Chapter 8 Monitoring
Monitoring, particularly of the cardiovascular and respiratory systems, is an integral part of the care of critically ill patients. Advances in technology have resulted in the widespread use of integrated monitoring systems capable of displaying multiple parameters simultaneously on bedside screens. Although most observers would agree that patient care is improved by sophisticated monitoring, it has proven difficult to confirm this objectively. For instance, the value of pulse oximetry is almost universally accepted, but a large randomized trial involving more than 20,000 patients was unable to demonstrate a survival benefit from using this monitoring tool.1,2 Thus, it is not surprising that for complex, user-dependent monitors such as echocardiography and the pulmonary artery catheter (PAC), an outcome benefit has not been clearly demonstrated and, at least in the case of the PAC, considerable controversy has resulted regarding its ongoing use.3–5
Monitoring can be harmful in a number of ways. First, the monitoring device can cause direct patient injury. For example, vascular catheters can cause a variety of complications at the time of their insertion and removal and present an ongoing risk for infection. Second, inappropriate interventions may be undertaken based on misleading data or the misinterpretation of accurate data, resulting in patient harm. Good patient care involves the integration of data from a range of sources: history, examination, monitoring, and investigations. Overreliance on a single parameter is potentially harmful. Conversely, a multitude of complex numeric data, particularly data involving derived or calculated indexes, creates “noise” that can confuse and overwhelm the clinician.
In this chapter, a number of monitors that are used in the intensive care unit (ICU) are discussed. Additional topics are discussed elsewhere: blood gas monitoring in Chapter 31; respiratory monitoring in Chapter 27; echocardiography in Chapter 7; neuromuscular monitoring in Chapter 4; and routine postoperative monitoring in Chapter 17. The techniques of insertion and the complications of intravascular catheters are outlined in Chapter 40.
Despite the absence of a demonstrable survival advantage, pulse oximetry has been identified as the single most useful monitor for the prevention of adverse patient events,6 and it is used routinely on virtually all patients in the ICU. Pulse oximetry utilizes the fact that the absorption spectra of blood vary depending on its oxygen saturation: oxygenated blood appears red, and deoxygenated blood appears blue. A standard oximeter probe contains two light-emitting diodes: one that emits red light (wavelength 660 nm) and one that emits near-infrared light (wavelength 940 nm). The ratio of light absorption at the two wavelengths is detected and used to calculate oxygen saturation. Light that passes through tissues is absorbed by arterial blood, capillary blood, venous blood, and nonblood components (bone, muscle, etc.). By eliminating the nonpulsatile component of light absorption, the oxygen saturation of arterial blood can be estimated. Arterial oxygen saturation obtained from a pulse oximeter is designated SPO2 to distinguish it from arterial oxygen saturation obtained from a blood gas analyzer, which is designated Sao2. In addition to SPo2, pulse oximeters measure heart rate and generate a pulse waveform, which provides a crude measure of peripheral perfusion. These secondary functions are useful when the pulse oximeter is used as the sole monitor.
Despite the obvious advantages of being able to rapidly and noninvasively assess arterial oxygen saturation, it must be remembered that pulse oximetry does not guarantee the adequacy of either oxygen delivery (see Equation 1-14) or ventilation (see Equation 1-17). In the presence of profound anemia, marked tissue hypoxemia can arise despite a normal SPo2. In patients to whom supplemental oxygen is being administered, profound hypoventilation and respiratory acidosis can be present in spite of a normal SPo2.
Occasionally, SPo2 readings are unreliable. Sources of error include poor peripheral perfusion, movement artifacts, electrical interference, dyes (e.g., methylene blue), and the presence of abnormal hemoglobin. Abnormal forms of hemoglobin include methemoglobin, which can occur in high concentrations due to nitric oxide or nitroprusside overdose, and carboxyhemoglobin, which is caused by carbon monoxide poisoning. Measurements of SPo2 may be unreliable in patients with extremely low arterial oxygen saturation (e.g., <70%).
The electrocardiograph (ECG) is essential for the diagnosis of cardiac arrhythmias and is extremely useful for the identification of myocardial ischemia and infarction. Also, specific ECG abnormalities provide supporting evidence for a wide range of cardiac disorders. The physiologic basis of the ECG and its relationship to the action potential is discussed in Chapter 1. Specific ECG abnormalities are covered in the relevant chapters, particularly 8 and 21.
