Basics of Mechanical Ventilation

Key points

• At end inspiration ( inspiratory pause), there is no flow and hence, airway pressure (plateau pressure) = 0 x resistance + alveolar pressure = alveolar pressure 
• Flow (v̇) = Tidal Volume / Inspiratory time. Hence, in PC-CMV, when Inspiratory time is fixed and if tidal volumes are increased, that means flow rate is increased.  
• Compliance = Δ Volume / Δ Pressure  
• Respiratory system resistance = (Paw – Pplat) / Peak inspiratory flow rate 
• Time constant: Compliance x Resistance 
• Work of breath = Volume x Pressure. It is the work required to overcome the mechanical impedance to respiration. In other words, it is the work needed to overcome both elastic and airflow resistance. 
• The time constant is a measure of the time needed for alveolar pressure to reach 63% of the change in airway pressure.  

Static compliance (Cst)	= Tv / (Plateau pressure – PEEP)  = 60-100 ml/cm H20
Decreased by pneumonia, edema, atelectasis, pneumothorax, or restrictive lung disease.
Dynamic compliance(Cdyn)	= Tv / (Peak pressure – PEEP)  = 50-80 ml/cm H20)
Airflow resistance becomes a factor. Decreased by bronchospasm, mucus plugging, kinked tube, or decreased static compliance.

1. Volume Controlled (volume limited, volume targeted) and Pressure is variable 
2. Pressure Controlled (pressure limited, pressure targeted) and Volume is variable 
3. Dual Controlled (volume targeted (guaranteed) pressure limited) 

1. Time cycled – such as in pressure controlled ventilation 
2. Flow cycled - such as in pressure support 
3. Volume cycled - the ventilator cycles to expiration once a set tidal volume has been delivered: this occurs in volume controlled ventilation. If an inspiratory pause is added, then the breath is both volume and time cycled 

• In pressure control, a pressure limited breath is delivered at a set rate. The tidal volume is determined by the preset pressure limit. This is a peak pressure rather than a plateau pressure limit.  
• The key advantage of pressure targeted ventilation is unlimited flow during inspiration to satisfy the patient’s demands. The harder the patient draws in, the greater the pressure gradient, and the higher the flow.  

• Advantages 
  • Lower Paw for a given Tv but higher MAP 
  • Lower VE, i.e. less dead space 
  • Spontaneous breathing 
  • Decreased sedation 
• Potential Disadvantages 
  • Volumes change with changes in compliance and resistance 
  • New technology 
  • Limited research and clinical experience. Limited studies didnot show any benefit with outcomes, except for oxygenation.  

• Rationale 
  1. Sustained elevations in airway pressure may more effectively recruit collapsed alveoli. 
  2. I:E ratio of > 1:1 may achieve higher mean airway pressure with lower peak alveolar pressure and lower PEEP than conventional mechanical ventilation (provided that excessive gas trapping does not occur). 
• Methods 
  1. Pressure controlled ventilation (PCV) : prolong inspiratory time 
  2. Volume controlled ventilation : prolong inspiratory time indirectly by  
     • ​Slow, constant inspiratory flow rate 
     • Constant flow, with end-inspiratory pause 
     • Decelerating flow 
• Problems 
  • Marked increase in gas trapping (PEEPi) 
  • Decreased Tv with increased PCO2 , if there is insufficient time for expiration. 
  • Discomfort (need deep sedation + paralysis) 

• increased mean airway pressure 
• increased FRC (prevention of airway collapse) 
• increase PaO2: increased capillary-alveoli interface for gas exchange, extra-vascular lung water displaced from alveolar interstitium to peribronchial interstitium 
• maximizes recruitment of alveoli by preventing cyclic de-recruitment on expiration 
• decreased airway resistance, especially with auto-PEEP
• reduced V/Q mismatch 
• improved distribution of inspired gas 
• reduced work of breathing by counteracting both intrinsic PEEP, overcoming airway resistance and improving compliance
• prevention of surfactant aggregation reducing alveolar collapse 
• reduction in LV afterload (due to increased LV transmural pressure) — decreased preload and WOB

• impaired CO2 elimination due to increased dead space 
• decreased RV preload, increased RV afterload, decreased LV compliance (due to intra-ventricular septum displacement) 
• reduced urine output through increased ANP, decreased GFR and increased ADH 
• increased pulmonary vascular resistance (PVR) (in West’s zone I and II where increased alveolar pressure exceeds venous pressure) 
• decreased flow in West’s zone I causing increased dead space (PA > Pa >Pv) 
• may worsen right to left intracardiac shunt by increased pulmonary vascular resistance
• decreased hepatic artery and portal venous flow (liver congestion and LFT changes) 
• increased ICP 
• decreased peribronchial lymphatic flow (? decrease pneumonia) 
• Decreased splanchnic blood flow (at >20cmH2O PEEP) due to decreased cardiac output. 

