Easily applied disposable electrodes use a combination of wet gel and silver/silver chloride sensors to detect electrical activity from the myocardium. This electrical activity is amplified and displayed continuously (it can also be printed or stored as a permanent record). In addition, variations in the electrical impedance are detected, which allows a respiratory rate to be calculated. Alarm parameters may be set on bedside monitors for extremes in heart rates or for subtle ST segment changes. The initial default lead viewed on the bedside monitor is usually lead II. The size (gain) is automatic but may be altered to allow the components of complexes to be more prominent.

This noninvasive, continuous modality identifies heart rate abnormalities, ischemic changes, and rhythm disturbances. Associated changes in blood pressure or atrial pressure tracings can lend additional weight to the interpretation of rhythm disturbances perhaps prompting an earlier investigation. Similarly, they may convey reassurance during technical problems such as dislodged ECG electrodes or electrical interference giving rise to a spurious visual display.

Deciphering any underlying rhythm abnormality with bedside monitoring may be difficult (see Chapter 77). High heart rates and limited monitor fidelity may conceal p waves, blur QRS morphology, and conceal A-V dissociation. Note that paying careful attention to invasive monitoring such as the CVP waveform or arterial pulse contour may help unmask these abnormalities. Running the ECG speed at 50 mm/s rather than 25 mm/s and altering the gain may be useful but ultimately any concerns should be investigated further with a 12-lead ECG. Additionally, interrogating atrial wires if present or using an esophageal probe may reveal a more accurate picture of the underlying rhythm.

A reduction in the size of the complexes may be significant. A fluid interface between the myocardium and chest wall (e.g., pericardial effusion) or poor electrical generation due to myocarditis or cardiomyopathy can reduce the size of the complexes and should prompt further investigation. ECG abnormalities should be promptly and thoroughly investigated and may be the first indication of impending circulatory dysfunction.

Incorrect lead placement is the most common technical problem during ECG monitoring. Distortions or “noise” created by electrical interference from the power grid, adjacent equipment, or muscle movements are reduced by using highfrequency filters.

The CO₂ concentration is measured by infrared spectroscopy and sampled by one of two methods: aspiration from the breathing circuit (sidestream analyzer) or measured inline (mainstream analysis) by a flow-through adapter and sensor. The normal baseline on the capnogram should have a CO₂ concentration of zero, reflecting inspiratory as well as early expiratory (anatomic dead space) gas; this is followed by a sharp upstroke, reflecting mid-exhalation and increasing alveolar gas; this is followed by the plateau phase, which represents a leveling off of alveolar gas. The capnogram then abruptly falls to zero, as the expiratory phase is terminated and inspiratory gas dilutes out the remaining CO₂. The point on the capnogram plateau just prior to the abrupt fall-off is called the end-tidal CO₂ (ETCO₂) concentration and approximates the arterial PCO₂ (PaCO₂) under conditions of normal ventilation to perfusion matching in the lung.

Normally, the end-tidal CO₂ level approximates the arterial CO₂ level and the arterial to end-tidal CO₂ gradient (PaCO_2-ETCO₂) is <2-3 mm Hg. Hypercapnia that results from hypoventilation is associated with a normal arterial to ETCO₂ gradient. Hypercapnia that results from wasted or dead space ventilation is associated with an elevated arterial to ETCO₂ gradient. The arterial to ETCO₂ gradient rises because pulmonary perfusion (Q) is low compared to ventilation (V) (an increased V:Q ratio). Diseases characterized by a decreased V:Q ratio and intrapulmonary shunt (perfusion without ventilation) do not contribute significantly to the arterial to ETCO₂ gradient. These principles make ETCO₂ monitoring a useful hemodynamic monitor. Low CO (and therefore low pulmonary blood flow) or congenital heart disease with relatively low pulmonary perfusion will exhibit low ETCO₂ concentration and an increased end-tidal to arterial PCO₂ gradient. End-tidal CO₂ monitoring can also be used to assess the effectiveness of chest compressions and the return of circulatory function during cardiac arrest. A sudden reduction in pulmonary blood flow (e.g., Blalock-Taussig shunt obstruction or pulmonary embolus) will suddenly decrease the ETCO₂ concentration.

Technical factors such as gas sampling method as well as the nature of the respiratory circuit can affect the accuracy of ETCO₂ measurements. The most common technical problem is a leak around the endotracheal tube, which lowers the ETCO₂ measurement and increases the arterial to ETCO₂ gradient.