The standard 12-lead ECG involves the placement of 10 electrodes on the patient in specific positions: one on each limb and six across the chest (Fig. 8-1). To ensure good contact between skin and electrode, the skin should be first cleaned with alcohol, gently abraded with fine sandpaper and, if necessary, shaved. From these 10 electrodes, 12 leads are recorded. A lead is obtained by recording the difference in electrical potential between two electrodes. Leads may be either bipolar or unipolar. With a bipolar lead, the signal is obtained from two active electrodes: one connected to the positive pole and one connected to the negative terminal of the ECG machine. With a unipolar lead, the signal is obtained using one active electrode (connected to the positive pole of the ECG machine) and an indifferent electrode, recorded at zero potential by connecting two or three limb electrodes through a resistor to the negative terminal of the electrocardiograph.
Figure 8.1 The chest leads. The top diagram shows the correct placement of the chest leads. The bottom diagram shows the orientation of the chest leads to the heart in the horizontal plane when looking from above. The arrow identifies the net direction of current flow during ventricular depolarization in the horizontal plane.
Six leads view the heart in the frontal plane (I, II, III, aVR, aVL, aVF) and six leads (V1 through V6) view the heart in the horizontal plane. The three standard leads (I, II, III) are bipolar leads; each lead records the potential difference between two limbs (Fig. 8-2). The augmented limb leads (aVR, aVL, aVF) are unipolar leads that record the potential difference between one limb and an indifferent composite electrode: aVR is obtained from the right arm; aVL from the left arm, and aVF from the left leg. The standard and augmented limb leads record the magnitude of the electrical signal in specific directions within the frontal plane, as shown in Fig. 8-3. The chest leads are unipolar leads that record the potential difference between the surface of the chest and an indifferent composite electrode. The orientation of the chest leads to the heart in the horizontal plane is shown in Figure 8-1.
Figure 8.2 The standard bipolar limb leads (I, II, and III). Each lead records the potential difference between two limbs. With lead I, the negative terminal of the ECG machine is connected to the right arm (RA) and the positive terminal, to the left arm (LA). With lead II, the negative terminal of the ECG machine is connected to the right arm and the positive terminal to the left leg (LL). With lead III, the negative terminal of the ECG machine is connected to the left arm, and the positive terminal is connected to the left leg.
Figure 8.3 The axes of the three bipolar standard limb leads (I, II, and III) and three unipolar augmented limb leads (aVL, aVF, and aVR). The direction from which each lead “looks” at the heart in the frontal plane is shown. If the direction of ventricular depolarization is toward a lead (i.e., toward the arrow), the QRS complex in that lead is positive. The size of the QRS deflection is dependent on the magnitude and direction of ventricular depolarization.
For accurate diagnosis of myocardial ischemia or cardiac arrhythmias, a standard 12-lead ECG should always be obtained. In patients who have undergone recent cardiac surgery, the sternal dressing may preclude obtaining leads V1, V2, and V3. For continuous ECG monitoring in the intensive care unit (ICU) or coronary care unit it is usual to use a 5-electrode system involving electrodes attached to each of the four limbs and a chest electrode attached at the V5 position. For convenience and to reduce motion artifact, the limb leads are normally placed on the shoulders and hips. From these five electrodes, seven leads can potentially be obtained (I, II, III, aVR, aVL, aVF, V5); it is usual to display simultaneously leads II and V5 on the patient monitor. (Somewhat confusingly, this arrangement is commonly referred to as a 5-lead ECG.) P waves are usually most clearly identified in lead II, therefore this lead is usually the best for diagnosing cardiac arrhythmias. V5 is the most sensitive lead for diagnosing myocardial ischemia.
Three-electrode systems (often called 3-lead ECG) are also used. In the standard form, electrodes are attached to the left and right arms and left leg, allowing the standard and augmented limb leads to be obtained. Various modifications of the three-electrode systems have been developed to improve the detection of ischemia.
All ECG machines use filters to reduce artifacts. High-frequency filters reduce electrical interference; low-frequency filters reduce movement artifact and signal distortion resulting from poor electrode contact. The lower frequency limit must be sufficiently low to display accurately low-frequency waveforms such as the P and T waves, and the higher limit must be sufficiently high to record high-frequency waveforms such as the QRS complex and to display rapid tachycardias. To display a range of ECG waveforms accurately, a frequency range of 0.05 to 100 Hz should be used, although this may be reduced if there is marked interference.
