Tinni Trihartini Maskoen
Departemen Anestesiologi Dan Terapi Intensif Fakultas Kedokteran Universitas Padjadjaran, Rumah Sakit Hasan Sadikin Bandung

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Journal : Majalah Anestesia dan Critical Care

Acid-Base Balance: Stewart’s Approach Pradian, Erwin; Maskoen, Tinni Trihartini; Destiara, Andy Pawana
Majalah Anestesia dan Critical Care Vol 33 No 2 (2015): Juni
Publisher : Perdatin Pusat

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Abstract

The Henderson-Hasselbalch approach to acid-base balance allows explanation and quantification of many disorders of acid-base phisiology and is still widely used in clinical practice. However, complex metabolic disorders, such as those present in critically ill patients, can be difficult to define and treat using this approach. Peter Stewart proposed a different approach to acid-base physiology based upon physicochemical principles, which are electrochemical neutrality, conservation of mass and law of mass action. According to Stewart, there are only three variables influence the dissociation of water. These independent variables are pCO2, total concentration of weak acid [ATot] and strong ion difference (SID). Another different is if in Henderson-Hasselbalch approach pointed on bicarbonat ion, Stewart use chloride ion as the important anion as the causatif factor so there are also known the terms hyperchloremia acidosis, dilutional acidosis and contraction alkalosis.
Clinical Manifestations of Iscehaemic and Reperfusion Injury Pradian, Erwin; , Rizki; Maskoen, Tinni Trihartini
Majalah Anestesia dan Critical Care Vol 33 No 2 (2015): Juni
Publisher : Perdatin Pusat

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Abstract

Although restoration of blood low to an ischaemic organ is essential to prevent irreversible tissue injury, reperfusionper se may result in a local and systemic inlammatory response that may augment tissue injury in excess of thatproduced by ischaemia alone. Cellular damage after reperfusion of previously viable ischaemic tissues is deinedas ischaemia-reperfusion (I-R) injury. I-R injury is characterized by oxidant production, complement activation,leucocyte endothelial cell adhesion, platelet-leucocyte aggregation, increased microvascular permeability anddecreased endothelium-dependent relaxation. In its severest form, I-R injury can lead to multiorgan dysfunctionor death. Although our understanding of the pathophysiology of I-R injury has advanced signiicantly in the lastdecade, such experimentally derived concepts have yet to be fully integrated into clinical practice. Treatment ofI-R injury is also confounded by the fact that inhibition of I-R-associated inlammation might disrupt protectivephysiological responses or result in immunosuppression. Thus, while timely reperfusion of the ischaemic areaat risk remains the cornerstone of clinical practice, therapeutic strategies such as ischaemic preconditioning,controlled reperfusion, and anti-oxidant, complement or neutrophil therapy may signiicantly prevent or limit I-Rinducedinjury in humans.