5–10 ml/kg), fresh frozen plasma (FFP; 10–20 ml/kg), or whole blood (10–20 ml/kg) may be indicated for patients with anemia and/or coagulopathy. While there is no absolute PCV below which a transfusion is required, consideration of the chronicity of anemia, cardiovascular stability, continuing losses, anticipated surgical intervention, and pulmonary function all impact the decision of whether or not to transfuse a patient. It is also important to remember, that in many critically ill patients, even after control of hemorrhage, coagulopathy may persist due to dilution, consumption, delayed liver production of clotting factors, and liver dysfunction, so repeated dosing of FFP may be needed even once coagulation parameters have normalized.
Regardless of the fluid type chosen for cardiovascular resuscitation, it is imperative that frequent reassessment of the patient's cardiovascular parameters in response to treatment be performed. That same physical exam parameters and initial diagnostics used to diagnose shock should be reevaluated. Additional diagnostics that may be helpful for determining whether a patient is appropriately or maximally fluid resuscitated, especially if shock persists, include central venous pressure (CVP) and central venous oxygen saturation (SCVO2). CVP, which is a measure of the hydrostatic pressure within the intrathoracic (cranial or caudal) vena cava, is used to approximate right atrial pressure, or preload. Normal CVP is 0–5 cm H2O. CVP values less than 0 cm H2O are consistent with hypovolemia or decreased venous tone secondary to vasodilation [55]. Increased CVP (> 7–10 cm H2O) can be seen with volume overload, pleural space disease (pneumothorax, pleural effusion), pericardial disease (restrictive pericarditis, pericardial effusion), tricuspid valve disease, myocardial disease, and intraabdominal hypertension [55, 56]. The value of CVP monitoring for guiding fluid resuscitation has been questioned in both human and veterinary critical care in recent years. In addition to CVP, central catheters can also be used to measure SCVO2, which is an assessment of global tissue oxygenation and is the percentage of saturated hemoglobin within the cranial or caudal vena cava or right atrium. Alterations in SCVO2 reflects imbalance between oxygen delivery and consumption. Decreased SCVO2 is seen with increased oxygen consumption relative to delivery, as with hypovolemia, anemia, cardiac dysfunction, pulmonary dysfunction, fever, and hyperthermia. Increased SCVO2 is seen with decreased oxygen consumption relative to delivery, as with hypothermia and mitochondrial dysfunction [57–59]. In critically ill dogs, a decrease in SCVO2 below 68% within the first 24 hours of hospitalization was associated with poor outcome with progressive increase in mortality with decrease in SCVO2 [59]. In septic dogs that underwent surgery for pyometra, survivors had lower lactate, base deficit and their average SCVO2 was 74.6%. Non‐survivors in this study had an average SCVO2 of 62.4% [33]. Co‐oximetry, which is not widely available, is needed for SCVO2 determination; this is likely the reason for its limited clinical use in veterinary patients.
Cardiogenic Shock
It is important to differentiate hypovolemic shock from cardiogenic shock, as many of the physical exam findings can overlap but the treatment is usually vastly different. Fluid therapy is generally contraindicated in most patients with cardiogenic shock. Cardiogenic shock can be due to forward (left‐sided) or backward (right‐sided) failure of blood flow. Common causes of cardiogenic shock include congestive heart failure, systolic dysfunction, as with dilated cardiomyopathy, diastolic dysfunction, as with hypertrophic cardiomyopathy, and arrhythmias [25, 26]. Clinical signs of cardiogenic shock include pale mucous membranes, heart murmur and/or arrhythmias, poor or variable pulse quality, pulse deficits, and tachycardia or bradycardia. Findings consistent with right‐sided heart failure include decreased ventral lung sounds consistent with pleural effusion, jugular venous distension, ascites, and hepatomegaly. Clinical signs seen with left‐sided dysfunction and left‐sided heart failure include increased respiratory rate or effort, respiratory distress, pulmonary crackles (pulmonary edema), and decreased lung sounds ventrally consistent with pleural effusion (cats).
In addition to history and physical examination findings, other diagnostics often needed to diagnose cardiogenic shock include ECG, blood pressure, pulse oximetry (SpO2), thoracic radiography, and TFAST. TFAST can be used to determine cardiac contractility, myocardial thickness, and cardiac chamber (atria and ventricle) size. Focused echocardiography training for emergency veterinarians has been shown to improve their diagnostic capabilities for determination of several cardiac abnormalities [59]. Treatment may involve oxygen supplementation, pericardiocentesis, diuretic therapy, anti‐arrhythmics, vasopressors, or vasodilators depending on the etiology of cardiogenic shock.
Distributive/Septic Shock
Distributive shock is defined as a maldistribution of blood flow, most commonly due to altered systemic vascular resistance (SVR). Decreased SVR is the most common SVR alteration, and vasodilatory shock secondary to sepsis is one of the most readily recognized forms of distributive shock. Distributive shock can also be secondary to obstructive disease processes, such as gastric dilation and volvulus, pericardial effusion, and neoplasia causing vascular obstruction (such as adrenal tumors with invasion into the vena cava) [25]. The clinical signs of distributive shock in dogs are often very different from other forms of shock. In dogs, the mucous membranes are often bright pink (Figure 1.5), CRT is decreased (< 2 seconds), and peripheral pulses can be bounding or more prominent than normal. Cats with septic shock generally do not demonstrate the hyperdynamic signs seen in dogs and instead have pale mucous membranes, bradycardia, and decreased rectal temperature [60].
Many patients with distributive shock also have a component of hypovolemic shock (absolute or relative), so fluid therapy to correct intravascular volume deficit is essential. In humans with severe sepsis and septic shock, early goal‐directed therapy is shown to improve patient outcome when compared to traditional management strategies. In two landmark human studies, hemodynamic parameters such as direct arterial blood pressure, CVP, and SCVO2 measurement, and treatment with crystalloids, colloids, pRBC, and catecholamines to improve cardiac contractility and/or vasomotor tone were used until prescribed endpoints were achieved [61, 62]. Standardized goal‐directed therapy does not yet exist for veterinary patients, therefore, normalization of routinely monitored cardiovascular and perfusion parameters, including heart rate and rhythm, rectal temperature, mucous membrane color and CRT, blood pressure, CVP, PCV/TS, lactate and base deficit are recommended [31, 63, 64].
Figure 1.5 Bright pink mucous membranes in a dog with septic peritonitis.
When fluid therapy fails to normalize hemodynamic parameters, particularly blood pressure in septic patients, vasoactive catecholamines may be necessary [65, 66]. Commonly used vasoactive catecholamines used in critical care are dopamine, dobutamine, and norepinephrine (Table 1.1). Vasopressin, also known as antidiuretic hormone, is a peptide synthesized in the pituitary that binds vasopressin specific receptors on vascular smooth muscle. Vasopressin stores can become depleted with prolonged shock or sepsis resulting in vasoplegia despite intravenous fluid and vasoactive catecholamine therapy. Vasopressin deficiency has been documented in people with refractory hypotension, and positive benefit has been shown with the addition of intravenous administration of vasopressin. Experience with vasopressin is growing in veterinary medicine [67, 68].
Early administration of broad‐spectrum antibiotics has been shown to improve survival in human patients with sepsis and septic shock when combined with early goal‐directed therapy. When antibiotics were given within one hour of triage in combination with early goal‐directed therapy, mortality decreased from 33.3% to 19.5% [69]. In veterinary patients with septic shock, antimicrobials should be given as soon as reasonably possible, especially for those that will undergo emergency anesthesia