Introduction

Mechanical ventilation is a common indication for intensive care unit (ICU) admission. This chapter will provide an overview of mechanical ventilation: its indications, basic physiology, ventilator settings, and issues that arise in caring for patients on mechanical ventilation.

Understanding mechanical ventilation requires a review of normal breathing. Ventilation occurs when fresh gas enters the alveolus, carbon dioxide diffuses from the blood across the alveolar-capillary membrane, and the carbon dioxide is exhaled. Oxygenation occurs simultaneously as oxygen diffuses from the inhaled gas into capillary blood. Total ventilation is divided into alveolar ventilation, that portion which participates in gas exchange, and dead-space ventilation, that portion that does not reach a functioning alveolar unit and is exhaled unchanged.

The functional residual capacity (FRC) is the resting volume at which the elastic recoil pressure of the lung inward equals the elastic recoil pressure of the chest wall outward, alveolar and mouth pressure are both zero, and there is no airflow. FRC increases with low lung elastic recoil pressure (such as in emphysema) and decreases when lung recoil pressure is high (such as in pulmonary edema or fibrosis).

Inspiratory muscles lower pleural pressure, generating a negative alveolar pressure while mouth pressure remains constant. Gas follows the pressure gradient and enters the lung. Expiration occurs when the lung returns to FRC with the relaxation of the inspiratory muscles although expiratory muscles can be used to speed the flow of gas out of the lung or to reduce lung volume below FRC down to residual volume.

Tidal volume is the volume of gas entering and leaving the lung during a respiratory cycle. It is determined by the pressure gradient from airway to alveolus and the mechanical properties of the lung and airways. Modern ICU ventilators deliver tidal volume by applying positive pressure to the airway. Negative pressure devices that lower the pressure outside of the chest wall, akin to the iron lung of historical note, are still used for some patients with chronic respiratory failure, but these devices are rarely used in the acute setting.

The history of mechanical ventilation is replete with famous figures in pulmonary physiology, anesthesia, and surgery.¹ Ventilators have been used in the operating room since the end of the 1900s, but widespread use in respiratory failure began in the 1950s treating patients with paralysis from polio. Advances in oxygen delivery and blood gas analysis allowed the treatment of patients with increasingly complex pulmonary and chest wall diseases over the next decade. Modern ventilators continue to advance with improvements in reliability and responsiveness and increasing ability to control all phases of the inspiratory cycle.

Impact of Positive Pleural Pressure on Hemodynamics

The complex interactions between the cardiac and pulmonary systems are well known to the cardiologist. Lowering of alveolar and pleural pressure during normal spontaneous breathing augments venous return, explaining the varying split of the S₂ heart sounds and the variation in right ventricular murmurs with inspiration. Analogously, the Valsalva maneuver, sustained forced expiration against a closed glottis raising pleural pressure, lowers cardiac output and left ventricular size accentuating the murmur of hypertrophic cardiomyopathy; release of the Valsalva restores venous return accentuating right-sided murmurs.

Transitioning from negative pressure in the pleura to positive has important hemodynamic consequences affecting both the right- and left-sided cardiac circulations.² A complete review of this topic is beyond the scope of this chapter, but understanding basic cardiopulmonary interactions allows the reader to predict the impact of positive pressure breathing on a given patient’s condition.^3,⁴

Positive alveolar pressure affects blood circulation in two important ways:

1. A portion of the alveolar pressure is transmitted to the pulmonary capillaries and veins, as increasing alveolar volume compresses the pulmonary capillary. The extent of transmission is dependent on lung elastance; more compliant lungs distend more easily, increasing stretch of the alveolar wall and increasing transmission of pressure. Increased capillary pressure has two net effects. Blood already within the capillary and pulmonary veins is ejected forward into the left atrium, increasing left ventricular preload acutely. The increased pressure acts as increased afterload for the right ventricle, decreasing left ventricular preload during the next cardiac cycle.

2. Rise in alveolar pressure distends the lung raising pleural pressure. Using the analogy of a balloon being inflated within a box, pleural pressure reflects distention of the lung up against the chest wall. The extent of transmission of alveolar pressure to the pleura is dependent on both chest wall and lung compliance; index of transmission = (lung compliance)/(lung compliance) + (chest wall compliance) defines this relationship. The lower the chest wall compliance compared to lung compliance, the more pressure is transmitted. Patients with stiff lungs and a normal chest wall have smaller increases in lung volume and therefore pleural pressure changes little; conversely, patients with normal lungs and stiff chest walls have lungs that push against the stiff chest wall, raising pleural pressure more steeply.⁵^–⁷

A rise in pleural pressure directly affects right ventricular preload and left ventricular afterload. Venous return is affected by central venous pressure as described by Guyton, and this determines right ventricular preload. Blood drains from the systemic veins down the pressure gradient from the mean systemic pressure down to central venous pressure; any increase in central venous pressure reduces the gradient, lowering venous return. Pleural pressure is also a determinant of left ventricular afterload. Increased intrathoracic pressure ejects blood out of the thoracic aorta; this decreases afterload and facilitates left ventricular emptying. This can also be expressed as decreased myocardial work, which is determined in large part by transmyocardial pressure.

