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Primary Survey (Triage) and Resuscitation

By Andrew Linklater, DVM, DACVECC, Lakeshore Veterinary Specialists, Glendale, Wisconsin

Triage is the art of assigning priority to emergency patients and their problems based on rapid assessment of historical and physical parameters (see Table: Parameters to Evaluate During Triage). Several historical or observed problems warrant transfer of the animal to the treatment area regardless of physical findings. These problems include known or suspected trauma, poisonings, profuse vomiting or diarrhea, urethral obstruction, labored breathing, cardiopulmonary arrest, seizures, loss of consciousness, severe alterations in mental state, acute inability to walk, excessive bleeding, prolapsed organs, potential snake bite, heat prostration, open wounds exposing extensive soft tissue or bone, anemia, burns, dystocia, shock, and disease that may rapidly decompensate such as gastric dilatation and volvulus and allergic reactions.

Parameters to Evaluate During Triage




Mucous membrane color


Normal PCV and adequate perfusion

Pale or white

Anemia or shock


Severe hypoxemia


Increased serum bilirubin due to hepatic disease or hemolysis

Capillary refill time

1–2 sec

Normal perfusion and rapidity with which capillaries refill with blood

>2 sec

Poor perfusion or peripheral vasoconstriction

<1 sec

Hyperdynamic states; could be associated with fever, heat stroke, distributive shock, or early compensatory stage of hypovolemic shock

Heart rate

70–120 bpm (small dogs)

60–120 bpm (large dogs)

120–200 bpm (cats)

Normal heart rates; indicate that at least one component of cardiac output is normal


Decreased cardiac output and subsequent poor perfusion; cats in particular develop bradycardia (<120 bpm) in shock; an irregular, slow heart beat can be associated with imminent cardiac arrest, severe arrhythmias, or metabolic derangements ( hyperkalemia, hypocalcemia, etc)

Tachycardia (dogs >180 bpm, cats >220 bpm)

Compromised diastolic filling; sinus tachycardia often results from hypovolemic shock or pain; tachycardia that is irregular or associated with pulse deficits usually indicates an arrhythmia, and an ECG is indicated

Pulse rate and quality

Strong and synchronous with each heart beat

Normal; both femoral and digital pulses should be palpated


Usually indicative of a cardiac arrhythmia


Hyperdynamic (compensatory) state of shock

Weak or absent

Decreased cardiac output, peripheral vasoconstriction, decreased pulse pressure, or thromboses

Level of consciousness

Alert and responsive to surroundings

Normal overall neurologic and metabolic state

Depressed or obtunded (less responsive to visual and tactile stimuli, sleepy appearance but still arousable)

Can be caused by any illness or decreased perfusion; may be mild, moderate, or severe

Stupor (arousable only with painful stimuli)

Severe neurologic or metabolic derangements

Comatose (unarousable with any stimuli) or seizures (usually associated with whole body convulsions, salivation, facial tremors, possibly involuntary urination and defecation)

Abnormal cerebral electrical activity from primary neurologic disease or secondary to metabolic derangements seen in diseases such as diabetes, hepatic encephalopathy, hypoglycemia, or toxin exposure; accurate history or prior health problems, current medications, and possible toxin exposure important

Level of pain

Vocalization, changes in behavior (avoidance, aggression), or physical changes (tachycardia, dilated pupils, etc)

Clinical signs can be similar to those seen in compensatory stage of shock; pain delays healing and must be treated.

Airway, breathing, and circulation are evaluated sequentially, followed by examination for sources of hemorrhage, and determination of the level of consciousness and level of pain. The most common reasons for an animal in catastrophic distress include 1) airway—airway obstruction or disruption; 2) breathing—cyanosis from tension pneumothorax, alveolar flooding (edema fluid or blood), severe bronchoconstriction with air trapping or brain-stem pathology affecting ventilation; and 3) circulation— shock (decreased perfusion), cardiopulmonary arrest, extreme bradyarrhythmias or tachyarrhythmias, cardiac tamponade, and acute intravascular volume loss usually due to internal or external hemorrhage.


Life-threatening airway pathology (catastrophic or severe) includes complete large airway obstruction and partial obstruction of the large and small airways.


