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2 Shock and dehydration

Shock and dehydration are both commonly seen in emergency practice and both require fluid therapy as a crucial part of their management (see Ch. 4). However, they represent different pathophysiological processes and have different clinicopathological findings. Understanding these differences is essential to ensuring that the most appropriate management is implemented.

Body Fluid Compartments

Total body water typically constitutes approximately 60% of a healthy non-obese adult dog or cat’s body weight. A basic understanding of the way in which the total body water is distributed is central to appreciating the concepts of perfusion, volume status, shock and hydration. The total body water is distributed as follows:

Intracellular compartment (40% body weight)
Extracellular compartment (20% body weight):
Interstitial space including lymph (15% body weight)
Intravascular space (4% body weight)
Transcellular compartment (e.g. cerebrospinal and synovial fluid; approximately 1%).

Active and/or passive movement of fluid occurs continuously between the intravascular and interstitial compartments at the capillary membrane. The most important factor that determines the size of each fluid compartment is the amount of solutes it contains.

Hypoperfusion and Shock

Organs and peripheral tissues rely on an adequate intravascular fluid space (adequate perfusion) for the delivery of oxygen and nutrients and the removal of by-products of tissue metabolism. ‘Hypoperfusion’ describes a situation in which there is a decrease in the blood supply to an organ or tissue. Although this can occur solely on a local level, it is seen most commonly in the context of a global (systemic) reduction in blood supply.

The term ‘shock’ is used clinically to describe the condition of a patient in which this global hypoperfusion has reached a certain level of severity, sufficient for the patient to manifest a number of characteristic clinical findings. This usually occurs when the reduction in blood supply is severe enough to cause inadequate oxygen delivery to the cells and thereby inadequate energy production. If the degree of shock is sufficiently severe or prolonged, irreversible cell damage can occur and treatment is invariably unsuccessful.

Clinical Tip

Systemic hypoperfusion is common in emergency patients and being able to recognize and treat this abnormality is crucial for successful stabilization.

Causes of hypoperfusion

The mechanisms of hypoperfusion and shock can be divided into four categories. However, it is important to remember that more than one type can exist in the same patient at the same time, and that they share some common changes and derangements at a cellular level.

Hypovolaemic shock

Hypovolaemia is a reduction in the effective circulating intravascular volume and is the most common cause of hypoperfusion in companion animals. It can be subdivided into absolute and relative hypovolaemia. Absolute hypovolaemia is the most common type and occurs as a result of loss of fluid from the intravascular space. This fluid loss may affect just the intravascular space (e.g. haemorrhage) or the extravascular space as well (e.g. salt and water loss, for example in vomiting and diarrhoea).

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Maldistributive shock

With maldistributive shock, the fluid in the intravascular space (the absolute volume of which may or may not be reduced) is distributed across the body in an abnormal way. This occurs as a result of inappropriate generalized vasodilation and can potentially be viewed as a form of relative hypovolaemia. Maldistributive shock is seen in animals with systemic inflammatory response syndrome (SIRS) which may occur for example in sepsis, severe pancreatitis or major tissue injury. Maldistribution also occurs in anaphylactic/anaphylactoid shock.

Cardiogenic shock

Primary cardiac dysfunction (e.g. from organic heart disease or severe dysrhythmia) results in failure of the heart to pump adequately. This compromises cardiac output causing hypoperfusion (see Ch. 31).

Obstructive shock

Systemic hypoperfusion occurs due to obstruction of blood flow from the heart or venous return to the heart; the most common example of this in small animals is pericardial tamponade.

Causes of systemic hypoperfusion in companion animals are listed in Table 2.1.

Table 2.1 Causes of systemic hypoperfusion in dogs and cats

Type of hypoperfusion Causes
Hypovolaemia
Blood loss (trauma, coagulopathy, ruptured neoplasm)
Vomiting and diarrhoea
Severe dehydration
Third space fluid loss (peritoneal, pleural, interstitial, gastrointestinal)
Neoplasia
Burn injury
Severe polyuria
Maldistributive
Systemic inflammatory response syndrome (SIRS):
Sepsis
Severe pancreatitis
Major tissue trauma
Neoplasia
Burn injury
Anaphylaxis/anaphylactoid reaction
Cardiogenic
Cardiomyopathy (especially dilated and hypertrophic)
Valvular disease
Severe dysrhythmia
Obstructive
Pericardial tamponade
Constrictive pericarditis
Pulmonary thromboembolism (PTE)

Hypovolaemia

The two most common causes of hypovolaemia in companion animals are haemorrhage and salt and water loss. Haemorrhagic hypovolaemia may cause some extravascular fluid deficits, while animals presenting with hypovolaemia due to salt and water loss (e.g. from vomiting and diarrhoea) will certainly have extravascular fluid deficits.

