Insertion and Allen Test. 

Several major peripheral arteries are suitable for receiving a catheter and for long-term hemodynamic monitoring. The most frequently used site is the radial artery.² The femoral artery is a larger vessel that is also frequently cannulated. Other smaller arterials such as the dorsalis-pedis, axillary, or brachial arteries are avoided if possible, and only used when other arterial access is unavailable.

The major advantage of the radial artery is the supply of collateral circulation to the hand provided by the ulnar artery through the palmar arch in most people. Before radial artery cannulation, collateral circulation must be assessed by using Doppler flow or by the modified Allen test according to institutional protocol.2,7 In the Allen test the radial and ulnar arteries are compressed simultaneously. The patient is asked to clench and unclench the hand until it blanches. One of the arteries is then released, and the hand should immediately flush from that side. The same procedure is repeated for the remaining artery.

Infection. 

Infection was once believed to be rare in arterial catheters because of the rapid arterial blood flow. New evidence suggests that arterial catheters are associated with the same risk of bloodstream infections as central venous catheters (CVCs).⁹ This means that infection prevention measures must be just as meticulous for arterial catheters as for CVCs.⁹

Perfusion Pressure. 

A MAP greater than 60 mm Hg is necessary to perfuse the coronary arteries. A higher MAP may be required to perfuse the brain and the kidneys. A MAP between 70 and 90 mm Hg is ideal for the cardiac patient to decrease left ventricular (LV) workload. After a carotid endarterectomy or neurosurgery, a MAP of 90 to 110 mm Hg may be more appropriate to increase cerebral perfusion pressure. Systolic and diastolic pressures are monitored in conjunction with the MAP as a further guide to the accuracy of perfusion. If CO decreases, the body compensates by constricting peripheral vessels to maintain the blood pressure. In this situation, the MAP may remain constant but the pulse pressure (difference between systolic and diastolic pressures) narrows. The following examples explain this point:

Mr. A: BP, 90/70 mm Hg; MAP, 76 mm Hg

Mr. B: BP, 150/40 mm Hg; MAP, 76 mm Hg

Both patients have a perfusion pressure of 76 mm Hg, but they are clinically very different. Mr. A is peripherally vasoconstricted, as is demonstrated by the narrow pulse pressure (90/70 mm Hg). His skin is cool to touch, and he has weak peripheral pulses. Mr. B has a wide pulse pressure (150/40 mm Hg), warm skin, and normally palpable peripheral pulses. Nursing assessment of the patient with an arterial line includes comparison of clinical findings with arterial line readings, including perfusion pressure and MAP.

Pulse Pressure. 

A clinical example of hemodynamic nursing assessment can be seen in patient JW 1 day after coronary artery bypass grafting (CABG). JW recently has been weaned from dopamine (Intropin) and sodium nitroprusside (Nipride) and received an IV diuretic, 20 mg of furosemide (Lasix). He has voided 800 mL of urine via the urinary catheter during the past 2 hours. JW’s MAP remains at 80 mm Hg, but his pulse pressure has narrowed by 30 mm Hg from 120/60 to 100/70 mm Hg. His heart rate (HR) has increased from 90 to 110 beats per minute. This clinical situation is not uncommon after furosemide administration, but the narrowed pulse pressure and increased HR may indicate hypovolemia. The nurse caring for JW will monitor the trend of the MAP. If the MAP begins to decrease and JW shows signs of a low CO, his physician will be notified. In most nonemergency situations, following the trend of the arterial pressure is more valuable than an isolated measurement.

Cuff Blood Pressure. 

If the arterial line becomes unreliable or dislodged, a cuff pressure can be used as a reserve system.¹⁰ In the normotensive, normovolemic patient, little difference exists between the arm cuff blood pressure and the intravascular catheter pressure, and differences of 5 to 10 mm Hg do not generally alter clinical management. The situation is different if the patient has a low CO or is in shock. The concern is that the cuff pressure may be unreliable because of peripheral vasoconstriction, and an arterial line is generally required. It is usual practice to compare a cuff pressure after the arterial line is inserted. A recent study in hypotensive patients found that a MAP calculated from the arm cuff blood pressure was comparable to the intravascular arterial MAP.¹¹ However, blood pressure cuffs placed on the thigh or ankle were less accurate in hypotensive patients.¹¹

Decreased Arterial Perfusion. 

Specific problems with heart rhythm can translate into poor arterial perfusion if CO decreases. Poor perfusion may be seen as a single, nonperfused beat after a premature ventricular contraction (PVC) (Fig. 14-3) or as multiple, nonperfused beats (Fig. 14-4). In ventricular bigeminy, every second beat is poorly perfused (Fig. 14-5). A disorganized atrial baseline resulting from atrial fibrillation creates a variable arterial pulse because of the differences in stroke volume (SV) between each beat (Fig. 14-6). All of these examples illustrate that when two beats are close together, the left ventricle does not have time to fill adequately, and the second beat is inadequately perfused or is not perfused at all.

