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26 Cards in this Set

  • Front
  • Back
How were the first mechanical ventilators designed to work?
-through pressure-cycled ventilation, where the lungs were inflated until a preset pressure was reached
Why did pressure-cycled ventilation fall out of favor?
Because the inflation volume varied with changed in the mechanical properties of the lungs
So what has become the standard method of positive-pressure ventilation, and why?
-volume-cycled ventilation: which inflates the lungs to a predetermined volume, and delivers a constant volume despite any changes in lung compliance
Volume-cycled ventilation waveforms
************24.1*********

-the lungs are inflated at a constant flow rate, producing a steady increase in lung volume
-the tracings are uniquely different for the proximal airways (Pprox) vs. the alveoli (Palv)
Pprox waveform
**********24.1********

-proximal airway pressure shows an abrupt initial rise, then a gradual rise the rest of lung inflation
What is the initial abrupt rise a reflection of?
Flow resistance in the airways
Palv waveform
-the pressure in the alveoli shows only a gradual rise throughout inflation

************24.1
Changes in the tracings when there is an increase in airway resistence?
-it will magnify the initial rise in proximal airway pressure, but the alveolar pressure will remain unchanged, meaning higher inflation pressures are needed to deliver the set volume, but the alveoli are not exposed to higher pressures

****************24.1
How does this compare to if the compliance of the lungs is reduced?
-there's an increase in both the proximal airway and alveolar pressure, thus the higher pressures needed to deliver the set volume is transmitted to the alveoli

**************24.1
Why is this significant?
The increase in alveolar pressure in noncompliant lungs can lead to pressure-induced lung injury
Influence of PPV on cardiac performance
-is complex, but involves changes in preload and afterload, and is explained by exploring the changes to transmural pressure created by PPV
What is the significance of transmural pressure?
It's the pressure that determines the ventricular filling (preload), and the resistance to ventricular emptying (afterload)
influence of lung mechanics on transmural pressure transmission
****************24.2**********

-the left shows what happens in a normal lung when inflated to 700 ml, the alveolar pressure is completely transmitted into the pulmonary capillaries, and there is no change in transmural pressure across the capillaries
-on the right is inflation in less compliant lungs, where the increased pressure is not transmitted fully to the capillaries, and results in compression of the vessels
what is the significance of this?
-in conditions which cause decreased lung compliance, such as pulmonary edema or pneumonia, PPV compresses the heart and intrathoracic blood vessels (which is sometimes detrimental, sometimes beneficial)
ways PPV decreases preload
*******************24-3*****************

does so in multiple ways:
-decreases the pressure gradient for venous inflow into the thorax (decreases the difference between pressure in and out of the thorax, which is driving venous return into the thorax)
-pressure on the outer surface of the heart reduces cardiac distensibility, reducing filling during diastole
-compression of pulmonary vessels increases pulmonary vascular resistance, which can impede RV output, which causes dilation of the right ventricle and pushes the intraventricular septum toward the left ventricle, reducing LV size and filling (ventricular interdependence)
positive intrathoracic pressure and afterload
-compression facilitates emptying during systole, like a hand squeezing the ventricle during ejection
-afterload, or the impedence to ventricular emptying, is a function of the peak systolic transmural wall pressure, and incomplete transmission of positive intrathoracic pressure into the ventricular chambers will decreases transmural pressure across the wall during systole, which decreases afterload
overall effect of PPV on cardiac output
-since it reduces vetricular filling during diastole, but also reduces afterload during systole, the effect on CO depends on which predominates
what factor determines which predominates?
-volume status
what happens in euvolemia?
-the effect on afterload predominates, and PPV increases CO, which causes an increase in BP during inflation, known as reverse pulsus paradoxus

(this may explain how chest compression increase CO)
PPV effect on CO during hypovolemia
-the predominant effect of positive intrathoracic pressure is to reduce preload and decrease CO, thus avoiding hypovolemia during PPV is important
some rules about the indications for mechanical ventilation
1. the indication for mechanical ventilation is thinking of it: we tend to delay it as long as possible hoping it wont be necessary, but this only creates the potential need to intubate emergently rather than in an elective controlled setting, putting the patient at risk

2. intubation is not an act of weakness, but rather shows strength of conviction in making a difficult decision

3. initiating mechanical ventilation is not a kiss of death, and the fallacy that once on a vent always on a vent should never influence the decision to intubate
old model of mechanical ventilation
-they used to recommend large tidal volumes to prevent alveolar collapse giving 10-15 ml/kg with PPV even though during spontaneous respiration ppl only take 5-7 ml/kg, and the volumes are even greater if using a mechanical sigh
new model of mechanical ventilation
-the conventional large volumes can damage the lungs, and promote injury to distant organs through release of inflammatory cytokines
-ventilator induced lung injury is a new concept changing the way mechanical ventilation is done
ventilator-induced lung injury
-in the lung diseases that most often require mechanical ventilation, like pneumonia or ARDS, the pathology is not evenly distributed to the lungs (even in ARDS where it looks like it is on CXR), so there are areas of diseased lung and areas of normal lung
-inflation volumes delivered by the ventilator are distributed preferentially to the normal lung, which gets hyperinflated, causing stress fractures at the alveolar-capillary interface due either to barotrauma or volutrauma
3 adverse consequences of alveolar rupture
1. accumulation of alveolar gas in either the lung parenchyma (pulmonary interstitial emphysema), mediastinum (pneumomediastinum), or pleural cavity (pneumothorax)
2. an inflammatory lung condition similar to ARDS
3. multiorgan injury from the release of inflammatory mediators into the bloodstream- called biotrauma
lung-protective ventilation
-a large study of ARDS patients showed tidal volumes of 6 ml/kg of predicted body weight to have reduced mortality compared to 12 ml/kg, so this is now recommended for all pts with acute respiratory failure