Case Scenario
A 69-year-old man was transported to the ED via emergency medical services after a family member discovered him alone at home and confused. His wife stated that her husband had been sick with the flu and had been febrile for the previous several days. The patient’s blood pressure taken on the scene by the emergency medical technician was 80/40 mm Hg, and 1 L normal saline was infused during transport. Upon arrival to the ED, his vital signs were: temperature, 103.3°F; heart rate,130 beats/minute; BP, 90/48 mm Hg; and respiratory rate, 24 breaths/minute. Oxygen saturation was 92% on nasal canula. An electrocardiogram showed sinus tachycardia with nonspecific changes.
Based on the patient’s symptoms, the emergency physician (EP) suspected sepsis and ordered the appropriate laboratory studies and radiographic images. During evaluation, the patient’s systolic BP decreased to 70 from 80 mm Hg, and the EP ordered another fluid bolus and considered assessing the patient’s volume status.
Introduction
There is a long-standing debate as to the most accurate method of determining the volume status of a critically ill patient, as well as the physiological ability to respond to fluid therapy. In the assessment of a critically ill patient receiving volume replacement, a wide variability of assessment options are available; however, the current literature has yet to determine which method is the best. This article reviews multiple approaches to estimating the intravascular volume status of critically ill patients and the use of modalities to determine a patient’s physiological response to fluid therapy.
Basic Physiology
Central venous pressure (CVP) is the pressure in the thoracic vena cava adjacent to the right atrium. The heart functions as a two-sided pump; the right side pumps volume at low pressure and the left side pumps against systemic arterial pressure. The major determinant of the filling pressure of the right ventricle (RV) at the end of diastole is CVP, which is affected by the initial stretching of the ventricles before contraction (preload).
Frank-Starling Mechanism
The Frank-Starling mechanism describes the relationship between cardiac performance and intravascular volume. Stroke volume increases in response to an increase in preload volume. The increased volume of blood stretches the ventricular wall, causing the cardiac muscle to contract more forcefully. The change in volume (∆V) of blood divided by the change in pressure (∆P) is termed compliance
(∆V/∆P).
The venous system is the major reservoir within the vascular system and is markedly more compliant than the arterial system. Thus, CVP will increase with a decrease in venous compliance and/or an increase in the venous volume. These relationships can be quite dynamic depending on the disease state.
History of CVP Monitoring
The resuscitation of hemodynamically unstable patients historically stressed the use of intravenous (IV) fluid boluses. However, measuring the efficacy of this approach has been difficult. This issue was first addressed in the 1960s and 1970s when clinicians began to use central venous catheters (CVCs) to measure CVP as a surrogate measure of right atrial volume, which had been interpreted as a measure of the amount of blood returning to the heart. However, CVP measurements were static measurements of a dynamic filtration, and derivation of cardiac output required a long and complex calculation. The Swan-Ganz pulmonary artery catheter was the first catheter that enabled continuous monitoring and allowed clinicians to obtain cardiac index calculations at the bedside.1
The CVP is an approximation of the right atrial pressure and is an indicator of RV preload, which is a major determinant of RV filling pressure. Both RV preload and RV filling pressure correlate with intravascular volume. Lower CVP may occur with vasodilation or hypovolemia, which decreases the volume returning to the right atrium. This volume depletion creates a need for fluid replacement.
To illustrate this point, picture the body’s blood supply contained within a 6-L expandable tank. Vasodilation may expand the tank to a 9-L capacity, with a 3-L volume deficit. Similarly, blood loss from the 6-L tank may drain 3-L from the tank, leaving a 3-L deficit. Both mechanisms may cause a 3-L deficit, with the tank partially empty. Although it might make sense to replace the loss or “fill the tank in both scenarios,” fluid replacement may have risks. Overly aggressive fluid resuscitation may cause multiorgan dysfunction such as pulmonary edema, abdominal compartment syndrome, altered mental status, dilutional anemia, or dilutional coagulopathy. However, suboptimal fluid treatment may cause inadequate resuscitation that may be complicated by persistent hypotension, hypoperfusion, and end-organ damage and failure.