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Hypovolemic Shock - a Review J Review Article Hypovolemic shock - A review J. A.Shagana1, M. Dhanraj1, Ashish R. Jain1*, T. Nir osa2 ABSTRACT Shock is described traditionally as tissue hypoxia due to inadequate perfusion which is classified as hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic shock is an important life-threatening emergency. In hypovolemic shock, there is decreased circulating blood volume due to the loss of intravascular fluid. Hemorrhagic shock is the most common form of hypovolemic shock and must be recognized early which prevent progression, morbidity, and mortality. Hence, this article will discuss about the causes, clinical features, diagnosis, and treatment of hypovolemic shock. KEY WORDS: Blood pressure, Cardiac output, Circulating blood volume, Hypovolemic shock and organ dysfunction INTRODUCTION The systemic vascular resistance (SVR) is typically increased in an effort to compensate for the diminished Shock is defined as the state in which profound and CO and maintain perfusion to vital organs. The early widespread reduction of effective tissue perfusion stage of recognition and intervention will help to leads first to reversible, and then if prolonged, prevent death.[4] to irreversible cellular injury. It is classified as hypovolemic/hemorrhagic shock, cardiogenic ETIOLOGY shock, obstructive shock, and distributive shock.[1]. Hypovolemic shock is defined as the rapid fluid loss or Hypovolemic shock is caused by sudden blood or fluid blood loss which results in multiple organ dysfunction losses within your body. The most common clinical due to inadequate circulating blood volume and causes of hypovolemic shock are hemorrhage, vomiting, perfusion. It is caused by a loss of intravascular diarrhea, severe burns, and excessive sweating.[5] Since fluid which is usually whole blood or plasma. Whole arterial blood pressure (BP) is dependent on the CO blood loss from an open wound is an obvious cause and SVR, marked reduction in either of these variables for hypovolemic shock. An intravascular volume without a compensatory elevation results in systemic depletion may occur with any condition which leads to hypotension. In hypovolemic shock, the volume excessive extracellular fluid loss with or without loss loss is exogenous or endogenous. Restoration blood of plasma protein.[2] Hypovolemic shock is secondary volume is both simple and effective if applied before to hemorrhagic shock (rapid blood loss) which is irreversible tissue damage occurs.[6] The external fluid rare but cause serious complications and mostly losses and the internal sequestration will cause reduced occurs in obstetrical situations. Hypovolemic shock venous return and decreased CO. This leads to set of is associated with disorders that cause an underlying reflex responses designed to maintain the oxygen hemodynamic defect of a low intravascular volume to critical organs such as brain and heart. However, and a reduction in myocardial contractility.[3] It is a these responses may limit perfusion of other organs consequence of decreased preload due to intravascular such as gut as to produce necrosis. The consequences volume loss. The decreased preload diminishes stroke of reduced tissue perfusion are similar in all forms of volume, resulting in decreased cardiac output (CO). shock.[7] SYMPTOMS Access this article online The symptoms can vary with the previous level of Website: jprsolutions.info ISSN: 0975-7619 organ function, compensatory mechanisms, severity of 1Department of Prosthodontics, Saveetha Dental College and Hospital, Saveetha University, Chennai, Tamil Nadu, India, 2Department of Public Health Dentistry, Saveetha Dental College and Hospital, Saveetha, University, Chennai, Tamil Nadu, India *Corresponding author: Dr. Ashish R. Jain, Department of Prosthodontics, Saveetha Dental College and Hospital, Saveetha University, Poonamalle High Road, Chennai - 600 127, Phone: +91-9884233423. E-mail: [email protected] Received on: 09-02-2018; Revised on: 06-04-2018; Accepted on: 17-05-2018 1102 Drug Invention Today | Vol 10 • Issue 7 • 2018 J. A. Shagana, et al. organ dysfunctions, and the cause of shock syndrome. chemoreceptors as well as hypoperfusion of the The symptoms of hypovolemic shock include pallor, medullary respiratory center results in increased minute tachycardia, hypotension, dyspnea, diaphoresis, volume (tachypnea and hyperpnea), hypocapnia, and tachypnea, cyanosis, faint heart sounds, agitation, primary respiratory alkalosis. With increased minute mental status changes, pinpoint pupils, cool and clammy volume and decreased CO, the V/Q ratio is increased. skin, lactic acidosis, and poor urine output.