What do we mean by shock?
The NHS describes shock as a life-threatening condition that arises when the circulatory system fails to supply enough oxygenated blood to the body. This lack of oxygen can cause vital organs to not receive the support they need. Patients showing signs of shock require immediate intervention, as untreated shock can lead to cell death, which may ultimately progress to multi-organ failure and death (Koya and Paul, 2023).
Aetiology
A decrease in oxygen delivery, oxygen consumption or inadequate oxygen use can lead to tissue or cellular hypoxia (Boag, 2015). Oxygen delivery occurs when oxygen molecules bind to haemoglobin within red blood cells (Wemple, 2010). The red blood cells then circulate through the body, releasing oxygen to the cells, where it is used for energy production (Edwards et al, 2021). This delivery system relies on sufficient tissue perfusion. Therefore, if a patient is poorly perfused, there will be an inadequate supply of oxygen to the tissues.
Shock is a condition that is categorised as circulatory failure and most frequently manifests as as hypotension, defined as a systolic blood pressure of less than 90 mmHg (Talbot et al, 2023). It is a fatal manifestation of a complex list of aetiologies (Edwards et al, 2021). There are four main categories of shock, including: distributive, hypovolaemic, cardiogenic and obstructive.
The different types of shock
Distributive shock is characterised by hypovolemia caused by the pathological redistribution of fluid (Dell'Anna et al, 2019). In this condition, the body struggles to maintain vasoconstriction of blood vessels due to the release of inflammatory mediators (Koya and Paul, 2023). This issue is often observed in cases of sepsis, systemic inflammatory response syndrome or anaphylaxis (Keefe, 2011).
Hypovolemic shock is defined as a reduction in intravascular volume, which results in decreased cardiac preload and, consequently, diminished cardiac output (NHS, 2019). This condition is the most common form of shock observed in veterinary patients, making it essential to understand (Talbot et al, 2023).
Hypovolemic shock can be categorised into two types: hemorrhagic and non-hemorrhagic. Hemorrhagic shock is caused by bleeding, which can occur due to trauma, such as in a road traffic accident, or because of non-traumatic reasons, such as a ruptured splenic mass (Standi et al, 2018). In contrast, non-hemorrhagic hypovolemic shock is related to excessive fluid loss, which can result from persistent vomiting or diarrhoea, or may occur due to traumatic events, such as burns.
Cardiogenic shock occurs as a result of an intracardiac disease process that results in decreased cardiac output and systemic hypoperfusion (Boag, 2015). This condition leads to hemodynamic abnormalities, which in turn causes reduced tissue perfusion and increased pulmonary venous pressures. Cardiogenic shock can result from various cardiac diseases, including advanced cardiomyopathies, severe arrhythmias, and valvular disease (Talbot et al, 2023).
Obstructive shock occurs when a mechanical or vascular blockage hampers blood flow (Dell'Anna et al, 2019). This blockage can result from various conditions, such as tension pneumothorax, thromboembolism, gastric dilated volvulus or other obstructive diseases. The severity and location of the obstruction are crucial factors in determining whether a patient will progress to shock (Boag, 2015).
Signs of shock and what to look out for
A diagnosis of shock is determined through a comprehensive physical examination, which includes assessing the patient's hemodynamic parameters, such as blood pressure and blood work (Dell'Anna et al, 2019). Therefore, being familiar with the clinical signs associated with shock in veterinary patients is essential. Veterinary nurses play a crucial role in identifying the early signs of shock through regular patient monitoring (Tabor, 2015). Early recognition is vital, as it can often mean the difference between life and death. Tables 1 and 2 detail the clinical signs of shock observed in dogs and cats. There are subtle differences in the clinical signs exhibited by both animals, with bradycardia being a notable difference observed in some cats.