Pulse Deficit. 

A pulse deficit occurs when the apical HR and the peripheral pulse are not equal. In the critical care unit, this can be seen on the bedside monitor. Normally, there is one arterial upstroke for each QRS, and if there are more QRS complexes than arterial upstrokes, a pulse deficit is present, as shown in Figures 14-3 and 14-6. To identify a pulse deficit in an unmonitored patient, a stethoscope is placed over the apex of the heart. The heartbeat can be heard, but it cannot be felt as a radial pulse. To determine whether a pulse deficit is significant, it is necessary to evaluate the clinical impact on the patient and whether any change in MAP or pulse pressure has occurred. Generally, the more nonperfused beats, the more serious the problem.

Pulsus Paradoxus. 

Pulsus paradoxus is a decrease of more than 10 mm Hg in the arterial waveform that occurs during inhalation (inspiration). It is caused by a fall in CO as a result of increased negative intrathoracic pressure during inhalation. As pressure within the thorax falls, blood pools in the large veins of the lungs and thorax, and SV is decreased. The procedure for identification of pulsus paradoxus is discussed in Chapter 13 (see Box 13-9).

In certain clinical conditions, the pulsus paradoxus is obvious and can be clearly seen on an arterial waveform. It can be used as a clinical diagnostic test in a patient with cardiac tamponade, pericardial effusion, or constrictive pericarditis.¹² Pulsus paradoxus commonly occurs in hypovolemic surgical patients who are mechanically ventilated with large tidal volumes (see Fig. 14-3).

Pulsus Alternans. 

In pulsus alternans, every other arterial pulsation is weak. This sometimes occurs in individuals with advanced LV heart failure.

Damped Waveform. 

If the arterial monitor shows a low blood pressure, it is the responsibility of the nurse to determine whether it is a patient problem or a problem with the equipment, as described in Table 14-2. A low arterial blood pressure waveform is shown in Figure 14-7. In this case, the digital readout correlated well with the patient’s cuff pressure, confirming that the patient was hypotensive. This arterial waveform is more rounded, without a dicrotic notch, compared with the normal waveform in Figure 14-2. A damped (flattened) arterial waveform is shown in Figure 14-8. In this case, the patient’s cuff pressure was significantly higher than the digital readout, representing a problem with equipment. A damped waveform occurs when communication from the artery to the transducer is interrupted and produces false values on the monitor and oscilloscope. Damping is caused by a fibrin “sleeve” that partially occludes the tip of the catheter, by kinks in the catheter or tubing, or by air bubbles in the system. Troubleshooting techniques (see Table 14-2) are used to find the origin of the problem and to remove the cause of damping.

Underdamped Waveform. 

Another cause of arterial waveform distortion is underdamping, also called overshoot or fling. Underdamping is recognized by a narrow, upward systolic peak that produces a falsely high systolic reading compared with the patient’s cuff blood pressure, as shown in Figure 14-9. The overshoot is caused by an increase in dynamic response or increased oscillations within the system.

Fast-Flush Square Waveform Test. 

The monitoring system’s dynamic response can be verified for accuracy at the bedside by the fast-flush square waveform test, also called the dynamic frequency response test.⁵ The nurse performs this test to ensure that the patient pressures and waveform shown on the bedside monitor are accurate.⁵ The test makes use of the manual flush system on the transducer. Normally, the flush device allows only 3 mL of fluid/hr. With the normal waveform displayed, the manual fast-flush procedure is used to generate a rapid increase in pressure, which is displayed on the monitor oscilloscope. As shown in Figure 14-10, the normal dynamic response waveform shows a square pattern with one or two oscillations before the return of the arterial waveform. If the system is overdamped, a sloped (rather than square) pattern is seen. If the system is underdamped, additional oscillations—or vibrations—are seen on the fast-flush square wave test. This test can be performed with any hemodynamic monitoring system. If air bubbles, clots, or kinks are in the system, the waveform becomes damped, or flattened, and this is reflected in the square waveform result.

This is an easy test to perform, and it should be incorporated into nursing care procedures at the bedside when the hemodynamic system is first set up, at least once per shift, after opening the system for any reason, and when there is concern about the accuracy of the waveform.⁵ If the pressure waveform is distorted or the digital display is inaccurate, the troubleshooting methods described in Table 14-2 can be implemented. The nurse caring for the patient with an arterial line must be able to assess whether a low MAP or narrowed perfusion pressure represents decreased arterial perfusion or equipment malfunction. Assessment of the arterial waveform on the oscilloscope, in combination with clinical assessment, and use of the square waveform test will yield the answer.

