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A clinical overview of how NIMV works in specific disease states, the negative effects of mechanical ventilation, and the physiology of respiratory mechanics. 

A clinical overview of how NIMV works in specific disease states, the negative effects of mechanical ventilation, and the physiology of respiratory mechanics.
by Jeffrey Sankoff, MD


Respiratory distress is commonly encountered in the emergency department. In most cases, aggressive management aimed at reversing the underlying process is sufficient. However, the emergency physician must occasionally turn to more intensive means of supporting a patient. With respect to the failing respiratory system, the EP has several options including endotracheal intubation with mechanical ventilation and non-invasive mask ventilation (NIMV) in the form of either continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP). Each of these may be beneficial but intubation may also be deleterious and should be avoided if possible.
This article will outline how NIMV works in specific disease states. The negative effects of mechanical ventilation will be reviewed and the physiology of respiratory mechanics discussed.


The Patient With A Failing Respiratory System

Before considering how NIMV helps patients, it is useful to consider why it is that they need this help in the first place.
The act of respiration encompasses two distinct processes: oxygenation and ventilation. Oxygenation involves the movement of oxygen from the atmosphere to the alveoli and subsequent diffusion into the blood while ventilation relates to the removal of carbon dioxide from the alveoli after diffusion from the blood. Both of these processes are dependent on gas moving in and out of the lungs. Unfortunately, air will not flow into the lungs unless there is a force driving it and it takes work to generate this force. The work of breathing creates a pressure gradient from the atmosphere into the lungs down which air can passively flow. Exhalation follows as a passive phenomenon secondary to the fact that at end inhalation, pressure in the lungs is greater than that of the atmosphere.
There are three forces that must be overcome before air can flow into the lungs. These are resistance (determined by the mean cross-sectional diameter of the airways) elastance, (the stiffness of the pulmonary circuit including the lungs, pleura and chest wall) and threshold load (intrinsic positive end expiratory pressure, (intrinsic PEEP or PEEPi)). Various respiratory disease processes impact differently on these three forces necessitating a larger gradient, and hence, more work, in order to provide a higher driving force for airflow to occur. Other medical problems may impair the ability to do even normal amounts of work. A mathematical representation of the work of breathing (WOB) is helpful in understanding this concept (figure 1).
The equation demonstrates how the WOB performed by the respiratory muscles is the amount of work required to generate a negative pressure gradient great enough to overcome the three forces opposing flow. This equation also explains how diseases result in a need for more work to be done in order to generate airflow. For example: A patient with pneumonia has fluid filled, stiff lungs. They may also have some bronchospasm. Thus both elastance and resistance are elevated. The patient will therefore need to generate a higher gradient to overcome both PR and PE by applying more Pmusc. If the patient cannot generate sufficient work, they will fail. Alternatively, a patient with Guillain Barre syndrome may have perfectly normal lungs but is simply unable to generate sufficient work on the left side of the equation and thus will fail (Figure 2).
There are other reasons for patients to have respiratory failure that are independent of the work of breathing. Some disease states impair the ability of the lungs to adequately oxygenate the blood while others impair the ability to remove carbon dioxide. Finally, there are those processes that spare the lungs but result instead in a loss of protective airway reflexes and subsequent airway obstruction. In these instances, mechanical ventilation provides other important benefits.
For patients who have hypoxemic respiratory failure, mechanical ventilation allows for the delivery higher amounts of FiO2 than are possible by mask alone. Mechanical ventilation also allows for the provision of positive end-expiratory pressure (PEEP). PEEP improves oxygenation both by increasing functional residual capacity, (FRC) and by improving the recruitment of alveoli leading to better ventilation perfusion (V/Q) matching.
Mechanical ventilators benefit patients with hypercarbic respiratory failure by improving minute ventilation. Additional benefits of mechanical ventilation are restricted to those patients who are intubated and include the possibility of improved toilet and maintaining the upper airway.
Unfortunately though, invasive mechanical ventilation also confers significant risks. These include barotrauma and volutrauma-physical forces that can injure the lung and lead to the acute respiratory distress syndrome, oxygen toxicity from high levels of FiO2, ventilator associated injury and/or pneumonias as well as difficulty or inability to wean. Finally, the endotracheal tube itself may damage the tracheal mucosa leading to long-term damage.
For these reasons it is important to consider alternatives to intubation and mechanical ventilation whenever time and circumstances allow. One such alternative that is widely in use and can often forestall if not completely obviate the need to intubate is NIMV.
NIMV: The basics

The mechanical means by which NIMV works is fairly simple. High flow air or an oxygen-enriched mixture passes into a circuit in which a pop-off valve dictates the enclosed pressure. A mask tightly fitted to the patient is an integral part of the circuit.
As the patient inspires, the valve closes until flow in the circuit generates the set pressure once more. Exhalation augments pressure in the circuit opening the release valve. Expired gases are removed by the continuous flow through the circuit and out the valve.
BiPAP differs from CPAP in that an electronic sensor detects when pressure falls due to inhalation and then augments the pressure to a preset inspiratory level. At end inhalation, pressure rises and the machine cuts off the inspiratory assist and resets to the baseline level.
Although NIMV may be suitable in various clinical settings, it has been experimentally shown to confer the most benefits in two types of patients: those with acute exacerbations of either congestive heart failure, (CHF) or chronic obstructive pulmonary disease, (COPD).


