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INTRODUCTION The heart and lungs are both driven by pressure, share space in the thorax and are anatomically contiguous. It should not be surprising that therapeutic modalities that target the chest and lungs by alterations in pressure, surgery or radiation may affect the heart in a negative manner, inducing iatrogenic complications. Furthermore, certain inhaled gases and both inhaled and oral medi­ cations used to treat pulmonary symptoms and diseases may also have undesirable cardiovascular effects. This chapter ­ will review how therapy directed to improve or cure thoracic disease and dysfunction may induce iatrogenic complications to the heart thereby causing unwanted morbidity. This review ­ will not include complications of invasive diagnostic pulmonary procedures resulting in cardiac harm, e.g., fiberoptic bronchoscopy with transbronchial biopsy causing pneumomediastinum and cardiac tamponade, since ­ these are operator dependent and the cardiac complications are to a major extent preventable. CARDIOVASCULAR IATROGENICITY FROM PRESSURE-­ALTERING PULMONARY THERAPY CPAP and PEEP Normal lung inflation is accomplished by the generation of increasingly negative intrathoracic pressure (ITP). This benefits normal circulation by increasing the pressure gradient for peripheral venous return into the thorax. During respiratory failure, positive pressure ventilation (PPV) is often instituted to provide assistance to breathing. This may be in the form of noninvasive ventilation with applied continuous positive airway pressure (CPAP) or PPV with varying degrees of positive end-­ expiratory pressure (PEEP), delivered to an intubated patient by a mechanical ventilator. Applications of ­ these modalities ensure that intrathoracic pressure is increased over normal throughout the breathing cycle, with CPAP giving the least increment for any given pressure (1). Depending on the patient’s intravascular volume status CHAPTER 24 Cardiovascular Iatrogenicity of Respiratory Therapeutic Modalities Michael S. Nolledo, Pauline O. Lerma, and Teodoro V. Santiago 288 / Cardiovascular Iatrogenicity of Respiratory Therapeutic Modalities tory failure and is now the recommended mode of ventilation (9). This advantage has been attributed to less volutrauma to the airways and lung structures (10). Largely overlooked are the relative salutary effects of this mode of ventilation on the cardiovascular system and their pos­ si­ ble contribution to improved outcomes. It should be noted that PPV is acutely beneficial in congestive heart failure (CHF) ­ because peripheral venous pressure is already elevated in this condition and both the diminished RV preload and LV afterload are of benefit to the failing heart. Adaptive Servo-­Ventilation in Congestive Heart Failure and Central Sleep Apnea Cheyne-­ Stokes respiration (CSR) and central sleep apnea (CSA) occur in 25% to 40% of patients with chronic CHF with reduced left ventricular ejection fraction (LVEF) (11). Their occurrences generally indicate a poor prognosis and are in­ de­ pen­ dent risk markers for death (12). CSA is characterized by repetitive apneic episodes of 10 seconds or longer due to loss of the central breathing signal. It is accompanied by repeated arousals from sleep, insomnia, and hypoxemia. The genesis of this periodic breathing in CHF is unclear, although a prolonged circulation time to the brain coupled with hypocapnia and enhanced chemosensitivity to carbon dioxide may play a role in creating an unstable respiratory controller (13).­ Because of the poor prognosis for CSA, adaptive servo-­ ventilation (ASV), a form of PPV, was introduced as therapy. ASV introduces servo-­ controlled positive respiratory pressures on top of positive expiratory pressures. It prevents the apneic episodes during sleep ­ because it provides servo-­ controlled breaths if no spontaneous respirations occur (14). Initial studies of CHF patients with CSA who ­ were treated with ASV showed improvement in plasma B-­ type natriuretic peptide , functional outcomes, LVEF, and mortality (15,16). However, a ­ later British study involving 1,325 patients with reduced LVEF (45% or less) and apnea plus hypopnea index of 15 events or more per hour of sleep showed that ASV increased all-­ cause and cardiovascular mortalities ­ after 12 months of therapy (17). The mechanism for the increase in mortality is currently unknown. One hypothesis is that periodic breathing may be beneficial to the failing heart by increasing sympaand peripheral venous pressure, such therapeutic modalities not uncommonly decrease cardiac output and arterial blood pressure. As heart rate is unaffected by PPV, the fall in cardiac output is due to a fall in stroke volume (2). The mechanism for this reduction primarily revolves around the diminishing pressure gradient between the peripheral veins and intrathoracic vessels reducing venous return to the chest. Some compensation to minimize the changes in venous return may involve partial preservation of this pressure gradient by sympathoadrenal stimulation or increases in stressed intravascular volume (3). However, the normal right...


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