1. LOW CARDIAC OUTPUT SYNDROM IN CHILDREN AFTER CARDIAC SURGERY
Hala EL-Mohamady, professor of anaesthesia,
Ain Shams University

2. 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.

3. reducing cardiac output
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

4. 6–18 h after cardiopulmonary
This occurs typically
6–18 h after cardiopulmonary
bypass, which is usually in the middle of the night!

5. Causes of
postoperative LCOS

6. -Inflammatory cascade triggered by (CPB)
-Aortic cross-clamp
-Hypothermia
-Reperfusion injury
-Pericardial tamponade
-Residual cardiac lesions, even when minor

7. 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

8. Diagnosis OF
LCOP SYNDROM

9. Anticipation So is the key to the diagnosis and management of LCOS
Diagnosis relies on anticipation, clinical features and investigation

10. CLINICAL Features - low blood pressure - oliguria (0.5 ml/kg/h)OF
LOW COP SYNDROM
- tachycardia
- oliguria (0.5 ml/kg/h)
- poor peripheral perfusion
- low blood pressure

11. The ability of clinicians to assess cardiac output from clinical
examination alone is poor

12. INVESTIGATIONS

13. - Metabolic acidosis
- Lactate
- Mixed venous oxygen saturation
- Echocardiography

14. aimed at achieving the optimal balance between
Management
aimed at achieving the optimal balance between
oxygen delivery and oxygen consumption

15. A check list of immediately treatable causes is useful, as is a flow diagram to lead staff through a logical approach.

16. Check list of causes of
postoperative LCOS

17. -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)

18. Preload measuring filling pressures from right and left atrial lines.
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.

19. Left ventricular afterload
Reduction in LV afterload will improve cardiac output, as long as an adequate diastolic pressure is maintained for coronary perfusion.

21. Right ventricular afterload pulmonary hypertension

22. Preventive treatment strategies PULMONARY HYPERTENSION
For
PULMONARY HYPERTENSION

23. -optimal sedation
-neuromuscular blockade
-induced 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

24. 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.

25. Nitric Oxide ?
Rebound pulmonary
hypertension

26. Pharmacological treatment of systolic and diastolic dysfunction

27. 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.

28. Terms used for cardiovascular drugs

29. Term Meaning Inotropy Increased force of myocardial
contraction not related to preload or afterload
Chronotropy Increased rate
Dromotopy Increased speed of electrical
conduction
Lusitropy Increased effectiveness of active diastolic relaxation

30. Main effects Agent b14b2 1–15 Dobutamine B14a1 a14b1 1–5 (low)
Stimulate
Dose range (mcg/kg/min)
Agent
Inotropy, chronotropy, dromotopy,VD
b14b2
1–15
Dobutamine
Inotropy, chronotropy, dromotopy
Vasoconstriction inotropy, chronotropy
B14a1
a14b1
1–5 (low)
5–15 (high)
Dopamine
Vasoconstriction with some inotropy
a1bb1
0.1–0.5
Noradrenaline

31. Main effects Stimulates Agent a14b14b2 0.1–1 (high) Adrenaline
Dose range (mcg/kg/min)
Agent
Inotropy, chronotropy, dromotopy,
bronchodilation, multiple endocrine
effects (increased glucose, lactate)
As above plus potent vasoconstrictio
a1 ¼ b1 ¼ b2
a14b14b2
0.05–o.1(low)
0.1–1 (high)
Adrenaline

32. Main effects Stimulates Agent Dose range (mcg/kg/min
Inotropy, lusitropy and vasodilation
Inhibits
phosphodiesterase III
75 mcg/kg load,
0.25–1
Milrinone
Potent vasoconstriction
V1, V2
0.02 U/min (not kg)
Vasopressin
Ca2+ sensitivity of troponin C
25 mcg/kg load, 0.2
for 24 h
Levosimendan

33. Lack of evidence to demonstrate benefit.
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.

34. 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.

35. Non-pharmacological treatment Systolic and diastolic dysfunctionof
Systolic and diastolic dysfunction

36. 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.

37. 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

38. 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.

39. 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.

40. the consequences of LCOS
Minimizing
the consequences of LCOS

41. Classically, a prolonged period of LCOS can lead to a
-ventilator-dependant
-oedematous child
-malnourished
-significant sedation problems
-vascular access difficulties.
Much can be done to minimize the effects of LCOS while awaiting intrinsic myocardial recovery.

42. 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.

43. 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.

44. 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.

45. Flow diagram
to guide management of
LCOS.

46. Evaluate and treat specific problem
Low Cardiac Output State
• Tachycardia, oliguria, poor perfusion, low BP
• Metabolic acidosis
• Rising lactate
• Low venous saturation
Exclude specific problem
• Airway/ventilation
• Pericardial tamponade
• Pulmonary hypertension
• Arrhythmia
• Residual lesion
• Electrolyte abnormality
Evaluate and treat specific problem
• ECHO
• Atrial ECG
• Surgical /medical intervention

47. Assess Preload clinical exam, CVP, LAP.
• Fluid challenge 5-10
ml/kg of 4% Albumin
or give blood if:
Hb<10-12
(acyanotic) or <12-14 (cyanotic)
• Reassess and repeat
• Consider effects of
ventilation on venous return
Assess Preload clinical exam, CVP, LAP.
low

48. Left Ventricle afterload Right Ventricle
• Short/long acting
vasodilators
• Inodilators
• Positive pressure
ventilation
• Sedation
• High FiO2
• iNO
• Optimal PEEP
high
Left Ventricle afterload Right Ventricle
high(PHT)

49. Inotropy • dobutamine Systolic function Diastolic function
• low dose adrenaline
• Increase preload
• Lusitopy (milrinone)
• Atrial “kick”
reduced
Systolic function
Diastolic function
reduced

50. Consider • Sternal reopening • Hypothermia • Mechanical support
Minimise effects of LCOS • Diuretics/PD • Optimal nutrition • Optimal ventilation
Consider • Sternal reopening • Hypothermia • Mechanical support
not improving

51. 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 non-pharmacological strategies should not be underestimated.