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Hypovolemic shock in Adults (at a glance) Introduction This article introduces the reader to hypovolemic shock. It discusses the risk factors, aetiology, investigations, staging, complications, principles of management, education and training, for hypovolemic shock. Shock Shock is generally classified according to its cause. There are four main pathological mechanisms that can result in a state of shock (Vincent and De Backer, 2013; Straton, 2017), being: hypovolemia (loss of intravascular volume form internal or external fluid loss, cardiogenic (pump failure), obstruction (barriers to cardiac filling or circulatory flow); and distributive shock (dur to vaso-regulation and loss of vascular tone). Shock is most commonly defined as âthe life-threatening failure of adequate oxygen delivery to the tissues and may be due to decreased blood perfusion of tissues, inadequate blood oxygen saturation, or increased oxygen demand from the tissues that results in decreased end-organ oxygenation and dysfunctionâ (Stratton, 2019). If left untreated, shock results in sustained multiple organ dysfunction, and end-organ damage with possible death. Tissue hypoperfusion may be present without systemic
hypotension, but at the bedside shock is commonly diagnosed when both are present (arterial hypotension and organ dysfunction) (Stratton, 2019). Hypovolemic Shock Hypovolaemic shock is characterised by a loss of intavascular volume of 15% or more leading to inadequate perfusion of the tissues (Peate, 2020). Hypovolemic shock occurs when the volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body (Rull and Bonsall, 2017). In summary, hypo means low, vol means volume and anaemic means blood translating as low blood volume. Patients with hypovolemic shock have severe hypovolemia with decreased peripheral perfusion. If left untreated, these patients can develop ischemic injury of vital organs, leading to multi-system organ failure. The first factor to be considered is whether the hypovolemic shock has resulted from haemorrhage or fluid losses, as this will dictate treatment. Pathophysiology and symptoms Hypovolemic shock results from depletion of intravascular volume, either by blood loss or extracellular fluid loss. The body compensates for this with increased sympathetic tone resulting in increased heart rate and cardiac contractility, and peripheral vasoconstriction. Changes in vital signs include; increase in diastolic blood pressure with narrowed pulse pressure. As volume status decreases, systolic blood pressure drops. Oxygen delivery to vital organs is unable to meet oxygen demand as a result and cells switch from aerobic metabolism to anaerobic metabolism, resulting in lactic acidosis. Blood flow is diverted from other organs to
is much greater as age increases because they often do not tolerate having low blood volume (Rull and Bonsall, 2017). Pathology in the cardiovascular, respiratory and renal systems increases risk. Aetiology The annual incidence of shock of any aetiology is 0.3 to 0.7 per 1000, with haemorrhagic shock being most common in the intensive care unit (Taghavi and Askari, 2019). Hypovolemic shock is the most common type of shock in children, most commonly due to diarrheal illness in the developing world. Hypovolemic shock occurs as a result of either blood loss or extracellular fluid loss. Haemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far the most common cause of haemorrhagic shock. Other causes of haemorrhagic shock include gastrointestinal (GI) bleed, bleed from an ectopic pregnancy, bleeding from surgical intervention, or vaginal bleeding (Taghavi and Askari, 2019). Hypovolemic shock as a result of extracellular fluid loss can be of the following aetiologies: Gastrointestinal Losses GI losses can occur via many different aetiologies. The gastrointestinal tract usually secretes between 3 to 6 litres of fluid per day. However, most of this fluid is reabsorbed as only 100 to 200 mL are lost in the stool. Volume depletion occurs when the fluid ordinarily secreted by the GI tract cannot be reabsorbed. This occurs
when there is retractable vomiting, diarrhoea, or external drainage via stoma or fistulas. (Taghavi and Askari, 2019). Renal Losses Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually excrete sodium and water in a manner that matches intake. Diuretic therapy and osmotic diuresis from hyperglycaemia can lead to excessive renal sodium and volume loss. In addition, there are several tubular and interstitial diseases beyond the scope of this article that cause severe salt-wasting nephropathy (Taghavi and Askari, 2019). Skin Losses Fluid loss also can occur from the skin. In a hot and dry climate, skin fluid losses can be as high as 1 to 2 litres/hour. Patients with a skin barrier interrupted by burns or other skin lesions also can experience large fluid losses that lead to hypovolemic shock (Taghavi and Askari, 2019). Third-Space Sequestration Sequestration of fluid into a third-space also can lead to volume loss and hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response (Taghavi and Askari, 2019). Blood Work Monitoring electrolytes and acid/base status in patients in hypovolemic shock is of utmost importance. Biochemical analysis will identify any electrolyte and acid-base
In the heart, reduced coronary perfusion and increased mediators (including tumor necrosis factor and interleukin-1) may depress contractility, worsen myocardial compliance, and down-regulate beta-receptors. These factors decrease cardiac output, further worsening both myocardial and systemic perfusion and causing a vicious circle often culminating in death. Arrhythmias may occur what ones? (Procter, 2019). In the gastrointestinal tract, ileus and submucosal hemorrhage can develop. Liver hypoperfusion can cause focal or extensive hepatocellular necrosis, transaminase and bilirubin elevation, and decreased production of clotting factors (Procter, 2019). Coagulation can be impaired, including the most severe manifestation, disseminated intravascular coagulopathy (Procter, 2019). Investigations ( Rull and Bonsall, 2017) Investigation Rationale Check Haemaglobin (Hb), Urea and Electrolytes (U&E), Liver Function Test (LFT) and, in haemorrhage and burns, group and save and crossmatch There is likely to be a significant drop in Hb in early stages of shock. Prompt administration of blood is essential in instances of severe or Aby Mitchell 1/4/2020 14: Comment [1]: Barry, I canât find this.