Alarms. 

All critically ill patients must have the hemodynamic monitoring alarms on and adjusted to sound an audible alarm if the patient should experience a change in blood pressure, HR, respiratory rate, or other significant monitored variable. The key issues concerning monitor alarms are presented in Box 14-2.

Insertion. 

The large veins of the upper thorax—subclavian (SC) and internal jugular (IJ)—are most commonly used for percutaneous CVC line insertion.⁴ The femoral vein in the groin is used when the thoracic veins are not accessible. All three major sites have advantages and disadvantages.

Air Embolus. 

The risk of air embolus, although uncommon, is always present for the patient with a central venous line in place. Air can enter during insertion¹⁵ through a disconnected or broken catheter by means of an open stopcock, or air can enter along the path of a removed CVC.^16,17 This is more likely if the patient is in an upright position, because air can be pulled into the venous system with the increase in negative intrathoracic pressure during inhalation. If a large volume of air is infused rapidly, it may become trapped in the right ventricular outflow tract, stopping blood flow from the right side of the heart to the lungs. Based on animal studies, this volume is approximately 4 mL/kg.¹⁸ If the air embolus is large, the patient will experience respiratory distress and cardiovascular collapse. An auscultatory clinical sign specifically associated with a large venous air embolism is the mill wheel murmur.^15,16,19 A mill wheel murmur is a loud, churning sound heard over the middle chest, caused by the obstruction to right ventricular outflow. Treatment involves immediately occluding the external site where air is entering, administering 100% oxygen, and placing the patient on the left side with the head downward (left lateral Trendelenburg position).¹⁹ This position displaces the air from the right ventricular outflow tract to the apex of the heart, where the air may be aspirated by catheter intervention or gradually absorbed by the bloodstream as the patient remains in the left lateral Trendelenburg position. Precautions to prevent an air embolism in a CVP line include using only screw (Luer-Lock) connections, avoiding long loops of intravenous tubing, and using closed-top screw caps on the three-way stopcock.

Thrombus Formation. 

Clot formation (thrombus) at the CVC site is unfortunately common. Thrombus formation is not uniform; it may involve development of a fibrin sleeve around the catheter,²⁰ or the thrombus may be attached directly to the vessel wall. Other factors that promote clot formation include rupture of vascular endothelium, interruption of laminar blood flow, and physical presence of the catheter, all of which activate the coagulation cascade. The risk of thrombus formation is higher if insertion was difficult or there were multiple needlesticks. Gradual thrombus formation may lead to “sudden” CVC occlusion. Usually, the CVC becomes more difficult to withdraw blood from, or the CVP waveform becomes intermittently damped over a period of hours or even 1 to 2 days and is reported as “needing frequent flushes” to remain patent. This situation is caused by the continued lengthening of a fibrin sleeve that extends along the catheter length from the insertion site past the catheter tip.²⁰ Some catheters are heparin coated to reduce the risk of thrombus formation, although the risk of HIT does not make this a benign option. Sometimes, CVC complications are additive; for example, the risk of catheter-related infection is increased in the presence of thrombi, where the thrombus likely serves as a culture medium for bacterial growth. Because of concerns over the development of HIT many hospitals use a saline-only flush to maintain CVC patency.^21,22

Infection. 

Infection related to the use of CVCs is a major problem. The incidence of infection strongly correlates with the length of time the CVC has been inserted, longer insertion times leading to a higher infection rate.4,23 CVC-related infection is identified at the catheter insertion site or as a bloodstream infection (septicemia). Systemic manifestations of infection can be present without inflammation at the catheter site. No decrease in bloodstream infections was found when catheters were routinely changed and this practice is no longer recommended.⁴ When a CVC is infected it must be removed and a new catheter inserted in a different site. If a catheter infection is suspected, the CVC should not be changed over a guidewire because of the risk of transferring the infection.⁴ Most infections are transmitted from the skin, and infection prevention begins prior to insertion of the CVC. Insertion guidelines state that the physician must use effective hand-washing procedures, clean the insertion site with 2% chlorhexidine gluconate in 70% isopropyl, use sterile technique during catheter insertion, and maintain maximal sterile barrier precautions.⁴ In many hospitals the nurse is authorized to stop the procedure if these insertion infection control guidelines are not followed. A daily review to determine whether the catheter is still required is recommended to ensure CVCs are removed promptly when no longer needed (Box 14-3).⁴

All clinicians must use good hand-washing technique and follow aseptic procedures during site care and any time the CVC system is entered to withdraw blood, give medications, or change tubing.⁴ Site dressings impregnated with chlorhexidine are recommended to lower CVC infection rates.⁴

Central Venous Pressure—Volume Assessment. 

