Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article. The opinions expressed in this paper do not reflect those of the Veteran’s Healthcare administration.
Dr Brant is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Niehaus is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Kobzik is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Goodmanson is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Skolnik is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Hamade is a critical care fellow, department of critical care, multidisciplinary critical care training program, University of Pittsburgh Medical Center, Pennsylvania. Dr Schott is an assistant professor, department of critical care medicine and emergency medicine, University of Pittsburgh and University of Pittsburgh Medical Center, Pennsylvania, and director of critical care ultrasonography, VA Pittsburgh Health Care Systems, Pennsylvania.
A return to a normalized serum lactate level is assumed to represent a transition back to aerobic metabolism. Lactate elevations, however, are not solely an indication of anaerobic metabolism and may only represent a small degree of lactate production.20 While the specific cellular mechanics are out of the scope of this article, it has been postulated that the increase in plasma lactate concentration is primarily driven by β-2 receptor stimulation from increased circulating catecholamines leading to increased aerobic glycolysis. Increased lactate levels could therefore be an adaptive mechanism of energy production—aggressive treatment and rapid clearance may, in fact, be harmful. Type A lactic acidosis is categorized as elevated serum levels due to tissue hypoperfusion.21
However, lactate elevations do not exclusively occur in severe illness. The use of β-2 receptor agonists such as continuous albuterol treatments or epinephrine may cause abnormal lactate levels.22 Other medications have also been associated with elevated serum lactate levels, including, but not limited to linezolid, metformin, and propofol.23-25 Additionally, lactate levels may be elevated after strenuous exercise, seizure activity, or in liver and kidney disease.26 These “secondary” causes of lactic acidosis that are not due to tissue hypoperfusion are referred to as type B lactic acidosis. Given these multiple etiologies and lack of specificity for this serum measurement, a failure to understand these limitations may result in over aggressive or unnecessary medical treatments.
Central Venous Pressure
Background
Central venous pressure (CVP) measurements can be obtained through a catheter, the distal tip of which transduces pressure of the superior vena cava at the entrance of the right atrium (RA). Thus, CVP is often used as a representation of RA pressure (RAP) and therefore an estimate of right ventricular (RV) preload. While CVP is used to diagnose and determine the etiology of shock, evidence and controversy regarding the use of CVP as a marker for resuscitation comes largely from sepsis-focused literature.5 Central venous pressure is meant to represent preload, which is essential for stroke volume as described by the Frank-Starling mechanism; however, its use as a target in distributive shock, a state in which it is difficult to determine a patient’s volume status, has been popularized by EGDT since 2001.2
Since the publication of the 2004 Surviving Sepsis Guidelines, CVP monitoring has been in the spotlight of sepsis resuscitation, albeit with some controversy.27 Included as the result of two studies, this recommendation has been removed in the most recent guidelines after 12 years of further study and scrutiny.2,27,28
Hypovolemic and hemorrhagic shock are usually diagnosed clinically and while a low CVP can be helpful in the diagnosis, the guidelines do not support CVP as a resuscitation endpoint. Obstructive and cardiogenic shock will both result in elevated CVP; however, treatment of obstructive shock is generally targeted at the underlying cause. While cardiogenic shock can be preload responsive, the mainstay of therapy in the ED is identification of patients for revascularization and inotropic support.29
Benefits
The CVP has been used as a surrogate for RV preload volume. If a patient’s preload volume is low, the treating physician can administer fluids to improve stroke volume and cardiac output (CO). Clinically, CVP measurements are easy to obtain provided a central venous line has been placed with the distal tip at the entrance to the RA. Central venous pressure is measured by transducing the pressure via manometry and connecting it to the patient’s bedside monitor. This provides an advantage of being able to provide serial or even continuous measurements. The “normal” RAP should be a low value (1-5 mm Hg, mean of 3 mm Hg), as this aids in the pressure gradient to drive blood from the higher pressures of the left ventricle (LV) and aorta through the circulation back to the low-pressure of the RA.30 The value of the CVP is meant to correspond to the physical examination findings of jugular venous distension.31,32 Thus, a low CVP may be “normal” and seen in patients with hypovolemic shock, whereas an elevated CVP can suggest volume overload or obstructive shock. However, this is of questionable value in distributive shock cases.
Aside from the two early studies on CVP monitoring during treatment of septic patients, there are few data to support the use of CVP measurement in the early resuscitation of patients with shock.2,28 More recent trials (PROMISE, ARISE, PROCESS) that compared protocolized sepsis care to standard care showed no benefit to bundles including CVP measurements.12-14 However, a subsequent, large observational trial spanning 7.5 years demonstrated improvements in sepsis-related mortality in patients who received a central venous catheter (CVC) and CVP-targeted therapy.33 Thus, it is possible that protocols including CVP are still beneficial in combination with other therapies even though CVP in isolation is not.
