Presentation on theme: "LOW CARDIAC OUTPUT SYNDROM IN CHILDREN AFTER CARDIAC SURGERY"— 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 clinicalsyndrome seen commonly (25%)after pediatriccardiac surgerybut also occurring secondary toacute myocarditis and septic shock.
3 reducing cardiac output Regardless of aetiology, the resulting effectsareshock and inadequate organ perfusionorgan dysfunctionCoincide With Postoperative decrease in cardiac index and increases in SVR and PVRreducing cardiac output
4 6–18 h after cardiopulmonary This occurs typically6–18 h after cardiopulmonarybypass, which is usually in the middle of the night!
6 -Inflammatory cascade triggered by (CPB) -Aortic cross-clamp-Hypothermia-Reperfusion injury-Pericardial tamponade-Residual cardiac lesions, even when minor
7 PREVENTIONBecause LCOS is common and contributes to postoperative morbidity and mortality, prevention of this predictable hemodynamic deterioration may have significant implications for clinical outcome
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 drugsFinally, positive pressure ventilation (PPV) will tend to reduce RV preload by inhibiting venousreturn.
19 Left ventricular afterload Reduction in LV afterload will improve cardiac output, as long as an adequate diastolic pressure is maintained for coronary perfusion.
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 Oxidea 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.
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.
29 Term Meaning Inotropy Increased force of myocardial contraction not related to preload or afterloadChronotropy Increased rateDromotopy Increased speed of electricalconductionLusitropy Increased effectiveness of active diastolic relaxation
30 Main effects Agent b14b2 1–15 Dobutamine B14a1 a14b1 1–5 (low) StimulateDose range (mcg/kg/min)AgentInotropy, chronotropy, dromotopy,VDb14b21–15DobutamineInotropy, chronotropy, dromotopyVasoconstriction inotropy, chronotropyB14a1a14b11–5 (low)5–15 (high)DopamineVasoconstriction with some inotropya1bb10.1–0.5Noradrenaline
31 Main effects Stimulates Agent a14b14b2 0.1–1 (high) Adrenaline Dose range (mcg/kg/min)AgentInotropy, chronotropy, dromotopy,bronchodilation, multiple endocrineeffects (increased glucose, lactate)As above plus potent vasoconstrictioa1 ¼ b1 ¼ b2a14b14b20.05–o.1(low)0.1–1 (high)Adrenaline
32 Main effects Stimulates Agent Dose range (mcg/kg/min Inotropy, lusitropy and vasodilationInhibitsphosphodiesterase III75 mcg/kg load,0.25–1MilrinonePotent vasoconstrictionV1, V20.02 U/min (not kg)VasopressinCa2+ sensitivity of troponin C25 mcg/kg load, 0.2for 24 hLevosimendan
33 Lack of evidence to demonstrate benefit. Thyroid hormoneThyroid hormone has an essential role in cellular metabolism and in maintaining haemodynamic stability.It is required for the synthesis of contractileproteins and to maintain normal myocardial contraction.Suppression of thyroid hormone levels has beendemonstrated 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 NesiritideB-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 dysfunction ofSystolic 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 hypothermiaReducing 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 supportThe major benefit of mechanical circulatory support in the treatment of LCOS is allowing time for myocardial recovery whilst preventing ongoing damage to other organ systemsVeno-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, orsignificantly affect heart rate, are common(425%) and poorly tolerated in the setting ofLCOS. Tachycardia can allow inadequate time forventricular filling, especially with a poorly compliantventricle; 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 Minimizingthe 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 failureRenal 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 failureRespiratory 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, SedationOptimal nutrition is often difficult due to fluidrestriction 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 venousaccess are always strived for but rarely achieved.
51 CONCLUSIONLCOS is a common problem in paediatric intensive care that is often predictable and sometimes preventable.Diagnosis relies on anticipation, clinicalfeatures 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.