ongoing blood loss. Coagulation screen Blood gases â arterial blood gas (ABG) or venous blood gas (VBG) These may show a metabolic acidaemia from poor perfusion; lactate levels particularly reflect hypoperfusion. Note: In clinical practice, an ABG is always preferred as the respiratory component is captured, and with patients who are in shock, it is inevitable that they will deteriorate. Monitor urine output, which may require a catheter. Urine output should be used to guide administration of fluids. Ultrasound This can be useful for differentiating hypovolaemic from cardiogenic shock; the vena cava can be assessed for adequate filling and echocardiogram can show any pump failure. Central venous pressure (CVP) Monitoring CVP may be useful where there is evidence of shock. Aby Mitchell 1/4/2020 14: Comment [2]: Barry can you add the rationale for this?
will begin to experience mental distress, including anxiety and agitation. The skin will be pale and cold, and they will begin sweating. Urine output drops to 20 millilitres/hour. Altered mental state will present in confusion, anxiety and/or agitation. Stage 4 A person with stage- 4 hypovolemia faces a critical situation. They will have experienced a loss of blood volume greater than 40 percent, or 2,000 ml. They will have a weak pulse but extremely rapid heart rate. Breathing will become be very fast and difficult. Systolic blood pressure will be under 70 millimetres of mercury (mm/Hg). They may experience the following symptoms:
- drifting in and out of consciousness
- sweating heavily
- feeling cool to the touch
- looking extremely pale
- Absent capillary refill
- Negligible urine output Principle of Managing Hypovolemic Shock Management of hypovolemia involves assessing and treating the underlying cause, identifying electrolyte and acid-base disturbances, and assessing and treating the volume deficit, all of which influence the choice of fluid and rate at which it should be administered (Mandel and Palevsky, 2019).
Clinicians should identify the aetiology (or aetiologies) contributing to hypovolemia so that therapies can be directed at the underlying cause of volume loss. Potential aetiologies of hypovolemia include gastrointestinal, renal, skin, haemorrhage, and third-space losses. Therapies may include anti-emetics to treat vomiting, cessation of diuretics, or controlling bleeding. Further details regarding aetiology and diagnosis of hypovolemia are discussed separately. Identify electrolyte and acid-base disturbances â Biochemical analysis will alert the clinician to electrolyte (e.g., hypo- or hypernatremia, hypo- or hyperkalaemia) and acid-base disturbances (e.g., contraction alkalosis, metabolic acidosis) which may affect choice of replacement fluid and rate of repletion. In some cases, an arterial blood gas may be needed if mixed acid-base disturbance is suspected. Fluid Resuscitation It is suggested that fluid resuscitation should be commenced immediately to restore circulating volume and improve cardiac output. NICE (2017) advise that crystalloids are most appropriate, unless the patient presents with active internal or external bleeding. In such cases, Red Blood Cells should be transfused as the patient would require haemoglobin to support the transportation around the body to prevent anaerobic respiration and cell death causing increase lactate (Dutton and Finch, 2018 ). Highlight carriage problems earlier and that respiratory rate and SaO2 may indicate this issue. Use of Crystalloids (NICE, 2017) Aby Mitchell 1/4/2020 15: Comment [3]: Barry, I canât answer this
Inadequate perfusion This leads to hypoxia and metabolic acidosis About 75% of the blood flow to the right ventricle and 100% to the left ventricle occurs in diastole A fall in diastolic pressure will predispose to cardiac arrhythmias and even arrest. Upset of acid-base balance, hypoxia and disturbance of electrolytes will aggravate the problem In those who are susceptible, dehydration This may lead to haemoconcentration and sludging of the circulation with such complications as venous sinus thrombosis. Vasoactive drugs Following the infusion of either crystalloids (fluid loss) or RBCâs (after blood loss), the patients vital signs should be remeasured. It is imperative that the patient has a normotensive blood pressure to perfuse the brain, heart, lungs and kidneys particularly, as otherwise they are likely to develop an Acute Kidney Injury or go into shock (REF). This is the goal of fluid resuscitation and has no mention of vasoactive drugs. Consider the audience for this paper. These drugs are most often administered in critical care areas. Pearls and Other Issues ( Taghavi and Askari, 2019) Aby Mitchell 1/4/2020 14: Comment [4]: Barry, do we still need this?
