Shock
Shock is a life-threatening condition in which acute circulatory failure leads to insufficient blood flow and oxygen supply to vital organs. At its core, it’s a mismatch between oxygen demand and oxygen supply in the tissues. Unlike in colloquial usage, shock is not a short-term event, but a progressive pathophysiological process that, if untreated, can lead to multiple organ failure and death.
In dogs and cats, shock progresses in characteristic phases. In the initial compensation phase, the body attempts to maintain blood pressure by activating the sympathetic nervous system and releasing stress hormones. This manifests as increased heart rate and vasoconstriction. This is followed by the decompensation phase, in which these mechanisms fail and blood pressure drops. Without adequate treatment, the irreversible phase finally occurs, in which organ damage can no longer be reversed.
Compared to dogs, cats often show more subtle clinical signs of shock, which can make early detection more difficult. Their physiological compensation mechanisms differ, which must be taken into account in diagnosis and therapy.
Causes
Shock occurs due to a sudden drop in blood pressure and associated reduced blood flow to vital organs.
Shock is potentially life-threatening. This sudden drop in blood pressure can be caused by heat, trauma, blood loss, fluid loss, allergic reactions, sepsis, burns, poisoning, and other factors (Fig.).
Supplements
Hypovolemic shock is the most common form and occurs due to an absolute volume deficiency in the vascular system. Causes include severe bleeding after trauma or surgery, severe dehydration from vomiting and diarrhea, extensive burns, or heatstroke. Particularly in dogs, gastric dilatation-volvulus or pyometra (uterine infection) in unspayed females can lead to rapid fluid loss.
Cardiogenic shock results from a weakening of the heart’s pumping ability, causing insufficient blood to enter the circulatory system. Triggers include heart muscle diseases such as dilated cardiomyopathy in large dog breeds, cardiac arrhythmias, heart valve diseases, or myocarditis. In cats, hypertrophic cardiomyopathy can be a cause.
Distributive shock encompasses several subtypes. Septic shock occurs due to severe bacterial infections with toxin release, such as in peritonitis or pyometra. Anaphylactic shock is triggered by severe allergic reactions, for example to medications or insect stings. Neurogenic shock can occur after severe spinal cord injuries.
Obstructive shock occurs due to mechanical obstructions of blood flow, such as in cardiac tamponade, pulmonary embolism, or pneumothorax.
Symptoms
- Pale mucous membranes
- Rapid heart rate
- Accelerated breathing
- Vomiting
- Weakness
- Staggering
- Unconsciousness
Additional symptoms appear due to progressive organ damage.
The clinical signs of shock vary depending on the cause, severity, and species of animal, but follow a characteristic pattern. In the early compensation phase, affected animals show restlessness, increased heart rate (tachycardia), and accelerated breathing (tachypnea). The mucous membranes initially appear hyperemic (reddened), later pale to blue-gray (cyanotic). The capillary refill time is prolonged (>2 seconds).
As the shock progresses, the extremities become cool, the pulse weak and thready. Body temperature drops (hypothermia). Affected animals show increasing weakness leading to collapse. Consciousness may be impaired or the animal may appear apathetic. Vomiting and diarrhea are common.
Cats often show more subtle symptoms of shock than dogs. They often become lethargic and withdraw initially. The heart rate can paradoxically be normal or even slowed (bradycardia), making detection more difficult. Extremely pale, sometimes slightly grayish mucous membranes and noticeable hypothermia are characteristic.
In cardiogenic shock, additional symptoms such as coughing, difficulty breathing, and cyanosis may occur. Anaphylactic shock often manifests with sudden onset of facial swelling, urticaria, and respiratory distress. In septic shock, fever or low body temperature, purulent discharges, and signs of an underlying disease may be present.
In the advanced decompensation phase, oliguria (decreased urine production) to anuria occurs, indicating kidney damage. If left untreated, shock leads to multiple organ failure and death.
First Aid
- Lay your pet down and keep it calm.
- Remove the collar.
