Changes in the ratio with treatment, whether intravenous fluids or diuretics, can be useful for monitoring response to therapy.
The use of point of care ultrasound techniques in dogs has been used to objectively assess vascular status and may be used as an adjunct diagnostic to guide fluid and/or vasopressor therapy. In normal dogs with furosemide induced hypovolemia, the caudal vena cava to aorta ratio measured from the right intercostal space in left lateral recumbency corresponded with decreasing body weight consistent with volume loss [38]. This ratio was also decreased after blood donation in healthy dogs [39]. In greyhounds, the iliac location for this ratio did not detect volume status changes before and after blood donation [40]. While additional work is needed in canine clinical cases of hypovolemia as well as normal and critically ill cats, this technique appears to be a promising method for non‐invasive volume assessment.
Hypovolemic Shock and Fluid Therapy
Hypovolemic shock, which is the most common type of shock seen in veterinary medicine, can be due to blood loss, fluid loss, or inadequate intake, and results in decreased tissue delivery of oxygen. Clinical signs consistent with hypovolemic shock are mental depression, weakness, pale mucous membranes, prolonged CRT, tachycardia, weak peripheral pulses, cool extremities, and tachypnea.
To treat hypovolemic shock, intravascular volume replacement is essential and generally accomplished with intravenous crystalloids, colloids, blood products, or a combination of the fluid replacement options. “Shock” doses of fluid therapy are based on the blood volume for a given species, and amounts for replacement are based on the percentages of volume loss to cause cardiovascular changes secondary to hypovolemic shock. Blood volume is approximately 90 ml/kg in dogs and 45–60 ml/kg in cats. Generally, patients are given portions of their shock dose of fluids, such as 10–30 ml/kg of balanced isotonic crystalloid solutions or 5–10 ml/kg of colloid solutions as a bolus over 15–20 minutes and assessed for improvement in perfusion parameters. The bolus is repeated if indicated. Hypertonic saline (7.5%, 3–5 ml/kg IV over 15–20 minutes in dogs, 2–3 ml/kg IV over 15–20 minutes in cats) is also effective for rapid volume expansion in hypovolemic shock but should only be used in patients with normal hydration. The decision about whether crystalloids or colloids should be chosen as the initial resuscitation fluid is controversial and has yet to be determined in both human and veterinary medicine [41–47]. In veterinary patients, the decision is often based on availability, cost, and whether there are concerns about the patient's colloid osmotic pressure and the ability to maintain fluid within the intravascular space. In June 2013, a boxed warning was placed on hydroxyethyl starch (HES) solutions, such as hetastarch, due to concerns for increased mortality, severe renal injury, and risk of bleeding associated with their use in critically ill adults, including those with sepsis and admitted to the intensive care unit. VetStarch® (Abbott Laboratories, Chicago, IL), a veterinary specific HES solution, is commercially available as a synthetic colloid for plasma volume expansion. Preliminary veterinary studies have conflicting evidence on association between the use of synthetic colloids and acute kidney injury in dogs; they should be used with caution until further research is available [48, 49].
Hypovolemic resuscitation or controlled intravascular volume replacement titrated to a mean arterial blood pressure (MAP) of 60 mmHg is widely used for human and veterinary patients with hemorrhagic shock [50–54]. The goal is to preserve perfusion to the vital organs, particularly the kidneys and cerebral circulation, without supranormalizing blood pressure, to prevent disruption of any clots tempering further hemorrhage. Experimental evidence in a swine model shows that rebleeding occurs when MAP is greater than 60 mmHg, while maintaining the MAP at approximately 60 mmHg maintains renal and cerebral blood flow [54]. Recommendations for decreased volume fluid resuscitation for crystalloid boluses are between 20 and 30 ml/kg and 5 ml/kg for colloid boluses titrated to effect and target blood pressure [52].
Transfusion with packed red blood cells (pRBC; 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
