53 Ventilatory strategies in acute heart failure

Ventilatory support and positive end-expiratory pressure (PEEP) are pivotal treatments of cardiogenic pulmonary oedema. As recently recommended, it should be introduced within minutes of admission at hospital for acute heart failure (HF) and ideally at home in case of prehospital management. Ventilatory support is one of the few tools that have been proven to change short-term outcome in acute HF.

The primary cause of hypoxaemia in cardiogenic pulmonary oedema is the intrapulmonary shunt related to the filling of alveolar by oedema fluid. PEEP will keep the alveoli open during inspiration and expiration. PEEP will augment functional residual capacity (FRC) thereby decreasing intrapulmonary shunting. As a consequence, arterial oxygen content will rise, leading to a greater oxygen transport. Furthermore, the increase in airway and alveolar pressure toward positive values tends by itself to reduce pulmonary oedema.

Pulmonary oedema also worsens the work of breathing. Indeed, oedema fluid reduces pulmonary compliance and engorgement of blood vessels—by reducing the caliber of the peripheral airways—increases airway resistance. This may lead to hypercapnia and impaired consciousness might occur as the consequence of respiratory exhaustion. Ventilatory support and PEEP can allow the alveoli and bronchi to stay open and ultimately improve pulmonary compliance by reducing lung water. Those effects of PEEP will improve oxygenation, reduce congestion of the small airways, and reduce hypercapnia.

PEEP and ventilator support will have two beneficial effects on the heart: (1) decreasing left ventricular preload by reducing venous return and (2) reducing left ventricular afterload.

Heart–lung interactions during mechanical ventilation have been extensively described. By increasing intrathoracic pressure, PEEP reduces right ventricular preload. Thus, when the heart is congestive, PEEP will reduce the venous return to the right and ultimately the left ventricles. Indeed, PEEP also increases the right ventricular afterload leading to a reduction of left ventricular preload.

PEEP and ventilator support have also direct beneficial effects of left ventricular function. PEEP reduces transmural pressure of both the left ventricle and the initial ‘intrathoracic’ portion of the aorta. Those effects will lead to reduced left ventricular afterload, improved myocardial oxygen consumption, and a better left ventricular contraction. The latter may lead to improved cardiac index.

In most cases of acute HF, pulmonary congestion is the main clinical sign and left ventricular function is often maintained. Accordingly, only moderate levels of PEEP (5–10 cmH₂O) are needed to improve Pao₂ by increasing alveolar recruitment, thereby increasing FRC and reducing intrapulmonary shunt. In few patients with signs of congestion and reduced cardiac output, PEEP might improve cardiac index. By contrast, in patients with low pulmonary capillary wedge pressure (PCWP), PEEP may reduce cardiac index.

Noninvasive ventilation (NIV) is a modality of ventilatory support without endotracheal intubation and sedation. It is usually delivered through a face mask but sometimes through a helmet. NIV is now recognized as a very simple and efficient treatment of acute pulmonary oedema due to acute HF. NIV has a rapid and tremendous effect on severe pulmonary oedema and is associated with a low cost-effectiveness ratio. NIV improves dyspnoea, oxygenation, and hypercapnia. Many NIV techniques require less than 1 h training and can be used by every physician or nurse in charge of patients suffering from acute HF and pulmonary oedema.

Two NIV techniques are particularly effective in cases of cardiogenic pulmonary oedema: noninvasive pressure support ventilation (NIPSV) and continuous positive airway pressure (CPAP). NIPSV provides (1) pressure support during the inspiratory phase and (2) PEEP. Of note, NIPSV is similar to bilevel positive airway pressure (BiPAP). Pressure support actively helps the patient during the inspiration. It requires the use of a mechanical ventilator with energy, air, and oxygen inputs. Thus during NIPSV, the patient makes a very small effort that triggers the inspiratory flow. CPAP is less sophisticated (no ventilator is required) and the most widely used NIV technique. Unlike NIPSV, in CPAP there is no active help in the inspiratory phase of respiration (no pressure support) and breathing is entirely spontaneous. CPAP requires a device that provides a high air/oxygen flow into the face mask. A flow higher than the patient’s maximum instantaneous inspiratory flow allows maintenance of a constant positive pressure.

CPAP and NIPSV are both indicated as soon as possible after admission for cardiogenic pulmonary oedema. Three recent meta-analyses showed that early application of NIV in patients with acute cardiogenic pulmonary oedema reduces both the need for intubation and short-term mortality; however, in a large randomized controlled trial, NIV improved clinical parameters but not mortality. NIV should not be used in patients who cannot cooperate or if there is an immediate need of endotracheal intubation as a result of progressive life-threatening hypoxia.

A PEEP of 5–7.5 cmH₂O should be applied first and titrated to clinical response up to 10 cmH₂O; Fio₂ delivery should be at least 0.40. Usually NIV is applied 30 min/h until the patient’s dyspnoea and oxygen saturation remain improved without NIV.

The two potential adverse effects of NIV are worsening of severe right ventricular failure and pneumothorax.

Sometimes, intubation and invasive mechanical ventilation are needed in case of respiratory exhaustion, haemodynamic instability, cardiogenic shock, impaired consciousness, and/or severe cardiac arrhythmias. Some of the ventilator parameters should be carefully chosen.

Under mechanical ventilation, arterial oxygenation, and hypercapnia should be improved within the first hour. In case oxygenation worsens, Box 53.1 provides an algorithm that should be followed to detect any complication relating to mechanical ventilation.

When the patient’s condition is improved (e.g. if the patient is awake with Fio₂ 〈40–50%), discontinuation of mechanical ventilation should be considered as soon possible to minimize related complications. However, patients must also satisfy a number of criteria before extubation is contemplated. The classical criteria for extubation are absence of uncontrolled ongoing infection (temperature ≤38°C), haemodynamic stability without vasopressors or moderate levels of dopamine or dobutamine, no sedation or sedative infusion, adequate cough, and adequate neurological status.

When patients meet these described criteria, enteral feeding should be stopped within 6 h preceding the weaning trial. A 30-min T-piece trial helps evaluate a patient’s ability to sustain spontaneous breathing. The patient is disconnected from the ventilator, and left to breathe spontaneously through an endotracheal tube with oxygen added laterally through an adaptor at the upper extremity of the tube (hence the term T-piece or T-tube). The first successful T-piece trial should be followed by extubation.

It is recommended to apply NIV, essentially CPAP, as early as possible in patients suffering from acute cardiogenic pulmonary oedema. CPAP should be applied 30 min/h until dyspnoea and oxygenation is improved. NIV improves both lung and heart functions.