Equipment and cannulation

The arterial catheter is placed in a peripheral artery or the femoral artery, with the radial artery being the most commonly used cannulation site. Arterial spasm and thrombosis, local infection and hematoma, distal ischemia, hemorrhage, and air embolism are the main complications. A 20G cannula is appropriate for the cannulation of a small artery, and an 18G for a larger one. Aseptic technique should always be applied. The arterial cannula is connected to a pressure transducer via high-pressure tubing. The pressure transducer should usually be located at the level of the right atrium, or at the level of the external auditory meatus for the sitting patient who is undergoing a neurosurgical procedure. Air should be thoroughly evacuated from the entire system. Zeroing to atmospheric pressure is done before first use and as needed afterward. The continuous flash device is connected to a bag of normal saline under a pressure of 300 mm Hg that brings a continuous flash of 1 to 3 mL/h to prevent clot formation at the tip of the arterial cannula. Heparin (1-2 μ/mL or 10-20 μgr/mL) can be added to the flush solution, but this is not mandatory, and the risk of heparin-induced thrombocytopenia should be kept in mind.

Waveform interpretation

The arterial waveform provides valuable and continuous hemodynamic information. It changes as the measuring catheter is located more distally from the heart. The pulse pressure increases, and the dicrotic notch is delayed and then disappears. The systolic pressure is higher in a peripheral artery, compared with the ascending aorta, but the mean pressure is minimally affected or slightly reduced. The heart rate and rhythm can be determined from the arterial tracing. The effect of ectopic beats on arterial pressure and waveform can be evaluated. The pulse pressure may help to evaluate the patient’s hemodynamic status. High pulse pressure can be seen after exercise and in patients with hyperthyroidism, aortic insufficiency, peripheral vasodilatation, arteriovenous malformation, increased stiffness of the aorta (most common in older patients), and mild hypovolemia. Narrow pulse pressure can be seen in patients with hypovolemia, pericardial tamponade, congestive heart failure, aortic stenosis, and shock states. The area under the arterial curve, from the onset of systole to the dicrotic notch, can estimate the stroke volume (SV), and the systolic rise may reflect myocardial contractility. However, the arterial curve changes as the location of the arterial cannula insertion moves distally from the ascending aorta.

Dynamic indexes of fluid responsiveness

The SPV and PPV derived from the arterial waveform during a mechanical breath (Figure 16-1) are more pronounced during hypovolemia because the left ventricle operates on the steep portion of the Frank-Starling curve. Changes in right and left ventricular preload, which are highly sensitive to changes in intrathoracic pressure induced by a mechanical breath, cause the variation in the left ventricular SV. Observing the various components of SPV and PPV can establish the presence and cause of hypovolemia, with dynamic changes in the arterial waveform predicting the response to fluid challenge. SPV, PPV, and SVV (measured by pulse contour analysis) are currently the most accurate indicators for fluid responsiveness in patients in the intensive care unit and in many surgical patients. Given that only 50% of patients in the intensive care unit respond to fluid loading, this measurement may provide valuable data for determining which patients should be first treated with fluids and which may benefit from inotropic support as the first intervention to increase CO. Although simply viewing the arterial waveform on the arterial pressure tracing can provide information about the presence of respiratory variation, an accurate electronic measurement can quantify the pressure variation and its components, allowing the effect of fluid loading to be continually assessed.

Measurements of SPV, SVV, and PPV are currently limited to the sedated mechanically ventilated patient who is in normal sinus rhythm. Spontaneous breathing, frequent arrhythmia, high positive end-expiratory pressure, high airway pressure, high and low tidal volumes, low chest wall compliance, increased intra-abdominal pressure, and the use of vasodilators may all cause inaccurate representations of the dynamic indexes on tracings from arterial catheters.

Many studies have demonstrated the superiority of the dynamic indexes—as compared with the static indexes (central venous pressure, pulmonary capillary occlusion pressure, left ventricular end-diastolic area, and global end-diastolic volume)—in predicting patient response to fluid loading. The dynamic indexes of fluid responsiveness should be evaluated as a component of the entire clinical scenario related to a given patient. They should not be used as a single “best” index for clinical decisions but, rather, should be used in the context of the other clinical parameters.

Cardiac output derived from the arterial pressure waveform

Arterial pressure waveform analysis is now used in clinical practice with several commercially available devices that can be used to continuously measure CO, based on the arterial pressure waveform. These devices provide a CO value derived from pulse-contour measurements that correlates well with the value derived from the pulmonary artery catheter thermodilution technique (a bias of 0.03-0.3 L/min), but, under various clinical conditions and therapies, this correlation might be disrupted. Compared with the thermodilution technique, these devices are less invasive and their use is associated with potentially fewer complications. Examples of commercially available devices include the PiCCO (Pulsion Medical Systems, Munich, Germany) and LiDCO (LiDCO, Ltd, Cambridge, UK), and the EV1000 Clinical Platform (Edwards Lifesciences, Irvine, CA) which require an invasive calibration and recalibration, and the FloTrac/Vigileo (Edwards Lifesciences) device, which uses individual demographic data to estimate arterial compliance and, therefore, does not require invasive calibration. These devices use pulse-contour analysis with various algorithms to estimate SV from the arterial waveform. The SV is calculated by a mathematical computation of the area under the systolic portion of the arterial pressure waveform. The algorithm incorporates parameters such as aortic impedance, arterial compliance, and peripheral vascular resistance. These devices can also calculate other hemodynamic variables (e.g., static preload parameters, peripheral resistance, oxygen delivery, and the dynamic indexes of fluid responsiveness [see earlier]). The hemodynamic profile is continuously displayed, with the option to follow trends and changes during patient care (Figure 16-2).