This article introduces the reader to hypovolaemic shock. It discusses the risk factors, aetiology, investigations, staging, complications, principles of management, education and training.
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; Stratton, 2019):
Shock is commonly defined as ‘the 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 dysfunction’ (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 arterial hypotension and organ dysfunction are present (Stratton, 2019).
Hypovolaemic shock
Hypovolaemic shock (hypo=low, vol=volume and anaemic=blood) is characterised by a loss of intravascular volume of 15% or more, leading to inadequate perfusion of the tissues (Peate, 2020). Hypovolaemic shock occurs when the volume of the circulatory system is too depleted to allow adequate circulation to the tissues (Rull and Bonsall, 2017). Patients with hypovolaemic shock have severe hypovolaemia with decreased peripheral perfusion. If left untreated, ischaemic injury of vital organs can occur, leading to multi-system organ failure. The first factor to be considered is whether the hypovolaemic shock has resulted from haemorrhage or fluid losses as this will dictate treatment.
Pathophysiology and symptoms
Hypovolaemic 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. Sympathetic tone is the condition of a muscle when the tone is maintained predominantly by impulses from the sympathetic nervous system. Changes in vital signs include an 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 demand as a result and cells switch from aerobic to anaerobic metabolism, resulting in lactic acidosis. Blood flow is diverted from other organs to preserve the flow to the heart and brain as sympathetic drive increases. This propagates tissue ischaemia and exacerbates lactic acidosis. If this is not corrected, there will be worsening haemodynamic compromise and, eventually, death (Gayet-Ageron et al, 2018).
Symptoms of hypovolaemic shock can be related to volume depletion, electrolyte imbalances or acid base disorders that accompany hypovolaemic shock. Patients with volume depletion may experience thirst, muscle cramps and/or orthostatic hypotension (decrease in systolic blood pressure of 20 mmHg or decrease in diastolic blood pressure of 10 mmHg within 3 minutes of standing compared to a sitting or supine blood pressure). In severe hypovolaemic shock, patients can experience abdominal or chest pain caused by mesenteric and coronary ischaemia. Brain malperfusion can cause agitation, lethargy or confusion.
Physical assessments as a result of volume depletion may find dry mucous membranes, decreased skin elasticity, low jugular venous distention, tachycardia, hypotension and decreased urinary output. Patients may also appear cold, clammy and cyanotic (Annane et al, 2013).
The clinical features of hypovolaemic shock can be seen in Box 1. A list of investigations and their rationales are shown in Table 1.
| Investigation | Rationale |
|---|---|
| Check haemoglobin (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 hypovolaemic shock. This is because, in the earliest stage of the condition, a person with will have lost up to 15%, or 750 ml, of their blood volume |
| Coagulation screen | The coagulation screen is a combination of tests designed to provide rapid information and allows an initial broad categorisation of haemostatic function. In hypovolaemic shock, the acute fall in clotting factors is likely due to increased haemostatic demands, plasma dilution from resuscitation, and extravascular relocation from shock-induced extravascular expansion |
| Blood gases: 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 |
Risk factors
A healthy adult can withstand the loss of 0.5 litre of fluid from a circulation of about 5 litres without ill effect (Rull and Bonsall, 2017); however, larger volumes and rapid loss cause progressively greater problems. Risk of shock is related to the degree of hypovolaemia and the speed of correction. In children and young adults, tachycardia is one of the earliest signs of hypovolaemia as the circulatory system is better able to cope with the rigours of loss. The risk of morbidity and mortality is much greater as age increases because older people 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). Hypovolaemic shock is the most common type of shock in children and is frequently due to diarrheal illness in the developing world. Haemorrhagic shock is hypovolaemic shock from blood loss and is mostly caused by traumatic injury. Other causes of haemorrhagic shock include gastrointestinal (GI) bleed, bleeding from an ectopic pregnancy, bleeding from surgical intervention, or vaginal bleeding (Taghavi and Askari, 2019).
Hypovolaemic 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 GI tract usually secretes between 3 to 6 litres of fluid per day. However, most of this fluid is reabsorbed as only 100–200 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 intractable vomiting, diarrhoea, or external drainage via stoma or fistulas (Taghavi and Askari, 2019).
Renal losses
Renal losses of salt and fluid can lead to hypovolaemic 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 can also experience large fluid losses that lead to hypovolaemic shock (Taghavi and Askari, 2019).
Third-space sequestration
Sequestration of fluid into a third-space can also lead to volume loss and hypovolaemic 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 hypovolaemic shock is of utmost importance. Biochemical analysis will identify any electrolyte and acid-base disturbances, for example contraction alkalosis, metabolic acidosis, which could affect choice of replacement fluid, and rate of repletion. In some cases, arterial blood gas is needed if mixed acid-base disturbance is suspected (Galvagno, 2014).