- Wrap your pet in a blanket or cover it to keep it warm.
- Do not give any fluids or food.
- If your pet vomits and there are no injuries to prevent it, support your pet so that its head is the lowest point of the body, allowing the vomited stomach contents to drain well and not enter the airways.
Diagnosis
The diagnosis of shock is primarily based on clinical examination and assessment of vital parameters. The veterinarian evaluates heart rate, respiratory rate, mucous membrane color, capillary refill time, pulse quality, and body temperature. These parameters allow an initial assessment of the severity and type of shock.
Laboratory tests are necessary for further diagnosis. A complete blood count can provide indications of blood loss (anemia), infections (leukocytosis), or dehydration (increased hematocrit). Blood chemistry helps assess organ functions, especially of the kidneys and liver. Elevated blood lactate levels are an important marker for tissue hypoxia and correlate with the severity of shock. Blood gas analysis allows assessment of acid-base balance and oxygenation.
If septic shock is suspected, blood cultures and, if necessary, swabs from infection sites are taken. ECG and echocardiography are essential for diagnosing cardiogenic shock. Imaging techniques such as X-ray, ultrasound, and in more complex cases, CT or MRI can help identify the underlying cause.
Particular diagnostic care is required for cats, as they often show shock symptoms more subtly than dogs. The so-called FAST ultrasound (Focused Assessment with Sonography for Trauma) can quickly detect free fluid in the chest and abdominal cavities in trauma patients.
To monitor the response to therapy and estimate prognosis, parameters such as central venous pressure (CVP), arterial blood pressure, and urine production are continuously monitored. Modern parameters such as mixed venous oxygen saturation or tissue oxygenation using near-infrared spectroscopy are increasingly being incorporated into intensive care monitoring.
Further veterinary measures
Shock in the medical sense is not a short-term event, but a disease process in which various causes have led to a mismatch between oxygen demand and oxygen supply in the tissues.
The treatment of shock is complex and extensive.
In small animal medicine, shock is usually caused by a loss of water and electrolytes due to vomiting and diarrhea (hypovolemic shock).
The primary goal of therapy is therefore to balance the fluid and electrolyte deficit using infusions, raise blood pressure, and improve tissue perfusion and oxygen supply.
Many laboratory diagnostic follow-up examinations are necessary to monitor organ functions and ensure the effectiveness of measures.
Furthermore, the cause of the volume deficiency must be identified and addressed.
Supplements
The treatment of shock follows the principle of goal-directed therapy and must be initiated immediately. The top priority is to ensure adequate oxygen supply to vital organs.
Basic measures include oxygen administration via nasal cannula, mask, or in severe cases through intubation and controlled ventilation. In parallel, a venous access is established, ideally through large-bore catheters, to enable rapid fluid therapy.
Fluid therapy is based on the type of shock. In hypovolemic shock, aggressive volume replacement is performed with crystalloid solutions (e.g., Ringer’s lactate) in boluses of 10-20 ml/kg for dogs and 5-10 ml/kg for cats, until circulatory parameters stabilize. In case of blood loss, colloids or blood transfusions may be necessary. In cardiogenic shock, however, fluid administration should be restrictive to avoid further cardiac strain.
Vasoactive medications are used when fluid therapy alone is insufficient. Dopamine, dobutamine, or norepinephrine are used depending on the form of shock and blood pressure situation. In septic shock, early administration of broad-spectrum antibiotics is crucial, ideally after obtaining samples for microbiological diagnostics.
Treatment of anaphylactic shock requires immediate administration of epinephrine, antihistamines, and glucocorticoids. In obstructive shock, the cause must be eliminated, for example, through pericardiocentesis in cardiac tamponade or chest drainage in pneumothorax.
Accompanying pain therapy with opioids that minimally affect circulation is provided. Body temperature is normalized using heating pads or lamps. Close monitoring of vital parameters, acid-base balance, and organ functions is necessary to continuously adjust therapy.
In advanced shock with organ failure, measures such as hemodialysis for acute kidney failure or special ventilation techniques for severe lung failure may be necessary.