Clinical signs in each stage of shock in dogs (Tabor, 2015; Talbot et al, 2023)
| Physical Examination | Compensatory Shock | Early decompensatory shock | Late decompensatory shock |
|---|---|---|---|
| Physical Examination | Compensatory Shock | Early decompensatory shock | Late decompensatory shock |
| Temperature | Normal to low normal | Slight to moderate hypothermia | Moderate to marked hypothermia |
| Heart rate | Tachycardia (>180bpm) | Tachycardia (>150 bpm) | Bradycardia (<140 bpm) |
| Mucous membrane colour | Normal to pale (hyperaemic in distributive) | Pale | Pale to grey |
| Capillary refill time | Normal to slightly prolonged | Prolonged | Prolonged |
| Blood pressure | Slight hypotension to normal (70 – 80 mmHg) | Mild to moderated hypotension (50 – 70 mmHg) | Marked hypotension refractory to fluid therapy (<60 mmHg) |
| Respiratory rate | Tachypnoea | Tachypnoea | Bradypnoea |
| Mentation | Responsive | Obtunded | Obtunded to stuporous |
Clinical signs of each stage of shock in cats (Tabor, 2015; Talbot et al 2023)
| Physical examination | Compensatory shock | Early decompensatory shock | Late decompensatory shock |
|---|---|---|---|
| Temperature | Normal to low normal | Slight to moderate hypothermia | Moderate to marked hypothermia |
| Heart rate | Severe tachycardia (>240 bpm) or mild bradycardia (160 – 180 bpm) | Moderate tachycardia (>200 bpm) or bradycardia (120–140 bpm) | Mild tachycardia (>180 bpm) or severe bradycardia (<120 bpm) |
| Mucous membrane molour | Pale (Hyperaemic in distributive) | Pale to white | Pale to grey |
| Capillary refill time | Normal to slightly prolonged | Prolonged | Prolonged |
| Blood pressure | Slight hypotension to normal (80–90 mmHg) | Mild to moderate hypotension (50–80 mmHg) | Marked hypotension refractory to fluid therapy (<50 mmHg) |
| Respiratory rate | Tachypnoea | Tachypnoea | Bradypnoea |
| Mentation | Responsive | Obtunded | Obtunded to stuporous |
The early stage of shock is known as the compensatory stage, during which the patient can adjust to the decreased oxygen delivery. The clinical signs in this stage are generally consistent across all types of shock because they reflect the body's response to inadequate tissue perfusion (Epstein et al, 2024). Patients experiencing the compensatory stage of shock may appear relatively well, making it easy for clinical signs to be overlooked (Porter et al, 2013).
If left unnoticed or untreated during the compensatory stage, the patient will progress into early decompensatory shock. During the early compensatory stage of all but distributive shock, patients undergo peripheral vasoconstriction to redistribute the circulating blood volume to the heart and brain (Standi et al, 2018). During this stage, the patients are at high risk of rapid deterioration and organ damage due to reduced blood flow (Dell'Anna et al, 2019).
If the patient continues to be left untreated, they will progress into late decompensatory stage. Once in this stage of shock, even with aggressive treatment, there is a high risk of multiple organ failure and, subsequently, death (Edwards et al, 2021).
Initial stabilisation
Treatment in these cases should focus on increasing the delivery of oxygen to the tissues. This is accomplished by increasing the effective circulating volume, supplying oxygen therapy, increasing the haemoglobin concentration, and increasing the cardiac output (Tabor, 2015).
Upon recognising the signs of shock, an attempt should be made to obtain vascular access. Ideally, a large-bore, short intravenous catheter should be placed to facilitate the delivery of fluid boluses (Epstein et al, 2024).
Oxygen therapy is crucial for patients experiencing shock, particularly those who are hypoxemic (Koya and Paul, 2023). There are several methods for delivering oxygen, including flow-by, face masks, nasal prongs, nasal cannulas, oxygen cages and oxygen hoods. The selection of the delivery method will depend on the patient's tolerance and the available resources.
In most forms of shock, fluid therapy is crucial for the initial stabilisation of the patient. The only exception is cardiogenic shock, where fluid therapy is contraindicated (Orme, 2016). The goal of fluid resuscitation is to elevate the systolic blood pressure to between 90 and 110 mmHg (Standi et al, 2018).
Fluid resuscitation typically starts with isotonic crystalloid fluids. These fluids have the same solute concentration as blood plasma, which prevents fluid shifts that could disrupt cell function (Cazzolli and Prittie, 2015). Isotonic fluids allow for volume resuscitation without disturbing cellular function. The veterinary surgeon determines the volume and rate of fluid administration based on the patient's clinical parameters.