Animals with complete large airway obstruction are unconscious and apneic. Partial large airway obstruction causes noisy breathing (stridor or stertor), heard without the aid of a stethoscope. Cyanosis and anxiety are often present with loud referred airway sounds heard throughout the thorax on auscultation. Compromise of the extrathoracic airway (nasal passages, pharynx, larynx, or cervical trachea) causes inspiratory stridor; compromise of the intrathoracic trachea or bronchi causes expiratory stridor. Stertor is most common with pharyngeal disease. Possible causes of large airway pathology include foreign bodies, edema, laryngeal paralysis or paresis, tracheal collapse, elongated soft palate, aspiration of stomach contents, neoplasia, and pharyngeal hematomas. Animals with severe small airway obstruction have labored breathing with an expiratory push of the diaphragm, cyanosis, and anxiety. Auscultation reveals high-pitched wheezes throughout the lung field. In severe life-threatening situations, the animal is cyanotic, open-mouth breathing, collapsed, and asphyxiating. Common causes include anaphylactic reactions; asthma (cats); and bronchial obstruction from edema, mucus, exudates, or foreign material.


Unconscious, apneic animals require immediate tracheal intubation. The clinician should be practiced in orotracheal intubation of animals in dorsal, lateral, and sternal recumbency. If an obstruction is present, it must be immediately relieved (with suction, manual removal, or the Heimlich maneuver) or bypassed via emergency tracheotomy. Once an airway is established, confirmed, and secured, ventilation is initiated with 100% oxygen via a bag-valve-mask. Should auscultation during ventilation detect absent or muffled lung sounds indicative of pleural fluid or air, immediate thoracocentesis is warranted. Heart sounds and pulses are checked and, when absent, cardiopulmonary resuscitation (see Cardiopulmonary Resuscitation) is initiated.

With partial large airway obstruction, flow-by oxygen is delivered through oxygen tubing at a high flow rate aimed at the open, panting mouth until an airway is secured or, if appropriate, a transtracheal or nasotracheal oxygen line is placed. Heavy sedation using a narcotic/tranquilizer (eg, butorphanol 0.2–0.4 mg/kg with or without acepromazine 0.01–0.05 mg/kg) combination may be used to relieve anxiety and struggling, to allow a cursory examination of the pharynx and larynx, and to remove pharyngeal foreign bodies. When tracheal intubation is necessary, general anesthesia should be induced using rapid-acting IV anesthetics such as etomidate (0.5–3 mg/kg), ketamine/diazepam combination (5–20 mg/kg and 0.1–0.4 mg/kg), or propofol (6–8 mg/kg to effect). The ability of the laryngeal cartilages to abduct during inspiration should be assessed during intubation and a full oropharyngeal examination performed when time allows. A tracheotomy is necessary when pharyngeal, laryngeal, or tracheal pathology prevents orotracheal intubation or when prolonged intubation is anticipated. A transtracheal catheter can be used to provide oxygen support during stabilization. When the airway pathology lies within the thoracic cavity, airway patency must be established down to the bifurcation of the trachea. Once the airway is established, it should be secured with a tie and inflation of the cuff mechanism, as well as confirmed with at least two of the following methods: palpation of the tube within trachea in the cervical region, ausculation of the lungs and visualization of chest wall movement when a breath is administered, visualization of the tube entering the airway, placement of an end-tidal CO2 monitor, or radiographs.

Cyanosis from small airway obstructive disease is treated by providing oxygen by flow-by, hood, or nasal cannula and sedation with a narcotic/tranquilizer combination. Epinephrine is given for its bronchodilatory effects both in anaphylaxis (0.01–0.02 mg/kg, IV) and in life-threatening asthma (0.02 mg/kg, IM). Corticosteroids (prednisone sodium succinate, 15 mg/kg, IV, or dexamethasone, 2–4 mg/kg, IM or IV) are given for allergic bronchitis, asthma, or severe swelling of the larynx or pharyngeal tissues. Other bronchodilators, such as aminophylline or terbutaline, are given IM, or albuterol can be given by nebulization in the case of an animal in crisis. Also see the calculator on this page for various emergency drug doses for dogs and cats.