The time-honored practice of using the CVP value to assess central volume status has now been challenged.²⁴ A landmark systematic review of the literature revealed a weak relationship between the CVP measurement and blood volume.²⁴ Nor was a low CVP value always reliable in predicting who would respond to a fluid challenge.²⁴ In patients with a CVP between 0 and 5 mm Hg, up to 25% do not respond to a fluid challenge as expected.²⁵ Overall only about half of critically ill patients respond as expected to a fluid challenge.²⁴ In this situation the clinician must look at other indices of poor tissue perfusion such as an elevated lactate level, low base deficit, or decreased urine output.²⁵

Water Versus Mercury Central Venous Pressure. 

CVP values are measured in millimeters of mercury (mm Hg) if bedside hardwire monitoring is used. If a patient is admitted from a medical–surgical unit with a water manometer CVP and clinicians want to know the relationship between the two values, it involves a straightforward calculation based on the following standard relationship: 1 mm Hg (mercury pressure) is equivalent to 1.36 cm H₂O (water pressure). Although the numeric value in cm H₂O will be higher, the values are clinically equivalent for the specific patient. To convert water manometer pressure to mercury pressure, the water-pressure value is divided by 1.36 (H₂O ÷ 1.36). To convert mercury pressure to water pressure, the mercury value is multiplied by 1.36 (mm Hg × 1.36).

Removal. 

Removal of the CVC usually is a nursing responsibility. Complications are infrequent, and the ones to anticipate are bleeding and air embolus. Recommended techniques to avoid air embolus during CVC removal include removing the catheter when the patient is supine in bed (not in a chair) and placing the patient flat or in reverse Trendelenburg position if the patient’s clinical condition permits this maneuver. Patients with heart failure, pulmonary disease, and neurologic conditions with raised intracranial pressure (ICP) should not be placed flat. If the patient is alert and able to cooperate, he or she is asked to take a deep breath to raise intrathoracic pressure during removal. After removal, to decrease the risk of air entering by a “track,” an occlusive dressing is applied to the site. If bleeding at the site occurs after removal, firm pressure is applied. If a patient has prolonged coagulation times, fresh-frozen plasma or platelets may be prescribed before CVC removal.

Patient Position. 

To achieve accurate CVP measurements, the phlebostatic axis is used as a reference point on the body, and the transducer or water manometer zero must be level with this point. If the phlebostatic axis is used and the transducer or water manometer is correctly aligned, any head of bed position of up to 60 degrees may be used for accurate CVP readings for most patients.⁵ Elevating the head of the bed is especially helpful for the patient with respiratory or cardiac problems who cannot tolerate a flat position.

Central Venous Pressure Waveform Interpretation. 

The normal right atrial (CVP) waveform has three positive deflections—a, c, and v waves—that correspond to specific atrial events in the cardiac cycle (Fig. 14-11). The a wave reflects atrial contraction and follows the P wave seen on the ECG. The downslope of this wave is called the x descent and represents atrial relaxation. The c wave reflects the bulging of the closed tricuspid valve into the right atrium during ventricular contraction; this wave is small and not always visible but corresponds to the QRS-T interval on the ECG. The v wave represents atrial filling and increased pressure against the closed tricuspid valve in early diastole. The downslope of the v wave is named the y descent and represents the fall in pressure as the tricuspid valve opens and blood flows from the right atrium to the right ventricle.

Cannon Waves. 

Dysrhythmias can change the pattern of the CVP waveform. In a junctional rhythm or after a PVC, the atria are depolarized after the ventricles if retrograde conduction to the atria occurs. This may be seen as a retrograde P wave on the ECG and as a large combined ac or cannon wave on the CVP waveform (Fig. 14-12). These cannon waves can be easily detected as large pulses in the jugular veins. Other pathologic conditions, such as advanced right ventricular failure or tricuspid valve insufficiency, allow regurgitant backflow of blood from the right ventricle to the right atrium during ventricular contraction, producing large v waves on the right atrial waveform. In atrial fibrillation, the CVP waveform has no recognizable pattern because of the disorganization of the atria.

Preload. 

Clinicians commonly describe the hemodynamic numbers related to preload as filling pressures. These values refer to the pressures resulting from the volumes in the atria and ventricles. These pressure numbers include pulmonary artery diastolic pressure (PADP) and PAOP (or wedge pressure), which measure preload in the left side of the heart, and CVP, which measures preload in the right side of the heart.

Preload is the volume in the ventricle at end-diastole. Because diastole is the filling stage of the cardiac cycle, the volume in the ventricle at end-diastole represents the presystolic volume available for ejection for that cardiac cycle. LV volume can be measured directly during cardiac catheterization but it is not generally measured in the critical care unit. The principle is that the presence of blood within the ventricle creates pressures that can be measured by the PA catheter and transducer and can be displayed on the bedside monitor.

