LOW CARDIAC
OUTPUT SYNDROM
IN CHILDREN
AFTER CARDIAC
SURGERY
Hala EL-Mohamady, professor of anaesthesia,
Ain Shams University
Low cardiac output syndrome
(LCOS)
is a clinical
syndrome seen commonly (25%)
after pediatric
cardiac surgery
but also occurring secondary to
acute myocarditis and septic shock.
Regardless of aetiology, the resulting effects
are
shock and inadequate organ perfusion
organ dysfunction
Coincide With Postoperative decrease in
cardiac index and increases in SVR and
PVR
reducing cardiac output
This occurs typically
6–18 h after
cardiopulmonary
bypass, which is usually
in the middle of the
night!
Causes
of
postoperative
LCOS
-Inflammatory cascade triggered by (CPB)
-Aortic cross-clamp
-Hypothermia
-Reperfusion injury
-Pericardial tamponade
-Residual cardiac lesions, even when minor
PREVENTION
Because LCOS is common and
contributes to postoperative
morbidity and mortality,
prevention of this predictable
hemodynamic deterioration may
have significant implications for
clinical outcome
Diagnosis
OF
LCOP SYNDROM
Anticipation
is the key to the diagnosis and
management of LCOS
So
Diagnosis relies on anticipation, clinical
features and investigation
CLINICAL Features
OF
LOW COP SYNDROM
- tachycardia
- oliguria (0.5 ml/kg/h)
- poor peripheral
perfusion
- low blood pressure
The ability of clinicians
to
assess cardiac output
from clinical
examination alone is
poor
INVESTIGATIONS
- Metabolic acidosis
- Lactate
- Mixed venous oxygen
saturation
- Echocardiography
Management
aimed at achieving the optimal balance
between
oxygen delivery and oxygen consumption
A check list of immediately
treatable causes is useful,
as is a flow diagram to lead
staff through a logical
approach.
Check list of
causes
of
postoperative
LCOS
-Adequate airway (tube position, size
and patency) and ventilation
(atelectasis, pneumothorax)
-Pericardial tamponade
-Pulmonary hypertensive crisis
-Arrhythmias (loss of AV synchrony,
tachycardia or bradycardia)
-Significant residual lesion
-Electrolyte abnormality (e.g.
hypocalcaemia)
Preload
Preload is traditionally assessed by:
measuring filling pressures from right and left
atrial lines.
In addition, venous capacitance also affects
venous return. Venodilatation often occurs on
rewarming and may be exacerbated by drugs
Finally, positive pressure ventilation (PPV) will tend
to reduce RV preload by inhibiting venous
return.
Left ventricular
afterload
Reduction in LV afterload will
improve cardiac output, as
long as an adequate diastolic
pressure is maintained for
coronary perfusion.
Left ventricular
afterload
Short Acting
Vasodilators
Nipride
GTN
Long Acting
Vasodilators
Phenoxybenzamin
Captopril
PPV
Right ventricular afterload
pulmonary hypertension
Pulmonary
hypertension
Right ventricular
Failure
poor COP
Preventive
treatment strategies
For
PULMONARY
HYPERTENSION
-optimal
sedation
-neuromuscular
-induced
blockade
respiratory or metabolic
alkalosis
-hyper-oxygenation
Avoiding or ablating stimuli
(trigger pulmonary hypertensive crises(e.g. administering fentanyl
bolus prior to airway suction).
-Nitric
oxide
Nitric Oxide
a potent endogenous vasodilator that
produces vascular relaxation via
increases in the intracellular
concentration of guanosine 3,5-cyclic
monophosphate.
It is a specific pulmonary vasodilator
when delivered by inhalation (iNO),
RV afterload is reduced, thereby
improving RV ejection fraction and
cardiac output.
Nitric Oxide
?
