The legs are inspected for signs of peripheral arterial or venous vascular disease. The visible signs of arterial vascular disease include pale, shiny legs with sparse hair growth. Venous disease creates an edematous limb with deep red rubor, brown discoloration, and, frequently, leg ulceration. A comparison of arterial and venous disease is presented in Table 11-1.

The nail beds are inspected for signs of discoloration or cyanosis. Clubbing in the nail bed is a sign associated with long-standing central cyanotic heart disease or pulmonary disease with hypoxemia.⁴ Clubbing describes a nail that has lost the normal angle between the finger and the nail root; the nail becomes wide and convex. The terminal phalanx of the finger also becomes bulbous and swollen, sometimes described as drumstick fingers.⁵ Clubbing is rare. It denotes long-standing severe central cyanosis (Figure 11-1). Platelet-derived vascular endothelial growth factor is thought to play a key role in the development of clubbing.⁶

Peripheral cyanosis, a bluish discoloration of the nail bed, is more commonly seen. Peripheral cyanosis results from a reduction in the quantity of oxygen in the peripheral extremities from arterial disease or decreased CO. Clubbing never occurs as a result of peripheral cyanosis.

The jugular veins of the neck are inspected for a noninvasive estimate of intravascular volume and pressure. The internal jugular veins are observed for jugular vein distention (JVD) (Figure 11-2 and Box 11-1). JVD is caused by an elevated central venous pressure (CVP).⁷ This occurs with fluid volume overload and right ventricular dysfunction, which elevates right atrial pressure.⁸ The right internal jugular vein can be used for measurement of CVP in centimeters of water (Figure 11-3 and Box 11-2).^9–11

The abdominojugular reflux sign can assist with the diagnosis of right ventricular failure. This noninvasive test is used in conjunction with measurement of JVD. The procedure for assessing abdominojugular reflux is described in Box 11-3. A positive abdominojugular reflux sign is an increase in the jugular venous pressure (CVP equivalent) of 4 cm or more sustained for at least 15 seconds.¹²

The thoracic cage is divided with imaginary vertical lines (sternal, midclavicular, axillary, vertebral, and scapular), and the intercostal spaces are divided with horizontal lines to serve as reference points in locating or describing cardiac findings (Figure 11-4). The anterior thorax is inspected for the apical impulse, sometimes referred to as the point of maximal impulse (PMI). The apical impulse occurs as the left ventricle contracts during systole and rotates forward, causing the left ventricular apex of the heart to hit the chest wall. The apical impulse is a quick, localized, outward movement normally located just lateral to the left midclavicular line at the fifth intercostal space in the adult patient (Figure 11-5). The apical impulse is the only normal pulsation visualized on the chest wall. In the patient without cardiac disease, PMI may not be noticeable (see Figure 11-5).

Seven pairs of bilateral arterial pulses are palpated. The examination incorporates bilateral assessment of the carotid, brachial, radial, ulnar, popliteal, dorsalis pedis, and posterior tibial arteries. The pulses are palpated separately and compared bilaterally to check for consistency. Pulse volume is graded on a scale of 0 to 3+ (Box 11-4). The abdominal aortic pulse can also be palpated. If a distal pulse cannot be palpated using light finger pressure, a Doppler ultrasound stethoscope can increase diagnostic accuracy.¹³ It is important to mark the location of the audible signal with an indelible ink marker pen for future evaluation of pulse quality. The radial and ulnar arterial pulses must be evaluated for collateral flow before an arterial line is inserted; this test, known as the Allen test, is described in Box 11-5.

Capillary refill assessment is a maneuver that uses the patient’s nail beds to evaluate arterial circulation to the extremity and overall perfusion. The nail bed is compressed to produce blanching, after which release of the pressure should result in a return of blood flow and baseline nail color within 2 seconds.14 The severity of arterial insufficiency is directly proportional to the amount of time required to reestablish baseline flow and color.