Noninvasive blood pressure monitoring is safe, simple, relatively reliable, reproducible, and inexpensive. It should be routinely performed in all children receiving inpatient care. The idea of sphygmomanometry was conceived by von Basch in the 1870s. However, the first indirect method, based on applying a known external pressure to occlude an artery, was developed in the 1890s. A cuff placed around the arm or leg abolishes the pulse when inflated above the patient’s systolic blood pressure. Deflating the cuff slowly allows turbulent blood flow in the artery to develop, which can be appreciated either by auscultation or by observing the oscillations of a manometer reflecting pulsatile flow. Automated oscillometric technology with cuff pressure sensors and a microprocessor controlling the sequence of inflation and incremental deflation is now the standard of care in critical care units. Maximal oscillation amplitude corresponds to the mean arterial pressure. A microprocessor algorithm derives the systolic and diastolic pressure from the change in slope of oscillation amplitude. Oscillation frequency readily yields the heart rate.

The frequency of obtaining blood pressure measurement depends on the severity of disease. Frequent measurements (every 1-3 minutes) are advised during resuscitation or procedures such as intubation. During these occasions care must be taken to ensure that an inflated cuff will not interfere with the administration of drugs from a distal IV or interrupt pulse oximetry monitoring. Ulnar nerve palsy is a potential complication when pressures are measured frequently for a prolonged period.

Technical difficulties can occur if the patient is small, obese, edematous, agitated (moving), shivering (local muscle contraction causes pseudohypertension), extremely tachycardic, or suffering from burns. Error may arise with an inappropriate size cuff. The cuff should cover at least two thirds of the upper arm, and one too small may overestimate blood pressure and vice versa. Petechial rashes have been noted in the area under the cuff usually reflecting repeated external pressure but may reveal an underlying coagulation defect. Oscillometric blood pressure is not suitable for pressure measurement during nonpulsatile flow such as extracorporeal membrane oxygenation. Finally, the oscillometric-derived blood pressure tends to underestimate or show a lower-than-actual diastolic pressure (12).

Invasive arterial monitoring is the “gold standard” but is not without risk. Its higher degree of complexity increases the chance of technical errors and complications. However, a number of advantages over its noninvasive counterpart exist: improved accuracy, continuous beat-to-beat measurement, waveform analysis, and frequent arterial blood sampling. The Reverend Stephen Hales first demonstrated invasive blood pressure monitoring in a horse, observing pressure as a column of blood in a glass tube connected to an artery. The principle for today’s measurement systems consists of a column of fluid that directly connects the arterial system to a strain gauge transducer, or Wheatstone bridge, which alters resistance to electron flow with variable pressure. Modern transducers utilize silicon crystals within a semiconductor that change electrical resistance in proportion to applied pressure.

To ensure accuracy and to counteract baseline drift, the transducer must regularly be zeroed to atmospheric pressure at the level of the right atrium (RA), which corresponds to the mid-axillary line. If the transducer is placed below the reference level, the arterial pressure reading will be falsely elevated and vice versa.

A transmitted arterial pressure waveform is converted into an electrical signal, amplified, and displayed continuously. The arterial pressure waveform represents the summation of a series of sine waves of different frequency, amplitude, and phase. It primarily consists of a fundamental wave (the pulse rate) and a series of further harmonics. Harmonics are smaller waves whose frequencies are multiples of the fundamental frequency. Fourier analysis, described by Lord Kelvin as “a great mathematical poem,” allows the waveform to be examined in terms of its constituent parts then reconstructed and displayed on the bedside monitor in a manner that is simple to interpret.

Monitoring systems are designed to have dynamic response characteristics brisk enough to ensure accurate reproduction of these waveforms across the wide range of heart rates and frequencies encountered in clinical practice. However, every substance has its own natural frequency at which it will oscillate freely. Any component sine wave of the arterial waveform close to that of the monitoring system’s natural (or resonant) frequency will cause resonance, which accentuates the waveform. This is of particular importance in pediatrics, because high heart rates can approach the system’s natural frequency resulting in an exaggerated and distorted signal, falsely elevating the systolic pressure.

