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

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Presentation on theme: "LOW CARDIAC OUTPUT SYNDROM IN CHILDREN AFTER CARDIAC SURGERY Hala EL-Mohamady, professor of anaesthesia, Ain Shams University."— Presentation transcript:

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 Regardless of aetiology, the resulting effects are shock and inadequate organ perfusion shock and inadequate organ perfusion organ dysfunction Coincide With Postoperative decrease in cardiac index and increases in SVR and PVR reducing cardiac output

4 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


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

10 CLINICAL Features OF LOW COP SYNDROM LOW COP SYNDROM - tachycardia - 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


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

14 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 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.

20 Left ventricular afterload Short Acting Vasodilators Nipride GTN Long Acting Vasodilators Phenoxybenzamin Captopril PPV

21 Right ventricular afterload pulmonary hypertension Right ventricular Failure poor COP Pulmonary hypertension

22 Preventive treatment strategies 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). (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 cardiovascula r drugs

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

30 Main effects Stimulate Dose range (mcg/kg/mi n) Agent Inotropy, chronotropy, dromotopy,VD b14b2 1 – 15 Dobutamine Inotropy, chronotropy, dromotopy Vasoconstriction inotropy, chronotropy B14a1a14b1 1 – 5 (low) 5 – 15 (high) Dopamine Vasoconstriction with some inotropy a1bb1 0.1 – 0.5 Noradrenalin e

31 Main effects Stimulates 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 a14b14b – o.1(low) 0.1 – 1 (high) Adrenaline

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

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

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

48 Left Ventricle afterload afterload Right Ventricle afterload Short/long acting Short/long actingvasodilators Inodilators Inodilators Positive pressure Positive pressureventilation Sedation Sedation High FiO2 High FiO2 iNO iNO Optimal PEEP Optimal PEEP high high(PHT)

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

50 Minimise effects of LCOS Diuretics/PD Diuretics/PD Optimal nutrition Optimal nutrition Optimal ventilation Optimal ventilation Consider Sternal reopening Sternal reopening Hypothermia Hypothermia Mechanical support 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.

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