How to read waveforms

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The flow waveform represents time dependence of blood flow velocity on cardiac activity [12]. Waveform recognition during Doppler examination starts with hearing the flow signal followed by visual analysis of the signal appearance on screen. Steps to optimize flow signals depend largely on this immediate recognition of the waveform and sonographer skills. Reading any ultrasound findings starts with orientation on screen and identification of machine settings. For Doppler examination, these simple and essential components include:

1 transducer and sample volume (gate) positioning;

2 flow direction;

3 angle of insonation;

4 scale settings; and

5 sweep speed.

For the purposes of this chapter, all Doppler recordings were obtained with a large (13-mm) sample volume at assumed zero angle of insonation. Flow signals towards the probe are displayed above baseline with a constant sweep speed. Scale settings, gain and baseline position were adjusted when necessary.

First, using the following five steps, identify the components of a cardiac cycle (Figure 5.1):

1 beginning of systole;

2 peak velocities during systole (peak systole);

3 diacrotic notch (closure of the aortic valve signalling the beginning of diastole);

4 end-diastolic velocities (end-diastole); and

5 the shape and magnitude of flow deceleration during the cardiac cycle.

Second, determine whether the measurements provided by automated software or manual placement are representative of the waveforms found. Doppler flow signal optimization is checked by the following:

1 signal-to-noise ratio (i.e. background should contain no or minimal noise);

2 envelope (or waveform follower) does not over- or underestimate velocities;

3 scale settings are adequate to display maximum velocities;

4 baseline (zero line) is positioned to avoid aliasing or sufficiently separate signals;

5 signal intensity is equal during recording sweep. Third, the waveform recognition will depend on

Figure 5.1 Keys to waveform presentation.

identification of the following components of an optimized Doppler signal:

1 early systolic upstroke (sharp or slow, delayed);

2 late systolic and diastolic deceleration (continuous, stepwise or flattened);

3 shape of the waveform (smooth, sharpened or flattened);

4 systolic/diastolic velocity difference (flow pulsatility); and

5 other components of the Doppler spectrum (bruit, spectral narrowing, embolic signals, etc.).

Specific waveforms

Normal findings

Case history. An asymptomatic 32-year-old man with arterial blood pressure 130/80 (Figure 5.2).

Interpretation. This waveform shows a sharp systolic flow acceleration and stepwise deceleration with positive end-diastolic flow. The end-diastolic velocity falls between 20 and 50% of the peak systolic velocity values, and this finding indicates low resistance to arterial flow.

Case history. An asymptomatic 32-year-old man with arterial blood pressure 130/80 (Figure 5.3).

Interpretation. This recording shows a bidirectional signal with simultaneous sharp systolic upstrokes and similar stepwise deceleration in both flow directions. Both waveforms show low-resistance flow patterns obtained at the ICA bifurcation.

Increased pulsatility of flow

Case history. A 65-year-old man with a new onset aphasia and chronic hypertension (Figure 5.4).

Interpretation. The waveform above baseline has a rapid systolic upstroke and a rounded peak systolic complex followed by a stepwise flow deceleration. The end-diastolic velocities below 30% of peak systolic values indicate relative increase in flow resistance. If flow

Figure 5.2 A low-resistance unidirectional flow signal.

Bidirectional Doppler Waveform Analysis

How to Reud Waveforms?

Velocity Seals (em O Background Signal Intensity

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I - beginning of systoli, 2 - peak lystolr, 3 - ciacrotic notch, 1 - end dutstoii Distances:

1 - 2 systolic acceleration. 2 3 late systolic deceleration. 3-4 diastolic deceleration


Figure 5.3 A low-resistance bidirectional flow signal.

Figure 5.3 A low-resistance bidirectional flow signal.

Envelope is a line tiivit follows the waveform

1 39



pulsatility is relatively similar in branching and contralateral vessels, a pulsatile waveform with normal or elevated mean flow velocity indicates normal vessel patency at the site of insonation and is not suggestive of a distal arterial occlusion. A weak flow signal below baseline in Figure 5.4 is not optimized and measurements are erroneous.

The effects of chronic hypertension on intracranial Doppler recordings may include:

1 increase in flow pulsatility [13] (pulsatility index values of >1.2 at the University of Texas STAT Neurosonology Laboratory); and

2 relative mean flow velocity increase above age-expected values.

Kidwell et al. showed that a relative increase in the

Figure 5.4 Increased resistance to flow with chronic hypertension.

Gosling pulsatility index above 1.17 correlates with the presence of silent brain damage on MRI in patients with chronic hypertension [14].