Prognosis and aftercare
The prognosis in shock depends significantly on the underlying cause, the timing of therapy initiation, and the response to initial treatment. Generally, the earlier the therapy begins, the better the prognosis. Hypovolemic shock due to acute blood loss has a more favorable prognosis with prompt treatment compared to septic or cardiogenic shock.
Crucial for establishing the prognosis is the monitoring of various parameters during intensive care. Decreasing lactate levels, normalization of acid-base balance, resumption of urine production, and stabilization of vital signs are positive prognostic indicators. Persistent hypotension despite maximal therapy, ongoing oliguria or anuria, and signs of multiple organ failure indicate a poor prognosis.
Aftercare following recovery from shock includes continuous monitoring of organ functions, especially of kidneys, liver, and lungs, as organ damage can occur with delay. Fluid and electrolyte balance must be closely monitored. Specific follow-up checks are necessary depending on the underlying condition.
For pets, gradual resumption of normal activity is important after discharge. Owners should watch for possible complications such as kidney dysfunction, neurological deficits, or wound healing problems. Regular follow-up checks with the veterinarian are essential to detect and treat any subsequent damage early.
The long-term prognosis after surviving shock varies greatly between individuals. While some animals recover completely, others may sustain permanent organ damage requiring lifelong therapy.
Summary
Shock in dogs and cats is a complex, life-threatening condition characterized by inadequate blood flow and oxygen supply to vital organs. It can have various causes, including blood loss, heart failure, severe infections, or allergic reactions, and is accordingly classified into hypovolemic, cardiogenic, distributive, and obstructive shock.
Clinical signs include tachycardia, tachypnea, pale mucous membranes, prolonged capillary refill time, and increasing weakness leading to loss of consciousness. Cats often show more subtle symptoms than dogs, which can make diagnosis more difficult.
Diagnosis is based on clinical examination, laboratory parameters, and imaging techniques. Therapy must be initiated immediately and includes oxygen administration, fluid therapy, vasoactive medications if necessary, and treatment of the underlying cause. Close monitoring of vital signs and organ functions is essential.
The prognosis depends on the underlying cause, the timing of therapy initiation, and the response to treatment. Aftercare includes continuous monitoring of organ functions and specific measures depending on the underlying condition.
Early recognition of shock symptoms by the pet owner and immediate transport to the veterinarian can be lifesaving. First aid measures such as keeping the animal warm, positioning with the head slightly lowered, and quick, careful transport to the veterinary practice significantly improve chances of survival.
Outlook on current research
Shock research in veterinary medicine continues to evolve. Current research focuses include optimizing fluid therapy through individual, targeted protocols instead of rigid volume formulas. Studies show that overly aggressive fluid administration can be harmful, while insufficient volume therapy does not restore tissue perfusion.
A promising approach is the development of species-specific biomarkers for early detection and progression assessment of shock. In addition to lactate, parameters such as procalcitonin, certain interleukins, and cell-free DNA are being investigated as potential markers for tissue damage and inflammatory reactions.
In the field of hemodynamics, new minimally invasive monitoring techniques such as transpulmonary thermodilution or pulse contour analysis allow for more precise control of circulatory therapy. These techniques are increasingly being adapted for use in dogs and cats.
Research into microcirculation using sidestream dark field microscopy provides insights into capillary perfusion, which can be disturbed despite normalized macrohemodynamic parameters. This could explain why some patients develop organ damage despite seemingly adequate therapy.
New therapeutic approaches focus on modulating the immune response in septic shock, as both excessive and insufficient immune reactions can contribute to organ failure. Experimental therapies with selective cytokine antagonists or immunomodulators show promising results in initial studies.
Research into mitochondrial dysfunction as a central mechanism of cellular damage in shock opens up new therapeutic perspectives. Substances that improve mitochondrial function could increase survival rates in the future.
These research approaches promise increasingly individualized and pathophysiologically based shock therapy that could further improve the survival and quality of life of affected animals.