In addition to the frequency response, the optimal dynamic capability and accuracy of a system also depends on its damping coefficient. All monitoring systems produce natural energy at rest through oscillation, which can create artifact and therefore possible distortion of the resultant waveform. This is counteracted by an inherent damping capability, dissipating this natural energy by frictional forces in the system. The degree of damping is rarely perfect. Too much (overdamping) or too little (underdamping) may falsely lower or elevate systolic pressures, which, if unrecognized, could influence therapeutic decision-making (Fig. 71.1). Overdamping is most commonly encountered in the ICU and occurs with obstruction or excessive compliance in the system resulting in a narrow pulse pressure and a flattened appearance on the displayed waveform. The mean arterial pressure is usually unaffected. Causes include large bubbles; clots; compliant, cracked, lengthy, or kinked tubing; soft transducer diaphragm; three-way taps; or a poorly secured transducer. If this picture emerges then it is worth examining the system for air bubbles and aspirating and flushing the cannula. Smaller-diameter cannula cause overdamping but this cannot be avoided in younger children. Underdamping has the opposite effect. Again, the mean pressure remains largely unchanged. Accurate invasive systems can be achieved by using a short length of wide, stiff tubing, filled with low-viscosity fluid, and free of air bubbles and clot. This ensures that the natural frequency is usually sufficiently high to overcome the problem of resonance and optimal energy dissipation and damping. The system is continuously flushed to reduce the chance of clotting. The ideal solution for this is dextrose due to its nonconducting properties; however; with children, and especially small babies, there is the risk of administering relatively large volumes of free water, which may lead to hyponatremia. Therefore, line patency is maintained by using saline (with or without heparin), which is driven by a 500-mL bag that is pressurized to 300 mm Hg, delivering ˜1-2 mL/h/lumen. A syringe driver (pump) is the
preferred method in smaller children due to improved accuracy of volume infused, which should be taken into account when calculating fluid balance. Infusion sets should be renewed every 72 hours to minimize line infections.

Invasive blood pressure monitoring provides a continuous display of the arterial waveform and additional information not available with the noninvasive modality (Fig. 71.2). The slope of the upstroke of the arterial waveform may be proportional to myocardial contractility. A slow upstroke can be indicative of poor cardiac function but is also seen in aortic stenosis and elevations in SVR. The area under the systolic portion of the waveform is proportional to the stroke volume. A low pulse pressure may reflect a low stroke volume. A widened pulse pressure due to elevated systolic and depressed diastolic pressures is seen in states characterized by poor systemic vascular tone, in patients with an aorta-to-pulmonary artery runoff (e.g., patent ductus arteriosus and aortopulmonary artery window), and in patients with aortic insufficiency.

A normal central venous or right atrial pressure in the spontaneously breathing patient is -2 to 5 mm Hg. The atrial pressure waveform (Fig. 71.3) normally demonstrates three
positive and two negative waves: the “a” wave follows the p wave on the ECG and is produced by atrial contraction; the “c” wave is produced by ventricular contraction and bulging of the tricuspid valve upward into the RA; the “x” descent results from atrial relaxation; the “v” wave results from right atrial filling and occurs in late systole before opening of the tricuspid valve; and the “y” descent results from opening of the tricuspid valve and passive filling of the right ventricle (RV). The CVP is the mean right atrial pressure, which approximates the right ventricular end-diastolic pressure, when right ventricular compliance and tricuspid valve function are normal. When ventricular function and compliance are diminished, atrial systole generates an end-diastolic pressure (reflected in the “a” wave) that is disproportionately higher than the mean pressure (14). Cannon “a” waves are produced when right atrial contraction occurs against a closed tricuspid valve, as in atrioventricular disassociation. Prominent “v” waves may be seen in tricuspid insufficiency and rapid “x” and “y” descents are suggestive of pericardial disease and restraint.

The relationship between CVP (ventricular filling pressure) and stroke volume is curvilinear. So long as volume administration produces an increase in stroke volume, the ventricle resides on the ascending portion of its Frank-Starling curve. The lack of a further increase in stroke volume after fluid administration suggests that preload reserve has been exhausted and the ventricle is now operating on the flat portion of its Frank-Starling curve (see Chapter 69). Any increase in stroke volume at this point would require inotropic support or afterload reduction.

Ventricular compliance is the ratio of the change of ventricular pressure (ΔP) to the change in ventricular volume (ΔV). One of the challenges of relying on the central venous (or ventricular filling) pressure as an indication of ventricular volume is that the relationship between volume and pressure (i.e., compliance) for a distensible chamber varies considerably from moment to moment in patients with cardiopulmonary disease (15). The effective compliance of the ventricle is affected by pericardial pressure and intrathoracic pressure. Thus, the end-diastolic transmural pressure (ventricular pressure-pericardial pressure) and ventricular compliance are the determinants of ventricular end-diastolic volume (Fig. 71.4). With a decrease in compliance, a greater distending pressure is needed to maintain ventricular filling. Ventricular compliance may be diminished as result of:

Ventricular compliance may also be affected as a result of diastolic ventricular interdependence. Ventricular interdependence defines a circumstance where changes in the volumes and pressures of one ventricle alter the volumes and pressures of the other ventricle. Under normal ventricular loading conditions and function, the interventricular septum deviates into the RV throughout the cardiac cycle because left ventricular
pressures exceed right ventricular pressures. If the interventricular septum shifts from its normal position, either due to an increase in right or left ventricular diastolic pressure, the compliance and therefore pressure and volume (filling) of the contralateral ventricle is altered.