Arterial, Central Venous, and Pulmonary Artery Catheters

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Arterial, Central Venous, and Pulmonary Artery Catheters

Jean-Louis Vincent

Chapter Outline

Arterial Catheters

What Do They Offer?

The placement of an arterial catheter permits (1) reliable and continuous monitoring of arterial pressure and (2) repeated blood sampling. Analysis of the arterial pulse pressure curve may also have other applications, including assessment of fluid responsiveness and estimation of cardiac output. The appearance of arterial pressure waves will vary according to the site at which the artery is sampled. As the arterial pressure wave is conducted away from the heart, three effects are observed: The wave appears narrower; the dicrotic notch becomes smaller; and the perceived systolic and pulse pressures rise and the perceived diastolic pressure falls.

Arterial Pressure Measurement

The optimal range of arterial pressure depends on individual patient characteristics, on underlying diseases, and also on treatment. Hence, it is impossible to give an optimal range of arterial pressure that is applicable in all patients. When arterial pressure needs to be evaluated accurately, oscillometric measurements become unreliable,¹ and insertion of an arterial catheter is indicated.

Four potential indications for insertion of an arterial catheter for measurement of arterial pressure are recognized:

1. Hypotensive states associated with (a risk of) altered tissue perfusion. Hypotension that is resistant to fluid administration requires the administration of vasopressor agents, and invasive measurement of arterial pressure is then necessary to titrate this form of therapy. Norepinephrine is the vasopressor agent most commonly used in this setting. A mean arterial pressure (MAP) of 65 to 70 mm Hg is usually targeted, but this level must be adapted to the individual patient and the clinical scenario; in particular, elderly patients with atherosclerotic disease may require higher levels than younger individuals with normal arteries.

2. Intravenous vasodilator therapy. Vasodilating therapy (e.g., nitrates and hydralazine) is a mainstay in the management of heart failure, because it can increase cardiac output. Close monitoring of arterial pressure is essential to avoid excessive hypotension.

3. Severely hypertensive states. Extreme hypertension may result in organ impairment, especially of the brain and the heart. Sodium nitroprusside or calcium entry blockers usually are used to lower arterial pressure, and careful, accurate monitoring is essential to titrate the antihypertensive therapy.

4. Induction of hypertension. Hypertension is sometimes induced in patients with neurologic diseases. Severe cerebral edema with intracranial hypertension, in particular, requires vasopressor support to maintain cerebral perfusion pressure (the gradient between the MAP and the intracranial pressure); likewise, hypertension may be used to treat or prevent the development of vasospasm secondary to subarachnoid hemorrhage, as part of the so-called triple-H therapy (hypertension, hypervolemia, hemodilution). Norepinephrine usually is used for this purpose.

Fluid Responsiveness

Variations in arterial pressure during positive-pressure ventilation have been used as a measure of fluid responsiveness. The transient increases in intrathoracic pressure influence venous return in patients who are likely to respond to fluid administration. This fluctuation in ventricular filling will translate into fluctuations in arterial pressure a few beats later. Accordingly, the greater the degree of systolic arterial pressure, or pulse pressure, variation during the respiratory cycle, the greater will be the increase in cardiac output in response to fluid administration (Fig. 4.1). However, this observation is valid primarily in patients without spontaneous respiratory movements and without significant arrhythmias, and only when a sufficient tidal volume is applied.^2,3

Figure 4.1 The systolic pressure variation (SPV) is the difference between the maximum and the minimum systolic blood pressures during one ventilatory cycle (A). The SPV is the sum of the ΔDown (B) and the ΔUp (C). (From Perel A, Pizov R, Cotev S: Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage. Anesthesiology 1987;67:498.)

Cardiac Output Assessment

The pulse contour analysis also can serve to estimate cardiac output less invasively than with the pulmonary artery catheter (PAC). Because the only determinants of arterial pressure are the stroke volume and the resistance and compliance factors of the blood and arteries, analysis of the pulse contour trace can help to monitor cardiac output over time. This can be done with regular calibrations whenever changes in vascular tone or blood volume occur, or even in the absence of calibration. These measurements are still approximations, so further technological developments can be expected to improve accuracy.

Blood Sampling

The presence of an arterial catheter can greatly facilitate blood sampling, especially in terms of enabling easy access to the circulation for regular monitoring of blood gases, such as may be required in severe respiratory failure or with acute metabolic alterations. Sensors can measure blood gases continuously, but widespread use of such sensors is limited by their cost.

Access

For placement of arterial catheters, usually the radial artery is used. The femoral artery can be easily cannulated and gives a better signal, but presence of a femoral catheter interferes more with patient mobility and warrants concern about infection.⁴ Use of other sites, such as the brachial or the axillary artery or even the dorsalis pedis artery,⁵ can be considered. An important point to keep in mind is that the pulse pressure increases from the core to the periphery. In other words, the systolic pressure is overestimated in smaller arteries (Fig. 4.2). Hence, it may be better to rely more on mean values than on systolic or diastolic pressures.