Unlike chronic CHF patients who are fluid overloaded, acute CHF patients are generally euvolemic and have an acute alteration in their cardiac physiology that precipitates the episode. The inciting event in these cases causes some degree of myocardial dysfunction due to ischemia, dysrhythmia or rarely, a sudden increase in blood pressure. Whatever the cause, the result is a decrease in cardiac output, (CO). This decreases oxygen delivery to the tissues. Cells then convert to anaerobic metabolism that produces lactic acid. Local and systemic acidosis stimulates a stress response with an ensuing catecholamine surge. This increases vascular tone increasing afterload that further worsens CO.
NIMV offers many physiologic benefits to the patient with an acute exacerbation of CHF the sum total of which actually contribute to reversing the underlying problem. The first of these is the application of positive pressure in the thoracic cavity.
Contrary to popular belief, NIMV does NOT push edema fluid out of the lungs. Patients with acute CHF have an imbalance in the CO of the right and left sides of the heart. With the inciting event (detailed above) the left ventricle becomes compromised but the right ventricle usually does not. So the right ventricle continues to pump forward a normal volume of blood but the left ventricle becomes unable to keep pace. Fluid backs up into the lungs resulting in capillary leak and pulmonary edema. With NIMV, the resultant positive intra-thoracic pressure decreases venous return. This reduces right-sided CO to a level that the left heart can equal or even exceed. Fluid ceases to back up and will even begin to be reabsorbed as left ventricular CO improves. Pulmonary edema ceases to worsen and may even diminish, often rapidly.
PEEP also improves oxygenation as previously described. This results in improvements in both peripheral and myocardial oxygen delivery. The end result of this is improved left ventricular function leading to better CO and improved peripheral oxygen delivery. This reduces the anaerobic stress on the peripheral tissues, leads to the clearance of lactate and decreases the systemic stress response. The end result is a fall in afterload that further improves CO.
A final means by which NIMV benefits patients with acute CHF relates to the decrease in the WOB required by the patient. CHF causes edematous, stiff, more elastic lungs and induces bronchospasm that increases airway resistance. As a result, patients with acute CHF need to perform substantially increased WOB. This means more and more CO being diverted to the respiratory muscles, further compromising peripheral perfusion and stressing the already failing heart. NIMV assists the patient with a resultant decrease in the proportion of CO being sent to the respiratory muscles and improved peripheral perfusion.
The use of NIMV decreases morbidity and mortality for CHF patients quite substantially. Studies have shown the best results with the use of CPAP but BiPAP too has been proven to be beneficial albeit less so, but this may be in part due to the fact that the absolute numbers of patients examined have differed substantially between the two therapies. There was one small study that seemed to suggest an increased risk of MI among patients treated with BiPAP but this has never been seen in any other study and there does not appear to be any physiological explanation as to why this would be so.
When using CPAP, 5 cm of water is a good starting point with sufficient FiO2 to maintain a saturation greater than 90-95%. 10/5 is a standard starting point for BiPAP.


Longstanding COPD causes architectural changes in the lungs. Terminal bronchioles become increasingly compliant so that they collapse before the alveoli empty resulting in PEEPi from gas trapping. In addition, bronchiolar walls become edematous, the smooth muscle surrounding them become hyper-reactive and, ciliary dysfunction leads to bronchial clogging. The lungs become progressively hyperinflated flattening the diaphragm and giving a more horizontal lie of the ribs, (barrel chest). With the increases in PEEPi, resistance and elastance (hyperinflated lungs are stiffer), WOB increases at the same time that the efficiency of the respiratory muscles is compromised by the anatomic changes they are subjected to. Referring back to the equation for WOB it is easy to see how this is an untenable situation: The left side of the equation is diminishing at the same time as the right side is increasing.
NIMV does NOT stent open the small airways, but, by augmenting the left side of the equation, helps restore a balance when the right side of the equation rapidly increases secondary to a COPD exacerbation. It cannot be overemphasized though, that unlike in those patients with acute CHF, NIMV is NOT a therapy for COPD. If measures are not instituted to alleviate the problems with resistance and gas trapping, the patient will eventually fail. NIMV simply allows more time for treatment to work.
Both CPAP and BiPAP have been shown to decrease the rate of intubation, the length of hospital stay and overall mortality in patients with acute COPD exacerbations. When NIMV is used, CPAP of 5 or BiPAP of 10/5 are good starting points. FiO2 should only be as high as needed to maintain oxygen saturation at or around 90% until it is determined if the patient is a chronic CO2 retainer or not.
Occasionally, NIMV may fail patients with either CHF or COPD exacerbations. Failure is generally due to patient inability to tolerate the tight fitting mask, or implementation at a point where the disease state is simply too far advanced or continuing to worsen. Observing patients carefully while simultaneously administering other indicated maximal therapies will be the best means of determining who is going to improve and who will need rescue intubation.
Jeffrey Sankoff, MD, is an assistant professor in the departments of emergency medicine and surgery at the University of Colorado Health Sciences Center


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