Adjusting the gain or calibration controls can alter the size of the displayed ECG. In certain situations, altering the default settings is useful: if the QRS complex is large, reducing the gain minimizes overlap between waveforms and reduces the likelihood of double-counting the heart rate; if the QRS complexes are small, increasing the gain may improve detection of the R wave, which is necessary for the calculation of heart rate and for the synchronization of shocks during electrical cardioversion.
The standard gain setting used when recording a 12-lead ECG is 10 mm = 1 mV. This setting must be used when the amplitude of ECG components, such as R wave height and ST segment deviation, are measured manually (parameters calculated automatically take the gain setting into account). The standard sweep speed is 25 mm/sec. A sweep speed of 50 mm/sec is occasionally useful to show waveforms more clearly, particularly the identification of P waves. The standard setting of 25 mm/sec must be used when the duration of various ECG components, such as PR interval or QT interval, are calculated manually.
ECGs are recorded onto a grid pattern composed of large and small squares. Large squares have dimensions of 5 mm by 5 mm and represent 0.5 mV on the vertical axis and 0.2 sec on the horizontal axis, assuming standard sweep and gain settings. Small squares have dimensions of 1 mm by 1 mm and represent 0.04 sec in the horizontal axis and 0.1 mV in the vertical axis. The various components of an individual ECG complex are shown in Figure 8-4. A normal 12-lead ECG is shown in Figure 8-5.
(Image modified from Wagner GS: Marriot’s Practical Electrocardiography, ed. 9. Fig. 2.10, p. 30. Philadelphia, Lippincott Williams and Wilkins, 1994.)
Heart rate is determined by dividing 300 by the number of large squares between each QRS complex (each large square represents 0.2 seconds, and there are 300 lots of 0.2 seconds in a minute). Once the heart rate is greater than 100, the number of small squares should also be considered, and the rate is calculated by dividing 1500 by the number of small squares.
The P wave represents atrial contraction. P waves are normally evenly rounded and either positive or negative in all leads except V1, where a biphasic wave is sometimes seen. Its duration should be less than 0.12 seconds and its amplitude less than 0.25 mV. Right atrial hypertrophy (e.g., due to pulmonary hypertension) results in peaked P waves. This is known as P-pulmonale and is best seen in leads II, III, and aVF. Left atrial hypertrophy (e.g., due to mitral stenosis) results in bifid P waves. This is known as P-mitrale and is also best seen in leads II, III, and aVF. Abnormalities of P-wave morphology also occur with atrial arrhythmias.
The normal PR interval is 0.10 to 0.22 seconds and is determined by the speed of conduction through the atrioventricular node. The PR interval varies inversely with heart rate and gradually lengthens with increasing age. A short PR interval is seen in some preexcitation syndromes, and a long PR interval is seen in first-degree and Wenckebach-type second-degree heart block (see Chapter 21).
The Q wave is a small negative deflection that precedes the R wave. Small Q waves (<0.03 seconds in duration) are a normal finding in all leads except V1 through V3, where they are always pathologic. Q waves of any size may be normal in leads III and aVR. Pathologic Q waves are indicative of transmural myocardial infarction (see Chapter 18). They develop within a few hours of infarction and are permanent.
The R wave is the first upward deflection that appears in the QRS complex. From leads V1 through V4 the R wave normally increases in amplitude and duration. Loss of this normal progression is indicative of loss of left ventricular muscle mass. The S wave is a downward deflection that follows the R wave and also reflects ventricular mass. The S wave is normally large in V1, larger in V2, and then decreases in size from V3 through V6.
The QRS complex represents ventricular depolarization and has a normal duration of 0.07 to 0.10 seconds. A wide QRS indicates abnormal conduction within the ventricles (e.g., bundle branch block) or a ventricular origin of an impulse (e.g., ventricular pacing or complete heart block).
The QRS amplitude has wide normal limits, ranging from as low as 5 mm in obese subjects to as high as 30 mm in slim males. Causes of large QRS amplitude include physical fitness and ventricular hypertrophy. Causes of low QRS amplitude include obesity, emphysema, and pericardial effusion.
The net direction of current flow in the heart at any moment can be represented as a vector. If the vector is directed toward a particular lead during ventricular depolarization, the QRS complex is predominantly positive (R wave > S wave). If the vector is directed away from that lead, the QRS is predominantly negative (S wave > R wave). If the vector is perpendicular to the lead, the R wave and S wave are equal. The direction of depolarization through the ventricles in the frontal plane is called the QRS axis and is determined by examination of the six limb leads (I, II, III, aVL, aVR, aVF). The following steps can be used to determine the frontal-plane QRS axis (see Fig. 8-3):
Figure 8-6 shows the normal range for the frontal-plane QRS axis along with the criteria for the diagnosis of left, right, and extreme axis deviation. Common causes of axis deviation are listed in Table 8-1.
