Chapter 23: Cardiac Failure

Cardiovascular disease is the leading cause of death in the United States. As a result, many patients present to the emergency department or general patient care units with congestive heart failure or acute myocardial infarction. Many of these patients benefit from the application of positive pressure ventilation. Increasingly the respiratory support is applied noninvasively.

Heart-Lung Interactions

The normal changes in intrathoracic pressure during spontaneous breathing facilitate venous return and maintains adequate preload to the right heart. In addition, the negative mean intrathoracic pressure reduces left ventricular afterload. Left ventricular dysfunction with myocardial infarction (MI) or severe congestive heart failure results in increased left ventricular preload, pulmonary edema, decreased cardiac output, hypoxemia, and work-of-breathing. Of particular concern is the increase in blood flow required by the diaphragm and accessory muscles as a result of ventricular dysfunction. The respiratory muscles receive as much as 40% of the cardiac output during stress, which can result in a reduction of blood flow to other vital organs.

Effects of Mechanical Ventilation

With positive pressure ventilation, the mean intrathoracic pressure is positive. During inspiration, intrathoracic pressure increases, whereas it decreases with spontaneous breathing. This decreases left ventricular preload and afterload. In the patient with acute left ventricular dysfunction, this may enhance the performance of a compromised myocardium. In the hypovolemic patient, however, these effects may further decrease cardiac output.

The response of the cardiovascular system to positive pressure ventilation is dependent on cardiovascular and pulmonary factors. From a pulmonary perspective, the compliance of the lungs and chest wall affects the transmission of alveolar pressure into the intrathoracic space. The most deleterious effect on hemodynamics occurs with compliant lungs and a stiff chest wall, which results in greater pressure in the intrathoracic space. Cardiovascular volume and tone, pulmonary vascular resistance, and right and left ventricular function determine the effect of intrathoracic pressure on hemodynamics (Table 23-1).

Positive End-Expiratory Pressure

Since positive end-expiratory pressure (PEEP) elevates intrathoracic pressure, it reduces venous return and decreases preload. In the presence of left ventricular dysfunction with an elevated preload, PEEP generally improves left ventricular function. PEEP may increase pulmonary vascular resistance, thus increasing right ventricular afterload and decreasing left heart filling. PEEP may decrease the compliance of the left ventricle by shifting the intraventricular septum to the left. By increasing the pressure outside the heart, PEEP may improve left ventricular afterload.

Indications

Severe heart failure leads to hypoxemia, increased myocardial work, and increased work-of-breathing (Table 23-2). Mechanical ventilation in this setting is indicated to reverse the hypoxemia, reduce the work-of-breathing, and decrease myocardial work. Some patients with severe heart failure develop acute hypercarbia. Therefore the initial treatment includes noninvasive continuous positive airway pressure (CPAP).

Continuous Positive Airway Pressure

The use of mask CPAP in the patient presenting with acute left ventricular failure and pulmonary edema reduces the work-of-breathing and the work of the myocardium. It also increases Pao₂, decreases Paco₂, reduces the need for intubation, and increases survival. In many patients, CPAP provides sufficient unloading of myocardial and respiratory work while pharmacologic treatment modifies cardiovascular function, avoiding invasive management. Generally, CPAP is most useful in patients who are awake, oriented, and cooperative. If the CPAP mask further agitates the patient, it should be removed and invasive ventilatory support considered. Initial CPAP settings are generally 10 cm H₂O with 100% oxygen.

Noninvasive ventilation (NIV) has also been used to avoid intubation of patients with acute congestive heart failure. For many such patients, the outcomes with CPAP or NIV are equivalent. The specific indication for NIV is hypercarbic ventilatory failure along with the hypoxemic ventilatory failure. However, NIV should be avoided in patients with acute MI, hemodynamic compromise, significant cardiac arrhythmias, and depressed mental status. In these patient presenting with respiratory failure, invasive ventilatory support should be provided rather than NIV.

Ventilator Settings

Since spontaneous breathing potentially diverts blood flow to the respiratory muscles, continuous mandatory ventilation (A/C) should be used (Figure 23-1). Either pressure-control or volume-control ventilation is acceptable. In spite of the pulmonary edema that may be present at the time of initiating ventilatory support, pharmacologic treatment results in rapid resolution. Tidal volumes of 6 to 8 mL/kg ideal body weight are usually adequate with respiratory rates greater than 15/min to achieve eucapnia. Plateau pressure should be less than 30 cm H₂O. Inspiratory time should be short (≤ 1 second). Fio₂ should initially be set at 1 and then titrated per Spo₂ and blood gases. PEEP of 5 to 10 cm H₂O should be applied as support for the failing heart. Care must be exercised with the titration of PEEP because of the complex effects of PEEP on cardiac function. However, most patients with severe left ventricular failure benefit by the application of PEEP (Table 23-3).

Monitoring

Hemodynamics are monitored during pharmacologic therapy and mechanical ventilation (Table 23-4). Pulse oximetry is used to ensure that patients are well oxygenated. Periodic arterial blood gases are needed. Plateau pressure should be monitored. In addition, urine output, and fluid and electrolyte balance should be carefully monitored.

Liberation

Provided no underlying chronic pulmonary disease or secondary pulmonary problems develop and the left heart failure is appropriately managed, weaning can be a relatively easy process. However, in these patients cardiovascular system function is most optimal with increased mean intrathoracic pressure. The elimination of mechanical ventilatory support during a spontaneous breathing trial might result in an increase in left ventricular preload and pulmonary edema. Weaning may progress rapidly to low level pressure support and CPAP, but pulmonary edema may develop when positive pressure ventilation is discontinued. Some patients may develop ischemic changes during weaning. In this case, ventilatory support must be continued until therapy is successful at improving cardiac function (eg, diuresis, afterload reduction).