In patients with hypovolemic shock due to extracellular fluid loss, the aetiology of fluid loss must be identified and treated. Monitoring electrolytes and acid/base status in patients in hypovolemic shock is of utmost importance. Trauma is the leading cause of haemorrhagic shock. The haemorrhagic shock should be treated with balanced transfusion of packed red blood cells, plasma, and platelets. Determining whether patients will be responsive to volume resuscitation should not rely on a single modality such as ultrasound, pulse pressure wave variation, passive leg raises, or central venous pressure. The decision for fluid administration should be based on a complete systematic assessment to help direct volume resuscitation. For patients with hypovolemic shock due to fluid loss, the crystalloid solution is preferred over colloid. Training and education (NICE, 2017) Hospitals should establish systems to ensure that all healthcare professionals involved in prescribing and delivering IV fluid therapy are trained on the principles covered in this guideline, and are then formally assessed and reassessed at regular intervals. Health care professionals need to be able to assess, identify and escalate care. Competence must be demonstrated in:
- understanding the physiology of fluid and electrolyte balance in patients with normal physiology and during illness
Dutton, H. Finch, J. (2018) Acute and Critical Care Nursing at a Glance. Wiley Blackwell publishers. Galvagno, S., 2014. Emergency Pathophysiology. Hoboken: Teton NewMedia, Inc. Gayet-Ageron A, Prieto-Merino D, Ker K, Shakur H, Ageron FX, Roberts I., Antifibrinolytic Trials Collaboration. Effect of treatment delay on the effectiveness and safety of antifibrinolytics in acute severe haemorrhage: a meta-analysis of individual patient-level data from 40 138 bleeding patients. Lancet. 2018 Jan 13; 391 (10116):125-132. Hooper N, Armstrong TJ. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 6, 2019. Haemorrhagic Shock. Lavoie, L. (2018) What to know about hypovolemic shock. Medical News Today. Available at: https://www.medicalnewstoday.com/articles/312348.php (Last Accessed: 24.01.2020). Mandel, J. Palevsky, P. (2019) Treatment of severe hypovolemia or hypovolemic shock in adults. Available at: https://www.uptodate.com/contents/treatment-of- severe-hypovolemia-or-hypovolemic-shock-in-adults (accessed on: 15.01.2020).
NICE (2017) Intravenous Fluid therapy in Adult in Hospital. NICE Clinical Guideline
- Available at: https://www.nice.org.uk/guidance/cg174/resources/composition-of- commonly-used-crystalloids-table- 191662813 (Last Accessed 24.01.2020). Procter, L. (2019) Shock. Available at: https://www.msdmanuals.com/en- gb/professional/critical-care-medicine/shock-and-fluid-resuscitation/shock (accessed: 16.01.2020). Rull, G. Bonsall, A. (2017) Resuscitation in Hypovolaemic Shock. Emergency medicine and trauma. Available at: https://patient.info/doctor/resuscitation-in- hypovolaemic-shock (Accessed on: 16.01.2020). Stratton, S. (2019) Shock. BMJ Best Practice. Available at: https://bestpractice.bmj.com/topics/en-gb/1013#referencePop4 (Accessed on: 15.01.202). Taghavi, S. Askari, R. (2019) Hypovolemic shock. Available at: https://www.ncbi.nlm.nih.gov/books/NBK513297/ (Accessed on: 15.01.2020). Vincent, J. De Backer, De. (2013) Circulatory Shock. NEJM. 2013: 369 (18); 1726-
