Mechanical Ventilation and Advanced Respiratory Support in the Cardiac Intensive Care Unit


Compared to initial coronary care units dedicated to the monitoring of and rapid intervention in life-threatening ventricular arrhythmias in the setting of acute myocardial infarction (MI), cardiac intensive care units (CICUs) have evolved into models providing care for a broader spectrum of acute cardiovascular conditions along with increasing prevalence of noncardiac comorbidities. Recent data suggested a further expansion in the role of CICUs to care for patients with secondary cardiovascular comorbidities presenting with acute noncardiac disease. The treatment of respiratory failure and use of advanced respiratory support has become a common indication for CICU admission. For example, an acute MI can be complicated by pulmonary edema in up to 40% of patients admitted to intensive care units. Likewise, there has been an increase in the use of mechanical ventilation in CICUs. This chapter provides a summary of commonly available modes of respiratory support, their physiologic effects, indications, and clinical issues related to cardiac patients. It focuses on the high-flow nasal cannula, noninvasive ventilation, and invasive mechanical ventilation. When available, data specific to patients with cardiogenic etiology of respiratory failure will be presented, although further studies are necessary to define best practices for these patients.

Basic Respiratory Physiology

Among the essential functions of the respiratory system, the two most commonly addressed in the critical care setting are ventilation and oxygenation. In normal respiration, the interplay between respiratory muscle action and chest wall compression with the compliance of the lungs, alveolar surface tension, and transpulmonary pressure determines the lung volumes at various stages of the respiratory cycle. Changes in lung volumes create a pressure differential that allows air to move in and out of the lungs. The tidal volume represents the volume of air inspired and expired with each breath. The tidal volume multiplied by the respiratory rate yields the minute ventilation. With each breath, part of the tidal volume occupies a portion of the respiratory system that is not involved in gas exchange, known as dead space ventilation, while the remaining portion that participates in gas exchange is known as alveolar ventilation. Alveolar ventilation allows gas exchange across the alveolar-capillary membrane down a pressure gradient. At the end of passive expiration, the outward recoil of the chest wall is counterbalanced by the elastic tendency of the lungs to collapse, maintaining the lung volume at the functional residual capacity (FRC). FRC not only helps to prevent atelectasis but also acts as an oxygen reservoir, maintaining steady partial pressure of oxygen (PaO 2 ). FRC can be affected by various physiologic and pathologic states. Pulmonary edema commonly encountered in the CICU is associated with reduced compliance of the lung and, therefore, decreased FRC.

Heart-Lung Interactions

The cardiovascular and respiratory systems are intimately coupled given their complex connection and anatomic containment within the closed space of the thorax. Both spontaneous breathing and positive pressure ventilation can affect cardiovascular parameters by altering intrathoracic pressures, lung volumes, and metabolic demands. Analyzing the respirophasic changes in cardiac preload and afterload as well as the effect of hypoxia and hypercapnia on vascular resistance and myocardial contractility can provide a simplified summary of the complex heart-lung interactions during critical illness ( Fig. 50.1 ). Understanding the hemodynamic alterations with positive pressure ventilation is essential for the management of complex patients in the CICU.

Fig. 50.1, Cardiopulmonary interactions during normal spontaneous inspiration and positive pressure ventilation. IAP, Intraabdominal pressure; ITP, intrathoracic pressure; LH, left heart; LV, left ventricle; RH, right heart; RV, right ventricle; SV, stroke volume.

Spontaneous Breathing

During spontaneous inspiration, the generation of a negative intrapleural pressure has multiple hemodynamic effects. It leads to an increase in the venous return and right ventricular (RV) preload and stroke volume owing to an increase in the pressure gradient between the right atrium (RA) and the mean venous systemic pressure. Such a simplified summary of the effect of spontaneous inspiration on right-sided chamber filling and stroke volume ignores the effects of the inspiratory increase in lung volumes on pulmonary vascular resistance (PVR) and RV afterload. Although alveolar distention during inspiration causes compression of adjacent alveolar vessels and, therefore, an increase in PVR, these changes do not become clinically significant until lung volumes start approaching extremes (residual volume or total lung capacity). Alternatively, being subjected to intrathoracic pressure changes, transmural aortic pressure, and left ventricular (LV) afterload increase with reduction in intrapleural pressure. Owing to ventricular interdependence, reduced LV diastolic filling coupled with the increased LV afterload result in a mild decrease in stroke volume and systemic blood pressure during inspiration. In healthy individuals, the change in LV stroke volume is not dramatic and is slightly offset by increased RV stroke volume during the next cycle. However, this effect can be amplified in conditions of exaggerated respiratory work or pathologic states with marked ventricular interdependence.

