LESS IS MORE- FLUID IN SEPSIS

Pathophysiology of sepsis explains that after fluid resuscitation with 20-30 ml/kg ( which is the pressure volume of intravascular space), it is unlikely that septic shock will respond to additional fluid resuscitation.

There may be transient response, as only five percent of the crystalloid will remain in the intravascular space, and rest of the fluid will accumulate in third space, giving rise to further organ damage.

Fluid resuscitation further exacerbates the deranged physiology including vasodilatation.

Multiple Clinical trials have suggested that positive fluid balance independently causes increased morbidity and mortality.

Vasopressors should not be delayed after initial fluid resuscitation with 20-30ml/kg. Thereafter further fluid boluses may be given based on dynamic parameters of fluid responsiveness.

Comments

Popular posts from this blog

FROM BICARBONATE TO STRONG ION DIFFERENCE- INTRIGUING STORY OF BLOOD ACID-BASE ANALYSIS “Life is struggle, not against sin, not against money power…. but against Hydrogen ion.” - H.L. Mencken, 1919 Since the understanding of similarity between fermentation of wine and respiration of animals, evolution of human physiology and measurement of carbon dioxide is coupled with studies of acids and bases. Alkalinity of blood was demonstrated by color indicators as early as eighteenth century by French chemist Hilaire Marin Rouelle, and one century later, its relation with gastric acid secretion was recognized by Henry Bence Jones. In 1831, William B. O’Shaughnessy, an Irish physician working in India, demonstrated that Cholera reduced the free alkali of blood. But the discovery of relationship between blood alkalinity and carbon dioxide was contained within the mystery of diabetic coma. 1. Story of Carbon Dioxide and Alkalinity of blood In Nineteen...

Vocal Cord Dysfunction (VCD ) or PARADOXICAL VOCAL CORD MOVEMENT (PVCM)

▪Inappropriate adduction of true vocal cords, mostly during inspiration. This results in dyspnoea and strider during inspiration. Rarely it may happen during expiration also. ▪15 Y F presenting with acute respiratory distress for 48 hours. For the past 2 years she was on inhaled bronchodialtors and steroids with short cources of oral/IV steroids for bronchial asthma. There was history of 4 hospital admissions and several emergency visits for symptoms attributed to asthma. Examination revealed apprehensive, tachycardic, tachpnoic girl with accessory muscle use and widespread rhonchi bilaterally, SPO2 93% on room air. Other systemic examination were normal. She was started on inhalation therapy but her conditioned worsened. Oxygen saturation felled to 78% ON 10 L face mask, ABG revealed pH 7.53, PaO2 58, PaCO2 28. She was intubated emergency and shifted TO ICU. She was treated as life threatening attack of bronchial asthma. She improved dramatically and successfully e...

REVERSE TRIGGERING: A newly classified though common form of double triggering

Reverse triggering is a recently defined type of double triggering where a controlled mechanical breath, stimulates receptors in the lung, eliciting inspiratory effort. Seen in patients who are deeply sedated with high mechanical ventilation rates. Reverse triggering could be explained by respiratory entrainment, a form of patient ventilator interaction, where diaphragmatic muscle contraction is triggered by ventilator insufflations, leading to breath initiation. Consequences of reverse triggering are large. Continuously induced muscle contraction of diaphragm cause cytokine release and muscle fibre damage. Additionally it increases inspiratory muscle load and oxygen consumption and may lead to cardiovascular instability. Reverse triggering also makes measurement of plateu pressure misleading as well as may generate high platue pressure and ventilator induced lung injury. Management is not entirely clear. Increasing sedation does not help. Increasing inspiratory time will cause the...

Learning Critical Care Medicine

Search This Blog