Measurement of Preload. 

When the PA catheter is correctly positioned with the tip in one of the large branches of the PA, the only valve between the PA catheter tip and the left ventricle is the mitral valve. During diastole, when the mitral valve is open, no obstruction exists between the tip of the PA catheter and the left ventricle (Fig. 14-14). The LV preload volume creates left ventricular end-diastolic pressure (LVEDP). This is measured clinically by the PAOP or “wedge” pressure. The PAOP and PADP are the values most often referred to in this chapter, because they are the values used in clinical practice. Normal left atrial pressure (LAP) or PAOP is 5 to 12 mm Hg.

Frank-Starling Law of the Heart. 

Clinically the PAOP has significance because a change in LV volume (preload) is reflected by a change in the measured PAOP (wedge pressure). Change in preload relies on the Frank-Starling law of the heart. This concept states that the force of ventricular ejection is directly related to two elements:

1. Volume in the ventricle at end-diastole (preload)

2. Amount of myocardial stretch placed on the ventricle as a result

If the volume in the left ventricle is low, CO is also suboptimal. If intravenous fluids (volume) are infused, CO increases as LV volume and myocardial fiber stretch increase. This is true up to a point. Past this point, more fluid volume overdistends the ventricle and stretches the myocardial fibers so much that CO decreases. This scenario is seen clinically in the setting of acute heart failure with pulmonary edema. The increased volume in the overdistended left ventricle raises pressure in the left ventricle, left atrium, and pulmonary veins (that drain into the left atrium), and it ultimately raises pulmonary capillary pressures measured as an increased wedge pressure (PAOP). The impact of preload on CO is represented in Figures 14-15 and 14-16, using the Frank-Starling curve as a model.

Pulmonary Hypertension. 

Specific clinical conditions can alter the normal PADP/PAOP relationship.³⁹ In ARDS with acute pulmonary hypertension, the pulmonary arterial systolic and diastolic pressures are independently raised above the LV pressures. In this clinical situation the PADP will not accurately reflect function of the left side of the heart. The numeric difference between the PADP and the PAOP value is called a gradient. If a large gradient exists between the PAOP and PADP when the PA catheter is inserted, the patient has pulmonary hypertension (Table 14-4, illustration C).

TABLE 14-4

CLINICAL INTERPRETATION OF PULMONARY ARTERY WAVEFORMS

PA PRESSURE	CLINICAL INTERPRETATION	WAVEFORM INTERPRETATION*
Pulmonary artery systolic (PAS) pressure	PAS pressure reflects the systolic pressure in the pulmonary vasculature. Waveform A is a normal waveform. The elevated values in pulmonary hypertension may be caused by idiopathic sources, some congenital heart defects, or lung disease.	A
Pulmonary artery diastolic (PAD) pressure	In the patient with healthy lung vasculature, PAD pressure reflects left ventricular end-diastolic pressure (LVEDP), as shown in waveform B. Even if the patient experiences heart failure, the pulmonary artery occlusion pressure (PAOP) and PAD increase together.	B
	In the presence of acute respiratory distress syndrome or pulmonary hypertension, PAD pressure is not an accurate reflection of PAOP, as shown in waveform C.	C
Mean pulmonary artery pressure (PAP mean or PAPM)	PAP mean pressure is used in the calculation of pulmonary vascular resistance (PVR) and pulmonary vascular resistance index (PVRI), as described in Table 14-1. High mean pressures can reflect cardiac or pulmonary disease. Low mean pressures reflect hypovolemia. Waveform D shows PAP mean placement.	D
Pulmonary artery occlusion pressure (PAOP) or pulmonary artery wedge pressure (PAWP)	In the healthy patient, PAOP reflects blood in the left ventricle at end-diastole (LVEDP). The normal PAOP waveform is a left atrial waveform, as shown in waveform E.	E
	If a patient has mitral valve regurgitation, the v waves are larger than normal, increasing PAOP and possibly not reflecting true LVEDP, as shown in waveform F. PAOP is elevated in many cardiac disease states in which LV function is compromised. PAOP is low in hypovolemic states.	F

^*Pressures on the y axis are given in millimeters of mercury (mm Hg).

Afterload. 

Afterload is defined as the pressure the ventricle generates to overcome the resistance to ejection created by the arteries and arterioles. It is a calculated measurement derived from information obtained from the PA catheter. As a response to increased afterload, ventricular wall tension rises. After a decrease in afterload, wall tension is lowered. The technical name for afterload is systemic vascular resistance (SVR).

Systemic Vascular Resistance. 

