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 H₂