Arterial Pressure Monitoring

Noninvasive measurement of blood pressure is one of the most widely undertaken procedures in clinical medicine. Invasive techniques are more commonly employed in intensive care patients for several reasons. Most importantly, the accuracy provided by intraarterial lines is vital to assess the mean arterial pressure in critically ill patients when they are hemodynamically unstable. In addition, continuous surveillance of arterial pressure is of paramount importance when vasoactive agents are used. Furthermore, frequent noninvasive arterial pressure monitoring adds to the discomfort of the patient. Finally, an arterial line also permits frequent arterial blood gas estimations. Historically it has been relatively easy to measure pressure in the major peripheral arteries. Reliance has therefore been put on the maintenance of systemic pressure under the assumption that adequate pressure will also provide adequate flow and thus adequate tissue perfusion.

Studies in intensive care patients where the focus has been the maintenance of blood pressure have not been particularly fruitful.⁴ Hypotension is defined as a systolic pressure less than 90 mm Hg or a mean pressure less than 65 mm Hg. Most intensivists accept that pressure needs to be kept at a level that allows adequate tissue perfusion, particularly of the major organs, but that maintenance of blood flow through these organs is paramount.

Interpretation of the changes seen in the arterial waveform in relation to changes in intrathoracic pressure can now also give information about whether the patient is likely to respond to a fluid challenge (Box 74-1).^6,¹⁴ A greater than 10% or 12% variability of systolic pressure, pulse pressure, and/or stroke volume caused by the regular and consistent positive pressure associated with positive-pressure inspiration indicates that the patient is probably hypovolemic and is likely to respond to fluid resuscitation. It should be stressed, however, that this technique can only be used in sedated and ventilated patients in whom there is no spontaneous breathing. This is an important technological development because occult hypovolemia is probably not uncommon in critically ill patients and if unrecognized is likely to contribute to an increase in both morbidity and mortality.

Central Venous Pressure

Central venous pressure (CVP) is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure. It is conventionally measured at the junction of the superior vena cava and the right atrium and provides an estimate of the right atrial pressure. The CVP is often used as a marker of volemic status or preload, although the ability of this measurement to provide this information is limited.

The CVP is influenced by the volume of blood in the central venous compartment and also the compliance of that compartment (Box 74-2). Starling¹⁵ demonstrated the relationships between CVP and ventricular contraction and Guyton the relationship between venous return and CVP. By plotting the two relationships on the same set of axes, it can be seen that the “ventricular function curve” and the “venous return curve” intersect at only one point, demonstrating that if all other factors remain constant in an individual patient, a given CVP can, at equilibrium, be associated with only one possible cardiac output (Figure 74-1). Both curves can of course be affected by a number of factors: total blood volume and distribution of that blood volume between the different vascular compartments (determined by vascular tone). The inotropic state of the right ventricle will affect the shape of the ventricular function curve. When any one of these factors is altered, there will be an imbalance between cardiac output and venous return that will persist for a short time until a new equilibrium is reached at a new central venous blood volume and/or an altered central venous vascular tone.

Figure 74-1 Ventricular function and venous return curves.

Normal CVP exhibits a complex waveform, illustrated in Figure 74-2. The a wave corresponds to atrial contraction and the x descent to atrial relaxation. The c wave that punctuates the x descent is caused by the closure of the tricuspid valve at the start of ventricular systole and the bulging of its leaflets back into the atrium. The v wave is due to continued venous return in the presence of a closed tricuspid valve. The y descent occurs at the end of ventricular systole when the tricuspid valve opens and blood once again flows from the atrium into the ventricle. This normal CVP waveform may be modified by a number of pathologic processes (Box 74-3).

Figure 74-2 Central venous pressure waveform from a ventilated patient (bottom), with time-synchronized electrocardiogram (ECG) trace (top). The a wave represents atrial contraction and occurs immediately after atrial depolarization, as represented by the p wave on the ECG. The c wave represents bulging of the tricuspid valve in early ventricular systole and is followed by the v wave, caused by atrial filling during ventricular systole.

Box 74-3

Disease States that Modify the Central Venous Pressure Waveform

In atrial fibrillation, the a wave is lost and the c wave may become more prominent.

In the presence of atrioventricular dissociation or junctional rhythm, when atrial contraction may occur during ventricular systole, extremely tall cannon a waves occur due to atrial contraction against a closed tricuspid valve.

In tricuspid regurgitation, blood is ejected backward during ventricular systole from the right ventricle into the right atrium. This produces a large fused c-v wave on the central venous pressure trace.

In tricuspid stenosis, forward movement of blood from the right atrium into the ventricle occurs against a greater than normal resistance, leading to an accentuated a wave and an attenuated y descent.

With pericardial constriction, a short steep y descent will also be seen that allows differentiation from cardiac tamponade, where the central venous pressure will be monophasic with a single x descent.

If the CVP is to be used as an index of cardiac preload, the end-diastolic pressure at end expiration must be identified. The c wave marks the closure of the tricuspid valve at the beginning of ventricular systole, and immediately before its onset, the measured pressure should be equivalent to the right ventricular end-diastolic pressure (except in the case of tricuspid stenosis, in which a pressure gradient will always exist between the two chambers). Where no c wave is clearly visible, it is conventional to take the average pressure during the a wave. Where no a wave is visible (e.g., in atrial fibrillation), the pressure at the Z point (that point on the CVP waveform that corresponds with the end of the QRS complex on the electrocardiogram) should be used.

Taking all these factors into account, it is perhaps not surprising that the CVP will not provide a reliable estimate of preload in critically ill patients. The CVP correlates poorly with overall volemic status, right ventricular end-diastolic volume, stroke index, or an individual patient’s response to a fluid challenge.¹⁶ It is perhaps best used in non–critically ill patients when it can provide an estimate of the components to right ventricular filling and venous return because their vasculature is behaving in a normal physiologic manner.

Pulmonary Artery Catheter

Continuous, reliable, and accurate pressure and flow monitoring of cardiac performance helps in the early initiation of appropriate therapy toward precise hemodynamic goals. The pulmonary artery catheter with its measured and derived parameters (Boxes 74-4 and 74-5) helps direct therapy in the critically ill who balance their physiology precariously. The first double-lumen, balloon-tipped, flow-directed catheter was designed by Swan and Ganz in 1970.¹⁷ Thereafter, there have been several modifications to the pulmonary artery catheter, which now enables continuous monitoring of cardiac output from a thermodilution technique, of intravascular pressures, and of mixed venous oxygen saturation (SvO₂).