Rebound pulmonary
hypertension
Pharmacological
treatment of systolic
and
diastolic dysfunction
It should be remembered that all of
these potent agents will increase
myocardial oxygen demand, and
that they should be titrated to the
minimal dose that achieves the
desired effect. They should not
be commenced or increased prior
to consideration of preload and
afterload.
Terms used for
cardiovascular
drugs
Term
Meaning
Inotropy
Increased force of myocardial
contraction not related to
preload or afterload
Chronotropy
Dromotopy
Lusitropy
Increased rate
Increased speed of electrical
conduction
Increased effectiveness of
active diastolic relaxation
Agent
Dobutamine
Dopamine
Noradrenalin
e
Dose range Stimulate
(mcg/kg/mi
n)
1–15
Main effects
b14b2 Inotropy,
chronotropy,
dromotopy,VD
1–5 (low)
5–15
(high)
B14a1
a14b1
Inotropy,
chronotropy,
dromotopy
Vasoconstriction
inotropy, chronotropy
0.1–0.5
a1bb1
Vasoconstriction with
some inotropy
Agent
Adrenaline
Dose range Stimulates
(mcg/kg/min)
0.05–o.1(low)
Main effects
a1 ¼ b1 ¼ b2 Inotropy,
0.1–1 (high) a14b14b2
chronotropy,
dromotopy,
bronchodilation,
multiple
endocrine
effects (increased
glucose, lactate)
As above plus
potent
vasoconstrictio
Agent
Dose range
(mcg/kg/min
Stimulates
Main effects
Milrinone
75 mcg/kg
load,
0.25–1
Inhibits
phosphodiester
ase III
Inotropy,
lusitropy and
vasodilation
Vasopressin
0.02 U/min
(not kg)
V1, V2
Potent
vasoconstrictio
n
Levosimendan
25 mcg/kg
load, 0.2
for 24 h
Ca2+
sensitivity of
troponin C
Inotropy,
lusitropy and
vasodilation
Thyroid hormone
Thyroid hormone has an essential role in cellular
metabolism and in maintaining haemodynamic
stability.
It is required for the synthesis of contractile
proteins and to maintain normal myocardial
contraction.
Suppression of thyroid hormone levels has been
demonstrated in children following CPB, maximal
between 12 and 48 h and lasting up to 7 days
after CPB.
Lack of evidence to
demonstrate benefit.
Nesiritide
B-type natriuretic peptide is
synthesized and excreted from the
ventricular myocardium in response
to myocardial stretch.
It results in natriuresis, diuresis and
vascular smooth muscle relaxation.
Clinically it is said to augment
preload and reduce afterload.
Nonpharmacological
treatment
of
Systolic and
diastolic
dysfunction
Delayed sternal closure
The aim is to allow the heart to recover, and
become less oedematous without the
added problem of ‘‘dry’’ tamponade.
Delayed closure is associated with an increased risk of
mediastinitis (particularly with gram negative
organisms), and thyroid suppression from iodine
absorption from iodine-based antiseptics. When the
sternum is closed, significant haemodynamic and
respiratory changes can occur and should be
anticipated.
Induced hypothermia
Reducing the body temperature results in a
reduction in metabolic rate, oxygen demand and
heart rate, and may have a direct beneficial
effect on cardiac function. SVR is increased and
stroke volume and MAP are maintained.
Although hypothermia is a useful rescue strategy, it is not
without risks, including sepsis, coagulation disorders
and altered pharmacokinetics. Neuromuscular paralysis
is usually required to prevent shivering which, if
unopposed, will increase oxygen consumption and
lactate production
Mechanical support
The major benefit of mechanical circulatory
support in the treatment of LCOS is allowing
time for myocardial recovery whilst preventing
ongoing damage to other organ systems
Veno-arterial (VA) ECMO, and LV and/or RV
assist devices are the two commonest methods of
mechanical support. Selection and assessment of
candidates for ECLS is extremely important. Bleeding is
the most common complication, particularly from the
wound, but intracranial haemorrhage can occur usually
resulting in withdrawal of therapy.
