Central Venous Pressure Monitoring: Learning How to Surf the Wave Forms

Richard Verstraete Level: Beginner

Content Description
Central Venous Pressure (CVP) is a common hemodynamic parameter used in the critical care setting. It is readily available for a patient with a central line and is the least invasive method for measuring cardiac filling pressures. CVP measures right atrial pressure, which reflects the blood return to the heart. The two most common uses for measuring CVP in the ICU are to assess volume status and assess preload of the heart. One of the most common misjudgments among practitioners is to rely on a single CVP measurement to guide volume therapy. This notion is fundamentally flawed, making it incumbent that the critical care nurse understands the physiology of CVP. In addition other principles of CVP monitoring are included in this coarse including: the rationale for the its use in the management of the acutely ill patient, factors that affect its measurement, wave form interpretation and analysis, and the use of central venous oxygenation ( ScVO2) to examine global tissue perfusion.

will result in a significant increase in CVP and cardiac output. The CVP is influenced by internal pressure i.e. compliance and external pressure i.e. pleural pressure. The difference between the two represents the transmural pressure. The difficulty with CVP is that it is referenced to the atmospheric pressure (zero reference) because it is not possible to measure pressures around the heart. So, in order to minimize this error measurement of CVP should be made at end expiration. 1. Factors influencing CVP a. Leveling b. Patient position c. Transmural pressure d. Where on waveform to make the measurement e. Cardiac rhythm f. Blood volume g. Tricuspid Valve disease h. Heart Compliance Interpretation of CVP a. Normal CVP 1-7 mm Hg b. Assumption: low CVP = hypovolemia; high CVP = hypervolemia c. Trends in CVP or response to therapy better indicator of volume status d. Starling curve plateau is highly variable (one size does not fit all) e. Most patients are volume limited at CVP 10-12 mm Hg CVP waveforms reflect the mechanical event of the cardiac cycle and consist of 5 phasic events. There are three peaks (a,c,v) and two descents (x,y). The CVP peaks are designated systolic (c,v) or diastolic (a) based on the phase of the cardiac cycle in which the wave begins. Likewise the descents are either systolic (x) or diastolic (y). The normal venous waveform can be remembered as follows: a. A wave atrial contraction b. C wave tricuspid valve closure c. V wave ventricular ejection d. X descent atrial relaxation e. Y descent ventricular filling The CVP waveform needs to be examined in conjunction with the ECG tracing to distinguish the different waveforms. There is a delay between the actual mechanical contraction as identified on the ECG tracing and the CVP waveforms. The a wave will occur after the P wave. The c wave (if present) will occur after the R wave as will the x descent, the v

Learning Outcomes
At the end of this session the attendee will be able to: 1. At the end of the coarse the participant will understand the physiological meaning of central venous pressure and its clinical application 2. At the end of the coarse the participant will be able to analyze the CVP waveform for abnormalities and how these abnormalities may impact the patients hemodynamic status 3. At the end of the coarse the participant will understand the meaning and usefulness of central venous oxygenation ( ScVO2) to examine global tissue perfusion

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Summary of Key Points

CVP is synonymous with right atrial pressure. CVP is a function of cardiac function and return function. Cardiac function is influenced by preload, afterload and contractility. Return function is influenced by the stressed vascular volume, venous compliance and venous resistance. The Frank-Starling curve is used to explain this interaction. Filling pressure and volume assume a curvilinaer relationship meaning that where the patients heart is on the pressure-volume curve can drastically alter the CVP measurement. For instance, when the heart is on the plateau of the curve a large increase in filling volume will result in a small increase in CVP and no change in cardiac output. Whereas, when the heart is on the up slope of the curve the same increase in filling volume

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wave will occur in adjacent with the T wave and the y descent will occur after the T wave. 5. Dysrhythmias, heart rate changes, and tricuspid valve disease can dramtically alter the CVP waveform morphology. For instance a short ECG P-R interval causes fusion of the a and c waves. Tachycardia reduces diastole time and the duration of the y descent, which cause the v and a waves to merge. Bradycardia causes each wave to become more distinct. At times there may be appearance of other waves forms to which one wants to attach a pathological significance. Many of these are simple artifacts related to the fluid-filled monitoring system. a. Atrial fibrillation - no a wave b. Junctional rhythm cannon a wave c. Tricuspid regurgitation tall v wave, loss of x descent d. Tricuspid stenosis tall a wave e. Ventricular Tacycardia no a wave, large v waves f. Pericardial constriction tall a and v waves, steep x and y descents g. Cardiac tamponade lose of y descent h. ScVO2 Interpreation i. Reflects upper body venous return and influenced by deoxygenated blood returning from the coronary sinuses. ii. Goal ScVO2 > 70% iii. ScVO2 < SvO2 iv. Shock states ScVO2 > SvO2 because of redistribution of blood flow v. In critically ill patients

Bibliography/Webliography
Magder, S: How to use central venous pressure measurements. Curr Opin Crit Care 2005; 11:264-270 Magder S, Erice F, Lagonidis D. Determinants of the y descent and its usefulness as a predictor of ventricular filling. J Intensive Care Med 2000; 15:262-269 Magder, S: Central venous pressure: A useful but not so simple measurement. Crit Care Med 2006; 34(8):22242227 Magder S: Central venous pressure monitoring. Curr opin crit Care 2006; 12(3):219-227 Barbeito A. Mark J. Arterial and central venous pressure monitoring. Anesthesiology Clin 2006; 24:717-735 Polanco M, Pinsky M. Practical issues of hemodynamic monitoring at the bedside. Surg Clin North America 2006: 86:1431-1456 Gellman,S. Venous function and central venous pressure A physiologic story. Anesthesiology 2008; 108:735-748 Magder, S. Invasive intravascular hemodynamic monitoring: Technical issues. Crit Care Clin 2007; 23:401414

AACN 2009 NTI & CRITICAL CARE EXPOSITION