Shock Assessment and Treatment (Basic)
World Small Animal Veterinary Association World Congress Proceedings, 2015
Amanda Boag1, MA, VetMB, DACVIM, DACVECC, DECVECC, MRCVS
1Vets Now, Dunfermline, Scotland, UK

The term "shock" refers to a clinical syndrome rather than a specific disease entity. Although different sources may differ in exactly how they define "shock," it is usually understood to mean a significant compromise in oxygen delivery to the tissues and particularly failure of the circulatory system to deliver blood flow to the tissues (circulatory compromise/tissue hypoperfusion). Tissue hypoperfusion, if untreated, leads to organ dysfunction and ultimately organ failure. Shock is present in the later stages of most fatal illnesses as circulatory failure is part of the final common pathway leading towards death. However, if shock is recognised and appropriately treated at an early stage, successful treatment is possible - these patients provide some of the most rewarding cases you may treat!

Circulatory shock may be further subdivided dependent on cause - this is important as different forms of shock require different treatments.

Shock is commonly categorised into:

 Hypovolaemic shock - Tissue hypoperfusion occurs secondary to a lack of circulating blood volume. This is the commonest form of shock seen in veterinary patients and can occur secondary to haemorrhage (internal or external) or severe acute fluid loss into the gastrointestinal tract, through the kidneys or into or a "third" space (peritoneal/pleural cavity).

 Distributive shock - The body displays generalised inappropriate vasodilation leading to alteration in distribution of blood flow between the tissues. Even in the face of a normal blood volume, tissue perfusion may be significantly reduced if all blood vessels are dilated. This kind of shock occurs with global release of inflammatory mediators such as in sepsis or SIRS (systemic inflammatory response syndrome) or rarely anaphylaxis. Other terms that may be used include septic or toxic shock but these are essentially subgroups of distributive shock.

 Cardiogenic shock - Failure of the heart as a pump. This occurs secondary to a number of cardiac diseases including advanced (late stage) cardiomyopathies and valvular disease and severe arrhythmias. However, in veterinary medicine, patients with cardiac disease more commonly present with signs of congestive heart failure and breathing difficulties rather than overt hypoperfusion and shock.

 Obstructive shock - Obstruction to blood flow. This form of shock is rare in veterinary patients but may be seen with pericardial effusion (where the pressure in the pericardial sac reduces venous return to the right side of the heart) or massive pulmonary thromboembolism.

Hypovolaemic shock is the commonest form of shock seen in veterinary patients and represents a loss of fluid from the circulating blood volume. It is very important that this form of fluid loss can be distinguished from that seen with dehydration. Both hypovolaemic shock and dehydration are treated with fluid therapy but the precise rate of fluid administration chosen depends on which is being treated.

To understand the difference between hypovolaemia and dehydration, a brief review of body fluid compartments is necessary. Roughly speaking 60% of the body is water and this is divided between intracellular and extracellular water. The extracellular water is further subdivided into interstitial and intravascular water. The relative distribution of the water is shown below:


 

Hypovolaemia occurs when fluid is lost primarily from the intravascular compartment - a relatively small total loss of fluid has profound physiological consequences with the development of hypovolaemic shock. In this circumstance, treatment with fluids centers around rapid replacement of the lost volume to restore tissue perfusion. Conversely dehydration represents fluid loss from all three body fluid compartments. It commonly occurs with more gradual fluid losses where there is time for water to move between body fluid compartments. Total body fluid losses may be much larger than with hypovolaemia but as the fluid losses are borne between all the compartments, it has much less profound and immediate physiological effects.

Diagnosis of Shock

The diagnosis of shock revolves around a careful physical examination which may be supplemented by measurement of haemodynamic parameters (e.g., blood pressure) or bloodwork (e.g., lactate - a marker of anaerobic respiration).

As a dog's blood volume reduces, a number of homeostatic mechanism act to maintain cardiac output and tissue perfusion by increasing heart rate and stroke volume (compensated shock). These will be successful up to a critical point where the blood volume is so decreased they are no longer effective (decompensated shock). Careful examination of a dog's perfusion parameters will allow an accurate assessment of the severity of hypovolaemic shock. The perfusion parameters are heart rate, pulse quality, mucous membrane colour and capillary refill time - all 4 perfusion parameters should be checked each time the patient is examined.