Edema is fluid accumulation in the extravascular spaces of the body. The dependent tissues within the legs and sacrum are particularly susceptible. The nurse should observe whether the edema is dependent, unilateral or bilateral, pitting or nonpitting. The amount of edema is quantified by measuring the circumference of the limb or by pressing the skin of the feet, ankles, and shins against the underlying bone. Edema is a symptom associated with several diseases, and further diagnostic evaluation is required to determine the cause. Although no universal scale for pitting edema exists, one example is a 0 to 4+ system (Table 11-2).

Blood pressure measurement is an essential component of every complete physical examination. Hypertension is diagnosed as a systolic blood pressure (SBP) of 140 mm Hg or higher, or a diastolic blood pressure (DBP) of 90 mm Hg or above.15 Prehypertension is defined as an SBP in the range of 120 to 139 mm Hg in association with a DBP between 80 to 89 mm Hg.^15,16 The incidence of hypertension in the United States has increased dramatically as a result of an aging population and an increasing prevalence of obesity. During the period from 1999 to 2000, 65 million adults in the United States were hypertensive, compared with 50 million in 1988 through 1994—an increase of 30%.¹⁷ Risk of hypertension increases with older age. More than 90% of people who have a normal blood pressure at 55 years of age eventually develop hypertension, according to findings from the Framingham Heart Study.¹⁶

In the critical care setting, systemic blood pressure can be measured directly or indirectly. Arterial monitoring devices that directly measure arterial pressure by means of an invasive catheter technique are considered the gold standard.¹⁸ Accurate use of a stethoscope and sphygmomanometer or electronic measuring devices can produce indirect blood pressure values that closely reflect direct measurements.¹⁹

When a healthy person stands, 10% to 15% of the blood volume is pooled in the legs; this reduces venous return to the right side of the heart, which decreases CO and lowers arterial blood pressure.20 The fall in blood pressure activates baroreceptors; the subsequent reflex increase in sympathetic outflow and parasympathetic inhibition leads to peripheral vasoconstriction, with increased heart rate and contractility.²⁰ Postural (orthostatic) hypotension occurs when the SBP drops 10 to 20 mm Hg or the diastolic BP drops 5 mm Hg after a change from the supine to the upright posture.^20,21 It is usually accompanied by complaints of dizziness, lightheadedness, or syncope. If a patient experiences these symptoms, it is important to complete a full set of postural vital signs before increasing the patient’s activity level (Box 11-6). Orthostatic hypotension can have many causes. The three most common causes of orthostatic vital sign changes (i.e., drop in blood pressure and rise in heart rate) observed in critical care are:

Box 11-6

Measurement of Postural (Orthostatic) Vital Signs

Guidelines

1. Record blood pressure (BP) and heart rate (HR) in each position.

2. Do not remove cuff between measurements.

3. Record all associated signs and symptoms.

4. Clearly document patient position.

Technique

1. Keep patient as flat as possible for 10 minutes before the initial assessment.

2. Patient supine: Obtain initial BP and HR measurements.

3. Patient sitting with legs hanging: Measure immediately and after 2 minutes.

4. Patient standing: Measure immediately and after 2 minutes. If BP and HR are stable but orthostasis is suspected, BP and HR can be repeated every 2 minutes. Note that this is rarely practical for the critically ill patient.

Results

Normal Changes

HR increases by 5 to 20 beats/min (transiently).

Systolic BP drops 10 mm Hg.

Diastolic BP drops 5 mm Hg.

Positive Orthostasis

Drop in systolic BP by more than 20 mm Hg.

Drop in diastolic BP by more than 10 mm Hg within 3 minutes.