Resistance to ejection from the left side of the heart is estimated by calculating the SVR. The formula, normally calculated by the bedside computer, is as follows:

SVR=MAP−CVPCO×80

The normal value is 800 to 1200 dyn·sec·cm⁻⁵. To index this value to the patient’s body surface area, the cardiac index (CI) is placed in the formula in the same position as the CO. The critical care nurse frequently manipulates prescribed vasoactive medications to therapeutically alter SVR. In general, the lower the SVR, the higher the CO.

Contractility. 

Many factors have an impact on contractility, including preload volume as measured by PAOP, SVR, myocardial oxygenation, electrolyte balance, positive and negative inotropic medications, and the amount of functional myocardium available to contribute to contraction. These factors can have a positive inotropic effect, enhancing contractility, or a negative inotropic effect, decreasing contractility. Significant factors related to contractility that can be measured by the PA catheter include preload filling pressures, SVR, and CO. Additional contractility numbers can be calculated and are displayed in the hemodynamic profile on the bedside monitor. These include left and right ventricular stroke work index values (LVSWI and RVSWI). These values estimate the force of cardiac contraction (see Table 14-1).

Preload has an impact on contractility by means of Starling’s mechanism. As volume in the ventricle rises, contractility increases. If the ventricle is overdistended with volume, contractility falls (see Figs. 14-15 and 14-16). SVR alters contractility by changes in resistance to ventricular ejection. If SVR is high, contractility is decreased. If SVR is low, contractility is augmented. Hypoxemia acts as a negative inotrope. The myocardium must have oxygen available to the cells to contract efficiently.

Right Atrial Lumen. 

The proximal lumen is situated in the right atrium and is used for intravenous infusion, CVP measurement, withdrawal of venous blood samples, and injection of fluid for CO determinations. This port is often described as the right atrial port, also called the CVP port.

Pulmonary Artery Lumen. 

The distal PA lumen is located at the tip of the PA catheter and is situated in the PA. It is used to record PAPs and can be used for withdrawal of blood samples to measure mixed venous blood gases (e.g., Svo₂).

Balloon Lumen. 

The third lumen opens into a balloon at the end of the catheter that can be inflated with 0.8 mL (7 Fr) to 1.5 mL (7.5 Fr) of air. The balloon is inflated during catheter insertion after the catheter reaches the right atrium to assist in forward flow of the catheter and to minimize right ventricular ectopy from the catheter tip. The balloon is also inflated to obtain the PAOP measurements when the PA catheter is correctly positioned in the PA.

Thermistor Lumen. 

The fourth lumen is a thermistor (temperature sensor) used to measure changes in blood temperature. It is located 4 cm from the catheter tip and is used to measure thermodilution CO. The connector end of the lumen is attached directly to the CO computer.

Additional Features. 

If continuous Svo₂ is measured, the catheter has an additional fiberoptic lumen that exits at the tip of the catheter (see Fig. 14-17C). If cardiac pacing is used, two PA catheter methods are available. One type of catheter has three atrial (A) and two ventricular (V) pacing electrodes attached to the catheter so that when it is properly positioned, the patient can be connected to a pacemaker and be AV paced. The other catheter method uses a specific transvenous pacing wire that is passed through an additional catheter lumen and exits into the right ventricle if ventricular pacing is required. A right ventricular volumetric PA catheter is available that measures SV in the right ventricle.

Right Atrial Waveform. 

As the PA catheter is advanced into the right atrium during insertion, a right atrial waveform must be visible on the monitor, with recognizable a, c, and v waves (see Fig. 14-18). The normal mean pressure in the right atrium is 2 to 5 mm Hg. Before passage through the tricuspid valve, the balloon at the tip of the catheter is inflated for two reasons. First, it cushions the pointed tip of the PA catheter so that if the tip comes into contact with the right ventricular wall, it will cause less myocardial irritability and, consequently, fewer ventricular dysrhythmias. Second, inflation of the balloon assists the catheter to float with the flow of blood from the right ventricle into the PA. It is because of these features and the balloon that PA catheters are described as flow-directional catheters.

Right Ventricular Waveform. 

The right ventricular waveform is distinctly pulsatile, with distinct systolic and diastolic pressures. Normal right ventricular pressures are 20 to 30 mm Hg systolic and 0 to 5 mm Hg diastolic. Even with the balloon inflated, it is not uncommon for ventricular ectopy to occur during passage through the right ventricle. All patients who have a PA catheter inserted must have simultaneous ECG monitoring, with defibrillator and emergency resuscitation equipment nearby.

Pulmonary Artery Waveform. 

As the catheter enters the PA, the waveform again changes. The diastolic pressure rises. Normal PA pressures range from 20 to 30 mm Hg systolic over 10 mm Hg diastolic. A dicrotic notch, visible on the downslope of the waveform, represents closure of the pulmonic valve.

Pulmonary Artery Occlusion Waveform (Wedge). 