Decrease in preload and afterload can occur cyclically during inspiration or can be continuous. For instance, patients ventilated with positive pressure breathing with positive end-expiratory pressure (PEEP) of zero have the normal negative pleural pressure at end-expiration that becomes positive during inspiration. Patients treated with continuous positive airway pressure (CPAP) continue to breathe unassisted spontaneously (i.e., lower their pleural pressure with each breath), but the baseline pressure is shifted upwards resulting in a continual hemodynamic effect. Often patients on mechanical ventilation receive positive inspiratory pressure on top of PEEP, thereby having cyclic decreases in preload on top of an already reduced baseline.

Manipulation of pleural pressure offers therapeutic options when patients are in the cardiac care unit, and it is important to remember these hemodynamic effects when initiating or withdrawing mechanical ventilation or adjusting settings. Patients who are preload dependent frequently develop hypotension after intubation, for instance those with hypovolemia, right ventricular infarction, pulmonary hypertension, or aortic stenosis; great care should be taken when initiating mechanical ventilation in patients with pericardial tamponade because deterioration in to pulseless activity (PEA) has been documented. Alternatively, the decrease in preload and afterload from intubation is beneficial for patients with congestive heart failure.

The interplay of breathing and hemodynamics offers an opportunity to determine preload responsiveness in critically ill patients. Combining the models of Guyton and Starling, Magder and colleagues showed that careful interpretation of the central venous pressure waveform during spontaneous breathing can differentiate those patients who are on the ascending portion of their Starling filling curves, thereby correctly predicting which patients will increase their cardiac output with a fluid challenge.^8,⁹ Similarly patients with large swings in arterial blood pressure with positive intrathoracic pressure are preload dependent and likely responsive to fluid.¹⁰ A thorough review of this topic has been published.¹¹

Indications for Mechanical Ventilation

The most common reason for mechanical ventilation in the cardiac care unit (CCU) is cardiogenic pulmonary edema. The underlying cardiac pathology may be a cardiomyopathy, valvular disease, or tachyarrhythmia. Whatever the cause, the resulting respiratory insult is the same: increased left atrial pressure and imbalance in Frank-Starling forces across the lung capillary membrane. This results in transudation of fluid into the lung interstitium and flooding of the alveoli. The lungs become stiff, and gas exchange is impaired across the thickened capillary membrane. In addition, the bronchi become edematous, so that airway narrowing may complicate the picture. All this leads to ventilation-perfusion () mismatch causing severe hypoxemia, and increased work of breathing causing ventilatory failure and CO₂ retention. Excess work of breathing increases the oxygen demand by the diaphragm, further stressing the heart. In this state, the goals of mechanical ventilation are to improve gas exchange and reduce the patient’s work of breathing. Settings for mechanical ventilation should reflect these dual goals.

Other indications for mechanical ventilation in the CCU include:

• Loss of upper airway reflexes and/or aspiration pneumonitis. This may be due to cardiac arrest, cardiogenic shock, or the need for heavy procedural sedation

• Acute and/or chronic pulmonary disease

• Concomitant neuromuscular disease

Finally, nosocomial and iatrogenic complications in the CCU may result in respiratory failure and the need for mechanical ventilation. These include pulmonary embolism, hospital-acquired pneumonia, critical illness polymyoneuropathy, and pneumothorax after placement of a central venous catheter.

Managing Gas Exchange and Oxygen Delivery

Oxygenation

The paramount goal of mechanical ventilation is to assure an adequate PaO₂ (arterial pO₂), such that hemoglobin saturation (SaO₂) is comfortably above 90%. It is important to recognize however that SaO₂ is only one of three factors whose product determines O₂ delivery to the tissues, the other two being cardiac output and the concentration of hemoglobin, as described by the equation:

From this it is clear that an increase in cardiac output from 5.0 to 6.0 liters/min or a rise in hemoglobin from 8 to10 mg% will have a greater impact on O₂ delivery than a rise in O₂-hemoglobin saturation (SaO₂) from 92% to 98%. Further, once SaO₂ is >92%, the patient is on the “flat portion” of the hemoglobin-O₂ saturation curve, such that small changes in PaO₂ will not greatly affect the SaO₂. For both of these reasons, keeping SaO₂ in the range of 92-95% is a reasonable goal when adjusting ventilator settings.

