Central venous pressure is a measure of pressure in the superior vena cava which can be used as an estimation of preload and right atrial pressure. Central venous pressure is often used as an assessment of hemodynamics in a patient, particularly in intensive care units. The central venous pressure can be measured using a central venous catheter placed in the superior vena cava near the right atrium. A normal central venous pressure reading is between 8 to 12 mmHg. This value can be changed depending on a patient’s volume status or venous compliance.
New evidence suggests no absolute direct correlation between central venous pressure and blood volume present in the circulation. Most importantly, as the concept of fluid responsiveness emerged and showed a crucial impact on patient outcome, the central venous pressure was found to be a poor predictor of fluid responsiveness. Accurate measurements of the central venous pressure were also challenged. A questionnaire revealed that about 75% of the respondents made an error in their measurement of central venous pressure. It also showed that many younger clinicians still use central venous pressure for management of cardiovascular scenarios despite the fact that they doubted the usefulness of central venous pressure. The questionnaire concluded that proper education regarding central venous pressure must be provided.
A systematic review from 2008 has indicated insufficient data to support that central venous pressure should be monitored in intensive care units, operating rooms, and emergency departments. The review also suggested that central venous pressure should only be used as a measure of right ventricular function and not volume status in certain patients, such as those undergoing a heart transplant, those who have had a right ventricular infarct, or those with an acute pulmonary embolism. Of note, The Surviving Sepsis Campaign no longer targets a central venous pressure of 8 to 12 mmHg as a gauge of fluid resuscitation. Due to the limitation of the central venous pressure as a static measure, the critical care society realized that parameters such as lactate clearance would more dynamically and accurately attest to the adequacy of end-organ perfusion.
The central venous pressure is an approximation of right atrial pressure. The central venous pressure, therefore, is directly affected by blood volume and the compliance of the central venous compartment. In terms of blood volume, the central venous pressure can be increased by cardiac output, total blood volume, changing to supine from a standing position, dilation of arteries, and any muscle contraction in the abdomen or limbs. These all increase the venous return, in turn, increasing the central venous pressure and showing that other organ systems besides the cardiovascular system can influence the central venous pressure. The renal system is involved because the total blood volume can be increased due to renal failure or fluid retention. The musculoskeletal system can increase venous return through muscle contractions which compress veins, forcing blood to rush into the vena cavae.
The central venous pressure has a positive influence on stroke volume and cardiac output by the Starling law. It also has a negative effect on venous return. The flow between the peripheral venous system and the central venous system can be guided by the flow equation Q = Delta-P/R where Q represents flow, Delta-P represents the drop in pressure between the two systems, and R represents resistance. If the peripheral venous system has a pressure that is equal to the central venous pressure, there will be no venous return. As central venous pressure decreases, there will be an increase in venous return because there will be a pressure drop in the venous resistance. However, another factor to consider is intrathoracic pressure. If the central venous pressure were to fall below the intrathoracic pressure, the central veins become compressed and limit venous return. The peripheral venous pressure can be affected by a change in volume, and because of their compliant nature, a change in total volume would have a greater effect on the amount of blood present in the veins. Venous tone also changes the peripheral venous pressure through the sympathetic nervous system or any outside force that compresses the vein. In normal physiologic states, the output of the right and left ventricles are equal. The central venous pressure affects cardiac output, usually meaning left ventricle output because changes in central venous pressure cause changes in the filling pressure of the left heart. Central venous pressure drives to reach a level where cardiac output and venous return are equal.
The central venous pressure is measured by a central venous catheter placed through either the subclavian or internal jugular veins. The central venous pressure can be monitored using a pressure transducer or amplifier. First, the transducer or amplifier must be zeroed to atmospheric pressure. Then, the transducer must be aligned to the horizontal plane of the tricuspid valve. The central venous pressure can also be measured using an ultrasound machine. The ultrasound can assess fluid responsiveness as measure the maximal inferior vena cava diameter, inferior vena cava inspiratory collapse, and internal jugular aspect ratio. Amongst these three, the measurement of the maximal inferior vena cava diameter was found to be the best estimate of the central venous pressure with an inferior vena cava diameter greater than 2 centimeters suggesting elevated central venous pressure and a measurement less than 2 centimeters, suggesting low central venous pressure.
Low Central Venous Pressure
Some factors that can decrease central venous pressure are hypovolemia or venodilation. Either of these would decrease venous return and thus decrease the central venous pressure. A decrease in central venous pressure is noted when there is more than 10% of blood loss or shift of blood volume. A decrease in intrathoracic pressure caused by forced inspiration causes the vena cavae to collapse which decreases the venous return and, in turn, decreases the central venous pressure.
Elevated Central Venous Pressure
Elevated Central Venous Pressure can occur in heart failure due to decreased contractility, valve abnormalities, and dysrhythmias. Any patients on ventilator assistance that have excessive positive end-expiratory pressure would have an increase in pulmonary arterial resistance which causes an increase in central venous pressure. However, an increased central venous pressure caused by increased pulmonary arterial resistance can also be affected by a decrease in the fraction of inspired oxygen, an increase in ventilation/perfusion abnormalities in the lung, an increase in pericardial pressure, or an increase in intra-abdominal pressure which would increase thoracic pressure. Increased juxta-cardiac pressure can also limit venous return, which can be due to tension pneumothorax and cardiac tamponade.
As mentioned, the central venous pressure can be used to assess the circulatory status of a patient. A high central venous pressure indicates that a patient has a cardiac pump dysfunction or is fluid overloaded. A high central venous pressure will present clinically as pulsation of the internal jugular vein when a patient is inclined at 45 degrees; however, it can be noted in an upright patient in severe cases. On the other hand, a low central venous pressure is indicative of a low volume status or decreased venous tone. The central venous pressure is used almost universally to guide fluid resuscitation. The Surviving Sepsis guidelines suggest targeting a central venous pressure between 8 and 12 mmHg during fluid resuscitation.
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