In normal physiology, the strength of the pulse fluctuates throughout the respiratory cycle. When the “pulse” is measured using the SBP, the pressure is observed to decrease slightly during inspiration and to rise slightly during respiratory exhalation. The normal difference is 2 to 4 mm Hg.8 One exception is cardiac tamponade, where the blood pressure decline is abnormally large during inspiration. In general, an inspiratory decline of SBP greater than 10 mm Hg is considered diagnostic of pulsus paradoxus.^22–24 The traditional technique for measuring pulsus paradoxus using a sphygmomanometer and a blood pressure cuff¹⁸ and pulse oximetry^22–24 is described in Box 11-7.¹⁸ If the patient is hypotensive, pulsus paradoxus is more accurately assessed in the critical care unit by monitoring a pulse oximetry waveform or an indwelling arterial catheter waveform.^22–24

Auscultation of the heart is the most challenging part of the cardiac physical examination, and, in an era of increasing technological demands, it is daunting to new clinicians.25 To summarize the advice given by most experts, the examiner must do the following:

First and Second Heart Sounds.

Normal heart sounds are referred to as the first heart sound (S₁) and the second heart sound (S₂). S₁ is the sound associated with mitral and tricuspid valve closure and is heard most clearly in the mitral and tricuspid areas. S₂ (aortic and pulmonic closure) can be heard best at the second intercostal space to the right and left of the sternum (see Figure 11-5). Both sounds are high-pitched and heard best with the diaphragm of the stethoscope (Box 11-8). Each sound is loudest in an auscultation area located downstream from the actual valvular component of the sound, as shown in Figure 11-6.

Box 11-8

Characteristics of the First and Second Heart Sounds

FIRST HEART SOUND (S1)	SECOND HEART SOUND (S2)
High-pitched	High-pitched
Loudest in mitral area (apex)	Loudest in aortic area (base)

SPLIT S1	SPLIT S2
Normal split less than 20 msec	Normal split less than 30 msec
Split heard best in tricuspid area	Split heard best in pulmonic area
Important to differentiate between split S1 and S4	↑ Split with inhalation
Occurs immediately before	↓ Split with exhalation
carotid upstroke

↑, increased; ↓, decreased.

The use of the anticoagulant heparin added to the normal saline (NS) flush setup to maintain catheter patency remains controversial. A systematic review of the literature showed that a heparinized flush solution is associated with a longer duration of catheter patency.31 Other units do not use heparin because of concern about development of the autoimmune condition known as heparin-induced thrombocytopenia (HIT). This is sometimes described as a “heparin allergy” and, when present, is associated with a dramatic drop in platelet count, and thrombus formation. Some trials have not found platelet counts or catheter duration to be influenced by heparin.^32,33 If heparin is used in the flush infusion, monitoring the trend in the platelet count is recommended.³⁴

The flush solutions and tubing are usually changed every 72 to 96 hours. There is variety; some hospitals change flush solutions every 24 hours. For this reason, it is essential to be familiar with the specific written procedures that concern hemodynamic monitoring equipment in each critical care unit.

To ensure accuracy of hemodynamic pressure readings, two baseline measurements are necessary:

All bedside hemodynamic monitoring systems have alarm limits that are preset to ensure patient safety. The alarms must be sufficiently distinctive and audible to be heard over the noise of a typical critical care unit. Patient safety guidelines are designed to promote clinical alarm goals. Some clinical situations create special challenges with respect to alarm safety. Nursing care actions that cause the patient to move in the bed will often trigger the alarms. Temporarily silencing the sound for 1 to 3 minutes while continuing to observe the bedside monitor is appropriate. The real challenge occurs when a patient is restless or fidgeting with IV tubing or electrodes, resulting in the alarms bring constantly triggered because the monitor is unable to evaluate the ECG rhythms and hemodynamic waveforms effectively. It is tempting to silence these “nuisance alarms” permanently. The alarms should not be turned off, however, because the patient is left in a vulnerable position if a dysrhythmia or hemodynamic complication arises. Clinical interventions to ameliorate the root cause of the problem (e.g., restlessness) are more appropriate. Education of nurses about the risk of becoming desensitized to the sound of beside alarms is also important.38 Key issues concerning monitor alarms are presented in the Patient Safety Priorities box on Clinical Alarms.