Importantly, the 3 factors in the equation above can interact with each other; for example increasing the intensity of mechanical ventilation to improve SaO₂ may over-pressurize the thorax, reduce venous inflow to the right ventricle and impair cardiac output. Excessive red blood cell transfusion to achieve a “normal” hemoglobin concentration is also ill advised, as it will increase blood viscosity and may impair C.O. Careful attention to these interactions will guide the clinician in choosing interventions to improve O₂ delivery to tissues.

The measurement of O₂ saturation by pulse oximetry (SpO₂) is a good estimate of SaO₂ in most situations, though it also records carboxyhemoglobin. When blood concentration of carbon monoxide is high (in heavy smokers or smoke-inhalation victims) the SpO₂ overestimates SaO₂.

In the mechanically ventilated patient, the two main parameters that affect the PaO₂ are the FiO₂ (fraction of O₂ in inspired air) and the mean airway pressure. A moderate increase in FiO₂ is often adequate to improve the PaO₂ in patients with respiratory failure due to mismatching of ventilation and perfusion in the lung (V/Q mismatch). This situation occurs commonly in patients with inhomogeneous airway diameter due to obstructive lung disease or early interstitial lung edema in patients with CHF.

Severe hypoxemia however may be refractory to increases in FiO₂ when it is due to pulmonary “shunting,” in which a significant fraction of the cardiac output passes through a lung capillary bed that is not aerated (not exposed to gas). This commonly occurs in patients with consolidated pneumonia, massive pulmonary edema or atelectasis due to airway obstruction or compression of lung tissue. In these scenarios, even FiO₂ levels approaching 100% will be unsuccessful in treating the cyanosis, just as in patients with an intra-cardiac shunt. Fortunately, there are alveoli at the margins of consolidated or atelectatic lung regions that can be “recruited” to function as gas exchange units if a high distending pressure is maintained. These higher airway pressures are commonly achieved by applying positive end-expiratory pressure (PEEP), which exerts its beneficial effect on PaO₂ by preventing the collapse of recruitable lung units during exhalation. The effect of PEEP on cardiac output is complex, as it reduces both RV preload and LV afterload. The result may be either beneficial or deleterious, depending on the patient’s volume status and lung compliance.^12,¹³ This is detailed in the preceding section.

Ventilation

Alveolar ventilation is the process by which the lungs excrete CO₂, and is thus inversely proportional to PaCO₂. So called “minute ventilation” (Ve) is the total volume of air exhaled per minute, and is the sum of alveolar ventilation (Va) and ventilation of the pulmonary “dead space” (Vd), which is the volume of exhaled air that did not participate in gas exchange at the alveolar membrane:

Elevated dead space may be present chronically, as in patients with emphysema, or acutely as in a patient who has suffered a pulmonary embolism. In either case however, if dead space is stable over time, control of minute ventilation will control alveolar ventilation and thus will regulate PaCO₂. Ve is measured as the product of respiratory rate (RR) and tidal volume (TV). Thus adjusting these two ventilator parameters will regulate PaCO₂. An important caveat to this is that patients on mechanical ventilation regulate their own RR via respiratory drive mechanisms, unless heavily sedated or paralyzed; therefore raising or lowering the ventilator “set” rate will not necessarily change the patient’s actual RR or alter PaCO₂.

The chief reason to control alveolar ventilation or PaCO₂ is to regulate pH. Marked acidosis can impair cardiac contractility and responsiveness to vasopressors ^14,¹⁵; marked alkalosis reduces the threshold for ventricular arrhythmias in susceptible patients.¹⁶ However mild derangements in pH (0.10 to 0.15 units either way) are generally harmless. Thus strict control of pH by adjusting Ve is often unnecessary, particularly if it requires harmful increases in the intensity of alveolar ventilation (see section on ARDS, below). Inadequate levels of Ve will however cause respiratory acidosis (low pH, high PaCO₂), stimulating the patient’s respiratory drive; in experimental studies this may divert up to 30% of cardiac output to the respiratory muscles.¹⁷ Conversely, excessive Ve causes respiratory alkalosis (high pH, low PaCO₂) which suppresses respiratory drive and can cause a patient to be apneic during a weaning trial, thereby prolonging the use of mechanical ventilation.

Delivery of Mechanical Ventilation

There is a rapidly expanding menu of options when delivering mechanical ventilation. Terminology is complicated by proprietary names entering bedside usage and by the retention of historical abbreviations that were nonideal. Although nomenclature standardization has been proposed, it has not reached universal usage, causing confusion at the bedside.^18,¹⁹ Another source of confusion is that different ventilators may require entry of a setting in different ways; for example, inspiratory time may be entered in seconds (e.g., 1.5 seconds) or as a percentage of cycle time (e.g., 25% of 6 seconds) or a ratio of inspiration to expiration (e.g., 1:3 of 6 seconds).

