Arterial pressure waveforms provide critical information during anesthesia beyond simple systolic and diastolic numbers. These tracings offer real-time insights into cardiovascular physiology, allowing anesthesiologists to assess hemodynamic status, guide interventions, and monitor treatment responses. Understanding these waveforms is essential for optimal patient management.
Arterial Waveform Components #
The arterial pressure tracing consists of several key components: the systolic upstroke, systolic peak, dicrotic notch (not seen at peripheral artery sites, any resembling trace is likely a pressure wave reflection off the narrowing peripheral arterial tree), and diastolic runoff. The systolic upstroke occurs during ventricular ejection, culminating in the systolic peak. The dicrotic notch (usually only seen with proximal aortic catheter placement) marks aortic valve closure, followed by the diastolic runoff as blood flows to the periphery against vascular resistance.
These morphological features change with physiologic alterations and pathological conditions, making waveform analysis valuable. Anesthesiologists must recognize normal waveform characteristics to identify abnormalities suggesting hemodynamic compromise.
Systolic Pressure and Myocardial Contractility #
Systolic pressure primarily reflects left ventricular contractility (inotropy) and stroke volume. Increased myocardial contractility produces steeper systolic upstrokes and higher systolic peaks, while decreased contractility results in slower upstrokes and lower peaks. The rate of pressure rise (dP/dt) within the systolic component serves as a surrogate marker for contractility.
During anesthesia, many agents directly depress myocardial contractility, with volatile anesthetics and some premeds like alpha-2 agonists being particularly significant. This effect manifests as less steep systolic upstrokes. Conversely, positive inotropes like ephedrine, epinephrine, and dobutamine increase contractility, elevating systolic pressure and steepening the upstroke.
Accurate interpretation requires consideration of preload status, as hypovolemia may present with decreased systolic pressure despite normal contractility. Similarly, increased systemic vascular resistance can elevate systolic pressure independent of contractility changes (eg dexmedetomidine).
Diastolic Pressure and Vascular Resistance #
Diastolic pressure primarily reflects systemic vascular resistance (SVR) and provides insight into afterload conditions. Higher SVR leads to elevated diastolic pressure as blood encounters greater resistance flowing through the arterial system. Lower SVR results in decreased diastolic pressure as blood flows more freely through the vasculature.
Several anesthetic agents, including volatile anesthetics, directly decrease SVR through vasodilation. Regional anesthesia techniques like epidurals and spinals similarly reduce SVR through sympathetic blockade. These effects typically present as decreased diastolic pressure readings and altered waveform morphology.
Diastolic pressure is particularly sensitive to vasopressor and vasodilator agents. Vasopressors like phenylephrine and norepinephrine increase SVR and elevate diastolic pressure, while vasodilators like nitroglycerine and sodium nitroprusside decrease SVR and lower diastolic pressure. Note that increased pressure as a result of increased resistance may not equate to improvement of tissue perfusion.
Mean Arterial Pressure and Tissue Perfusion #
Mean arterial pressure (MAP) serves as the driving pressure for tissue perfusion throughout the body. Organ perfusion depends on maintaining adequate MAP above autoregulatory thresholds. For most organs (esp kidney and brain), perfusion remains relatively constant when MAP ranges between 60-160 mmHg due to autoregulation, but drops precipitously below these thresholds.
The formula for calculating MAP is:
MAP = Diastolic Pressure + 1/3 (Systolic Pressure – Diastolic Pressure)
Notably, diastolic pressure contributes more significantly to MAP than systolic pressure. This weighted formula reflects the fact that the heart spends approximately two-thirds of the cardiac cycle in diastole and that the calculation of average of the curvilinear AUC pressure wave is not a algebraic average. Consequently, changes in diastolic pressure have greater effects on MAP and tissue perfusion than equivalent changes in systolic pressure.
During anesthesia, maintaining MAP above 60-65 mmHg is generally recommended to ensure adequate perfusion to vital organs, particularly the kidneys and brain. However, individualized targets should consider the patient’s baseline pressures and comorbidities, with higher targets often necessary for patients with chronic hypertension or cerebrovascular disease.
Area Under the Curve and Stroke Volume #
The area under the curve (AUC) of the arterial pressure waveform correlates with stroke volume and provides valuable information about cardiac output. The AUC represents the pressure-time integral, which serves as a surrogate marker for the volume of blood ejected during systole.
Increased stroke volume typically presents as a wider pressure wave with greater area, while decreased stroke volume manifests as a narrower wave with smaller area. This relationship forms the basis for various pulse contour analysis systems that estimate stroke volume and cardiac output from arterial waveforms.
Several factors influence this relationship during anesthesia. Changes in arterial compliance alter the pressure wave morphology independent of stroke volume changes. Increased arterial stiffness, common in elderly or hypertensive patients, can exaggerate pressure changes relative to volume changes. Conversely, increased compliance attenuates pressure changes for given volume changes.
Pulse pressure variation (PPV) and stroke volume variation (SVV), derived from arterial waveforms, help assess fluid responsiveness during mechanical ventilation. These dynamic parameters reflect cardiopulmonary interactions and predict whether stroke volume will increase with fluid administration.
Clinical Applications During Anesthesia #
Arterial pressure waveform analysis aids several clinical decisions during anesthesia. It helps distinguish between various causes of hypotension, such as differentiating hypovolemia (narrow pulse pressure, respiratory variation) from decreased contractility (reduced systolic upstroke, normal diastolic pressure) or vasodilation (decreased diastolic pressure, normal systolic upstroke).
Waveform changes often precede numerical blood pressure changes, allowing earlier intervention. For instance, progressively narrowing pulse pressure with increasing variation may signal developing hypovolemia before mean pressure decreases significantly.
The waveform analysis also guides vasoactive therapy selection. Patients with preserved systolic upstrokes but low diastolic pressures likely benefit from vasopressors to increase SVR, while those with decreased systolic components may benefit more from inotropic support.
Limitations and Considerations #
Several factors affect waveform interpretation during anesthesia. Damping from air bubbles, kinks, or excessive tubing length distorts waveforms and underestimates systolic while overestimating diastolic pressures. Resonance from underdamped systems artificially elevates systolic readings.
Measurement site impacts waveform morphology, with peripheral sites showing higher systolic and lower diastolic pressures compared to central measurements due to wave reflection phenomena. This site-dependency must be considered when interpreting absolute values.
Patient positioning can significantly impact readings through hydrostatic effects, particularly when transducers aren’t level with the heart. Each 10 cm vertical displacement introduces approximately 7.5 mmHg pressure difference.
Finally, pathophysiological conditions like aortic regurgitation, aortic stenosis, and atrial fibrillation produce characteristic waveform changes that must be differentiated from anesthesia-related alterations for accurate interpretation.