Case history. A 37-year-old man with closed traumatic brain injury (TBI) and intracranial pressure 52 mmHg (Figure 5.5).

Interpretation. The flow signal above baseline shows sharp systolic upstrokes followed by sharp deceleration indicating an overall increased resistance to flow.

Despite elevated pulsatility index (PI) in a young individual free of chronic hypertension (PI = 1.2), this high resistance waveform in the middle cerebral artery indicates normal patency of its proximal segment. This patient with traumatic brain injury (TBI) had

Tcd Waveforms
Figure 5.5 A complex waveform Indicating flow to both high-and low-resistance vascular beds.

intracranial pressure of 52 mmHg that produced increased resistance in the distal vascular bed. Elevated pulsatility index values were observed in patients with increased intracranial pressure [15]. The Doppler spectrum shows sharpening of the waveform due to faster flow deceleration. At the same time, the waveform above baseline also has a substantial diastolic flow indicating that some of this flow may be directed to a low-resistance vascular bed. This can happen in patients with TBI because both edematous (bruised) and normally perfused tissues may be present within the MCA territory. Furthermore, brain areas may be present with disturbed autoregulation or unequal distribution of ICP and mass effect. The waveform above baseline resembles a common carotid waveform because the CCA supplies both low- and highresistance vascular beds.

The flow signal below baseline has a low-resistance flow pattern flow seen in a vein. A loud thump-like early systolic sound (circled) is present due to vessel wall motion. This bright reflector disturbs spectral analysis and causes the envelope to spike (marked with *) leading to errors in automated velocity and pulsatility measurements below baseline.

Case history. A 35-year-old man with subarachnoid hemorrhage (Grade II, Day 2) and liver failure (Figure 5.6).

Interpretation. Both waveforms above and below the baseline have sharp systolic upstrokes and an abrupt flow deceleration. These pulsatile waveforms with the end-diastolic velocities within 20-25% of peak systolic values indicate high resistance to arterial flow. The difference in automated calculations of PI (PI below baseline is higher than above baseline) is attributable to the weakness of the signal directed away from the probe and the underestimation of the diastolic velocity by the envelope (last full cycle on the right).

This patient with subarachnoid hemorrhage has an even more pulsatile waveform (PI = 1.7). The differential diagnosis includes increased intracranial pressure, vasospasm and systemic conditions. Although hydrocephalus can be expected to develop by 48 h after the bleeding, this patient has normal ICP values (continuous ventricular drainage and invasive ICP monitor) at the time of TCD examination. A vasospasm that may produce these waveforms at Ml and A1 segment origins should affect both MCA and ACA territories and this will be an unlikely event on Day 2. Finally, the patient does not hyperventilate since he is alert and breathing room air at a normal pace. In this case, increased PI values and a sharp pulsatile waveform are seen due to autoregulatory vasoconstriction of the distal arterial bed in response to spontaneously increased cardiac output (cardiac index = 7) in a young patient with liver failure.

Case history. A 42-year-old woman with closed traumatic brain injury (Figure 5.7).

Interpretation. The waveforms above baseline show a regular heart rate with variable velocities (sharp systolic upstrokes, stepwise deceleration, low resistance). Marked velocity fluctuations can spontaneously occur every four cardiac cycles due to breathing. A cycle with the highest velocities (*) can be used for manual calculations.

Flow velocity and pulsatility fluctuations can also be caused by altered autoregulation (the patient has traumatic brain injury) and changes in the intracranial pressure. Blood flow velocity measurements can also be partially affected by changes in the angle of insonation (transducer positioning and, to a lesser degree, vessel pulsation and motion). Changes in flow pulsatility and waveform shape, as seen in this patient, are unlikely to be affected by the angle of insonation.

Figure 5.6 Increased pulsatility of flow at a bifurcation.

Transcranial Doppler Interpretation

Figure 5.6 Increased pulsatility of flow at a bifurcation.

Figure 5.7 Variable velocity and pulsatility.

Transcranial Doppler Interpretation

Figure 5.7 Variable velocity and pulsatility.

Transcranial Doppler Interpretation

Irregular heart rhythm

Case history. A 54-year-old man with an acute small cortical stroke and left ventricular hypertrophy (LVH) (Figure 5.8).

Interpretation. Waveforms above and below the baseline have sharp upstrokes, arrival of maximum systolic velocities towards the end of systole and stepwise flow deceleration. The end-diastolic velocities fall below 30% of peak systole due to irregular heart rate: this also affects estimation of flow resistance (increased values of PI calculated with envelope tracings) from only 2-5 cycles' averaged values. A single cycle may be selected for manual measurements.