Assessing perfusion and volume status

Clinical Tip

Physical examination is undoubtedly the most valuable and readily available means of assessing systemic perfusion in companion animals. The amount of information that can be derived from this examination should not be underestimated. Following initial assessment, repeated physical examination allows response to therapy and ongoing progress to be readily evaluated.

A number of physical examination parameters are used to assess perfusion:

Heart rate (HR)
Arterial (usually femoral and dorsal pedal) pulse quality
Mucous membrane (MM) colour
Capillary refill time (CRT)
(Mentation)
(Temperature of extremities.)

The dorsal pedal artery is located just distal to the hock on the craniomedial aspect of the pelvic limb. Being confident in palpating the arterial pulse at this site is useful for a number of reasons in addition to assessing perfusion status.

In animals with uncomplicated hypovolaemia, the perfusion parameters listed above are reliable indicators of volume status and tend to follow predictable trends both as hypovolaemia progresses, from compensatory through to early and then late decompensatory phases, and as normal perfusion is restored.

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Dogs

Compensatory phase of hypovolaemia

In this phase, hypovolaemia is mild. A compensatory increase in sympathetic activity causes both an increase in heart rate and cardiac contractility, and peripheral vasconstriction. The corresponding clinical picture is hyperdynamic:

HR 120–150 beats per minute
MM normal or pinker than normal with a rapid CRT of 1 second or less
Femoral pulses are bounding or snappy (hyperdynamic) with dorsal pedal pulses that are readily palpable
(Mentation and extremity temperature are typically normal.)

Note that most healthy adult dogs have a heart rate in the practice setting of 70–120 beats per minute. There is some variation in heart rate amongst dogs of different size (with bigger dogs usually having slower heart rates) and resting heart rate is also dependent on factors such as the individual animal’s level of fitness. It would be highly unusual to detect a resting heart rate in a calm healthy greyhound of 110 beats per minute; likewise a resting heart rate of 70 beats per minute in a Chihuahua. Thus the heart rate identified must be interpreted in the context of the patient in question as a heart rate within the normal range may in fact be an inappropriate finding.

Early decompensatory phase of hypovolaemia

In this phase, hypovolaemia is moderate and systemic perfusion has become compromised due to progressive failure of compensatory mechanisms:

HR 150–170 beats per minute
MM pale pink with an apparently normal CRT of 1–2 seconds
Femoral pulses are weak with dorsal pedal pulses that are only just palpable
(Mentation is depressed and extremity temperature is normal or cool.)

Late decompensatory phase of hypovolaemia

In this phase, hypovolaemia is severe and systemic perfusion is severely compromised. The corresponding clinical picture is markedly hypodynamic:

HR 170–220 beats per minute
MM extremely pale/white with a CRT that, if detectable, is more than 2 seconds
Femoral pulse very weak or ‘thready’ with a dorsal pedal pulse that is no longer palpable
(Mentation is severely depressed and extremities are cold.)

Some dogs in this final stage of hypovolaemic shock present with a heart rate that is inappropriately within normal limits or bradycardic. This is because the heart can no longer sustain its compensatory chronotropic response.

Clinical Tip

A heart rate in a dog of more than 220–240 beats per minute (more than 300 beats per minute in a cat) is unlikely to represent a physiological sinus tachycardia and is most likely to be the result of a tachydysrhythmia (see Ch. 12).

Cats

There are a number of important differences with respect to perfusion assessment and hypovolaemia in cats that lend further support to the notion that ‘cats are not small dogs’.

The heart rate of healthy cats in the veterinary setting is usually 160–200 beats per minute. However, cats are more susceptible to the stress of this environment and much higher heart rates (even up to 240 beats per min) can be seen in cats that are completely healthy.
Hypovolaemic cats are often found to have a hypodynamic clinical picture (inappropriate bradycardia, weak or absent pulses, pallor, prolonged or undetectable CRT, depression and hypothermia).
The oral mucous membranes can appear pale in normal cats and another site (usually the conjunctival membranes) should be used to clarify this finding.
Peripheral pulse assessment is not as reliable and repeatable in cats.