Positive Pressure Ventilation

To avoid alveolar derecruitment, many contemporary modalities of advanced respiratory support use and maintain positive airway pressure at end expiration. This baseline level of positive airway pressure is partially transmitted to the intrathoracic cavity at varying degrees depending on the compliance of the chest wall and lungs. The increase in intrathoracic pressure, in turn, is reflected as an increase in RA pressure, causing a reduction in the pressure gradient responsible for systemic venous return and ultimately a decrease in RV preload. These changes are not as drastic as would be expected owing to a lesser degree of increased mean venous systemic pressure. The increased intrapleural pressure and distention of the alveoli also lead to an increase in PVR and RV afterload. Both effects translate to a reduction in RV stroke volume in patients treated with positive pressure ventilation.

The effects of positive pressure ventilation on the LV can be more complex and variable. Although the reduction in RV preload could potentially allow the interventricular septum to shift to the right and possibly improve LV compliance, this is usually offset by the increased RV afterload causing RV dilation, which, along with decreased RV stroke volume and increased lung volumes, result in decreasing LV preload. Additionally, the increased intrapleural pressure leads to a reduction of LV afterload. These changes can improve cardiac output (CO) or affect it adversely depending on the patient's specific loading conditions, underlying cardiac disease, and myocardial performance. For example, in hypovolemic patients or those with preload-dependent cardiac conditions such as cardiac tamponade, RV infarction, or aortic stenosis, positive pressure ventilation is likely to decrease CO. However, by decreasing afterload, improving myocardial oxygen demand and shifting the preload to a more optimal relationship on the Starling curve, patients with LV systolic dysfunction may demonstrate improvement in CO. Last, patients with severe pulmonary hypertension and RV dysfunction can experience deleterious hemodynamic effects and possible circulatory collapse with positive pressure ventilation owing to multiple factors, including increased RV afterload and worsened RV ischemia, in addition to medications needed for induction and sedation of mechanically ventilated patients. Mechanical ventilation is also associated with major humoral and autonomic changes that can have a significant effect on the cardiovascular system. These effects can be complex and are beyond the scope of this chapter.

Indications for Advanced Respiratory Support in the Cardiac Intensive Care Unit

No studies have specifically evaluated the indications for mechanical ventilation and advanced respiratory support in CICUs. Several multicenter studies including medical and surgical intensive care units have been conducted in the past decade to shed light on the indications for mechanical ventilation. In the largest study of 412 ICUs, which included 1638 patients receiving mechanical ventilation, acute respiratory failure was the most common indication, accounting for 66% of the total study population (70% in the United States) with cardiogenic pulmonary edema being the third most prevalent cause of acute respiratory failure (13% of patients). Other causes for requiring advanced respiratory support included acute exacerbation of chronic respiratory disease (13%), coma, and neuromuscular disorders. More recent, smaller multicenter prospective studies conducted in single countries have shown similar trends. Despite a stable trend in the indications for mechanical ventilation, Esteban et al. showed an increase in the use of noninvasive ventilation (11.1% in 2004 compared to 4.4% in 1996).

The most common need for mechanical ventilation in the CICU continues to be cardiogenic pulmonary edema due to various myocardial, pericardial, arrhythmic, or valvular disorders. The increases in cardiac filling pressures can flood the alveoli with transudative fluids and lead to significant ventilation-perfusion mismatch that causes significant hypoxia, increased work of breathing, and possible ventilatory failure and hypercapnia that can be further exacerbated by bronchial edema. Other indications for mechanical ventilation in the CICU include the following:

  • States that result in loss of upper airway reflexes, increased risk of aspiration or hypoventilation/apnea, such as cardiac arrest, cardiogenic shock, or heavy sedation

  • Management of respiratory comorbidities with acute or chronic pulmonary disease

  • Concomitant neuromuscular disease

  • Nosocomial and iatrogenic complications leading to respiratory failure (pulmonary embolism, hospital-acquired pneumonia, critical illness polyneuropathy, pneumothorax)

  • Deep sedation required for procedures or in some patients with incessant unstable arrhythmias (ventricular tachycardia/electrical storm)

Common Modalities of Advanced Respiratory Support in the Cardiac Intensive Care Unit

As patients have presented with more complex cases and in attempts to reduce the need for endotracheal intubation, technological advancements have allowed the development of less invasive methods to treat respiratory failure. This was previously limited to noninvasive ventilation (NIV), but the more recent introduction of high-flow oxygen delivery via nasal cannula (HFNC) has provided a possible alternative in a select patient population.

High-Flow Nasal Cannula Oxygen

The limitations of conventional low-flow oxygen delivery (up to 15 L/min) provided by nasal prongs or face masks have been well recognized. In some patients with acute respiratory failure, the needed inspiratory flow could exceed 30 L/min and up to 120 L/min. This mismatch of flow provided by conventional low-flow devices results in an inconsistent fraction of inspired oxygen (FiO 2 ) and insufficient oxygenation for the demands of critically ill patients. A high-flow nasal cannula system delivers optimally heated and humidified oxygen at up to 60 L/min with an adjustable FiO 2 in the driving gas.