While the balloon remains inflated, the catheter is advanced into the wedge position. This maneuver produces the PAOP. The waveform decreases in size and is nonpulsatile, reflecting a normal left atrial tracing with a and v wave deflections. This is known as a wedge tracing, because the balloon is “wedged” into a small pulmonary vessel, but it is technically described as the PAOP (see Fig. 14-18). The balloon occludes the pulmonary vessel so that the PA catheter tip and lumen are exposed only to left atrial pressure (LAP) and are protected from the pulsatile influence of the right ventricle and PA. When the balloon is deflated, the catheter should spontaneously float back into the PA. When the balloon is reinflated, the wedge tracing should be visible. The normal PAOP ranges from 5 to 12 mm Hg.

After insertion, the introducer is sutured to the skin, the catheter, which lies within the introducer, is secured with tape or with a specialized catheter securement device. A chest radiograph is taken to verify placement. If the catheter is advanced too far into the pulmonary bed, the patient is at risk for pulmonary infarction. If the PA catheter is not sufficiently advanced into the PA, it will not be useful for PAOP readings. However, in many critical care units, if the patient’s PADP and PAOP values approximate (within 0 to 3 mm Hg), the PADP is reliably used to follow the trend of LV filling pressure (preload). This prevents possible trauma from frequent balloon inflation; in such a situation, the PA catheter is consciously pulled back into a nonwedging position in the PA.

After insertion of the catheter, the chest radiograph or fluoroscopy is used to verify the PA catheter position to make sure that it is not looped or knotted in the right ventricle and to rule out pneumothorax or hemorrhagic complications. A thin plastic sleeve is placed on the outside of the catheter when it is inserted to maintain sterility of the part of the PA catheter that exits from the patient. If the PA catheter is not in the desired position or if it migrates out of position, it can be repositioned. Use of this external sleeve on PA catheters has been associated with lower rates of bloodstream infection.⁴

Patient Position. 

The patient does not need to be flat for accurate pressure readings to be obtained. In the supine position, when the transducer is placed at the level of the phlebostatic axis, a head-of-bed position from flat up to 60 degrees is appropriate for most patients.⁵ It is important to know that PADP and PAOP measurements in the lateral position may be significantly different from those taken when the patient is lying supine. If there is concern about the validity of pressure readings in a particular patient, it is more reliable to take measurements with the patient on his or her back, with the head of bed elevated from flat to 60 degrees as tolerated. After a patient changes position, a stabilization period of 5 to 15 minutes is recommended before taking pressure readings.⁵ The stabilization period is usually longer if the patient has LV dysfunction or is hemodynamically unstable.

Respiratory Variation. 

All PADP and PAOP (wedge) tracings are subject to respiratory interference, especially when the patient is on a positive-pressure, volume-cycled ventilator.⁵ During the positive-pressure inhalation phase, the increase in intrathoracic pressure may “push up” the PA tracing, producing an artificially high reading (Fig. 14-19A). During inhalation with spontaneous breaths, negative intrathoracic pressure “pulls down” the waveform, producing an erroneously low measurement (see Fig. 14-19B). To minimize the impact of respiratory variation, the PADP is read at end-expiration, which is the most stable point in the respiratory cycle when intrapleural pressures are close to zero. If the digital number fluctuates with respiration, a printed readout on paper can be obtained to verify true PADP. In some clinical settings, ECG signals or airway pressure and flow are recorded simultaneously with the PADP/PAOP tracing to identify end-expiration.⁵

Positive End-Expiratory Pressure. 

Some clinical diagnoses, such as ARDS, require the use of high levels of PEEP set with the ventilator to treat refractory hypoxemia. If a PEEP of greater than 10 cm H₂O is used, PAOP (wedge) and PAPs will be artificially elevated, and CO may be negatively affected. Because of this impact of PEEP, in the past, patients in some critical care units were taken off the ventilator to record PAP measurements. It has since been shown that this practice closes alveoli, decreases the patient’s oxygenation level, and may result in persistent hypoxemia.

Because patients remain on PEEP for treatment, they remain on it during measurement of PAPs. In this situation, the trend of PA readings is more important than one individual measurement. The most important factor is not one individual measurement or the absolute number obtained; it is instead the trend of the measurements being used as a basis for clinical interventions to support and improve cardiopulmonary function in the critically ill.

Avoiding Complications. 

Potential cardiac complications include ventricular dysrhythmias, endocarditis, valvular damage, cardiac rupture, and cardiac tamponade. Potential pulmonary complications include rupture of a PA, PA thrombosis, embolism or hemorrhage, and infarction of a segment of lung. The PA catheter tracing is continuously monitored to ensure that the catheter does not migrate forward into a spontaneous wedge or PAOP position. A segment of lung can suffer infarction if the wedged catheter occludes an arteriole for a prolonged period. If the catheter is spontaneously wedged the catheter must be gently pulled back out of the wedge position to prevent pulmonary infarction.