Compromised breathing in both dogs and cats manifests with an increased respiratory rate and effort, immediately followed by a change in the respiratory pattern. Postural changes (orthopnea) follow; dogs stand with the elbows abducted and the back arched or high on the rear haunches with the head and neck extended, whereas cats may sit crouched on all four limbs with the sternum slightly elevated. Obvious labored, open-mouth breathing, and changes in mucous membrane color (gray and/or blue [cyanosis]) develop last and indicate significant loss of pulmonary function and impending pulmonary arrest.

The location of the pathology—pleural space or parenchymal disease—can be determined at presentation by careful observation of the breathing pattern and auscultation of the thorax. This will direct resuscitative efforts. Taking radiographs or performing stressful diagnostic procedures before the animal has been stabilized can lead to rapid decompensation.

Pleural space disease causes asynchronous breathing. The chest expands on inspiration as the abdomen is pulled inward, then the chest moves inward on expiration as the abdomen expands. In cats, breathing is slower and more deliberate than in dogs. The respiratory pattern is the same whether air, fluid, or abdominal contents are in the pleural space. Thoracic auscultation reveals muffled lung sounds over the affected regions.

Lung parenchymal disease causes quiet, smooth breathing, with the chest and abdominal wall moving in the same direction. Inspiration and expiration are equally labored unless concurrent small airway edema or constriction adds an expiratory push. Cats demonstrate rapid, shallow synchronous breathing, often with movement of the cupula. Thoracic auscultation reveals louder than normal lung sounds in early phases. As disease progresses, harsh lung sounds with moist crackles and rales are heard over the affected lungs. Pulmonary edema may be cardiogenic, often accompanied by a murmur, gallop, or arrhythmia noted on auscultation and mild hypothermia. Other differential diagnoses include CNS disease, pneumonia (viral, parasitic, fungal, or bacterial), aspiration, pulmonary contusions, or hemoglobin abnormalities. Noncardiogenic pulmonary edema may be caused by seizures, electrocution, after an acute airway obstruction (such as after choking or near-drowning) and acute lung injury, or respiratory distress syndrome.

Thoracic radiography should be performed only when the animal is able to tolerate the procedure. Radiographs can help differentiate many of these diseases; however, imaging should not delay therapy. Some animals may be more tolerant of ultrasonography. The thoracic focused assessment with sonography (TFAST) technique may be used to identify pleural fluid and air, examining both hemithoraces between the fifth and sixth ribs ventrally and between the seventh and ninth ribs dorsally. A pneumothorax may be present when the "slide sign" is absent; this is a linear movement noted between the visceral and parietal pleura and requires practice to identify.


Oxygen is administered immediately via flow-by, mask, hood, or oxygen cage techniques. Sedation with a narcotic/tranquilizer combination (butorphanol 0.2–0.4 mg/kg, IV or IM, with or without acepromazine, 0.05 mg/kg, IV or IM) can relieve struggling and anxiety. Longterm continuous supplemental oxygen is best provided by a nasal oxygen catheter. The intranasal oxygen catheter is placed after topical anesthetic has been instilled into the nostril where the tube is to be inserted. Humidified nasal oxygen flow rates of 50–100 mL/kg/min deliver 40%–60% inspired oxygen while allowing the animal to be examined and the underlying disease treated. Nasopharyngeal or nasotracheal catheters or bilateral nasal cannulas may provide higher percentages of inspired oxygen. If cyanosis and decompensation persist or work of breathing is profound, intubation and positive-pressure manual ventilation or mechanical ventilation with 100% oxygen is necessary.

Catastrophic pleural space disease with rapid cardiovascular decompensation, absent lung sounds throughout the thorax, and a barrel-shaped chest suggests tension pneumothorax. A routine thoracocentesis is often inadequate for these animals, so an intercostal incision or placement of a large-bore catheter is necessary: lidocaine is injected for local anesthesia, a small skin incision is made between ribs (at the seventh to eighth intercostal space), and hemostats are used to enter the pleural space, relieving the tension within the thorax. This allows cardiovascular filling and lung reexpansion. The open pneumothorax is then managed by placing a chest tube and surgically closing the intercostal incision.

