Instant Feedback:. The A wave starts just after the P wave ends and represents the atrial contraction. The high point of the A wave is the atrial pressure at maximum contraction. During the A wave the atrial pressure is greater than the ventricular diastolic pressure.
At that point, the atrium is contracted, the tricuspid is open. Therefore, the high point of the A wave closely parallels the right ventricular end diastolic pressure. Remember, when the tricuspid valve is open and the right ventricle is full, the ventricle, atrium and vena cavae are all connected. Pursuing a fixed value of CVP, such as 12 cm H 2 O, can be deleterious in a patient with ventricular dysfunction, whereas for a patient with intra-abdominal hypertension, this CVP could be associated with a decreased preload.
However, since a healthy heart is associated with low CVP values, a significant CVP raise after fluid administration should be interpreted as an early sign of RV dysfunction. Giving more fluids beyond this point could worsen cardiac function and impair venous return and capillary blood flow. Therefore, the role of CVP for guiding fluid therapy is not for defining how much, but rather when to stop giving fluids.
It has been explained that an isolated CVP value is difficult to interpret. As CVP is defined by the interaction between RV function and the venous return, CVP and CO changes are determined by a unique peripheral venous return and central cardiac function relationship. On the other hand, when changes in CO and CVP are in opposite directions, they usually result from a variation in cardiac function Fig.
An adequate use of CVP measurements requires a solid knowledge of its physiological basis and limitations. In this regard, we strongly believe that, understanding these physiological boundaries, CVP measurement may still have a role in the hemodynamic assessment.
Both authors contributed to the original idea and writing of this manuscript. The authors declare no conflict of interest regarding this paper. ISSN: Descargar PDF. Autor para correspondencia. Table 1. Central venous pressure CVP : use and misuse.. Texto completo. Introduction Central venous pressure CVP is still the most frequent hemodynamic variable for deciding when to administer fluids. Figure 1. Table 2. Cecconi, C. Hofer, J.
Teboul, V. Pettila, E. Wilkman, Z. Molnar, et al. Intensive Care Med, 41 , pp. Marik, R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. It is at this stage that the CVP is most helpful for these options can be separated by considering the actual CVP or even better, how it changed with the change in cardiac output.
Understanding the factors that determine CVP magnitude, mechanisms that produce the components of the CVP wave form and changes in CVP with respiratory efforts can also provide useful clinical information. In many patients, CVP can be estimated on physical exam. Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.
Please subscribe or login to access full text content. If you have purchased a print title that contains an access token, please see the token for information about how to register your code. For questions on access or troubleshooting, please check our FAQs , and if you can't find the answer there, please contact us. All Rights Reserved. In the fluid nonresponder, the same increase in blood volume and preload is associated with no change in cardiac output and major changes in CVP.
Accordingly, an increase in CVP cannot be used to suggest a positive response to fluids. Volume measurements better evaluate changes in preload in preload-responsive patients while pressure measurements better evaluate changes in preload in preload-nonresponsive patients. Considering changes in CVP without taking into account changes in cardiac output can be very misleading as one may erroneously consider that the greater the change in CVP the larger the increase in preload and thus potentially the greater the effect of fluids.
However, the opposite effect may be true, i. Changes in CVP during a fluid bolus can be used to predict the response to further fluid administration. In 80 surgical patients, Hahn et al. Hence, if anything, changes in CVP should be minimal, but accompanied by an increase in cardiac output; otherwise it implies that preload was not affected. CVP is an excellent variable to estimate the risk associated with extrathoracic organ congestion.
Limiting CVP in liver surgery is associated with less risk of bleeding and better perioperative outcomes [ 11 ]. Similarly, the incidence of acute kidney injury is increased in patients with sepsis or with congestive heart failure who have elevated CVP values [ 4 , 12 ].
In patients with sepsis, the risk of developing acute kidney injury increased with the mean CVP values over the first 12 h after admission [ 4 ]. In patients with congestive heart failure, those in the two upper quartiles of CVP had more severe renal impairment compared to the other quartiles, even though cardiac output was similar in the four quartiles [ 12 ].
