Low cardiac output syndrome is a postoperative complication caused by reperfusion and ensuing oxidative stress to the pulmonary and cardiac tissues. This syndrome is important to consider for its association with high morbidity and mortality due to impaired cardiovascular function.
Low cardiac output syndrome (LCOS) is a reduction in cardiac output often seen in postoperative situations, especially those of coronary artery bypass grafting (CABG), and cardiopulmonary bypass (CPB) [1] [2]. It happens on account of the oxidative stress caused by reperfusion after surgical manipulations. The oxidative stress, as well as inflammatory reactions, cause a disturbance of function in the myocardium resulting in a necessity of inotropic support [3]. Pulmonary tissues also undergo reperfusion that participates in the development of vascular reactivity and damage to the alveoli causing pulmonary edema; the latter is responsible for poor tissue oxygenation [4].
There are no strict clinical criteria for diagnosing the patient with possible LCOS. Strong indications for LCOS is hemodynamic instability and impaired tissue oxygenation occurring postoperatively. Additionally, one of the essential pointers is the need for administration of afterload reduction agents or inotropic agents e.g. dobutamine, epinephrine, and dopamine in order to maintain sufficient cardiac function [5]. Intra-aortic balloon counterpulsation support and positive pressure oxygenation are also important factors contributing to the diagnosis [3] [2].
On examination, the patient will reveal cold extremities, particularly in the most distal parts like toes, an absence of pedal pulse and a decrease in the systolic pressure measuring under 90 mmHg. Likewise, weakened perception of sensation may be noted [6]. LCOS is considered to be associated with high risk of morbidity and mortality, thus prompt recognition and preservation of adequate circulation are of immense importance [2].
Low cardiac output syndrome can be the cause of decreased tissue oxygenation and disturbance in the cardiovascular system. Parameters evaluating the dynamics of this syndrome are linked with measurements of the arterial blood gas, central venous pressure, blood pressure, and estimates of the cardiac output.
It is possible to assess cardiac output (CO) directly by thermodilution. This technique includes a placement of the pulmonary artery catheter and is considered a gold standard for measuring the CO. It also gives data of right ventricle activity, such as right ventricular ejection fraction and right ventricular end diastolic volume. Although there are some drawbacks to this method, firstly it is an invasive procedure and secondly, it is not meant for continuous measurement of the CO [7]. There are other less invasive techniques for measuring the CO e.g. with transthoracic (TTE) or transesophageal (TEE) echocardiography.
LCOS is considered if the cardiac index (which is calculated with CO as a variable) is less than 2.2 L/min/m2, pulmonary artery occlusion pressure (PAOP) is more than 16 mmHg, and oxygen saturation drops to less than 60% [6] [8].
In the case of poor oxygenation caused by LCOS, serum lactate levels increase to more than 2 mmol/L for at least 2 hours and metabolic acidosis is recognized. Compensatory mechanisms will be exhibited by oliguria with urine output of less than 1.0 mL/kg/h [6].
Arterial blood gas analysis may uncover changes in partial arterial oxygen tension with less than 100 mmHg and partial arterial carbon dioxide tension of value exceeding the normal range of 35–45 mmHg. Central venous pressure is also likely to deviate from the norm of 6–8 mmHg [6] [9].