Physiologic Effects of High-Flow Nasal Cannula Oxygen

In addition to improved patient comfort, evidence suggests that adequate heating and humidification of the inspired gas protects from some of the adverse effects of breathing dry and cold air, including mucosal inflammation, impaired mucociliary clearance, and bronchoconstriction. Moreover, HFNC oxygen appears to be associated with improved oxygenation compared to conventional oxygen therapy with low-flow nasal cannula or face masks. The ability of HFNC oxygen to maintain flow rates equivalent to the inspiratory rates of patients with acute respiratory failure minimizes the dilution of delivered oxygen by entrainment of room air and allows for sustaining a constant and more reliable FiO 2 . An additional advantage is the ability of the HFNC systems to generate a small amount of positive airway pressure attributed to the resistance to expiratory flow generated by the continuous high flow of delivered gas. Studies conducted on healthy volunteers, postoperative patients, and critical care patients demonstrated variable degrees of positive airway pressure, ranging from 3 cm H 2 O and up to 10 to 12 cm H 2 O depending on flow rates, open-mouth breathing, and specific vendors. Another benefit provided by HFNC therapy is to washout carbon dioxide from anatomic dead space, thus minimizing reinhalation of expired gas and improving alveolar ventilation. These physiologic effects, along with improving thoracoabdominal synchrony, are credited with the decreased work of breathing associated with the use of HFNCs.

Effect of High-Flow Nasal Cannula Oxygen on Clinical Outcomes

Although the evidence regarding the improvement in clinical outcomes with HFNC therapy is not conclusive, several studies have shown promising results. In a randomized, multicenter trial of 310 patients, Frat and colleagues compared the impact of HFNC therapy to conventional oxygen therapy through a low-flow face mask or noninvasive ventilation on the rate of invasive mechanical ventilation for acute hypoxic respiratory failure. Patients randomized to HFNC demonstrated the lowest need for invasive mechanical ventilations (38% for the HFNC vs. 47% and 50% for conventional therapy and NIV, respectively) and the highest rate of ventilator-free days at 28 days in addition to the lowest 90-day mortality rate. Another randomized trial comparing postextubation treatment with HFNC to NIV when used for postsurgical patients who were at high risk for or who developed acute respiratory failure showed that the HFNC was not inferior to NIV in regard to the requirement for reintubation. These findings were not replicated in a meta-analysis of 14 trials that demonstrated no difference in mortality and intubation rates when treating acute hypoxic respiratory failure with HFNC compared to usual care. The paucity of data about the use of the HFNC is more apparent in the CICU patient population. Patients with cardiogenic pulmonary edema were excluded from the randomized study by Frat et al. and were underrepresented in the other trials. However, given the improvement in oxygen delivery and generation of low levels of positive airway pressure, the HFNC would theoretically be of significant benefit in the treatment of cardiogenic pulmonary edema. In a small series reported by Carratala-Perales et al., five patients demonstrating persistent hypoxemia with conventional therapy were successfully treated for acute decompensated heart failure using HFNC therapy.

HFNC oxygen therapy is highly promising as a treatment for mild to moderate acute hypoxic respiratory failure in CICUs. Further trials are necessary to help define the patient population that would benefit from this therapy, optimal flow-rate titration, predictors of therapy failure to avoid delays in escalation of therapy to mechanical ventilation, best rescue measures, and possible contraindications or adverse effects.

Noninvasive Ventilation

NIV refers to forms of mechanical ventilatory support that do not require endotracheal intubation. These devices commonly use full oronasal masks or nasal masks that use a silicone rim to form a tight seal. NIV can be delivered in the form of continuous positive airway pressure (CPAP) providing a baseline supra-atmospheric pressure throughout the respiratory cycle improving alveolar recruitment, lung compliance, and oxygenation, or bilevel positive airway pressure (BiPAP) that adds noninvasive inspiratory positive airway pressure (IPAP) to the baseline expiratory positive airway pressure (EPAP), which would also improve ventilation.

Noninvasive Ventilation in Cardiogenic Pulmonary Edema

As NIV became more widely available, its role in the treatment of pulmonary edema was readily recognized and early data from small studies were promising. These studies suggested that the use of CPAP in patients with heart failure could be associated with improvement in oxygenation, reduction in work of breathing, and overall improvement in cardiac performance and CO. In addition to these physiologic effects, small randomized trials emerged associating the use of NIV for the treatment of acute decompensated heart failure and pulmonary edema with lower rates of invasive ventilation and improved surrogates of treatment failure. However, these trials were too underpowered to show an effect on mortality when compared to standard therapy. The conclusions of seven meta-analyses or systematic reviews, albeit with overlapping studies analyzed and different outcomes assessed, yielded similar encouraging results correlating the use of NIV with improved in-hospital mortality and a reduced need for invasive ventilation.