When breathing is severely compromised by pleural air or fluid without tension pneumothorax, the pleural space should be drained by thoracocentesis. The intended site is clipped and aseptically prepared (when time permits). If fluid is expected, the needle is inserted ventrally between the sternum and costochondral junction. When air is to be recovered, the needle is inserted into the dorsal half of the thorax, above the costochondral junction. A local anesthetic is placed into the skin, subcutaneous tissue, and intercostal muscle at the site to be tapped. After the needle is inserted just through the skin, a drop of saline is placed in the hub of the needle. The needle is then gradually inserted straight into the thorax (with the needle perpendicular to the chest wall) until the saline in the needle hub moves. The movement of the saline in the hub indicates that the pleural space has been entered, although this may not always occur. The needle is immediately directed so that it lies against the parietal pleura. This prevents laceration of the lung by the needle as the lung reexpands. As soon as the pleural space is entered, the evacuation apparatus (an IV extension set, 3-way stopcock, and syringe) is attached and aspiration begins. In animals in which the pleural space cannot be emptied (eg, tension pneumothorax, ongoing hemorrhage) or when repeated chest taps are required within minutes to hours, an indwelling chest tube should be placed for continuous closed suction until the problem resolves or futher therapy is performed.

Lung parenchymal disease is primarily treated using oxygen supplementation, sedation to relieve anxiety, and therapy directed at the underlying cause. Cardiogenic edema is usually associated with a gallop, murmur (determined by auscultation), arrhythmia, and/or mild hypothermia and responds well to furosemide administration (1–4 mg/kg, IV, every 1–2 hr) in all but the most severe of cases. Furosemide is more effective when delivered as a constant-rate infusion (1–2 mg/kg/hr). Cardiogenic edema can benefit from venodilation from nitroglycerin ointment (¼ in. for cats and ½ in. for larger dogs) applied topically to a shaved area of the abdomen, inguinal region, or directly to a mucous membrane; severely affected animals with normal blood pressure may benefit from a balanced vasodilator (nitroprusside, 0.5–10 mcg/kg/min), tapered up slowly and monitoring blood pressure continuously to keep the mean arterial pressure >85 mmHg. After initial stabilization, further diagnostic procedures (eg, thoracic radiography and echocardiography) aid in determining the cause and specific therapy. Animals with proteinaceous fluid (such as occurs with noncardiogenic pulmonary edema, respiratory distress syndrome, pneumonia, etc) will not respond to simple diuretic therapy. If oxygen supplementation does not maintain PaO2 >60 mmHg (pulse oximetry or SpO2 >90%), or if PaCO2 ≥60 mmHg, or if there is moderate to severe increases in work of breathing despite oxygen therapy, then manual or mechanical positive-pressure ventilation is required.

If respiratory failure is imminent with pulmonary fluid visible in mouth or nares, then intubation, airway suctioning, and manual bag-valve-mask ventilation with 100% oxygen are required. Elevated or postural pulmonary parenchymal evacuation (EPPE) can be performed with two or more people elevating the pet vertically, head down, while guarding the endotracheal tube. The thoracic cavity is manually compressed to assist airway and lung fluid drainage. Manual ventilation with 100% oxygen and suction of the airway should be performed between EPPE efforts.



Animals with circulatory compromise have alterations in their physical perfusion parameters (ie, heart rate, mucous membrane color, capillary refill time [CRT], rectal temperature, pulse quality, and level of consciousness). Careful auscultation of the heart for a murmur, gallop, arrhythmia, or muffled heart sounds and of the lungs for evidence of fluid is important to help identify heart failure as a cause of poor perfusion. Measurement of arterial blood pressure, central venous pressure, central venous PaO2, and serum lactate provide objective data for reaching resuscitation endpoints and monitoring trends of change after resuscitation.

In the early compensatory stages of hypovolemic shock in dogs, there is a rapid heart rate, pink to red mucous membranes, rapid CRT, and bounding pulses; the animal is most often alert and responsive. Animals with a significant amount of pain or anxiety may appear to be in compensatory shock; pain medications are warranted, and time for the animal to acclimate to the environment is helpful. This stage is rarely identified in cats. Tachycardia is often the first and only sign, so persistent tachycardia must be considered a sign of decreased perfusion and addressed as such. As the pathology progresses, dogs begin to have pale mucous membranes, prolonged CRT, weak pulses, tachycardia, and a decreased level of responsiveness—the classic signs of the middle or early decompensatory stage of shock. Cats have gray mucous membranes, slow CRT, weak or absent pulses, hypothermia, and a normal or low heart rate. As shock approaches the terminal stages, the heart rate slows in both dogs and cats, and animals begin to lose consciousness. Clinical signs in this terminal stage include heart failure, pulmonary edema, severe hypotension, oliguria, and abnormal respiratory patterns. Cardiopulmonary arrest is a common sequela.


