x-ray can be used to confirm that the tube is in good position and can be used to follow the progression of the patient’s disease process. Chest x rays may also be helpful if there are acute changes, such as a pneumothorax or right upper lobe collapse. The ventilator can also be a source of information. Is it delivering what it is set for? Has the PIP increased suddenly? Has the expired tidal volume dropped? A significant difference between the inhaled tidal volume and exhaled tidal volume may be indicative of a leak within the circuit.
- Just as examining the patient yourself is vital so is ventilating the patient yourself. Doing this allows you to decide if it is the patient or the ventilator that is the source of the problem. It is easy or hard to bag the patient? How long does it take for the lungs to exhale? Is it easy to bag after the patient has been suctioned or repositioned? This is a good example of one of the prime rules of critical care - always check your equipment.
- When trying to decide where the problem is, remember the ABC’s. ETTs can become obstructed with secretions or be dislodged if the patient moves (or is moved). Leaks can develop around the ETT, resulting in hypoventilation. Mucus plugs can block lower airways as easily as they can obstruct ETTs. Bronchospasm or a pneumothorax may cause more of an acute change as compared to pneumonia or atelectasis. If evidence of a tension pneumothorax is present (tachycardia, hypotension, absent breath sounds on one side, deviated trachea and distended jugular veins) needle thoracentesis is indicated emergently. Cardiovascular compromise can worsen pulmonary function. Cardiogenic shock may lead to pulmonary edema with worsening compliance. Tachypnea can be an early sign of sepsis; patients with impaired respiratory function may not be able to handle this burden and progress (or regress as the case may be) to respiratory failure. Just as an adequate amount of gas must be brought to the alveolus for exchange, so must an adequate blood supply be present. This is a rare cause of respiratory dysfunction due to the low resistance in the pulmonary bed. An extreme example is cardiac arrest - without any forward flow, there is no blood to oxygenate regardless of the alveolar PO2.
- If the patient is not responding in the way that you expect them to and you have ruled out the previously mentioned causes, you have to re-assess your original decisions. Does the patient need more support? Are they weaker than you expected? Are they still sleeping off the 20 mg of Ativan that the ER gave them for status epilecticus? Have you controlled the bronchospasm? Are there air leaks in the circuit? How about in the patient (pneumothorax, etc.) ? Can the patient work with the ventilator(see more below) ? Perhaps the patient is not working with the ventilator because they are ready to be extubated and would prefer to breathe without a tube in their throat. The work of breathing on a ventilator may be greater than the work of breathing imposed by the disease process. This can be seen especially with small infants. Lastly, is the vent working properly - check that equipment!
- In order for a patient to breathe comfortably on the ventilator, their demands must be recognized and quickly met. The delay between recognition of a patient’s effort and the opening of the inspiratory valve has decreased markedly with newer generation ventilators. The less work the patient needs to do to trigger the vent, the more work they can spend on generating a tidal volume. Also, the ventilator and patient should not conflict. That is to say that the ventilator should not try to give a breath when a patient is exhaling. You do not want a situation in which both the ventilator and the patient are working hard - one should be asked to work less. If the patient is ready to do more, than decrease the vent settings. If the patient is not ready, then increase the settings in order to decrease the patient’s distress.
- Okay, you have now dismissed the vent as the source of the problem; there doesn’t appear to be any patient-ventilator dysnchrony and any acute problems have been addressed. You are left with a patient that has unacceptable ventilation and/or oxygenation. What can you do? Recall the basics - you can increase the FiO2 or PEEP to improve oxygenation; you can increase the rate or tidal volume to increase ventilation. Before deciding what to do, you must first decide what the problem is. Is hypercarbia due to inadequate tidal volumes? Is there increased dead space? Has the metabolic production of carbon dioxide changed? Is the worsening oxygenation due to increased V/Q mismatch? Is this due to decreased ventilation? Is there increased dead space? Increasing the PEEP may improve alveolar ventilation to a greater extent than it increases dead space. Increasing the rate may improve alveolar ventilation such that both oxygenation and ventilation improve. Increasing the FiO2 may be all that is needed to bring the SaO2 back to an acceptable level.
- What is an acceptable level of PaO2 or PaCO2 ? Like so many things in life, an acceptable level is often determined by what you are willing to do to get there. Ideally, a patient should have a SaO2 greater than 95%. If this can be accomplished with a PEEP of 7 and an FiO2 of &lt;0.60, that would be acceptable. If achieving a SaO2 greater than 95% means that the PEEP is 12 and the FiO2 is 1.0, this is not acceptable. Along these same lines, if achieving a PaCO2 of 40 mmHg results in a peak pressure of 30 mmH2O, this is acceptable. Peak pressures greater than 35-40 mmH2O are not as acceptable. In general, the upper limit for an acceptable FiO2 is 0.60; peak pressures ideally would be less than 35-40 mmH2O; PEEP should probably be kept at 15 mmH2O or less. Recognize that these limits are arbitrary in nature and no study has ever demonstrated what a safe PIP or FiO2 is. Furthermore, these “limits” must be made in the context of the patient’s clinical situation and expected clinical course. When you reach your limits with the ventilator, you must decide to either exceed these limits or change your goals. PaCO2 is somewhat easier to deal with. Hypercarbia in of itself does not pose much danger (CO2 narcosis should not be of concern for a patient on a ventilator). It does result in a respiratory acidosis. One must decide what pH they will accept. Some may accept a pH of 7.20, other 7.30, still others in between or even lower than 7.20. You can buffer the pH with bicarbonate or let the kidneys do it for you and accept the metabolic alkalosis. Again, the clinical situation must be taken into account - you will not accept the same PaCO2 for the child with ARDS as you would for the child with head trauma. You may also want a normal pH if the patient is receiving vasopressor support. Oxygen can be somewhat trickier. The body has a significant ability to tolerate decreases in oxygen delivery without a change in oxygen consumption. When this changes however can be difficult to predict, especially in critically ill patients, who may have altered delivery-consumption relationships. Recall that contributes very little to oxygen content. Also, increasing the SaO2 from 90% to 95% increases oxygen content by 6% but may require significant increases in ventilatory support. If you increase the hemoglobin from 9 mg/dL to 12 then you have increased oxygen content by 33%. For this reason a SaO2, of 88-90% may be tolerated if an acceptable hematocrit is maintained. Again these numbers are arbitrary and this strategy has never been proven to decrease mortality. For the patient in shock, you may want a greater than 93%. For the patient with cyanotic heart disease, a of 70% may be acceptable. Decide what you want and what you will pay (or what the patient can pay).
