Parameters to Evaluate During Triage

Mucous membrane color

Pink

Normal PCV and adequate perfusion

Pale or white

Anemia or shock

Cyanotic or muddy

Severe hypoxemia or decompensatory shock

Yellow

Increased serum bilirubin due to hepatic disease or hemolysis

Local or systemic disease

Focal changes to mucous membranes, such as petechia or redness, swelling, sloughing of superficial layers, or very dark or black discoloration; can also indicate systemic disease.

Petechia may indicate thrombocytopenia or thrombocytopathy; redness and swelling or sloughing may indicate local chemical, thermal, or electrical injury; dark or black discoloration may indicate loss of blood supply with thrombosis, necrosis, etc.

Capillary refill time

1–2 seconds

Normal perfusion and rapidity with which capillaries refill with blood

> 2 seconds

Poor perfusion or peripheral vasoconstriction

< 1 second

Hyperdynamic state; could be associated with fever, heatstroke, distributive shock, or early compensatory stage of hypovolemic shock

Heart rate

70–120 bpm (small dogs)

60–120 bpm (large dogs)

150–220 bpm (cats)

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

Bradycardia:

< 60–70 bpm (dogs)

< 150 bpm (cats)

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

Tachycardia:

> 180 bpm (dogs)

> 220 bpm (cats)

Compromised diastolic filling; sinus tachycardia often results from hypovolemic shock, pain, or primary cardiac disease; 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 heartbeat

Normal; both femoral and digital pulses should be palpated

Irregular

Usually indicative of a cardiac arrhythmia

Bounding

Hyperdynamic (compensatory) state of shock; indicates an increase in pulse pressure (ie, an increase in systolic pressure, decrease in diastolic pressure, or both)

Weak or absent

Decreased cardiac output (including cardiopulmonary arrest), peripheral vasoconstriction, decreased pulse pressure, or thrombosis

Level of consciousness

Alert and responsive to surroundings

Normal overall neurological 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 neurological or metabolic derangements, including toxin ingestion

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

Abnormal cerebral electrical activity from primary neurological disease or secondary to metabolic derangements in diseases such as diabetes mellitus, 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). This is best recorded with a composite pain scale.

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