Measurements that are affected by irregular heart rate include:

Figure 5.8 Extrasystole.

1 velocity (underestimation); and

2 pulsatility (overestimation).

A prolonged pause between cardiac contractions (seen in the second cycle, Figure 5.8) leads to lower than usual end-diastolic velocities that artificially decrease the velocity and increase pulsatility index values. Avoid including in measurements the compensatory pauses after extrasystole; or, if extrasystoles are too frequent, a higher number of cardiac cycles should be averaged using slower sweep speeds or manual measurements of the highest velocity cycle should be used.

Case history. A 60-year-old woman with recent transient ischemic altack (TIA) and atrial fibrillation (Figure 5.9).

Interpretation. Waveforms towards the probe have irregular arrival of cardiac cycles with sharp upstrokes

Transcranial Doppler Interpretation
Figure 5.9 Atrial fibrillation.

and variable velocities. As a practical rule, a cycle with the highest velocities (marked as *) can be used for manual calculations. However, estimation of flow resistance and representative mean velocity is difficult since the pulse rate and cardiac output are affected.

This a typical waveform obtained from a patent middle cerebral artery in a patient with atrial fibrillation. This waveform can be easily recognized if there is no cardiac cycle similar to the other. Yet, overall it is a low-resistance flow recording since end-diastolic velocity exceeds 30% of peak systole during every cycle taken separately. PI values are overestimated since the envelope recognizes maximum peak systole and minimum end-diastole taken from separate cycles. Although averaging of 20 cardiac cycles may provide more representative velocity and pulsatility index values, it is impractical and difficult to accomplish. A less scientific but practical solution is to use manual measurements taken from a cycle with the highest peak and end-diastolic measurements that are often representative of a more synchronized cardiac contraction with better cardiac output. This approach also shortens time of examination and introduces a consistent way of recording velocities for serial studies.

Changes in the systolic flow acceleration

Case history. A 67-year-old man with resolving MCA stroke and carotid occlusion (Figure 5.10).

Interpretation. The waveform above baseline shows a delayed systolic flow acceleration, flattened systolic complex and slow diastolic deceleration. End-diastolic velocities above 50% of peak systole indicate very low flow resistance. This waveform is called a 'blunted' flow signal.

This waveform shows a delayed systolic flow acceleration that can be found in a patent vessel distal to a high-grade stenosis or occlusion [16]. The MCA usually receives either collateral flow around or residual flow through the ICA lesion and, in order to attract more flow, compensatory vasodilatation occurs to reduce overall resistance to flow (low (1.0 - 0.6) or very low (< 0.6) PI values). When these 'blunted' waveforms (with MFV generally above 20 cm/s) are found unilaterally, it is a sign of a proximal (ICA or terminal ICA) hemodynamically significant obstruction. If a delayed systolic flow acceleration is found in both internal carotid branches and the basilar artery, it may be a sign of reduced cardiac output (i.e. congestive heart failure).

Case history. A 73-year-old man with MCA stroke and carotid occlusion (Figure 5.11).

Interpretation. The waveform above baseline has an upward systolic upstroke. This waveform has to be compared to a non-affected vessel in order to decide if only a slight delay in systolic acceleration is present. In any case, this is not a blunted signal since a clear systolic complex is visualized.

This waveform shows only a slight delay in the systolic flow acceleration and a clear systolic complex. This type of flow acceleration can be found in patients with or without hemodynamically significant proximal arterial obstruction. When found at the MCA origin or just posteriorly to a 'blunted' MCA signal, this waveform may be attributable to the posterior communicating artery or the posterior cerebral artery with a normal systolic flow acceleration in the presence of an ICA obstruction.

Collateralization of flow

Case history. A 70-year-old woman with a recent TIA and carotid occlusion (Figure 5.12).

Normal Ica Waveform

Figure 5.10 A blunted signal.

Transcranial Doppler Velocities
Figure 5.11 Slightly delayed systolic flow acceleration.

Figure 5.12 Flow diversion.

Interpretation. This tracing displays a bidirectional signal with normal systolic upstrokes. The waveform below baseline shows higher velocities and lower resistance to flow. This may represent flow diversion to a branch directed away from the probe.