- There are options beyond adjusting the ventilator. We will briefly touch on the concept of proning. It is well established that atelectasis develops in the dorsal areas of the lung when patients are supine for any extended period of time. “Flipping” a patient can help re-expand these collapsed areas and improve alveolar ventilation and hence gas exchange. Additionally, the chest wall has a more favorable compliance curve in the prone position. Most patients will usually have improved oxygenation when prone and can tolerate being prone for 20 hours at a time. It has not been established that proning improves mortality but it can be useful in the patient that is difficult to oxygenate.
- Nitric oxide was originally thought to be the “magic bullet” for ARDS and other forms of severe respiratory failure. Given its ability to vasodilate blood vessels, be delivered as a gas (act on blood vessels that perfuse ventilated alveoli - selective pulmonary vasodilatation) and its short half-life (no systemic hypotension), it was studied with great interest. iNO does improve oxygenation in ARDS, it just doesn’t improve outcome. It does have more of a beneficial effect in patients with pulmonary hypertension, especially neonates with persistent pulmonary hypertension of the newborn or post-operative cardiac patients.
- Positive pressure ventilation can be injurious to the lungs, which were designed as a negative pressure circuit. What exactly qualifies as a dangerous pressure or even what is the best pressure to follow is not exactly known. Recently, a plateau pressure of &gt;35 mmH2O has been proposed as a limit. Plateau pressures are measured during an inspiratory “pause” - the lungs are kept inflated but there is no gas flow occurring. Also, recent studies have demonstrated that cyclic overdistention/collapse of an alveolus can contribute to lung injury by causing the release of inflammatory mediators. You want to keep the alveolus on the steep part of the compliance curve - not ride between the bottom plateau and the upper plateau (refer to slide #22). See below for the side effects of PEEP. What constitutes a safe FiO2 is also not exactly known. 0.60 is an acceptable limit to some, albeit arbitrary. Oxygen toxicity results in the production of free radicals with resulting cell damage and death.
- Increasing the intrathoracic pressure, as mechanical ventilation does, has several effects on the heart. First and foremost, it decreases venous return to the right side of the heart and subsequently to the left side of the heart. Patients may need a higher CVP to maintain cardiac output. Positive pressure also causes the interventricular septum to bow to the left, which decreases the filling capacity of the left ventricle and thus its output. Positive pressure does decrease the afterload the LV faces. This can be of use in patients with left heart failure. The effects on right sided afterload depend on the lung volumes. If positive pressure increases the total lung volume to FRC then pulmonary vascular resistance will decrease (as hypoxic vasoconstriction is relieved) and right sided afterload will decrease. If positive pressure increases lung volumes beyond FRC, then overdistended alveoli will compress blood vessels, increasing PVR and right sided afterload. More often than not, a patient will have decreased cardiac output when on positive pressure. This can often be ameliorated by fluid administration. The degree of cardiac compromise may often limit the amount of PEEP a patient can tolerate and hence what you are willing to use.
- Other complications from mechanical ventilation are as listed. [Should we discuss post-extubation stridor and laryngeal edema or leave that for the folks doing the airway talk?]
- In truth, you are always weaning a patient in the sense that you are always trying to minimize the ventilator settings. “True” weaning implies a different expectation - that the patient is improving and will soon not need mechanical ventilation. This usually happens when the disease process is improving or resolved and the patient has acceptable parameters. It is important to assess the ability of the heart to handle the increased demands that extubation may place upon it (e.g., pneumonia/ARDS has resolved but significant septic shock with cardiovascular collapse is present).
- Weaning is really the transfer of demands from the ventilator to the patient. By decreasing the rate, the FiO2 and the PEEP, you are asking the patient to do more. The rate at these parameters are decreased will often depend on the acuity of the disease process. The patient who was intubated because of sedation secondary to a drug overdose may wean rapidly when they are awake as compared to the child recovering from ARDS who may take weeks to completely wean from mechanical ventilatory support. The rate can be decreased in increments of 2-5 breaths/minute (or more) as dictated by the clinical situation. An arterial blood gas or end tidal CO2 monitor can be used to assess the PaCO2 after these changes. PEEP is generally lowered in increments of 1-2 mmH2O per change. As changes in oxygenation or ventilation may not be immediately apparent after a decrease in PEEP, these changes are not made more often than every 6-8 hours. [fair statement?]
- When is a patient ready to be extubated? First, they must be able to protect their airway. They should have an acceptable SaO2 on an FiO2 of no more than .30-.35. They should be breathing at a comfortable rate with a set ventilator rate of 5-8. Patients may be trialed on just pressure support/CPAP to make sure they are generating an adequate spontaneous minute ventilation. The amount of pressure support should be just enough to compensate for the added work of breathing imposed by the vent and ETT. The PEEP should be at 5 mmH2O. If these are the circumstances, then the patient is ready for an attempt at extubation and their time on mechanical ventilation (and this presentation) has come to an end.