The therapeutic goal is to deliver oxygen and substrate to the tissues. This requires a heart that effectively pumps blood and adequate hemoglobin, intravascular volume, vascular tone and patency, as well as sufficient oxygen and substrate for cellular metabolism. General guidelines for treatment of hypovolemic and distributive shock are described below, but modifications may be needed for specific animals or disease processes.

Oxygen Supplementation:

Oxygen (at least 40%–60% inspired concentration) should be administered by flow-by technique, mask, hood, nasal cannula, endotracheal tube, or transtracheal catheter.


Control of ongoing hemorrhage is essential for stabilization and often required before restoration of circulation. The animal must be carefully and thoroughly examined for any evidence of external hemorrhage. Direct pressure should be immediately placed over the bleeding skin site, and bleeding arteries clamped. When blood slowly oozes from a skin wound, a compression bandage should be placed. If more aggressive hemostasis is required, a blood pressure (pneumatic) cuff or tourniquet can be temporarily placed until coagulation occurs or surgical intervention is used to stop the bleeding. Tourniquets should not remain in place for >10 min.

Intrathoracic or abdominal hemorrhage may be dfficult to detect and may be exacerbated when blood pressure and circulation are restored. The focused abdominal sonography for trauma (FAST) technique may be used to rapidly identify free abdominal fluid, focusing the probe on the ventral midline caudal to the xiphoid, over the urinary bladder, and on the right and left dependent flank regions. A four-quadrant abdominocentesis can be performed if ultrasound is not immediately available. The TFAST may be used to identify pleural fluid as well.

Ongoing abdominal hemorrhage is initially managed by small volume fluid resuscitation to low-normal endpoints and abdominal counterpressure (see below). Ongoing intrathoracic hemorrhage should be managed with thoracocentesis or a thoracostomy tube to evacuate the blood and to allow measurement of the volume lost. Exploration of these body cavities may be required for assessment and definitive hemostasis if a coagulopathy is not present. PCV of thoracic or abdominal fluid the same or higher than that of peripheral blood confirms hemorrhage. Significant volumes of cavitary hemorrhage may be collected in sterile, empty IV bags or blood transfusion bags for autologous blood transfusion, if necessary.

Intravascular Volume Replacement:

Intravenous or intraosseous catheters are used, with multiple catheters placed for rapid, large-volume infusion in dogs >30 kg body wt. Isotonic crystalloids can be administered by repeated low-volume boluses (10–15 mL/kg) until desired endpoints of resuscitation are reached (eg, low-normal cardiovascular parameters). However, the interstitium is at risk of fluid overload with crystalloids alone. The concurrent use of colloids and crystalloids can reduce the amount of crystalloid required, rapidly expand the intravascular space with a smaller volume of fluid infused, and reduce the amount of fluid extravasating into the interstitial spaces of vital organs (eg, lung, brain). Isotonic crystalloids are given with hydroxyethylstarches (eg, hetastarch) or stroma-free hemoglobin. Whole blood, stroma-free hemoglobin, or packed red cells are necessary during initial volume resuscitation when hemorrhage has been significant.

Small volume resuscitation to low-normal endpoints (measured perfusion parameters) is used to avoid volume overload or hypertension and is ideal for animals with head injury, pulmonary edema or contusions, abdominal or intrathoracic hemorrhage, heart disease, and all cats in hypovolemic shock. Isotonic crystalloids are given (10–15 mL/kg, IV), followed by hetastarch or stroma-free hemoglobin (dogs 5 mL/kg, IV; cats 1–5 mL/kg, IV, slowly), repeating the colloid infusion, to effect. The least amount of crystalloids and colloids possible are used to obtain and maintain a systolic blood pressure of 90 mmHg, restore a normal heart rate, and improve CRT and pulses. For an in-depth explanation, see Fluid Therapy.

