SHOCK (Slides) - Vega 2025

Small Animal Emergency Medicine 2025 Laura Vega DVM, MS, DACVECC

Shock

Lesson objectives

Differentiate the underlying pathophysiological mechanisms of the major types of shock

Identify the clinical signs that allow for a rapid diagnosis of shock in small animals

Develop an appropriate initial treatment plan for shock in small animal patients

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Severe imbalance between oxygen supply and demand, leading to inadequate cellular energy production

Shock is...

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Oxygen delivery

Oxygen consumption

Severe imbalance between oxygen supply and demand, leading to inadequate cellular energy production

Shock is...

https://copd.net/clinical/home-oxygen-benefits

SaO2: oxygen saturationPaO2: arterial partial pressure of oxygen

Sympathetic vs parasympathetic nervous systems

Contractility

Afterload

Preload

Heart rate x Stroke volume

(1.34 x Hemoglobin x SaO2) + (0.003 x PaO2)

Oxygen delivery

Cardiac output

Arterial content of O2

• Na+/K+ - ATPase dysfunction
• Cellular necrosis and apoptosis
• Acidemia
• Endothelial dysfunction
• Activation of inflammatory and coagulation cascades
• Multiorgan dysfunction syndrome
• Death

https://www.brainkart.com/article/Conditions-Precipitating-Shock_31724/

Consequences of shock

https://www.oeveo.com/media/blog/358-no-more-shocks-puppy-proofing-your-cables-with-oeveo.html

Functional classification of shock

Cardiogenic

Obstructive

Distributive

Hypovolemic

Metabolic

Hypoxic

Circulatory

Types of shock

Decreased cardiac output

Decreased preload

• Hemorrhage
• Internal or external

• Severe dehydration
• Gastrointestinal
• Renal
• Third space fluid loss
• Severe burns

Decreased intravascular volume

Hypovolemic

"relative hypovolemia"

Decreased systemic vascular resistance +/- Preload +/- Contractility

• Anaphylactic shock: histamine-induced vasodilation
• Septic shock: cytokine-mediated endothelial dysfunction
• Neurogenic shock
• Pheochromocytoma or extreme fear

Maldistribution of fluid from changes in vascular tone and increased vascular permeability

Distributive

Decreased diastolic filling and preload

Decreased cardiac output

• Gastric-dilatation-volvulus
• Obstruction of vena cava
• Tension pneumothorax
• Cardiac tamponade from pericardial effusion
• Positive pressure ventilation

Compression of heart or great vessel that interferes with venous return

Obstructive

"Primary" decrease in cardiac output

• Systolic failure (e.g. dilated cardiomyopathy)
• Diastolic failure (e.g. hyperthrophic cardiomyopathy)
• Atrioventricular valve degeneration or defects
• Brady- or tachy-arrhythmias

Decrease in forward flow from the heart due to "pump failure"

Cardiogenic

Decreased tissue oxygen delivery

Decreased arterial oxygen content

Deranged cellular metabolism leading to inappropriate O2 tissue use

• Severe hypoglycemia

• Mitochondrial dysfunction

• Severe pulmonary disease
• Anemia
• Dyshemoglobinemias

Metabolic

Hypoxic

Compensatory mechanisms

⇧Renal water reabsorption

• Antidiuretic hormone

Peripheral vasoconstriction Renal Na+ reabsorption

Angiotensin II

⇧Respiratory rate and tidal volume

• RAAS activation

• Chemoreceptors

⇧Heart rate⇧Cardiac contractility Peripheral vasoconstriction

• Baroreceptor reflex

Compensatory mechanisms

• Clinical diagnosis
• One abnormality can be enough
• Compensatory vs decompensated shock
• Blood pressure?

Heart rate* Pulse quality Mucous membrane color Capillary refill time Peripheral temperature Mentation

PERFUSION PARAMETERS

Clinical manifestations

Characterized by initial vasodilation instead of vasoconstriction"hyperdynamic phase"

TachycardiaCRT < 1 secondRed to injected MMElevated temperatureBounding pulses

Anaphylactic & septic shock

https://todaysveterinarypractice.com/emergency-medicine-critical-care/systemic-inflammatory-response-syndrome-sepsis-part-1-recognition-diagnosis/

Unpredictable heart rate changesRarely manifest signs of vasodilatory shock Lungs = "shock organ"

Mucous membranes?Capillary refill time?Bradycardia*Hypothermia*

Cats ≠ Small dogs

Drastically different treatmentLook for clues to try attempt to diagnose

Signalment Heart murmurRespiratory distressCoughing (dogs)Jugular venous distension AscitesPleural or pericardial effusionPulmonary crackles Arrhythmias Syncope

Cardiogenic shock

• Head to tail examination - what is the cause?
• Point-of-care tests: PCV/TS, blood glucose, lactate, blood pressure, ECG, POCUS, acid-base and electrolyte panel
• Once more stable CBC/Chem/UA, chest x-rays, abdominal x-rays or ultasound, echocardiogram, fluid analysis, bacterial cultures, etc.

Further diagnostics

1. Flow-by oxygen2. Obtain IV access 3. IV fluid bolus resuscitation

Where to start ?

Restore O2 delivery to tissues as soon as possible

Goal =

Treatment

NOT if cardiogenic

1. Flow-by oxygen2. Obtain IV access 3. IV fluid bolus resuscitation

Where to start ?

Restore O2 delivery to tissues as soon as possible

Goal =

Treatment

Consider benefits vs risks in each patient

Immediate reassessment following bolus is key!

Hypertonic salineSynthetic vs natural colloids Whole blood vs component therapy

Additional options

Isotonic crystalloids 5-20ml/kg IV over 10-20 minutes Repeat as needed up to 90ml/kg in dogs or 66ml/kg in cats

Mainstay therapy

• Vasopressors (epinephrine)

• Anti-histamines

Anaphylactic

• Vasopressors (norepinephrine)

• Broad-spectrum antibiotics

Septic

Obstructive

Tap it!

Distributive

• Gastric trocarization
• Thoracocentesis
• Pericardiocentesis

• Congestive heart failure? Diuretics (furosemide), O2 therapy, +/- thoracocentesis

• Systolic dysfunction? Positive inotropes (dobutamine, pimobendan)
• Treat life-threatening arrhythmias? Lidocaine vs atropine, vs others

Correct underlying diseaseDepends on etiology O2 therapyNO IV fluids*Minimize stress

Cardiogenic

Clinical reassessment every 5 to 10 minutes or after every therapeutic intervention during stabilizationOnce normal perfusion parameters ⇒ successful resuscitation, can de-escalate monitoring and therapy

Resuscitation endpoints

Reassessment: static mentation, pulse quality, MM and CRT. Updated TPR: T 97.4, P 160, R 50.

Initial treatments: oxgen cage 40%, IV catheter placement, 0.2mg/kg butorphanol, 10ml/kg Lactated Ringer's IV over 40 minutes.

Clinical exam findings: quiet (previously reported to be spicy), T 97.8, P 150, R 48, MM pale pink tacky, CRT unable to determine, delayed skin tent, sunken eyes, weak pulses, III/VI parasternal systolic heart murmur (history of heart murmur on record), and some increased respiratory effort.

Spot the mistake!

Pearl, a 16 year old FS DSH, presented to the ER for anorexia, lethargy, and rapid breathing.