[8] Right-heart Coupled with an increased workload, respiratory, catheterization will usually reveal a low central venous and diaphragmatic muscle impairment caused by pressure (CVP), pulmonary artery occlusion pressure hypoperfusion may lead to early respiratory failure. (PAOP), CO, and mixed venous oxygen content. If shock is not promptly reversed and the initiating During spontaneous ventilation, pulsus paradoxus condition controlled, adult respiratory distress may occur, whereas during mechanical ventilation, syndrome may develop.[11] the systolic BP only transiently increases during the inspiratory phase followed by a rapid decrease (with Renal System a systolic pressure variation of >10 mmHg) being It responds to hemorrhagic shock by stimulating an suggested as a method to diagnose hypovolemia in a increase in renin secretion from the juxtaglomerular mechanically ventilated patient with normal pulmonary apparatus. Renin converts angiotensinogen to compliance.[9] The presence of cardiovascular disease, angiotensin I, which subsequently is converted to autonomic neuropathy or anemia, or prior treatment angiotensin II by the lungs and liver. Angiotensin II with β-adrenergic blockers or calcium channel blockers has two main effects, both of which help to reverse may worsen the cardiovascular response to blood loss.[10] hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone EFFECTS ON CEREBRAL secretion by the adrenal cortex. Aldosterone is AND OTHER REGIONAL responsible for active sodium reabsorption and subsequent water conservation.[11] CIRCULATIONS Neuroendocrine System Cerebral Circulation In neuroendocrine system, an increase in circulating Although central nervous system neurons are extremely antidiuretic hormone is responds to shock which is sensitive to ischemia, the vascular supply is highly released from the posterior pituitary gland in response resistant to extrinsic regulatory mechanisms. Patients to a decrease in BP (as detected by baroreceptors) and without a primary cerebrovascular impairment support a decrease in the sodium concentration (as detected by their cerebral function well until the mean arterial osmoreceptors). It leads to an increased reabsorption pressure falls below approximately 50–60 mmHg. of water and salt (NaCl) by the distal tubule, the At this point, irreversible ischemic injury may occur collecting ducts, and the loop of Henle.[11] to the most sensitive areas of the brain, i.e. cerebral cortex and watershed areas of the spinal cord. 58, 59 INVESTIGATIONS Before such injury, an altered level of consciousness varying from confusion to unconsciousness may be The diagnostic evaluation should occur as same seen depending on the degree of perfusion deficit. as resuscitation if patient is suspected of having Electroencephalographic recordings demonstrate non- shock. Laboratory tests may help identify the cause specific changes compatible with encephalopathy.[11] of shock and early organ failure.[12] They should be performed early in the evaluation of undifferentiated Cardiovascular System shock which include complete blood count with Initially, the cardiovascular system responds to differential, basic chemistry tests (sodium, potassium, hypovolemic shock by increasing the heart rate, chloride, and serum bicarbonate), blood urea constricting peripheral blood vessels, and increasing nitrogen, creatinine, liver function tests, amylase, myocardial contractility. This occurs secondary to an lipase, prothrombin time or international normalized increased release of norepinephrine and decreased ratio, partial thromboplastin time, fibrinogen, fibrin baseline vagal tone regulated by the baroreceptors split products or dimer, cardiac enzymes (troponin in the carotid arch, aortic arch, left atrium, and or creatine phosphokinase isoenzymes), urinalysis pulmonary vessels. Further redistribution of the blood with a detailed sediment analysis, arterial blood gas to the brain, heart, kidneys and the skin, muscle, (ABG), toxicology screen, and lactate level.[13] A and gastrointestinal tract, the cardiovascular system chest radiograph, abdominal radiograph for intestinal responses to shock.[11] obstruction, abdominal computed tomography (CT), head CT scan, electrocardiogram, echocardiogram, Respiratory System or urinalysis may also be helpful.[14] Gram stain of Increased respiratory drive resulting from peripheral material from sites of possible infection (sputum, stimulation of pulmonary receptors and carotid body urine, and wounds) may give early clues to the etiology Drug Invention Today | Vol 10 • Issue 7 • 2018 1103 J. A. Shagana, et al. of infection while cultures are incubating. Blood CONCLUSION should be taken from two distinct venipuncture sites and inoculated into standard blood culture media.[15] In general, people with milder degrees of shock tend to do better
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