1. Impaired cardiac function due to reduced right ventricular preload as a result of raised mean intrathoracic pressure and increased right ventricular afterload because of increased lung volume (which may not happen if gas trapping does not occur and if tidal residual volumes are physiologic). 
2. Marked increases in lung volume cause an increase in pulmonary vascular resistance. This increases right ventricular afterload, which may compromise the forward output of that chamber. The increase in right ventricular volume associated with raised pulmonary vascular resistance may in turn impair left ventricular function, since both ventricles share the interventricular septum, pericardial sac, and certain circumferential muscle fibers. 
3. Increase in juxtacardiac pressure that occurs as a result of the increase in intrathoracic pressure induced by positive pressure causes a functional reduction in left ventricular afterload.  
4. Positive-pressure ventilation does not always impair cardiac function, and in certain circumstances it may even improve it. Although the work of spontaneous breathing normally accounts for a small proportion of overall oxygen consumption, this may increase drastically during acute respiratory failure. When cardiac function is severely impaired, as in cardiogenic shock, the heart may not be able to meet the demands imposed by this excessive work of breathing.  
5. Increased intracranial pressure. Positive pressure ventilation can increase jugular venous pressure, which in turn can impede venous return from the brain and raise increased intracranial pressure (ICP). 

1. Decreased maximal static expiratory pressure (neuromuscular disease) 
2. increased airway resistance (asthma) 
3. decreased lung elastic recoil pressure (emphysema) 

1. The expiratory time is the key variable – it should be short enough to prevent derecruitment and long enough to obtain a suitable tidal volume. The expiratory time is set between 0.4 to 0.6 seconds – the tidal volume is your target (between 4 and 6ml/kg). If the tidal volume is inadequate, the expiratory time is lengthened; if it is too high (>6ml/kg) the expiratory time is shortened. 
2. The high CPAP (PEEP) level is set at plateau pressure or the mean airway pressure level from the previous mode (pressure control, volume control etc). If you are starting off with APRV then start high (28cmH2O of less) and work your way down. Higher transalveolar pressures recruit the lungs. 
3. Low PEEP is set at 0cmH2O. The large pressure ramp allows for tidal ventilation in very short expiratory times. 
4. The inspiratory time is set at 4-6 seconds (the respiratory rate should be 8 to 12 breaths per minute – never more). 
5. Neuromuscular blockade should be avoided: the patient should be allowed to breathe spontaneously (this is beneficial). The breaths can be supported with pressure support – but the plateau pressure should not exceed 30cmH2O. 
6. There are two different ways to wean patients from APRV. If lung mechanics rapidly return to normal, the patient should be weaned to pressure support. If ARDS is prolonged, then the high CPAP level is gradually weaned down to 10cmH2O, and then the patient is converted to a standard vent wean. 

• It is ventilation with small tidal volumes at high frequencies i.e. TV 1-4mL/kg at 60-100/min and is often used with high PEEP. It is essentially a vibrating CPAP. 
• 1 Hz = 1 cycle/sec = 60 breaths/min 
• The only indication is when conventional ventilation fails and if no ECMO is available. 
• Contraindications are severe airflow obstruction and raised intracranial pressure. 
• It maintains lung recruitment, avoids over distention, and does not rely on bulk flow for oxygenation and ventilation.  
• Mean airway pressure is very high and pressures oscillate around MAP. 
• TV is less than dead space -> normal bulk flow inadequate -> but gas delivery into the system still undergoes gas exchange by a number of mechanisms but not well understood. Both inspiration and expiration are active processes. 
• Utilize highest possible frequency to minimize tidal volume (only decrease for CO2 control if amplitude of oscillations maximal).  
• Factors that determine PaO2 are FiO2 and mean airway pressure.  
• Factors that determine PCO2 are amplitude (power) of oscillations, frequency of oscillations, inspiratory time and cuff leak. Increase in amplitude or reduction in frequency leads to increased tidal volumes. 
• Typical intial settings:  
  1. Bias flow 40 L/min 
  2. Inspiratory time 33% 
  3. mPaw 34 cm H2O ( also called a CPAP or PEEP in this mode) 
  4. FIO2 1.0 
  5. Amplitude (delta P) 90 cm H2O. It is pressure swing around MAP.  
• Initial frequency based on most recent arterial blood gas: 

• Complications include decreased venous return, intracranial hemorrhage from high MAP, pneumothorax, increased need for sedation and paralytics. 
• Oxygenation problems: Increase FiO2, increase MAP by 2-3cm every 30 mins, increase inspiratory time, repeat recruitment maneuver, consider ECMO and consider flolan or NO. 
• Inadequate ventilation: Increase delta P by 5-10cm upto a max of 90cm, decrease frequency by 1 hz every 2-3 hours and check for cuff leak 
• OSCILLATE trial: Increased mortality with early use of HFOV in moderate to severe ARDS. Also, there is higher risk of hemodynamic instability due to higher mean airway pressures. 