(Image redrawn from Galen S, Wagner GS: Marriot’s Practical Electrocardiography, ed. 9. Fig. 3.9, p. 45. Philadelphia, Lippincott Williams and Wilkins, 1994.)
|Left Axis Deviation|
|Left anterior hemiblock (Table 21-1)|
|Inferior myocardial infarction|
|Left ventricular hypertrophy|
|Right Axis Deviation|
|Left posterior hemiblock (Table 21-1)|
|Right ventricular hypertrophy (including COPD)|
|Lateral or apical myocardial infarction|
|Extreme Axis Deviation (rare)|
|Right ventricular hypertrophy|
|Apical myocardial infarction|
COPD, chronic obstructive pulmonary disease.
Given that the net direction of current flow during ventricular systole is from the base to the apex of the heart and is dominated by the left ventricle, then based on Figure 8-1 it can be appreciated that the QRS complexes in leads V1 and V2 are normally negative, and the QRS complexes in leads V5 and V6 are normally positive. With right ventricular hypertrophy, the electrical axis in the horizontal plane shifts rightward, resulting in a progressive increase in R wave amplitude in leads V1 and V2 such that with severe right ventricular hypertrophy, the QRS becomes positive in these leads. In contrast, with left ventricular hypertrophy there is accentuation of the normally dominant R wave in V5 and V6 and the development of deep S waves in V1 and V2. Ventricular hypertrophy may also result in ST segment depression and T wave inversion (strain pattern), which may be difficult to distinguish from ischemia. The ECG findings in right and left ventricular hypertrophy are summarized in Table 8-2.
|Abnormality||Left Ventricular Hypertrophy||Right Ventricular Hypertrophy|
|QRS conduction||Partial or complete left bundle branch block||Partial or complete right bundle branch block|
|Strain pattern (ST segment depression and T wave inversion)||Leads V3-V6||Leads V1-V3|
|Vertical plane||Leftward shift in QRS axis||Rightward shift in QRS axis|
|Horizontal plane||Large S waves in V2 and V3||Large R waves in V1 and V2 with severe hypertrophy, the QRS complex may become positive|
|Large R waves in V5 and V6|
|Atrial hypertrophy||P-mitrale: bifid P waves in II, II, aVF||P-pulmonale: peaked P waves in II, II, aVF|
The T wave represents ventricular repolarization. T waves are normally positive, but negative T waves are normal findings in leads aVR and V1 (and in young people, in V2). The causes of pathologic T-wave inversion include myocardial ischemia and infarction, ventricular strain, and treatment with digoxin. Following a myocardial infarction, T-wave inversion develops within 12 to 48 hours and is usually permanent. There is a wide variation in both the duration and the amplitude of the T wave. Flattening T waves are seen with hypokalemia, and peaked T waves are seen with hyperkalemia.
The ST segment is measured from the J point (the point where the ST segment meets the QRS complex) to the beginning of the T wave (see Fig. 8-4). Slight (<1 mm) upsloping, downsloping, or horizontal ST segment depression is a normal variant. Up to 4 mm of ST segment elevation in leads V1 through V3 may also be a normal finding, especially in young males.
Pathologic ST segment elevation may indicate myocardial infarction, left ventricular aneurysm, pericarditis, or bundle branch block. With myocardial infarction, ST segment elevation usually develops within a few minutes and resolves within 24 to 48 hours. The distribution of ST segment elevation can be used to help localize the zone of infarction (see Chapter 18). ST segment elevation across a wide range of leads is common following cardiac surgery and probably represents a pericardial reaction. A clue to this diagnosis is that the ST segment elevation is usually mild and is not limited to a specific coronary territory.
ST segment depression is commonly associated with myocardial ischemia but is also seen with ventricular strain, digoxin therapy, hypokalemia, and conduction abnormalities such as bundle branch block. Mild upsloping ST segment depression is seen with tachycardia. ST segment depression due to ischemia is typically horizontal or downsloping (Fig. 8-7). Upsloping ST depression is not usually indicative of ischemia. Unlike ST segment elevation, the distribution of ST segment depression does not reliably localize the region of ischemia.