Multiple organ dysfunction syndrome
The combination of direct and reperfusion injury may cause multiple organ dysfunction syndrome (MODS)—the progressive dysfunction of more than 2 organs consequent to life-threatening illness or injury (Procter, 2019). MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock. MODS also occurs in more than 10% of patients with severe traumatic injury and is the primary cause of death in those surviving longer than 24 hours (Procter, 2019).
During MODS, the permeability of lung parenchyma leads to inflammation and oedema collection within the alveoli. Lactate production and metabolic acidosis produces abnormal levels of hydrogen ions. This decreases the pH in the blood and the level of bicarbonate. To compensate for this the respiratory rate is increased, resulting in hyperventilation (Galvagno, 2014). Progressive hypoxia may be resistant to supplemental oxygen therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS) (Procter, 2019).
The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal insufficiency manifested by oliguria and a progressive rise in serum creatinine (Procter, 2019).
In the heart, reduced coronary perfusion and increased mediators (including tumour 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 (Procter, 2019).
In the GI tract, ileus and submucosal haemorrhage 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).
Staging
Lavoie (2018) recognises that there are four stages of hypovolaemic shock based on how much blood volume has been lost. All stages require early treatment, but it is helpful to recognise the stage of hypovolaemia in order to provide the appropriate treatment quickly due to the complications hypovolaemic shock presents (Table 2).
| Complication | Wider implication |
|---|---|
| Blood is directed away from the kidneys and gut | This can produce acute kidney injury and complications of gut ischaemia |
| Obstetric shock | Acute tubular necrosis can occur |
| 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 |
Stage 1
During the earliest stage of hypovolaemic shock, a person will have lost more than 15% (>750 ml) of their intravascular fluid volume. This stage can be difficult to diagnose. Blood pressure, urine output and breathing will still be normal. The most noticeable symptom at this stage is skin that appears pale. The person may also experience sudden anxiety.
Stage 2
In the second stage, the body will have lost up to 30% (1500 ml), of blood. The individual may experience increased heart and breathing rates. Blood pressure may still be within the normal range. However, the diastolic pressure may be high. The person may begin sweating and feeling more anxious and restless. At this stage, capillary refill is delayed, and urine output may be about 20–30 ml/hour.
Stage 3
By stage 3, a person with hypovolaemic shock will have lost 30–40% (1500–2000 ml) of blood. The systolic blood pressure will be 100 mmHg or lower. The patient's heart rate may increase to over 120 beats per minute. They will also have a rapid breathing rate of over 30 breaths per minute. The patient will begin to experience mental distress, including anxiety and agitation. Their skin will be pale and cold, and they will begin sweating. Urine output drops to 20 ml/hour.
Stage 4
A person with stage 4 hypovolaemia faces a critical situation. They will have experienced a loss of blood volume greater than 40% (2000 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 mmHg. They may experience the following symptoms:
Principles of managing hypovolaemic shock
Management of hypovolaemia involves assessing and treating the underlying cause, identifying electrolyte and acid-base disturbances, and assessing and treating the volume deficit. This will 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 hypovolaemia so that therapies can be directed at the underlying cause of volume loss. Therapies may include anti-emetics to treat vomiting, cessation of diuretics, or controlling bleeding.
It is important to identify electrolyte and acid-base disturbances. Biochemical analysis will alert the clinician to electrolyte (eg hypo-or hypernatremia, hypo- or hyperkalaemia) and acid-base disturbances (eg 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. The National Institute for Health and Care Excellence (NICE) (2017a) recommends the administration of intravenous (IV) crystalloids that contain sodium in the range 130–154 mmol/l, with a bolus of 500 ml over less than 15 minutes, unless the patient presents with active internal or external bleeding. In such cases, red blood cells should be transfused to support the transportation of haemoglobin around the body (Dutton and Finch, 2018). Hypovolaemia directly impacts circulating blood volume and therefore contributes to decreased oxygen carriage, increased lactate for anaerobic respiration, cell death, and potentially leads to pre-renal failure.
Clinical considerations
In patients with hypovolaemic shock due to extracellular fluid loss, the aetiology of fluid loss must be identified and treated (Taghavi and Askari, 2019):
Training and education
Hospitals should establish systems to ensure that all health professionals involved in prescribing and delivering IV fluid therapy are trained on the principles covered in the NICE (2017b) guideline, and are then formally assessed and reassessed at regular intervals. Health professionals need to be able to assess, identify and escalate care. Competence must be demonstrated in:
Hospitals should have an IV fluids lead, responsible for training, clinical governance, audit and review of IV fluid prescribing and patient outcomes.
Conclusion
Hypovolaemic shock is characterised by an imbalance between oxygen supply and demand. If left untreated patients can develop ischaemic injury of vital organs, which leads to multi-system organ failure. It is important for nurses to be able to assess, identify and escalate care to ensure patients receive correct and timely treatment.