In the largest multicenter randomized controlled study, the Three Interventions in Cardiogenic Pulmonary Oedema (3CPO) trial, Gray et al. compared the use of CPAP and noninvasive intermittent positive-pressure ventilation (NIPPV) with standard oxygen therapy in 1069 patients presenting to the emergency department with acute pulmonary edema with the primary endpoint being 7-day mortality and the composite outcome of mortality and need for invasive ventilation. As in smaller trials, NIV (CPAP or NIPPV) was associated with improvement in physiologic and subjective parameters but there was no statistically significant difference in 7-day mortality (9.8% for standard therapy vs. 9.5% for NIV, P = .87) compared to standard therapy. There were also no differences in the secondary outcomes of 30-day mortality (16.4% vs. 15.2%, P = .64) or in the need for intubation (2.8% vs. 2.9%, P = .90). However, the study was performed in patients undergoing treatment in the emergency department and did not enroll patients in other hospital settings. In addition, the overall mortality and intubation rates were lower than demonstrated in other studies, suggesting a less critically ill patient population. Most important, there was considerable crossover of about 15% from the standard therapy group to NIV that could have reduced adverse outcomes in the standard therapy group, particularly when assessing the need for intubation. Although some trials have suggested faster correction of gas-exchange abnormalities and improvement in dyspnea scores, the majority of meta-analyses and small randomized trials have demonstrated no difference in hospitalization outcomes, including mortality, when comparing CPAP to BiPAP. These results were replicated in the 3CPO trial.

Safety of Noninvasive Ventilation and Risk of Myocardial Infarction

The 3CPO trial reconfirmed the safety of using NIV in patients with cardiogenic pulmonary edema. Initial concerns about the increased risk of acute MI with NIPPV/BiPAP led to the termination of a trial by Mehta et al. Likewise, a weak signal was noted in a meta-analysis that included this study. However, subsequent studies that included the 3CPO trial did not find an association between the use of NIV and risk of acute MI. On the contrary, data have emerged to suggest comparable physiologic and clinical effects of NIV in the treatment of pulmonary edema complicating acute MI. In a retrospective study of 206 patients, including 26% who had an acute MI, NIV-associated improvement in oxygenation and reduction in the need for invasive ventilation was unaffected by the underlying cause of pulmonary edema.

Although the beneficial effect of NIV on mortality in patients with acute cardiogenic pulmonary edema is yet to be proven in a large randomized trial, NIV remains a valuable adjunct therapy with a favorable safety profile. Early introduction of NIV in the appropriate patient population (e.g., adequate level of consciousness, able to tolerate mask, acceptable level of secretions, synchronous breathing with respirator) remains a helpful and widely used rescue treatment for respiratory failure in the CICU. The modality used and the device-patient interface depends on patient-specific characteristics, gas exchange abnormalities, and system availability. Newer studies have evaluated the use of adaptive servoventilation (ASV) in acute cardiogenic pulmonary edema. ASV provides both positive expiratory pressure and pressure support during inspiration with automatic adjustments in the settings based on the analysis of the patient's breathing. Only limited data about the use of ASV in heart failure are available so far. Small trials have suggested a favorable hemodynamic effect, sympathetic modulation, and possible reduction in rate of intubation when compared to standard oxygen therapy in the treatment of acute pulmonary edema. These results are not conclusive and no trials comparing ASV to other forms of NIV have been conducted.

Invasive Mechanical Ventilation

Invasive mechanical ventilation requiring tracheal intubation remains the most commonly used method of advanced respiratory support in the CICU. The correction of gas exchange impairment is the paramount goal of mechanical ventilation as the underlying etiology of respiratory decompensation is addressed. To simplify the approach to mechanical ventilation, management of the impairments in gas exchange can be separated into oxygenation and ventilation.

Oxygenation

Maintaining adequate tissue oxygenation and efficient aerobic metabolism is of utmost importance in preserving tissue viability and improving outcomes of critically ill patients. When considering tissue oxygenation, oxygen delivery is determined as follows:


DO 2 = CO × [ ( 1.3 × Hb × SaO 2 ) + ( 0.003 × PaO 2 ) ]

Since most of the oxygen content in blood is bound to hemoglobin, the oxygen delivery rate (DO 2 ) is therefore directly proportional to CO, hemoglobin concentration (Hb), and hemoglobin oxygen saturation (SaO 2 ). Thus, the optimization of CO and oxygen-carrying capacity of blood are as essential as increasing SaO 2 or PaO 2 in critically ill patients. Likewise, it is crucial to consider the interactions between these factors. In some patients, changes in mechanical ventilation to improve SaO 2 could lead to a decrease in CO that would overall adversely affect tissue oxygenation.

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