These data strongly demonstrate an association between an elevated CVP and an increased risk of developing acute kidney injury, but they do not demonstrate a causal link. Importantly, the CVP may fail to reflect the risk of developing pulmonary edema, which depends on capillary pressure and hence on left atrial pressure. This is a difficult question, as no clear cut-off value can be identified.
In a study by Boyd et al. This individually determined upper limit can be used as a value at which further fluid administration should be restricted. Nevertheless, one should try to keep CVP as low as possible as long it remains associated with adequate tissue perfusion.
This concept is the basis of some resuscitation algorithms including that used by Rivers et al. Of note, the same CVP targets were used in the goal-directed and control arms so that no conclusions can be made on the effectiveness of this approach based on these trials. No difference in survival or organ dysfunction was reported between the usual care arm and the two other arms, but it should be noted that a central line was inserted in the majority of patients in the usual care arm and we do not know whether a CVP value was targeted in these patients.
Physiologically, it does not seem reasonable to target a specific CVP value because the CVP value above which a patient would not respond to fluids is highly variable.
As indicated earlier, each patient follows their own Frank-Starling curve, and only extreme CVP values carry some predictive value for fluid responsiveness. Hence, targeting a specific CVP value is only valid at the population level.
Applying bootstrap analysis on data obtained from critically ill patients submitted to a fluid challenge, Biais et al. Nevertheless, it would be dangerous to target such high values of CVP as many patients would be exposed to the detrimental effects of fluids while still being nonresponsive.
These values represent a reasonable target as the majority of patients respond to fluids when CVP is less than 8 mmHg and only a minority when it is greater than 12 mmHg [ 7 , 8 ]. Nevertheless, using these values of CVP to guide fluid administration is far from perfect and should only be applied when more accurate predictors of fluid responsiveness cannot be obtained.
In stabilized patients, it is clear that no attempt should be made to increase CVP to specific target values. There were no differences in survival between the groups, but patients in the conservative strategy group were more rapidly weaned from mechanical ventilation. In a recent exploratory analysis of this trial, the risk of death was increased in the liberal group compared to the conservative group when basal CVP was between 0 and 10 mmHg but not at higher values of CVP [ 19 ], suggesting a harmful effect of fluid administration to target a given CVP value when this was not needed.
The reliability of CVP measurements has been questioned, with errors related both to positioning of the zero level as well as reading errors. Although these potential errors should be acknowledged as a clear limitation, they are not restricted to CVP measurements and, more importantly, adequate training should limit the risk of such errors occurring.
Indeed, measurements of end-diastolic volume by transpulmonary thermodilution or echocardiography reflect cardiac preload better than do intravascular pressures, including CVP.
In healthy volunteers, changes in stroke volume during fluid loading correlated better with changes in cardiac volumes than with CVP [ 20 ].
Of note, volumes better predict fluid responsiveness on the steep part of the Starling relationship, whereas on the plateau pressures indicate better that the patient has reached the limits of filling Fig. In addition, measurements of intravascular pressures are more physiologic in terms of the Starling relationship of the vessels; indeed, edema formation depends on intravascular pressures and not on volumes. Relationship between preload, end-diastolic volumes, and pressures.
Volume measurements better evaluate changes in preload in preload-responsive patients a while pressure measurements better evaluate changes in preload in preload-nonresponsive patients b. The only exception is probably the abdominal compartmental syndrome, in which CVP is markedly increased due to the increase in intrathoracic pressure, while cardiac volumes are markedly reduced.
Dynamic indices of fluid responsiveness, such as pulse pressure variation PPV or stroke volume variation SVV , or changes in cardiac output during a passive leg raise, reflect that the heart is on the ascending part of the Starling relationship. Given their excellent predictive capacities for fluid responsiveness, these tests are now included in recent guidelines [ 21 , 22 ]. Unfortunately, PPV or SVV can only be used reliably in a minority of the patients, who are mechanically ventilated, sedated and without arrhythmias.
0コメント