Clinical parameter

Mild hypovolaemia

Moderate hypovolaemia

Severe hypovolaemia

Heart rate

130–150

150–170

170–220

Mucous membrane color

Normal to pinker than normal

Pale pink

Gray, white or muddy

Capillary refill time

Rapid (< 1 second)

Approximately normal (1–2 s)

Prolonged (> 2 s) or absent

Pulse amplitude

Increased

Mild to moderate decrease

Severe decreased

Pulse duration

Mildly reduced

Moderately reduced

Severely reduced

Metatarsal pulse

Easily palpable

Just palpable

Absent

The table above provides a fairly accurate assessment of what happens to the perfusion parameters as a dog progresses through hypovolaemic shock and can be adapted for other species. Pulse quality is assessed by both the amplitude (height) and duration (width) of the pulse. Many different terms are used to describe pulse quality. The tall and narrow pulses found in early hypovolaemic shock are sometimes called "bounding" or "hyperkinetic" whereas the very short and narrow pulses seen in late shock may be described as "weak" or "thready."

The tachycardia seen with hypovolaemia is a sinus tachycardia (i.e., on an ECG complexes all appear normal). Maximum rate for a sinus tachycardia is approximately 220 bpm as at heart rates higher than this cardiac output will actually start to fall as there is insufficient time for ventricular filling.

Other forms of shock can be distinguished by how they differ from uncomplicated hypovolaemic shock as described in the table:

 Distributive shock: The hallmark of distributive shock is inappropriately red mucous membranes. For example consider a dog with a heart rate of 200 bpm and poor pulse quality. If this animal had uncomplicated hypovolaemic shock their mucous membranes should be pale as they undergo peripheral vasoconstriction with diversion of the remaining blood volume to the important internal organs. Red mucous membranes in this patient should suggest inappropriate vasodilation and the presence of distributive shock.

 Cardiogenic shock: Animals with cardiogenic shock typically have respiratory signs as well due to concurrent congestive heart failure. However, occasionally animals with tachyarrhythmias present in shock without concurrent heart failure - their heart rates are likely to be higher than the maximum achieved during hypovolaemia (a sinus tachycardia). Inappropriate bradycardia in a collapsed patient with poor pulse quality should also prompt assessment for an underlying cause (e.g., hyperkalaemia).

 Obstructive shock: This is the least common kind of shock. Diagnosis relies on an index of suspicion for an underlying disease such as pericardial effusion that may lead to obstructive shock.

More than one kind of shock may coexist in the same patient and although assessment of uncomplicated hypovolaemic shock is relatively straightforward, some patients present more of a challenge.

Treatment of Shock

Hypovolaemic shock: The treatment of hypovolaemic shock revolves around replacing intravascular volume. Isotonic replacement crystalloid fluids (e.g., Hartmann's, lactated Ringers) are generally the first choice fluid. When treating shock, bolus doses of fluids are used with the size and duration of the bolus being determined by the clinical signs of the patient. Most animals with moderate to severe shock will receive a bolus of 20–40 ml/kg over 15–30 minutes which may be repeated. Very severely compromised patient may receive a "full" shock bolus of 60–90 ml/kg in a dog and 40–60 ml/kg in a cat although it is rare to use this as the initial dose especially in cats. This is approximately the same as the animal's blood volume. Unfortunately there are no precise rules that allow accurate judgement of the correct amount of fluid to give in each patient; the most important thing is that following administration of the bolus the perfusion parameters of the patient are rechecked. If the perfusion parameters are within normal limits, the treatment has been effective; if the perfusion parameters are still abnormal, further fluid boluses may be required. The patient should also be monitored for complication of fluid therapy, especially evidence of dyspnoea. This is an especial concern in animals with concurrent heart disease which may not be able to tolerate a rapid increase in their intravascular volume. Other fluid therapy options for hypovolaemic shock include hypertonic saline, colloid therapy or blood products.

Distributive shock: In patients with distributive shock the underlying cause for the inflammatory stimulus should be aggressively sought as successful treatment involves addressing the underlying problem. Fluid therapy is also important in these patients and occasionally specific medications including blood pressure support with inotropes or pressors (e.g., dopamine) is required.

Cardiogenic shock: Cardiogenic shock is treated dependent on the underlying heart disease - fluid therapy is generally contraindicated in these patients.

Obstructive shock: Obstructive shock is treated by removal of the cause of vascular obstruction e.g., pericardiocentesis in a patient with pericardial effusion.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Amanda Boag, MA, VetMB, DACVIM, DACVECC, DECVECC, MRCVS
Vets Now
Dunfermline, Scotland, UK


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