Assessing perfusion – the holistic approach

Animals with hypovolaemia may have concurrent abnormalities that preclude their perfusion parameters changing in the predictable way described above. When assessing a patient’s perfusion status it is therefore important to adopt a holistic approach that takes changes in all the perfusion parameters into account and correlates them in the context of the patient in question. For example:

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A dog in an Addisonian crisis may have a heart rate in the normal range despite other findings suggestive of moderate or severe hypovolaemia. This heart rate is in fact an inappropriate bradycardia due to hyperkalaemia that would be overlooked were it not interpreted in the context of all the other perfusion parameters.
Mucous membranes may remain pale despite appropriate fluid therapy in an animal with severe anaemia.
Mentation may remain depressed in an animal with head trauma despite appropriate fluid therapy as a result of raised intracranial pressure.

In addition to physical examination, other measures of perfusion, if available, include blood pressure measurement, venous lactate concentration and urine output. Again these findings must be interpreted in the context of the patient’s physical examination parameters.

Clinical Tip

Bradycardia in dogs with signs of hypoperfusion is usually the result of primary heart disease (primary cardiac bradydysrhythmia – see Ch. 12), brain disease, severe hyperkalaemia (or hypocalcaemia) or drug toxicity (e.g. digoxin).

Pain management

The majority of causes of hypovolaemia will also result in pain that can interfere with cardiovascular and respiratory function, and confuse clinical assessment. Adequate analgesia is therefore extremely important. The use of opioids initially is the mainstay of pain management and nonsteroidal antiinflammatory agents should be avoided until hypovolaemia and dehydration have been corrected (see Ch. 5).

Maldistributive shock

Early on when intravascular volume remains adequate, dogs in maldistributive shock typically have a hyperdynamic vasodilatory cardiovascular picture, i.e. tachycardia, hyperdynamic pulses, markedly hyperaemic mucous membranes and a fast capillary refill time. With the onset of concurrent severe hypovolaemia, tachycardia progresses but pulses become weaker and CRT more prolonged. However, unlike dogs with uncomplicated severe hypovolaemia, dogs in severe hypodynamic maldistributive shock are likely to retain colour in their mucous membranes that may be normal in appearance or hyperaemic. By cross-referencing perfusion findings it is often possible to identify this retained mucous membrane colour as a discrepant finding that suggests the presence of a distributive component to the hypoperfusion.

Cats in maldistributive shock are more likely to present with a hypodynamic cardiovascular picture.

Dehydration

For clinical purposes, dehydration can be defined as the process whereby an animal loses more salt and water from its body than it takes in. This loss of body fluid is predominantly extravascular and the effect on intravascular volume depends on both the degree of fluid loss and the tonicity (isotonic or hypotonic) of the fluid. The tonicity is related to the sodium concentration.

Assessing hydration status

The physical examination parameters that are used to assess hydration are related to interstitial volume. They are the moistness of the mucous membranes, skin turgor (elasticity), and the presence and degree of globe retraction. The perfusion parameters described above also become relevant if dehydration is severe enough to cause hypovolaemia.

Clinical Tip

Guidelines for estimating dehydration on the basis of physical examination findings must only be used as an approximation of fluid loss in the dehydrated patient to facilitate the initial fluid plan as there are a number of potential inherent inaccuracies.

Guidelines similar to those in Table 2.2 are generally used to estimate dehydration on the basis of physical examination findings. However, these guidelines must only be used as an approximation of fluid loss in the dehydrated patient to facilitate the initial fluid plan (see Ch. 4) as there are a number of potential inherent inaccuracies. For example, skin turgor can be affected by the degree of subcutaneous fat present (with obese animals having increased turgor), and mucous membrane moistness can be affected by salivation (e.g. due to nausea).

Table 2.2 Guidelines for estimating dehydration on the basis of physical examination

Severity of dehydration (estimated % of body weight) Progression of physical examination findings
<5% Normal
Mild (5–6%) Skin turgor mildly reduced
Moderate (6–10%)
Skin turgor progressively reduced
Mucous membranes dry
Eyes sunken
Severe (10–15%)
Complete loss of skin turgor
Mucous membranes very dry
Eyes severely sunken and dull
Progressive signs of hypovolaemia, ultimately leading to shock and death
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Additional measures of dehydration

In addition to physical examination, a number of other parameters can readily be evaluated to determine the presence and severity of dehydration. Given the inaccuracies of assessing hydration status based on physical examination, it is recommended that these additional measures are utilized as much as possible especially for monitoring rehydration (see Ch. 3). They include:

Packed cell volume and serum total solids
Blood urea and creatinine concentrations in conjunction with urine specific gravity.

Short-term changes in body weight may also provide useful information with respect to fluid balance in hospitalized patients.