1. Trigger insensitivity.  
2. Missed trigger or ineffective or wasted efforts. Common causes are inadequate respiratory efforts or increased flow to the ventilator circuit during nebulizer treatments or Auto PEEP in COPD 
3. Double triggering due to coughing, low tidal volumes as in ARDS, low flow states or increased ventilatory demand 
4. Trigger delay due to decreased respiratory drive, sleep, hypocapnia and sedation. 
5. Auto trigger due to increased sensitivity or leaks in the system 
6. Flow starvation 
7. Inadequate volumes 
8. Premature cycling due to short i-time or coughing 
9. Too fast or too slow pressurization rate 

• When present, intrinsic PEEP can increase work of breathing. It can be offset by applying extrinsic PEEP ( upto 80% of iPEEP). 
• Ramp style flow pattern results in lower peak airway pressure and higher mean airway pressures compared to square wave pattern. 
• In ramp style pattern, peak airway pressure is the plateau pressure as flow returned to zero at end inspiration. There is no need to put an inspiratory pause.  
• The plateau pressure is the pressure applied to the small airways and alveoli. It is believed that control of the plateau pressure is important, as excessive stretch of alveoli has been implicated as the cause of ventilator induced lung injury. The peak pressure is the pressure measured by the ventilator in the major airways, and if plateau pressure is normal, it strongly reflects airways resistance. 
• In pressure controlled ventilation, the pressure limit is (usually) the plateau pressure due to the dispersion of gas in inspiration. In volume control, the pressure measured by the ventilator is the peak airway pressure, which is really the pressure at the level of the major airways.  
• Dyssynchrony is a term which describes a patient fighting the ventilator. If it persists after adquate sedation, in the majority of cases it is due to inadequate flow delivery from the ventilator. If the flow of gas is inadequate, the patient attempts to suck gas out of the ventilator – which is extremely unpleasant. This only occurs in volume control modes. In pressure control, flow is unlimited – the reason is that flow is related to the pressure gradient between the upper and lower airway – a deeper attempted inspiration makes the pressure in the alveoli more negative in relation to the upper airway, and the pressure gradient is larger – and the flow greater. 
• Removal of positive pressure ventilation may unmask LV failure and may precipitate pulmonary congestion by increasing venous return. 
• PEEP less than 10 is unlikely to affect CVP  
• There is no evidence that a gradual reduction of ventilation support accelerates the ventilator discontinuation process. Patient either pass weaning trial or not. 
• RSBI (Tobin Index) is a measure of readiness for weaning trial. It is applied before starting the weaning process. Score of < 105 signifies that patient is ready for weaning trial. 
• Causes of failed extubation: Upper airway resistance (supraglottic edema), poor cough and excessive secretions, poor airway reflexes leading to aspiration, respiratory weakness masked by pressure support, increased cardiac load induced by removal of CPAP, and onset of new pathology.  
• Minimal vent. Settings for weaning: Martin Tobin has argued that adding either 5 cm H2O as “physiologic” PEEP or pressure support of 7 cm H2O to overcome the resistance in an endotracheal tube (or both, as is usually done) may actually reduce the “spontaneously” breathing patient’s workload by >40% and may result in failure once extubated. An alternative is to have the ventilator set on “flow-by,” with pressure support and PEEP set at zero 
• Failure of exhaled tidal volume to match inhaled tidal volume may be due to auto-PEEP or leak around ET cuff or chest tubes or broncho pleural fistula. 
• Extubate high risk patients to NIPPV, which would reduce reintubation rates, especially in COPD. 
• Single Lung ventilation: Eg. Single lung transplant, bleeding in unilateral lung. Set initial tidal volume at 4 ml/kg and adjust RR to maintain normocapnia. PEEP in normal lung may help in preventing atelectasis but at the same time, the shunt on non ventilated lung increases due to increased diversion of blood flow from normal to abnormal lung induced by PEEP. 
• Low tidal volume strategy is good in even non ARDS but those at risk for ARDS like multiple transfusions, sepsis, pancreatitis, trauma or high risk surgery.  
• Cardiac oscillations as trigger: base line of pressure time wave forms moves up and down with the heart beat thereby triggering synchronized breaths.  
• We measure gas partial pressure in mmHg, and ventilator gas pressures in cmH2O. 1mmHg = 1.36 cm of H2O. Measured in cmH2O, sea level pressure is 1033. Thus, we ventilate our patients with pressure differences which are minute in comparison to the total pressures in play in the environment around them, or even to the pressures in their own cardiovascular system. 
•  Weaning from ventilator is a wrong concept. Liberation from ventilator is the right concept. Weaning with decreasing pressure support day by day is a poor strategy. When the primary lung pathology is reversed, we should aim for liberation from ventilator. 
• Changing from square wave to ramp pattern increases the I-time, if the flow rate is constant. Hence, E-time may be lessened and pt. may go into dyssynchrony. Hence, if the pt. is tachypneic and you want to keep long enough E-time, increase the flow rate when changing from square wave to ramp pattern. 
• In normal patients, expiratory time constant is around 0.3 seconds and hence would need about 1.5 secs for expiration i.e. 5 time constants. 
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