Heart–lung interactions result from changes in intrathoracic pressure and lung volume that affect preload, contractility and afterload.
Intrathoracic pressure: the heart is a pressure chamber within a pressure chamber. There is a pressure gradient for venous return between the venous reservoirs and right atrial pressure. An increase in mean intrathoracic pressure (transmitted through the compliant right atrial wall) increases right atrial pressure and impedes venous return.
Preload and contractility – right ventricle (RV) output and left ventricle (LV) output are in series, therefore changes in RV preload alter LV preload and end-diastolic volumes. Left ventricular end-diastolic volume (LVEDV) is the main determinant of the position of the LV on the Frank–Starling curve. If end-diastolic volume falls, cardiac output falls. Some of these changes can be modified by infusion of fluid (to increase central venous pressure) when mechanical ventilation begins. With spontaneous ventilation, the decrease in mean intrathoracic pressure on inspiration increases venous return, LVEDV and stroke volume.
Lung volumes: changes in lung volume affect autonomic tone and pulmonary vascular resistance (PVR). In the normal range (Vt < 10 ml/kg) heart rate increases as vagal tone decreases (sinus arrhythmia). PVR increases if lung volume decreases below normal end-expiratory levels (e.g. ARDS, pneumonia). As lung volume decreases, lung interstitial radial tone decreases, small airways collapse, alveolar hypoxia follows and hypoxic pulmonary vasoconstriction (HPV) increases (alveolar recruitment such that FRC increases may reverse this process). When lung volume increases there is a point at which increased alveolar pressure relative to capillary pressure collapses small vessels and increases PVR (emphysema, hyperinflation, gas trapping).
Contractility and afterload – as PVR increases, changes in pulmonary hypertension and RV ejection result in a fall in cardiac output. If the right ventricular end-diastolic volume (RVEDV) becomes significantly raised, bulging of the intraventricular septum into the left ventricular cavity can occur, LV compliance is reduced (ventricular interdependence – changes in RVEDV inversely change LV compliance). LVEDV and stroke volume fall in a fashion analogous to cardiac tamponade. Increased RV wall tension can compromise RV coronary perfusion and lead to a further reduction in cardiac output. Very large tidal volumes can restrict absolute cardiac volume by direct compression of the heart (biventricular free wall can collapse into the septum) and limit end-diastolic volumes.
Patients with gas trapping: hyperinflation can occur from premature airway closure on expiration (emphysema, acute COPD or asthma) or when expiratory time is too short to allow complete exhalation – gas trapping (inverse ratio ventilation). Cardiac output can fall because of an exaggeration of the effects described above. The immediate manoeuvre if cardiac output is falling acutely is to allow a longer expiratory time and to consider bronchodilator therapy, reduced tidal volumes and judicious use of PEEP or CPAP to splint airways open in expiration.
Patients with heart failure: in patients with existing heart failure, the increase in intrathoracic pressure and reduction of preload can increase cardiac output. If RVEDV is increased (e.g. associated with COPD cor pulmonale or excessive negative pressures on inspiration in spontaneous respiration) the reduction in preload by intermittent positive-pressure ventilation (IPPV) can reduce RVEDV and through ventricular interdependence lead to an improvement in LV compliance and LVEDV.
Afterload reduction can also occur because raised intrathoracic pressure is transmitted through the walls of the ventricle and thoracic aorta causing a reduction in the work of the left ventricle to maintain a specific systolic arterial pressure (i.e. pressure in the ventricle is supplemented by the actual intrathoracic pressure).
The ultimate cardiovascular reponse to acute respiratory failure is a balance of the basal cardiovascular function of the patient, the respiratory pathophysiology and the ventilatory pattern.
Mechanical ventilation with positive airway pressure leads to a reduction in renal water and sodium excretion. The increase in intrathoracic pressures results in a decrease in cardiac output and mean arterial pressure. Low pressure baroreceptors discharge leads to increased sympathetic activity, raising plasma antidiuretic hormone (ADH) concentration (lower urine output). The reduction in renal perfusion and increase in renal sympathetic activity stimulate the renin–angiotensin system. Angiotensin II formation stimulates aldosterone production with a resultant increase in reabsorption of water and sodium. Reduced venous return and less stretch of the right atrium decrease atrial natriuretic peptide (ANP) release, contributing to increased sodium reabsorption and less diuresis. The higher mean intrathoracic pressure increases venous pressure and causes some kidney congestion, an additional problem when associated with low renal perfusion pressure from reduced cardiac output. These effects are not significant in a healthy kidney but may exacerbate the situation if associated with other co-morbidities.
Hepatic blood flow depends on a balance of flow through the hepatic artery and portal circulation. The reduction in cardiac output associated with IPPV leads to a proportional reduction in hepatic blood flow. In addition, raised mean intrathoracic pressure leads to increased hepatic venous congestion, which has a deleterious effect on portal vein blood flow (a relatively low pressure system). Hepatic cellular function may be compromised especially if associated with other co-morbidities.
An increase in intrathoracic pressure and use of PEEP is accompanied by an increase in intracranial pressure. The raised mean intrathoracic pressure obstructs venous return from the jugular veins. This, combined with the fall in cardiac output leads to a fall in cerebral perfusion pressure. In the healthy brain, autoregulation ensures adequate cerebral perfusion despite changes in arterial pressure and intracranial pressures. This autoregulation may be disrupted by cerebral pathologies with a risk of hypoperfusion. Therefore, PEEP should be used with caution in these patients.