PubMed · 9777873
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P A Andrews. 1998-10-10. Heart failure.. https://doi.org/10.1016/s0140-6736(05)60573-9
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A low cardiac output state is an important cause of morbidity and mortality following repair of tetralogy of Fallot (ToF). This is often refractory to conventional measures. The cardiac output of these patients is highly dependent on diastolic pulmonary arterial flow which is enhanced during spontaneous respiration, but much reduced by intermittent positive pressure ventilation (IPPV). We report the successful use of negative pressure ventilation (NPV) as haemodynamic therapy in three children with a low output secondary to restrictive right ventricular (RV) physiology following ToF repair. NPV produced a significant haemodynamic improvement, with increases in cardiac output of greater than 100 % in two of the children. By augmenting pulmonary blood flow, and hence cardiac output, NPV has a role as adjunctive haemodynamic therapy in patients with a low output secondary to diastolic RV dysfunction, in whom early extubation is not possible.
Cardiac transplantation provides the best option for neonates with congenital heart disease that is not amenable to surgical repair or palliation. The scarcity of suitable organs for this group has resulted in prolonged waiting times; many infants die awaiting transplantation. We present the case of a newborn with severe Ebstein's anomaly and low cardiac output who was supported with extracorporeal membrane oxygenation for 1,126 hours, until an appropriate organ became available.
Myocardial function is determined by preload, afterload, contractility and heart rate. Pathologic changes of these variables may result in decrease of blood pressure, acute heart failure or cardiogenic shock. Hyperdynamic septic shock is associated with systemic hypotension despite increased cardiac output. Mediators of sepsis induce both myocardial depression and pulmonary arterial hypertension. Moreover, sepsis is characterized by microcirculatory disturbances and dysbalance in regional oxygen delivery and consumption. Severe systemic hypotension is a symptom often requiring catecholamine therapy to restore systemic circulation and to avoid organ damage. As the use of catecholamines is not a causal therapy administration should be limited to an initial measure until correction of the underlying abnormalities can be achieved. Different etiologies of shock as well as diseases requiring specific interventions as pulmonary embolectomy, systemic lysis or coronary angioplasty have to be considered. First line intervention consists of optimizing preload by fluid resuscitation as appropriate and use of dopamine (4-12 micrograms/kg.min) as primary catecholamine to increase contractility and blood pressure. In acute left heart failure inotropic support with dobutamine (4-12 micrograms/kg.min) or epinephrine (0.05-1 microgram/kg.min) may be necessary, frequently combined with a vasodilator (sodium nitroprusside 0.2-5 micrograms/kg.min or nitroglycerine 0.5-2.5 micrograms/kg.min) or phosphodiesterase-III-inhibitor (milrinone 0.3-0.8 microgram/kg.min). In right heart failure norepinephrine is preferred to increase coronary perfusion pressure. Hyperdynamic septic shock with decreased vascular resistance is treated with norepinephrine to restore mean arterial pressure and to improve right ventricular dysfunction induced by pulmonary hypertension.