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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.

Pathophysiology
A 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.

Diagnosis
Prevention, 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

Management
The treatment of LCOS aims at providing adequate
oxygen delivery to meet the demands of end
organs.

A balance between Increasing


O2 supply
and
demand!
Decreasing the
O2
delivery:
Oxygen delivery
can be improved by
oxygen therapy, red
blood cell
transfusions,
intravenous fluids,
and inotropic
support +
Mechanical
respiratory support

demand:
By basic critical care
therapies such
intubation and
mechanical support
for respiratory
insufficiency
analgesia and
sedation, treatment
of anemia and
temperature control.

Look for the Cause!


Adequate airway (tube position, size and patency)
and ventilation
(atelectasis, pneumothorax)
Pericardial tamponade
Pulmonary hypertensive crisis
Arrhythmias (loss of AV synchrony,
bradycardia)

tachycardia or

Significant residual lesion


Electrolyte 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 tx
Mechanical Circulatory Support
When medical treatment is ineffective.
By extracorporial life support (ECLS) or extracorporial
membrane oxygenation (ECMO) or ventricular assist device
(VAD).

Thank You