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Advances in Vasodilatory Shock: a Concise Review Sandeep Lahiry1, Sayanta Thakur2, Dwaipayan S Chakraborty3

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Advances in Vasodilatory Shock: a Concise Review Sandeep Lahiry1, Sayanta Thakur2, Dwaipayan S Chakraborty3 REVIEW ARTICLE Advances in Vasodilatory Shock: A Concise Review Sandeep Lahiry1, Sayanta Thakur2, Dwaipayan S Chakraborty3 ABSTRACT Vasodilatory shock is a critical manifestation of cardiovascular failure. There is uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing the failure of physiologic vasoregulatory mechanisms. Unfortunately, only few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to the standard approach of managing vasodilatory shock. The present review offers the latest updates in management of this important clinical entity and a guidance framework for future research. Keywords: Hypotension, Sepsis, Shock, Vasodilatory shock Indian Journal of Critical Care Medicine (2019): 10.5005/jp-journals-10071-23266 INTRODUCTION 1–3Department of Pharmacology, Institute of Postgraduate Medical Shock, a common clinical manifestation of circulatory compromise, Education and Research, Kolkata, West Bengal, India results in decreased delivery of oxygenated blood to tissues Corresponding Author: Sandeep Lahiry, Department of Pharmacology, culminating in decreased organ perfusion as well as cellular Institute of Postgraduate Medical Education and Research, Kolkata, dysfunction. Table 1 provides an overview of different types of West Bengal, India, e-mail: [email protected] shock. Approximately one-third of patients in the intensive care How to cite this article: Lahiry S, Thakur S, Chakraborty DS. Advances unit (ICU) can be diagnosed harboring the clinical condition,1 which in Vasodilatory Shock: A Concise Review. Indian J Crit Care Med can broadly be classified into four categories: 2019;23(10):475–480. 1. Hypovolemic shock (due to external or internal fluid loss, such Source of support: Nil as hemorrhage) Conflict of interest: None 2. Cardiogenic shock (due to acute myocardial infarction, cardiomyopathy, arrhythmias, and valvular heart diseases) 3. Obstructive type of shock (due to cardiac tamponade and VASODILATORY SHOCK AND SEPSIS pulmonary embolism), and Sepsis is the most common cause of vasodilatory shock affecting 4. Vasodilatory shock (due to sepsis or anaphylaxis). more than 1.5 million Americans each year at an annual burden of Septic shock, a form of vasodilatory shock, is the most common cost of more than $20 billion.2 Sepsis is also a significant challenge form of shock in critically ill patients, followed by cardiogenic and in India in context of the healthcare facility, health education and hypovolemic shocks.1 In most other subtypes, there is inadequate awareness, and limitation in resource. The findings of mortality oxygen transport attributed to low-cardiac output. However, in from sepsis have been diverge in different age groups, ranging vasodilatory shock, clinical manifestation ensues due to decreased from as low as 9% in neonates to as high as 63% in the elderly.3 systemic vascular resistance (SVR) with alteration in oxygen delivery One study raised definite apprehension indicating that 25% of to cells. the total patients admitted in ICU developed severe sepsis or Table 1: Overview of different types of shock Shock (Hypotension + decreased tissue perfusion and oxygenation) Low CO + fluid responsiveness Low CO (+) fluid responsiveness Low CO (+) fluid responsiveness High CO (+) fluid responsiveness Hypovolemic shock Cardiogenic shock Obstructive shock Vasodilatory shock Hemorrhage excessive diuresis Myocardial compromise, e.g., AMI, Cardiac tamponade, tension Sepsis “Third-spacing” under-resuscitated stress cardiomyopathy pneumothorax, pulmonary Anaphylactic shock sepsis embolism, dynamic hyperinflation Drugs: Propofol, vasodilators Metabolic acidosis Hypocalcemia • Blood diagnostics • Imaging: echo, PAC • Imaging: Chest radiograph, • Diagnostics: Blood cultures, • Imaging to identify suspected • Consider inotropes echo, pleural USG procalcitonin, ionized calcium, bleeding sites • Consider MV support • Bladder pressure ABG, lactate • Cardiac filling pressure • MV waveforms • Discontinue offending • Fluid challenge • Fluid challenge = correction of medications • Blood transfusion, if bleeding underlying cause • Increase vasopressors ABG, arterial blood gas; AMI, acute myocardial infarction; CO, cardiac output; echo, echocardiography; MV, mechanical ventilation; PAC, pulmonary artery catheter; USG, ultrasonogram © The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons. org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Advances in Vasodilatory Shock: A Concise Review septic shock with an estimated mortality >50%.4 The surge in the K+-ATP channels are physiologically activated by decreases death toll of sepsis is representative of the overall burden of the in the cellular ATP concentration and by increases in cellular hospital-acquired infection (HAI) in the country. Paucity in resource concentrations of hydrogen ion and lactate. The opening of K+-ATP is a further hindrance over the propagation of sepsis research channels allows an efflux of potassium and, thus, hyperpolarizing infrastructure throughout the country. In this regard, an example the plasma membrane. This causes closer of voltage-gated calcium of the initiation of research infrastructure was promulgated by channels with subsequent vasodilation. Indian Society of Critical Care Medicine by developing a “cloud-based NO production is increased due to the expression of the database” called “Customized Health in Intensive Care, Trainable “inducible form” of NO synthase in many types of cells, including Research and Analysis” (CHITRA) (http://www.isccm.org/chitra. vascular smooth muscle cells and endothelium. Involvement aspx).5 of several cytokines (e.g., interleukin-1β, interleukin-6, tumor necrosis factor-α, interferon-γ, and adenosine) is predicted, as the PATHOPHYSIOLOGY mechanism is not well established. In response to hypotension, such as that due to hemorrhage The pathophysiology of vasodilatory shock could range from or sepsis, vasopressin releases from the neurohypophysis, and its multiple contributory states, including systemic inflammatory concentration in plasma markedly increases, which contributes to response syndrome (SIRS), anaphylaxis, pancreatitis, hepatic the maintenance of arterial pressure. As shock worsens, the initially failure, neurologic shock due to spinal cord injury, glucocorticoid very high concentrations of vasopressin in plasma decrease. The deficiency, and various toxins. Vasodilatory shock can occur solely exact mechanism responsible for these low concentrations remains or in combination with all other types of shocks. Put simply, to be determined, but it is known that neurohypophyseal stores of vasodilatory shock can be the final common pathway for severe vasopressin may be depleted after profound osmotic stimulation. shock of any cause (Flowchart 1).6 In all the forms of vasodilatory shock, plasma catecholamine concentrations are markedly increased, and the renin–angiotensin HEMODYNAMIC CHANGES system (RAS) gets activated. However, vasodilation and hypotension Hemodynamically in any kind of vasodilatory shock, initially cardiac results in less oxygen being supplied to the peripheral tissues. The output and heart rate are increased to compensate of reduced three cardinal mechanisms underpinning the pathologic state are oxygen supply to tissues. There is also hyperdynamic left ventricular the following: systolic contraction to propel blood to tissues. Despite the inotropic 1. Activation of adenosine triphosphate (ATP)-sensitive potassium and chronotropic stimulation, SVR decreases due to vasodilatation. channels (K+-ATP channels) in the plasma membrane of vascular This results in increase in venous capacitance and pooling of blood smooth muscle. in the venous system, prompting a dip in cardiac output. As a 2. Activation of the inducible form of nitric oxide (NO) synthase, sequel, various counterregulatory systems, such as the sympathetic and nervous system, the renin–angiotensin–aldosterone system gets 3. Deficiency of the hormone vasopressin. activated to counterbalance the state. But typically, SVR and preload Flowchart 1: Pathophysiology of vasodilatory shock 476 Indian Journal of Critical Care Medicine, Volume 23 Issue 10 (October 2019) Advances in Vasodilatory Shock: A Concise Review remain decreased. Therefore, compromised tissue oxygenation in Table 2: The Surviving Sepsis Campaign Bundles Update 2018: Elements the context of adequate or even increased cardiac output can be with strength of recommendations and underpinning quality of a characteristic feature of typical vasodilatory shock (Flowchart 1).6 evidence When sepsis-induced hypotension remains refractory to initial Grade of recommendation with management with fluid resuscitation, septic shock ensues. Septic Hour 1 - Bundle Element level of evidence shock is distinguished from other shock states as a distributive type Measurement of lactate level; Weak recommendation, low of shock. At an early “compensated” stage of shock, blood pressure
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