The recommended total shock bolus volume of isotonic fluids is 60 to 90 ml/kg for dogs and 40 to 60 ml/kg for cats. This volume is usually divided into smaller boluses (Cazzolli and Prittie, 2015). After each bolus, the patient's perfusion parameters should be reassessed to guide decisions about repeating boluses. Treatment is considered effective once the patient has regained normal perfusion parameters.
If administering a large volume of fluid rapidly enough for resuscitation becomes difficult or if large volumes are contraindicated, hypertonic crystalloids may be considered (Edwards et al, 2021). Hypertonic crystalloids cause fluid to shift from the intracellular space to the extracellular space, thereby expanding intravascular volume and improving venous return, cardiac output, and tissue perfusion (Cazzolli and Prittie, 2015).
Once the volume has been restored, it is important to continue fluid therapy to prevent dehydration. Additionally, blood products may be necessary for patients in shock, particularly those experiencing hemorrhagic shock or who have low total protein levels (Epstein et al, 2024).
If the patient is persistently hypotensive with a normal cardiac volume, it can be assumed this is caused either because of a decrease in cardiac contractility or vasodilation. At this point, the veterinary surgeon may consider the use of either positive inotropes for cardiac contractility or vasopressors for adjustments of vascular tone (Koya and Paul, 2023).
The endpoint for the initial resuscitation of patients in shock has not been clearly defined in veterinary medicine, so it often relies on the veterinarian's judgment (Dell'Anna et al, 2019). Common endpoints include a normalised heart rate, improved mental status, stabilisation of blood pressure, the improved colour of mucous membranes, enhanced capillary refill time and better peripheral pulses (Boag, 2015). Even if the patient appears to have stabilised, close monitoring is still essential for any signs of deterioration, while the underlying causes of shock are identified and addressed.
Nursing considerations in the shock patient
During the resuscitation phase, these patients require intensive monitoring and nursing care due to their dynamic state (Tabor, 2015). Monitoring of these patients should be carried out both during and following resuscitation. Parameters that should be assessed regularly include:
When assessing a patient's pulse, it is essential to also auscultate the heart to check for any asynchronous pulses (Standi et al, 2018). To facilitate the monitoring of these parameters, the patient may be connected to a multi-parameter monitor, if available. Attaching the patient to a continuous electrocardiogram provides the medical team with valuable information regarding the heart rate, rhythm and electrical activity. This is crucial because if the myocardium experiences hypoxia, ventricular premature contractions may occur (Edwards et al, 2021). Additionally, monitoring oxygen levels can be done non-invasively through pulse oximetry, which measures the amount of oxygen bound to hemoglobin (SpO2) in the blood.
Monitoring of urine output is important in these patients as a decrease could indicate either inadequate fluid resuscitation or a decrease in renal function (Orme, 2016). A normal urine output for a patient on fluids should be at least 1ml/kg/hr (Boag, 2015). Close monitoring of the patient's USG is another indicator of whether there is adequate fluid resuscitation. When a patient is adequately hydrated and receiving fluid therapy, a normal USG is between 1.008 and 1.012 (Epstein et al, 2024).
Regular blood analyses should be conducted for shock patients during their treatment. The parameters that need to be regularly checked include packed cell volume (PCV), total protein (TP), electrolytes, blood glucose (BG), urea, creatinine and lactate.
PCV measurements indicate the potential oxygen-carrying capacity of the blood, as it is estimated that one-third of the PCV reflects the haemoglobin content. A haemoglobin concentration of more than 8 g/dL is necessary for adequate oxygen delivery. If a patient's PCV falls below 24%, blood products may be required (Koya and Paul, 2023; Standi et al, 2018).
Lactate levels are also crucial to monitor. When tissues experience hypoxemia or hypovolemia, anaerobic metabolism occurs, leading to the production of lactate. Elevated blood lactate levels suggest a degree of hypoperfusion, allowing for the assessment of the patient's response to resuscitation through serial lactate monitoring (Edwards et al, 2021).
Additionally, monitoring blood urea and creatinine levels can help to indicate renal function. Increased levels of these markers suggest a decline in function, indicating that the patient may be beginning to decompensate (Koya and Paul, 2023).
Conclusions
Shock is a complex condition that encompasses a wide variety of factors and treatments. Veterinary nurses play a crucial role in recognising early signs of shock through proper training and vigilant monitoring. Early intervention in shock cases significantly increases a patient's chances of survival and helps to prevent more severe complications.