3. Central Venous Pressure and Cannulation

Three upstrokes (the ‘a’, ‘c’ and ‘v’ waves) and two descents (the ‘x’ and ‘y’) that relate to the cardiac cycle

‘a’ wave: this occurs at the end of diastole and is caused by increased atrial pressure as the atrium contracts (occurs at end-diastole) Atria

‘x’ (or ‘x”) descent: this reflects the fall in atrial pressure as the atrium relaxes relaX

‘c’ wave: this supervenes before full atrial relaxation, and is caused by the bulging of the closed tricuspid valve into the atrium at the start of isovolumetric right ventricular contraction. (closed contraction)

‘x’ descent: this is a continuation of the ‘x” descent (interrupted by the ‘c’ wave) and represents the pressure drop as the ventricle and valve ‘screw’ downwards at the end of systole.

‘v’ wave: this is the increase in right atrial pressure as it is filled by the venous return against a closed tricuspid valve. Venous Valve

‘y’ descent: this reflects the drop in pressure as the right ventricle relaxes, the tricuspid valve opens and the atrium empties into the ventricle.

‘y’ descent: this reflects the drop in pressure as the right ventricle relaxes, the tricuspid valve opens and the atrium empties into the ventricle.

Any event that alters the normal relationship between these events will alter the shape of the waveform. For example, in atrial fibrillation the ‘a’ wave is lost; in tricuspid incompetence, a giant ‘v’ wave replaces the ‘c’ wave, the ‘x’ descent and the ‘v’ wave. ‘Cannon’ waves are seen when there is atrial contraction against a closed tricuspid valve (as occurs at a regular interval if there is a junctional rhythm, or at an irregular interval if there is complete atrioventricular conduction block).

CVC catheters are used for the monitoring of central venous pressures, for the insertion of pulmonary artery catheters and to provide access for haemofiltration transvenous cardiac pacing. Central venous lines also allow the administration of drugs that cannot be given peripherally, such as inotropes and cytotoxic agents, and the infusion of total parenteral nutrition. It is suggested that they can be used to aspirate air from the right side of the heart after massive air embolism, although very few anaesthetists have ever used them for this purpose

Function of CVP monitoring – intravascular volume: the CVP is the hydrostatic pressure generated by the blood within the right atrium (RA) or the great veins of the thorax. It provides an indication of volaemic status because the capacitance system, including all the large veins of the thorax, abdomen and proximal extremities, forms a large compliant reservoir for around two-thirds of the total blood volume. Hypovolaemia may be actual or effective, caused, for example, by subarachnoid block or sepsis, in which loss of venoconstrictor tone or venodilatation decreases venous return and reduces CVP. A single reading may be unhelpful, whereas trends are more useful, particularly when combined with fluid challenges.

Function of CVP monitoring – right ventricular function: CVP measurements also provide an indication of right ventricular (RV) function. Any impairment of RV function will be reflected by the higher filling pressures that are needed to maintain the same stroke volume (SV).

Normal values: the normal range is 0–8 mmHg, measured at the level of the tricuspid valve. The tip of the catheter should lie just above the RA in the superior vena cava.

CVP decreases: if the blood volume is unchanged, then the CVP will alter with changes in cardiac output (CO). It will fall as the CO rises because the rate at which blood is removed from the venous reservoir also increases

CVP increases: potential causes for an increase in CVP include a fall in CO (the converse of the effect described previously). Ventilatory modes may also cause the increase which is seen with IPPV, PEEP and CPAP. The CVP also rises in response to volume overload, if there is RV failure, pulmonary embolus, cardiac tamponade or tension pneumothorax. Rarer causes include obstruction of the superior vena cava (assuming that the catheter tip lies proximally) and portal hypertension leading to inferior vena caval backpressure.

These are numerous and include arterial puncture (carotid and subclavian), haemorrhage, air embolism, cardiac arrhythmias, pneumothorax, haemothorax, chylothorax, neurapraxia, cardiac tamponade and thoracic duct injury Anatomically proximate structures such as the oesophagus and trachea can also be damaged. Parts of catheters or entire guidewires can embolise into the circulation. Ultrasound guidance can reduce complications associated with catheter insertion Endocarditis and cardiac rupture have been reported. Venous thrombosis is common, but the risk may be reduced by the use of heparin-bonded catheters. Infection is a problem, and occurs in up to 12% of placements. Its risk is reduced by full aseptic precautions, by the use of antiseptic- and antibiotic-coated catheters (in high-risk patients) and by using the subclavian approach approach. There is no definite evidence of benefit for tunnelling, for prophylactic line changes or for the use of prophylactic antibiotics. These complications can be fatal: the confidential maternal mortality reports alone have documented three deaths caused by central catheterization

If the CVP is measured from the accurate reference point of the tricuspid valve, then a sustained negative intravascular pressure is impossible. Certainly, the negative intrathoracic pressure during inspiration will be transmitted to the central veins, and if there is respiratory obstruction this negative pressure will be high. It will, however, be transient. If a mean CVP reading is consistently negative it can only be because the transducer has been placed above the level of the right atrium

The right atrial pressure reflects the right ventricular end-diastolic pressure (RVEDP), and it is frequently assumed that this also reflects the left ventricular end-diastolic pressure (LVEDP). This means that, for a given fluid load, the increase in SV of each ventricle is identical, but the rise in filling pressure in the left ventricle exceeds that in the right. This discrepancy is accentuated by LV dysfunction, and under these circumstances accurate diagnostic information has to be obtained by other means.