Acute cardiac failure
In acute left ventricular failure there is oedema of the small airways which increases the airway resistance, and ventilation-perfusion mismatching which causes hypoxia. Pulmonary oedema reduces the lung compliance and lung volumes, and increases the work of breathing. The myocardial oxygen supply falls, due to hypoxia, and there may also be a metabolic acidosis. The sympathetic activity increases the heart rate and blood pressure.
Treatment with diuretics, nitrates and opiates reduces sympathetic activity and leads to vasodilatation. Nevertheless intubation and ventilation may still be required, although the intubation rate can be reduced by around 30% by the application of continuous positive airway pressure. This reduces ventilationperfusion mismatching, offsets intrinsic PEEP, reduces the work of breathing, and reduces the left ventricular afterload and preload. Continuous positive airway pressure is safe if the left ventricular end-diastolic pressure is greater than 12 cmH2O, but if it is less than this it may cause hypotension and possibly myocardial infarction. Bilevel pressure support ventilation may be better tolerated with a lower expiratory pressure, but is more likely to reduce the arterial Pco2.
Drug therapy. Standard drug therapy, apart from beta blockers, has little effect on the arousal index, sleep quality or ventricular dysrhythmias. Respiratory stimulants, such as theophyllines and acetazolamide, may have some benefit.
Oxygen. This reduces the hypoxic drive to breathe and thereby may increase the arterial Pco2 and reduce the frequency of central apnoeas as well as the after-load due to peripheral vasoconstriction.
Continuous positive airway pressure (CPAP) treatment. 1 Central sleep apnoeas. A level of at least 10 cmH2O is required to have a significant effect on preload. CPAP is in effect a left ventricular assist device, which reduces the cardiac diameter and thereby by Laplace's law reduces the wall tension. It reduces sympathetic activity which leads to a fall in heart rate and blood pressure, with less peripheral vasoconstriction, and this reduces the left ventricular afterload. The left ventricular ejection fraction may increase and, if this reduces the circulation time, Cheyne-Stokes respiration will be less evident. Any reduction in pulmonary oedema also reduces ventilation-perfusion mismatching, reduces the respiratory drive, increases arterial Pco2 and tends to relieve any central apnoeas and Cheyne-Stokes respiration.
Central apnoeas may not be abolished immediately and CPAP should be reassessed after around 1 month with a repeat sleep study. Abolition of central apnoeas may not be sufficient to have the desired effect on preload, which makes it difficult to assess the optimum level of CPAP.
2 Obstructive sleep apnoeas. CPAP acutely relieves upper airway obstruction, reduces sympathetic drive and thereby reduces blood pressure. This reduction in left ventricular afterload increases the ejection fraction, reduces pulmonary oedema, and increases the arterial P02. In the long term the left ventricular ejection fraction increases and the left ventricle becomes smaller.
Non-invasive ventilation. Conventional pressure or volume present nasal ventilation increases the functional residual capacity and lung compliance by recruitment of alveoli through relief of pulmonary oedema. It also reduces ventilation-perfusion mismatching, but impairs venous return. It reduces the work of breathing and the metabolic rate so that there is less oxygen requirement and carbon dioxide elimination.
Nasal ventilation should not be used if there is unstable cardiac ischaemia or low blood pressure. If there is a low filling pressure its main effect is to reduce cardiac output by impairing venous return. Nasal pressure support ventilation is indicated if the arterial Pco2 is raised, if CPAP is poorly tolerated, or if the breathlessness persists despite CPAP. Inspiratory pressures of 10-15 cmH2O and 5 cmH2O expiratory pressure are usually effective.
Adaptive servoventilation has been proposed as a method of providing sufficient pressure to have the benefits of CPAP without leading to overventilation and a lowering of the Pco2. This type of ventilator adjusts the applied pressure frequently during sleep, with the aim of stabilizing the respiratory pattern. It reduces brain natriuretic peptide and urinary cate-cholamine excretion and improves daytime sleepiness.
Cardiac pacing. Cardiac resynchronization therapy may be indicated in heart failure with left bundle branch block. This delays left ventricular contraction and leads to desynchronization of the two ventricles, and a reduction in cardiac output. Insertion of a pacemaker resynchronizes ventricular function and can be combined with an implanted defibrillator. It increases the cardiac output, improves left ventricular failure and central sleep apnoeas and Cheyne-Stokes respiration in sleep.
Was this article helpful?