Figure 4.2 Schematic representation of an arterial pressure tracing showing that the pulse pressure increases as arterial size decreases.

Complications

The most feared complication with use of arterial catheters is ischemia. With any suspicion of ischemia, the catheter must be removed immediately. Allen’s test, to determine occlusive arterial lesions distal to the wrist, is unreliable and is no longer widely used. The accidental disconnection of arterial lines can be associated with severe hemorrhage and even exsanguination. Infectious complications are rare.

Central Venous Catheters

What Do They Offer?

The central venous catheter can facilitate fluid administration. It also allows measurement of the central venous pressure (CVP) and enables access to central venous blood for sampling.

Fluid Administration

The large-bore central venous catheter allows fluids to be administered fast and reliably in the presence of acute hemorrhage. Placement of a central catheter is therefore essential in patients with hemorrhage due to polytrauma or with other forms of acute bleeding. It also allows irritant or hypertonic fluids to be administered, such as parenteral solutions, potassium-enriched solutions, and some therapeutic agents. Central venous lines also can be convenient in patients who need prolonged intravenous therapy when peripheral venous access becomes problematic.

Measurement of Central Venous Pressure

CVP is identical to right atrial pressure (RAP) (in the absence of vena cava obstruction) and to right ventricular (RV) end-diastolic pressure (in the absence of tricuspid regurgitation). It is thus equivalent to the right-sided filling pressure. CVP is determined by the interaction of cardiac function and venous return, which is itself determined by the blood volume and the compliance characteristics of the venous system. Hence, an elevated CVP can reflect an increase in blood volume as well as an impairment in cardiac function. Because the CVP evaluates the right-sided filling pressures, CVP can be increased in the presence of pulmonary hypertension, even if left ventricular (LV) function is normal. The normal value in healthy persons is very low, not exceeding 5 mm Hg. Thus, the CVP value may not be much lower than normal in the presence of hypovolemia. In general, a CVP below 10 mm Hg can be considered to indicate that the patient is more likely to respond to fluid resuscitation, but exceptions to this rule exist. A high CVP suggests a certain blood volume but does not guarantee sufficient LV filling.

Clinically, CVP can be assessed by evaluation of the degree of jugular distention ⁶ or liver enlargement. A single CVP measurement is not very useful and is not a good indicator of a positive response to fluids; an increase in CVP without a concurrent increase in cardiac output is not only useless but also harmful, because it will lead to increased edema formation.

Access to Blood in Superior Vena Cava

Measuring the central venous oxygen saturation (ScvO₂) is a surrogate for measurement of the true mixed venous oxygen saturation (). Although absolute values of ScvO₂ are not identical to single values, trends in ScvO₂ over time follow the same pattern as trends in , making ScvO₂ a useful measure in patients who do not require an arterial catheter.⁷ ScvO₂ can be obtained either intermittently (by withdrawal of blood samples) or continuously (with the use of a catheter equipped with fiberoptic fibers).

Trace Analysis

Analysis of the CVP waveform can provide some interesting information. In particular, a large y descent indicates a restrictive cardiac state, but not all restrictive patterns are associated with this finding.

Access

The central venous catheter generally is introduced via the internal jugular vein; the subclavian vein also can be used, although the risk of pneumothorax may be somewhat higher with this route. Peripherally inserted central catheters can also be placed, via the cephalic vein, basilic vein, or brachial vein. Introduction of a femoral catheter through the abdominal inferior vena cava to the right atrium can also yield reliable CVP measurements.⁸ The use of femoral catheters, however, is associated with a greater risk of infections and thrombophlebitis.⁹

Complications

Complications of central venous catheterization are related primarily to puncture of the central vein: Hemothorax can be life-threatening, especially in the presence of severe respiratory failure. In the presence of unilateral pathology, the catheter must be introduced on the affected side. Arterial puncture resulting in a local hematoma is not uncommon, but hematoma formation usually is without major consequences. Bedside ultrasonography can help guide the introduction of the catheter into the vein. Excessive advancement of a long catheter in a small patient can result in arrhythmias; such arrhythmias have been described with advancement of the catheter tip into the right ventricle, but this problem can be identified by the presence of an RV trace on the monitor display.

Catheter-related infections constitute the major long-term complication. Adherence to basic hygiene guidelines can decrease the incidence of catheter-related sepsis. Triple-lumen catheters may be associated with a higher incidence of catheter-related infection,¹⁰ primarily as a result of increased catheter manipulation. The use of antimicrobial-coated catheters may decrease the risk of infections,¹¹ but fears remain about the risks of development of resistant organisms.¹² Routine replacement of catheters after 3 to 7 days is not recommended.¹³

Pulmonary Artery Catheters

What Do They Offer?

PACs allow collection of data on right atrial, pulmonary artery, and pulmonary artery occlusive pressures (Fig. 4.3); flow (cardiac output); and oxygenation ().

