Effect of One Lung Ventilation on Cardiac Output
One lung ventilation (OLV) typically reduces cardiac output by 10-25% through multiple mechanisms including increased pulmonary vascular resistance, impaired venous return, and ventricular interdependence, with patients having pre-existing cardiovascular disease experiencing substantially greater hemodynamic compromise.
Primary Hemodynamic Mechanisms
Pulmonary Vascular Resistance and Right Ventricular Afterload
OLV increases pulmonary vascular resistance (PVR) in direct proportion to mean airway pressure, with tidal forces and positive end-expiratory pressure (PEEP) consistently elevating PVR during the respiratory cycle 1.
Transpulmonary pressure changes are the fundamental mechanism by which mechanical ventilation affects pulmonary artery pressure and right ventricular afterload during OLV 1.
During positive pressure inspiration, alveolar pressure increases, causing PVR to rise, with higher mean airway pressures producing greater cyclic variations in mean pulmonary artery pressure 1.
West Zone 2 and Zone 1 conditions develop during OLV, where alveolar pressure exceeds pulmonary venous or arterial pressure respectively, causing microvascular collapse and substantially increasing RV afterload 1.
Venous Return and Preload Effects
Positive pressure ventilation during OLV reduces right ventricular preload by increasing intrathoracic pressure and decreasing the pressure gradient for venous return 2.
The normal pressure gradient from systemic venous reservoir to heart is only 4-8 mmHg, so positive pressure ventilation substantially impairs venous return and consequently reduces cardiac output 3.
PEEP-induced increases in central venous pressure further compromise venous return, with the entire fall in cardiac output being a consequence of reduced left ventricular stroke volume since heart rate typically remains unchanged 4.
Ventricular Interdependence
Right ventricular overdistension from increased afterload causes the interventricular septum to shift leftward, constraining left ventricular filling and reducing LV preload through ventricular interdependence 3, 2.
This diastolic interaction between ventricles is a critical mechanism reducing cardiac output during OLV, particularly when RV afterload is elevated 4.
High-Risk Patient Populations
Pre-existing Cardiovascular Disease
Patients with chronic heart failure experience abnormal ventilatory responses and reduced cardiac output for metabolic rate, with increased pulmonary vascular resistance and subclinical pulmonary edema making them particularly vulnerable to OLV 5.
Patients with coronary artery disease have reduced peak cardiac output and ventilatory reserve, though chronicity rather than acute flow changes appears responsible for the severity of compromise 5.
Pulmonary Vascular Disease
Patients with pulmonary hypertension, pulmonary embolism, or chronic thromboembolic disease demonstrate substantially greater hemodynamic compromise from positive pressure ventilation-induced PVR increases 5, 1.
These patients develop pathologic cardiovascular limitation depending on extent of pulmonary vascular involvement, underlying pathology, disease progression, and the heart's inability to maintain adequate cardiac output against increased pulmonary vascular resistance 5.
Pulmonary vascular resistance remains constant or may even rise during exercise in these patients, compared to normal subjects where it falls due to vascular recruitment and distension 5.
Right-to-left shunting across a patent foramen ovale occurs in approximately 20% of patients with pulmonary vascular disease and elevated right-sided heart pressures, further compromising oxygenation and cardiac output 5.
Single Ventricle Physiology
Patients with single ventricle anatomy who have undergone Stage I procedure or Fontan physiology experience substantially greater hemodynamic compromise from positive pressure ventilation effects on PVR 5.
These patients remain in a chronic preload-deficient state, operating on the steep portion of the Frank-Starling curve, making them exquisitely sensitive to any reduction in venous return 3.
Magnitude of Cardiac Output Reduction
Typical Response
Cardiac output during OLV is reduced to approximately 50% of what a normal subject could achieve at peak exercise in patients with severe lung disease, though the cardiac output-to-metabolic rate relationship typically remains normal 5.
The reduction in cardiac output is entirely due to decreased stroke volume, as heart rate at a given oxygen consumption is actually higher than normal in these patients 5.
Factors Amplifying Reduction
In ARDS, acute cor pulmonale develops in 20-25% of cases, partly driven by mechanical ventilation effects on pulmonary vascular resistance, with substantially greater cardiac output reductions 1.
The magnitude of pressure transmission depends on lung compliance, with approximately 50% of alveolar pressure changes transmitting to pleural pressure in normal lungs, but diseased lungs with reduced compliance transmit less 1.
Patients with decreased lung compliance and reduced pulmonary vascular reserve experience particularly prominent West Zone effects and greater cardiac output reductions 1.
Clinical Management Considerations
Ventilator Settings
Configure tidal volume of 6-8 mL/kg predicted body weight to minimize ventilator-induced lung injury and excessive increases in mean airway pressure 6.
Initiate with PEEP of 5 cmH₂O and individualize according to response, maintaining driving pressure <18 cmH₂O to limit PVR increases 6.
Avoid excessive PEEP (>15 cmH₂O) as this causes overdistension and worsens right ventricular function 6.
Hemodynamic Optimization
Extreme caution with fluid administration is required, as aggressive volume expansion worsens right ventricular function when afterload is elevated 6.
Do not administer >500 mL of fluids in patients with RV dysfunction, as this causes RV overdistension and hemodynamic collapse 6.
Consider vasopressors to maintain systemic perfusion rather than volume loading when cardiac output is reduced 6.
Monitoring
Pulse pressure variation can predict fluid responsiveness even at low tidal volume ventilation during OLV 7.
Echocardiographic evaluation should focus on right ventricular size, thickness, and systolic function, as the RV is most affected by positive pressure ventilation 2.
Dynamic methods such as end-expiration occlusion test, passive leg raise, and fluid challenge are preferable to assess fluid responsiveness, as inferior vena cava assessment is unreliable in mechanically ventilated patients 2.
Critical Pitfalls to Avoid
Do not routinely hyperventilate, as this worsens global perfusion by excessive increases in intrathoracic pressure and cerebral vasoconstriction 5.
Recognize that hypoxemia may be refractory due to right-to-left shunt through patent foramen ovale when right atrial pressure exceeds left atrial pressure 6.
Avoid assuming adequate oxygen delivery based solely on arterial blood gases, as cardiac output reduction may critically impair oxygen delivery despite adequate arterial oxygen content 8.
Do not delay consideration of extracorporeal support in high-risk patients with single ventricle physiology or severe pulmonary hypertension who develop cardiovascular collapse during OLV 5.