Pain Control:

Analgesia is provided during initial fluid resuscitation for optimal cardiovascular response and relief of anxiety. Narcotics are administered systemically, and local anesthetics can be infiltrated into the affected area. (Also see Pain Assessment and Management.)


Animals in shock should be warmed during fluid resuscitation until rectal temperatures are >98°F. This is best accomplished by increasing the environmental temperature using warm air blowers or hot water bottles with blankets, warm water blankets, and IV fluid line warmers. Gastric, peritoneal, or urinary lavage may be needed for severe hypothermia. Surface warming is instituted only after initial volume resuscitation has provided enough intravascular volume to offset the peripheral vasodilation. Care must be taken in animals with cardiogenic shock or pericardial disease to avoid excessive peripheral vasodilation, because this may exacerbate a relative hypovolemia (due to decreased cardiac output).


Corticosteroids are administered when a deficiency is suspected (ie, Addisonian crisis, critical illness–related corticosteroid insufficiency). High-dose steroid administration has not been proved to reduce mortality in hypovolemic, septic, or cardiogenic shock and has been associated with increased morbidity, so it is not recommended.

Cardiovascular Support:

Pharmacologic agents (positive inotropes, systemic vasodilators, and vasopressors) can be used when fluid infusion has adequately replaced intravascular volume (ie, central venous pressure >5–8 cm H2O) but fails to restore blood pressure and perfusion, or when poor cardiac contractility is thought to contribute to hypotension. A positive inotropic agent can be administered to increase cardiac contractility in diseases such as sepsis and dilated cardiomyopathy (eg, dobutamine, initially at 2–5 mcg/kg/min, and the dosage titrated for optimal cardiac output). Stroma-free hemoglobin (dogs 5 mL/kg; cats 1–3 mL per cat, slowly) can be administered, and repeated as indicated, for its colloid effect as well as its mild vasopressor effect; it is particularly useful in animals with concurrent anemia. The initial resuscitation doses may be followed by a slow constant-rate infusion (dogs 10–15 mL/kg/day; cats 1–3 mL/hr up to 5 mL/kg/day) to maintain perfusion if the initial dose was successful and further support is anticipated. Pressor agents delivered as an IV constant-rate infusion such as dopamine (5–20 mcg/kg/min), norepinephrine (0.05–2 mcg/kg/min) or vasopressin (extra-label, 1–4 mU/kg/min) are other options to support blood pressure; they should be delivered in the smallest dosage needed to maintain arterial systolic pressure >90 mmHg. The blood flow to the kidneys and GI tract, as well as other organs, may have been significantly impaired during shock. Urine output, heart rate, blood pressure, ECG, pulse intensity, and mucous membrane color should be closely monitored, because further vasoconstriction can worsen organ blood flow and function. If organ function declines or if arrhythmias become a problem, the IV drip should be stopped.

Hindlimb and Abdominal Binding:

When ongoing abdominal hemorrhage is suspected from trauma, hindlimb and abdominal counterpressure can improve perfusion. This procedure compresses the arteries and arterioles within the bound regions, increasing regional vascular resistance, and produces abdominal tamponade, thereby effectively slowing or arresting hemorrhage and redirecting blood flow from the venous capacitance vessels in the caudal half of the body to the more central (core) circulation. Hindlimb and abdominal counterpressure can be performed by placing a rolled towel or rolled cotton between the legs and along the ventral midline of the abdomen. This prevents the wrap from impairing ventilation or fracturing the spleen or liver. If time permits, a urinary catheter is placed. The hindlimbs and abdomen are then firmly wrapped with padded bandage material or towels, beginning at the toes of the hindlimb and moving cranially toward the xiphoid, taking care not to impede respiration. The bandage should be secured with tape or stretch bandage material wrapped in a spiral pattern starting caudally and moving cranially. Abdominal binding should be avoided in cases of intrathoracic or intracranial hemorrhage. Once perfusion has stabilized, the wrap is removed slowly by sections (releasing one section every 15 min) from the abdomen, starting at the most cranial portion and moving caudally. Any signs of decompensation warrant rapid rebinding of the region last unwrapped.

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