Figure 4.3 Pressure waveforms. A, The normal right atrial (RA) tracing. The a wave is the RA pressure rise resulting from atrial contraction and follows the P wave of the electrocardiogram (ECG). On simultaneous ECG and RA tracings it usually occurs at the beginning of the QRS complex. The c wave, caused by closure of the tricuspid valve, follows the a wave and is coincident with the beginning of ventricular systole. Atrial relaxation (x descent) is followed by a passive rise in RA pressure resulting from atrial filling during ventricular systole and occurs during the T wave of the simultaneously recorded ECG. The y descent reflects the opening of the tricuspid valve and passive atrial emptying. B, The normal right ventricular (RV) tracing. The sharp rise in RV pressure (1) is due to isometric contraction and is followed by a rapid pressure decrease (2) as blood is ejected through the pulmonary valve. This rapid ejection is followed by a phase of more reduced pressure decrease, which is often reflected in a small step in the downslope of the RV pressure waveform (3). The subsequent sharp decline in RV pressure (4) occurs as a result of isometric relaxation and is noted once the RV pressure falls below the pulmonary artery (PA) pressure (with consequent closure of the pulmonary valve). As RV pressure falls below RA pressure, the tricuspid valve opens, and passive refilling (5) of the right ventricle occurs, followed by atrial contraction, causing a biphasic wave of ventricular filling to appear on the RV tracing (6). C, The normal pulmonary arterial waveform. A pulmonary artery systolic elevation is caused by ejection of blood from the right ventricle, followed by a decline in pressure as RV pressure falls. As RV pressure falls below pulmonary artery pressure, the pulmonary valve closes, which causes a momentary rise in the declining pulmonary artery pressure. This is the dicrotic notch characteristic of the pulmonary arterial (and also the systemic arterial) waveform. The pulmonary artery systolic wave usually occurs in synchrony with the T wave of the ECG. Pulmonary artery diastolic pressure (PADP) does not fall below RA pressure and therefore is higher than right ventricular end-diastolic pressure (RVEDP): it is an approximation to left ventricular end-diastolic pressure (LVEDP). D, The normal pulmonary artery occlusion pressure (PAOP) waveform. The waveform of the pulmonary capillary wedge pressure (PCWP) is subject to the same mechanical variables as the RA waveform, but because of the damping that occurs through the pulmonary circulation, the waves and descents often are less distinct. Similarly, the mechanical events are recorded later in the cardiac cycle, as seen on the ECG. Thus, the a wave is not seen until after the QRS complex, and the v wave occurs after the T wave of the ECG. The PCWP is a closer approximation to LVEDP than is PADP. (From Grossman W: Cardiac catheterization. In Braunwald E (ed): Heart Disease: A Textbook of Cardiovascular Medicine, 3rd ed. Philadelphia, WB Saunders, 1992.)

Pressures

Right Atrial Pressure

As indicated earlier, the RAP is identical to the CVP in the vast majority of cases.

Pulmonary Artery Occlusion Pressure

When the balloon on the catheter is inflated, it causes an obstruction (becomes wedged) in a small branch of the pulmonary artery, interrupting the flow of blood locally (but blood flow continues normally in the rest of the pulmonary circulation), so that (assuming the absence of an abnormal obstacle) a continuous column of blood is present between the tip of the PAC and the left atrium. This pulmonary artery occlusion pressure (PAOP), or pulmonary artery wedge pressure (PAWP), generally reflects the left atrial pressure well. Nevertheless, a number of steps must be taken to ensure the adequacy of the measurement.

A first question is whether the PAOP reflects the pressure in the pulmonary veins and not the alveolar pressure. The tip of the catheter should be in a West zone III position, where a continuous column of blood exists between the catheter tip and the left atrium (Fig. 4.4). These considerations are less important with fluid optimization and with today’s lower positive end-expiratory pressures (PEEPs).

Figure 4.4 The position of the pulmonary artery catheter tip in relation to the zones of the theoretical lung model described by West. For pulmonary artery occlusion pressure (PAOP) to be a valid estimate of “left heart” filling pressure, a continuous column of blood must exist between the catheter tip and the left atrium. In zones I and II, pulmonary vasculature is either totally or partially compressed by the intra-alveolar pressure, and measurements of PAOP will be misleading. PA, alveolar pressure; Pa, pulmonary artery pressure; Pv, pulmonary venous pressure. (From Marini JJ: Respiratory Medicine and Intensive Care for the House Officer. Baltimore, Williams & Wilkins, 1991.)

To exclude a possible influence of airway pressure on PAOP readings, the changes in PAOP can simply be compared with the changes in pulmonary artery pressure (PAP) during the respiratory cycle. If PAOP reflects the pressure within the pulmonary veins, these changes should be identical, because the pulmonary artery and vein should be subjected to identical changes in intrathoracic pressures. If, on the other hand, the catheter tip is not in a West zone III, the changes in PAOP will be more significant than the changes in PAP. In these latter conditions, either fluid administration or some reduction in the PEEP level may abolish the differences.

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