Pacing and arrhythmia management
Arrhythmias that result in loss of AV synchrony, or
significantly affect heart rate, are common
(425%) and poorly tolerated in the setting of
LCOS. Tachycardia can allow inadequate time for
ventricular filling, especially with a poorly compliant
ventricle; bradycardia is also poorly tolerated.
AV synchrony is particularly important in LCOS as the
effects of atrial systole (atrial kick) on ventricular
preload can be significant, and contributing up to 20%
of stroke volume. AV synchrony is particularly
important in LCOS as the effects of atrial systole (atrial
kick) on ventricular preload can be significant, and
contributing up to 20% of stroke volume.
Minimizing
the
consequences
of LCOS
Classically, a prolonged period of LCOS can
lead to a
-ventilator-dependant
-oedematous
-malnourished
child
-significant sedation problems
-vascular access difficulties.
Much can be done to minimize the effects
of LCOS while awaiting intrinsic
myocardial recovery.
Renal failure
Renal failure and fluid retention are common due
to poor renal perfusion and low mean blood
pressure.
Diuretics are usually necessary after the first 24
h.
Early peritoneal dialysis (PD) started prior to
significant oedema formation, can prevent
excessive fluid bolus administration, ionotrope
escalation and frusemide toxicity.
Respiratory failure
Respiratory failure following LCOS is
usually multifactorial, resulting from
fluid overload, malnutrition, muscle
weakness, critical illness
polyneuropathy, atelectasis, upper
airway oedema and intrinsic lung
disease, with significant reduction in
FRC secondary to sternotomy.
Appropriate ventilation strategies
that optimize PEEP, minimize tidal
volume (6-8 ml/kg) and avoid
paralysis are optimal.
Nutrition, Sedation
Optimal nutrition is often difficult due to fluid
restriction and gut failure.
Early enteral nutrition and the early use of
jejunal feeding strategies are important.
TPN is sometimes required but can often be
avoided by jejunal feeding. It is often worth
starting PD to make space for increased caloric
intake.
Optimal sedation and uncomplicated venous
access are always strived for but rarely achieved.
Flow diagram
to guide
management of
LCOS.
Low Cardiac Output
State
Exclude specific problem
• Airway/ventilation
• Tachycardia, oliguria,
poor perfusion, low BP
• Metabolic acidosis
• Rising lactate
• Low venous saturation
• Pericardial tamponade
• Pulmonary hypertension
• Arrhythmia
• Residual lesion
• Electrolyte abnormality
Evaluate and treat specific problem
• ECHO
• Atrial ECG
• Surgical /medical intervention
• Fluid challenge 5-10
Assess Preload
clinical exam,
CVP, LAP.
ml/kg of 4% Albumin
or give blood if:
Hb<10-12
(acyanotic) or <12-14
(cyanotic)
low
• Reassess and repeat
• Consider effects of
ventilation on venous
return
Left Ventricle
afterload
Right
Ventricle
afterload
high
high(PHT)
• Short/long acting
vasodilators
• Inodilators
• Positive pressure
ventilation
• Sedation
• High FiO2
• iNO
• Optimal PEEP
Systolic function
Diastolic function
reduced
reduced
Inotropy
• dobutamine
• low dose
adrenaline
• Increase preload
• Lusitopy
(milrinone)
• Atrial “kick”
Minimise effects of
LCOS
• Diuretics/PD
not improving
• Optimal nutrition
• Optimal ventilation
Consider
• Sternal reopening
• Hypothermia
• Mechanical
support
CONCLUSION
LCOS is a common problem in paediatric
intensive care that is often predictable
and sometimes preventable.
Diagnosis relies on anticipation, clinical
features and investigation.
Management is aimed at achieving the
optimal balance between oxygen delivery
and oxygen consumption.
Preload and afterload should be optimized
prior to escalation of inotropic support.
The effects of PPV and nonpharmacological strategies should not be
underestimated.