Frequently asked questions (FAQs)
- What is the difference between shock and a short-term circulatory weakness in my pet?
Shock is a life-threatening condition with insufficient blood flow to vital organs, while short-term circulatory weakness is usually temporary and less severe. In shock, pale mucous membranes, weak pulse, and increasing loss of consciousness are observed. - What emergency measures can I take as a pet owner if I suspect shock?
Keep your pet warm, calm it down, position it with the head slightly lowered and the hindquarters elevated. Remove collars and transport it immediately to the veterinarian. Do not administer any fluids or food. - How long does it take for my pet to recover from shock?
Recovery time varies greatly depending on the cause and severity of the shock, as well as the age and health condition of the animal. It can range from a few days to several weeks. Some animals may suffer permanent organ damage. - Are certain dog or cat breeds more susceptible to shock?
In general, any animal can experience shock. Brachycephalic breeds like pugs or Persian cats can go into shock more quickly due to heat stress. Dobermans and Boxers are predisposed to cardiogenic shock due to their tendency towards heart diseases. - Can shock have long-term consequences for my pet?
Yes, surviving shock can lead to permanent organ damage, particularly to the kidneys, liver, brain, and heart. Regular follow-up checks are important to detect and treat consequential damages early. - How can I prevent shock in my pet?
Avoid situations that can lead to overheating. Ensure prompt treatment of injuries and infections. For known allergies, keep appropriate emergency medications on hand. Have chronic diseases regularly checked. - Why is shock harder to recognize in a cat than in a dog?
Cats often show more subtle symptoms and can have a normal or even slowed heart rate despite being in shock. They withdraw and become quiet, which can be misinterpreted as normal behavior. - How does the veterinarian decide which fluid my pet should receive in shock?
The choice of fluid depends on the type of shock, laboratory values, and clinical condition. Blood transfusions may be necessary for blood loss, crystalloid solutions for dehydration. In case of heart problems, the fluid amount is limited. - What does it mean if my pet in shock stops producing urine?
Reduced or absent urine production (oliguria/anuria) indicates kidney damage due to insufficient blood flow. This is a serious warning sign and requires intensive therapeutic measures.
Literature
- Sigrist, N. (Ed.): Emergency Medicine for Dogs and Cats. Immediate Measures and Safe Management. 2017, 544 pp., Enke Verlag
- Dörfelt, R.: Common Emergencies in Dogs and Cats. Prepare, Recognize, and Manage. Paperback: 232 pages, Schluetersche GmbH & Co. KG Verlag, 2019
- Löwe, G. and Löwe, O. (2021). Emergencies in Dogs and Cats – A Veterinary Guide. Kynos-Verlag. 208 p.
- Silverstein, D.C. and Hopper, K. (2022). Small Animal Critical Care Medicine. 3rd Edition. St. Louis: Elsevier Saunders. ISBN 978-0323676694.
- Boller, M. and Boller, E.M. (2020). “Shock: Pathophysiology, Classification, and Approach to the Trauma Patient.” In: Drobatz, K.J., et al. (Eds.) Textbook of Small Animal Emergency Medicine. 2nd Edition. Hoboken: Wiley-Blackwell, pp. 986-995. ISBN 978-1119028949.
- Adamantos, S. and Hughes, D. (2021). “Fluid Therapy in Patients with Cardiovascular Disease.” Veterinary Clinics of North America: Small Animal Practice, 51(6), pp. 1121-1136. DOI: 10.1016/j.cvsm.2021.05.002.
- Keir, I. and Dickinson, A.E. (2022). “Septic Shock in Dogs and Cats: Recognition and Treatment.” In Practice, 44(1), pp. 5-16. DOI: 10.1002/inpr.108.
- Reineke, E.L. and Drobatz, K.J. (2021). “Pathophysiology and Management of Distributive Shock in Dogs and Cats.” Journal of Veterinary Emergency and Critical Care, 31(2), pp. 171-184. DOI: 10.1111/vec.13058.