Infection is always a risk with a PA catheter. The risks are similar to those discussed in the section on CVCs (see Box 14-3).

Pulmonary Artery Catheter Removal. 

PA catheters can be safely removed from the patient by critical care nurses competent in this procedure.5,46 Removal is not usually associated with major complications. Sometimes there are PVCs as the catheter is pulled through the right ventricle.⁵

Thermodilution Cardiac Output Bolus Method. 

The bolus thermodilution method is performed at the bedside and results in CO calculated in liters per minute. Three CO values that are within a 10% mean range are obtained at one time and are averaged to calculate CO. A known amount (5 mL) of iced or, more typically, 10 mL of room-temperature NS solution is injected into the proximal lumen of the PA catheter. The injectate exits into the right atrium and travels with the flow of blood past the thermistor (temperature sensor) located at the distal end of the catheter in the PA. The injectate can be delivered by hand injection using individual syringes of saline. Frequently, a closed in-line system attached to a 500-mL bag of NS is used as a reservoir to deliver the individual injections.

Sometimes, the right atrial (proximal) port is clotted and not usable. If another right atrial port is available, it can be substituted. However, if a usable port is not available, to ensure accurate CO data, a new PA catheter is inserted.

Cardiac Output Curve. 

The thermodilution CO method uses the indicator-dilution method, in which a known temperature is the indicator. It is based on the principle that the change in temperature over time is inversely proportional to blood flow. Blood flow can be diagrammatically represented as a CO curve on which temperature is plotted against time (Fig. 14-20A). Most hemodynamic monitors display this CO curve, which must then be interpreted to determine whether the CO injection is valid. The normal curve has a smooth upstroke, with a rounded peak and a gradually tapering down-slope. If the curve has an uneven pattern, it may indicate faulty injection technique, and the CO measurement must be repeated. Patient movement or coughing also alters the CO measurement (see Fig. 14-20B).

Injectate Temperature. 

If the CO is within the normal range, it is equally accurate whether iced or room temperature injectate is used. However, if the COs are extremely high or very low, iced injectate may be more accurate. To ensure accurate readings, the difference between injectate temperature and body temperature must be at least 10° C, and the injectate must be delivered within 4 seconds, with minimal handling of the syringe to prevent warming of the solution. This is particularly important if iced injectate is used. With all delivery systems, the injectate is delivered at the same point in the respiratory cycle, usually end-exhalation.

Patient Position and Cardiac Output. 

In the normovolemic, stable patient, reliable CO measurements can be obtained in a supine position (patient lying on his or her back) with the head of the bed elevated up to 60 degrees.⁵ If the patient is hypovolemic or unstable, leaving the head of the bed in a flat position or only slightly elevated is the most clinically appropriate choice. CO measurements performed when the patient is turned to the side are not considered as accurate as those performed with the patient in the supine position.

Clinical Conditions That Alter Cardiac Output. 

Two clinical conditions produce errors in the thermodilution CO measurement: tricuspid valve regurgitation and ventricular septal rupture. If the patient has tricuspid valve regurgitation, the expected flow of blood from the right atrium to the PA is disrupted by backflow from the right ventricle to the right atrium. This creates a lower CO measurement than the patient’s actual output. If the person has an intracardiac left-to-right shunt, as occurs after ventricular septal rupture, the thermodilution CO measures the large pulmonary volume and records a higher CO than the patient’s true systemic output.

Continuous Invasive Cardiac Output Measurement. 

The bolus thermodilution method is reliable but performed intermittently. Continuous CO monitoring using a PA catheter is also frequently used in clinical practice. One method employs a thermal filament on the PA catheter to emit small energy signals (the indicator) into the bloodstream. These signals are then detected by the thermistor near the tip of the PA catheter. The equivalent of an indicator curve is created, and a CO value is calculated from this data.

Calculated Hemodynamic Profiles. 

For the patient with a thermodilution PA catheter in place, additional hemodynamic information can be calculated using routine vital signs, CO, and body surface area (BSA). These measurements are calculated using specific formulas that are indexed to a patient’s body size using the DuBois body area surface chart or the computer program associated with the current generation of hemodynamic monitors.

The calculated values used in the hemodynamic profiles are described in Table 14-1. Clinical use of these profiles is described in two case studies. In Hemodynamic Profile 1 (Box 14-4), the example is a step-by-step interpretation of the hemodynamic profile to familiarize the reader with use of calculated values. In Hemodynamic Profile 2 (Box 14-5), the example uses only values indexed to body weight and illustrates the impact of treatment on these values over time.