Low Cardiac Output Syndrome (LCOS)

Definition A clinical and biochemical state where there is inadequate systemic oxygen delivery (DO2) to meet the metabolic demands of the patient. 

When Does it Happen?In patients with severe sepsis, myocarditis,

and cardiomyopathies and after pediatric cardiac surgery!

It affect up to 25% of infants and children. Between 6 and 18 hours after cardiac

surgery.Results in longer intensive care stay and

increased mortality.

Why & How?Postoperative physiologic changes resulting

from cardiopulmonary bypass, residual lesions, cardioplegia, ventriculotomy, changes in the loading conditions of the myocardium, or myocardial ischemia during aortic cross-clamping all may contribute to the development of LCOS.

PathophysiologyA variety of proinflammatory triggers are

activated during cardiopulmonary bypass as a result of blood contact with foreign surfaces, ischemia, reperfusion, tissue trauma, and temperature changes.

“inflammatory response” >> complement activation, cytokine release, leukocyte and platelet activation, and the expression of adhesion molecules.

DiagnosisPrevention, early recognition, and

optimal treatment are essential components for reversing its course.

When unrecognized or inadequately treated, LCOS can result in irreversible end organ failure, cardiac arrest, and even death!

Clinical features- Tachycardia- Oliguria (0.5 ml/kg/h)- Poor peripheral perfusion - Low blood pressure

Investigations Arterial lactate.Mixed or central venous saturation.Echo

ManagementThe treatment of LCOS aims at providing adequate

oxygen delivery to meet the demands of end organs.

A balance between O2 supply and demand!Decreasing the demand:By basic critical care therapies such intubation and mechanical support for respiratory insufficiency analgesia and sedation, treatment of anemia and temperature control.

Increasing O2 delivery: Oxygen delivery can be improved by oxygen therapy, red blood cell transfusions, intravenous fluids, and inotropic support + Mechanical respiratory support

Look for the Cause!Adequate airway (tube position, size and patency)

and ventilation (atelectasis, pneumothorax)Pericardial tamponadePulmonary hypertensive crisisArrhythmias (loss of AV synchrony, tachycardia or

bradycardia) Significant residual lesionElectrolyte abnormality (e.g. Hypocalcaemia)

Pharmacologic tx

 Epinephrine, dobutamine and dopamine all increase myocardial oxygen consumption (MVO2) postoperatively. However, only with dobutamine is this matched by a proportional increase in coronary blood flow, suggesting that the other agents may impair coronary vasodilatory reserve postoperatively.

The incidence of postoperative myocardial infarction was significantly lower (0%) with amrinone compared to dobutamine (40%) because it decreases LV wall tension without increasing MVO2, despite increases in heart rate and contractility.

The PRIMACORP study

Milrinone: a phosphodiesterase III inhibitor, improves cardiac muscle contractile force and vascular muscle relaxation through positive inotropic and vasodilatory effects. 

Levosimendan has been shown to decrease the time to extubation compared to milrinone. Compared to dobutamine, levosimendan decreases the incidence of postoperative atrial fibrillation and myocardial infarction, ICU length of stay, acute renal dysfunction, ventricular arrhythmias, and mortality in the treatment of postoperative LV dysfunction. 

Non Pharmacologic txMechanical Circulatory SupportWhen medical treatment is ineffective.By extracorporial life support (ECLS) or extracorporial

membrane oxygenation (ECMO) or ventricular assist device (VAD).

Thank You