Despite the rapid increase in options, there are little randomized controlled data showing a benefit to a particular style of ventilation. There are significant differences in comfort and muscle unloading depending on the mode selected, but no mode has been shown superior in regards to patient outcome.^20,²¹ Ventilator setting in most ICUs remains dependent on local expertise and the model of mechanical ventilator available. Improved understanding of the available modes allows finer control over ventilation and a better understanding of how a change in patient status will affect the setting. Most important to the patient is whether ventilation is assured, the respiratory muscles are effectively unloaded, and whether the tidal volume and end-expiratory volume are appropriate for the disease.

Mechanical ventilators allow manipulation of nearly every aspect of inspiration; expiration however, is not controlled except for airway pressure (PEEP). Usually discussed first is the pattern of breathing, or mode. A mode will allow different types of breath: each with its own name, options, and settings. These issues will be introduced in this chapter but full discussion requires a textbook and is beyond the scope of this chapter.²²

Most breaths on mechanical ventilation can be classified as either mandatory or spontaneous. The ventilator exerts more control during mandatory breaths; settings include when to start the breath, what to control during the breath, and when the breath ends. Common mandatory breaths include: volume control, pressure control, and demand-flow volume control. A hallmark of mandatory breaths is the required setting of inspiratory time. During spontaneous breathing, the ventilator does not control inspiratory time but rather supports the inspiratory efforts. Common spontaneous breaths include pressure support and unsupported.

Some ventilators allow breaths that are not easily classified as mandatory or spontaneous. One example is volume-assured pressure support, which is a hybrid with spontaneous breathing that converts to mandatory if a tidal volume target is not reached.²³ Another example is biphasic positive airway pressure (BIPAP) in which there are two asynchronous cycles as the ventilator maintains a background pattern of varying positive pressure breathing interspersed with patient effort.²⁴

Mode

Generally the first decision in ventilator setting is the mode. The most common modes are continuous mandatory ventilation (CMV), intermittent mandatory ventilation (IMV), and spontaneous ventilation (CPAP).¹⁸ CPAP, standing for continuous positive airway pressure, describes a mode which is continuously spontaneous and therefore never mandatory. The name is intrinsically confusing, as the acronym CPAP also signifies a therapy for sleep apnea, a type of mask, and delivery of positive airway pressure. It is also inaccurate as airway pressure is not constant (when used in conjunction with pressure support) or necessarily positive as CPAP can be set to zero. Despite attempts at renaming, CPAP remains entrenched in bedside and ventilator manufacturer usage.

CMV allows only mandatory breaths, the shape and size is determined by the settings described below. There is a minimum set rate. Patients can increase ventilation by “triggering” additional breaths; the ventilator senses either a drop in airway pressure across a closed inspiratory valve or inspiratory flow from a bias flow circuit. Regardless if the breath is time-triggered (i.e., at the minimum set rate) or patient-triggered (i.e., above the minimum set rate), every breath is mandatory and largely controlled by the ventilator.

CPAP allows only spontaneous breaths. There is no minimum set rate; each breath is started and stopped by the patient, and the patients breathes at the tidal volume and respiratory rate determined by their drive and respiratory mechanics. The ventilator can mimic unassisted breathing or can provide “support” during each breath; the level of support can vary from minimal support, to low levels of support to overcome the inherent added work of the ventilator, to higher levels of support that can actually be sufficient to essentially take over the entire work of breathing except for the initial trigger. It is important to remember that the ventilator is adjusting the inspiratory flow continuously over the breath to allow a spontaneous breath; it is not that the ventilator is just standing by passively. The ability of the ventilator to mimic unsupported breathing has improved significantly over the last decade; prior ventilators had high levels of imposed work that are much lower today.

IMV delivers a set number of mandatory breaths delivered per minute. Patient triggering above this set rate delivers spontaneous breaths. As such, IMV requires setting of two distinct parameters: a full description of the mandatory breaths and the level of support to deliver during spontaneous breaths. Careful attention to both the mandatory and spontaneous breaths is needed to appropriately adjust the amount of ventilatory support delivered to the patient. Most ventilators attempt to synchronize the mandatory breaths with patient effort so a patient trigger may yield a mandatory or a spontaneous breath. This can lead to instability in the respiratory center as identical phrenic nerve output results in different tidal volumes. During IMV, patients may be performing more work during the mandatory breaths than during the spontaneous ones.²⁵