10th September 2010
|Word Count 2740 |
Congenital heart disease (CHD) accounts for a large portion of clinically significant birth defects, and remains the leading cause of infant deaths (M. Torres, Pharm, & Nieves, 2008). Advances in paediatric cardiology, cardiothoracic surgery and intensive care have dramatically improved survival for these children. However, even with this progress there remains to be an expected and reproducible fall in cardiac output, low cardiac output syndrome (LCOS), after cardiac surgery (Bailey et al., 2004; Ravishankar, Tabbutt, & Wernovsky, 2003; M. Torres, et al., 2008).
In the following assignment I will be reviewing the evidence relating to the use of milrinone, a phosphodiesterase inhibitor that is commonly used to increase cardiac output in children after cardiac surgery. I will focus on LCOS in children and the pathophysiology surrounding this. I will also examine the biological action of milrinone and how it has been shown to increase cardiac output in children after surgery. This will include the review of three studies that support this finding. To conclude, I will include other relevant literature and discuss their relevance within the New Zealand setting.
The prevention and initial treatment of LCOS is now a key priority of intraoperative practice and postoperative intensive care. It is a clinical syndrome that complicates 25% of infants and children early after cardiopulmonary bypass (CPB). Consequences of LCOS are the need for prolonged mechanical ventilation, longer intensive care stay and increased risk of sepsis and mortality [pic](Jones, Hayden, Fraser, & Janes, 2005; Ravishankar, et al., 2003; Stocker et al., 2007).
Although there have been advances in myocardial protection, surgical and CPB techniques, an expected fall in cardiac output occurs between 6 and 18 hours after surgery (Ravishankar, et al., 2003). Causes of LCOS have been described as being multifactorial, including myocardial ischemia during aortic cross clamping, alterations in systemic and pulmonary vascular reactivity, reperfusion injury, hypothermia and activation of the inflammatory and complement cascades. Residual cardiac lesions may also contribute to LCOS in the post operative course (Costa Auler Jr, Costa Barreto, Gimenez, & Abellan, 2002; Hoffman et al., 2002; Jones, et al., 2005; Ravishankar, et al., 2003).
Cardiac output is the volume of blood ejected by the heart in one minute. Heart rate and stroke volume determine cardiac output (Hazinski, 1992; McCance & Huether, 1998). Preload, ventricular fibre shortening and afterload determine the stroke volume (Kulasekaran K, Sargent PH, & Flenady V, 2004).
The clinical characteristics of LCOS are low blood pressure, tachycardia, oliguria and poor peripheral perfusion. Laboratory parameters such as blood gas analysis looking at lactate, mixed venous oxygen saturations and acidosis may also give an indirect assessment of cardiac output and oxygen delivery....