This bidirectional signal represents a typical finding at the MCA/ACA bifurcation with flow diversion to the ACA being present. When the ACA becomes the donor vessel for the anterior cross-filling to compensate for a contralateral carotid obstruction, the ACA starts to supply both A2 segments and often the contralateral MCA via contralateral A1 segment reversal. This cross-filling may manifest on the donor site as the mean flow velocity difference ACA > MCA and pul-satility index ACA < MCA due to compensatory flow volume increase and vasodilatation. It is important to optimize both MCA and ACA signals to make sure that maximum Doppler shifts are compared at these vessels and not between the terminal ICA (TICA) and ACA. Simultaneous display of the terminal ICA/ACA signals may yield similar velocity differences due to a suboptimal angle of insonation with the TICA.

Aliasing and signal optimization

Case history. A 72-year-old man with a recent TIA and a moderate proximal carotid stenosis (Figure 5.13).

Interpretation. This recording shows a waveform that exceeds one half of the velocity scale (i.e. an artifact called 'aliasing'). Both envelopes show automated

Figure 5.13 Aliasing.

Tcd Waveforms


Transcranial Doppler Interpretation

recognition of the velocity values that are erroneous. This waveform also contains a low-frequency bidirectional signal heard as a bruit (circled).

This waveform is a typical pulse wave Doppler artifact [ 17]. This artifact inappropriately displays, or cuts off, the systolic frequencies from the top or the bottom of the spectral display. There is often an overlap in maximum velocities between the flow signals towards and away from the probe. This artifact is linked to a pulsed Doppler system handicap in velocity detection posed by the half of pulse repetition frequency (PRF) threshold (or the Nyquist limit) [17]. Steps to optimize this signal should include:

1 adjustment of the velocity scale to maximum possible values;

2 moving baseline ('drop the baseline', or converting the recording into a unidirectional display); and

3 reducing sample volume or gate (this may help to focus the beam at one vessel thus avoiding or reducing the impact of aliasing on the velocity measurements).

Case history. A 68-year-old man with a recent MCA stroke and MCA stenosis (Figure 5.14).

Interpretation. This waveform is an optimized signal with high velocities, bruits, normal systolic acceleration and low-resistance flow pattern. Background contains no noise and the envelope shows a good automated waveform tracing. Other data are needed to confirm whether this is a stenotic signal, i.e. focal changes in velocity along the MCA stem and comparison to the contralateral MCA velocity values.

Differential diagnosis includes a compensatory velocity increase if another large vessel lesion is present. From a single depth tracing in the intracranial vessels, it is impossible to tell whether this waveform represents a focal significant velocity increase due to stenosis, or it represents hyperemia with collateraliza-tion of flow. Shown in this figure, the MCA flow signal with a mean flow velocity of 117cm/s was found at the site of a 50% MCA narrowing unilateral to the hemisphere affected by an ischemic stroke. If found contralateral to a proximal ICA obstruction, similar velocity findings may represent Ml MCA stenosis or flow diversion. A focal MCA stenosis is likely to be found if the distal M1 MCA velocity decelerates by more than 30%.

Case history. A 59-year-old man with an acute stroke and carotid occlusion contralateral to the side of insonation (Figure 5.15).

Interpretation. This tracing displays a bidirectional signal with minimal aliasing. Both waveforms show normal systolic upstrokes, bruits and low resistance

Figure 5.14 A stenotic signal.

Abnormal Transcranial Doppler

Figure 5.15 Aliasing or optimized signal?

Figure 5.15 Aliasing or optimized signal?

patterns. Envelopes indicate reasonable signal optimization. Other data are needed to determine whether this is a compensatory or stenotic velocity increase.

This recording shows that bidirectional signals with elevated velocities may not be completely separated by adjustment to the maximum velocity scale values, yet both signals are reasonably optimized for measurements. These signals are both abnormal in terms of being above the age-expected velocities, and further adjustments of Doppler setting may insignificantly improve the velocity values obtained at bifurcation. The waveforms were found at the ICA bifurcation contralateral to a complete proximal ICA occlusion mostly indicating laminar flow (note changes in the intensity spectrum of the MCA waveform above baseline) and bruits at bifurcation due to compensatory flow diversion. In acute ischemic stroke, the abrupt development of carotid thrombosis may cause a significant flow diversion and opening of collateral channels. This process may result in acutely elevated velocities in the donor vessels followed by velocity decrease in the subacute and chronic phases when stroke is completed or vessel dilatation is accomplished.

Case history. A 42-year-old woman with subarachnoid hemorrhage (Day 8) (Figure 5.16).

Interpretation. This simultaneous display of four waveforms is due to a large sample volume (or gate) of insonation of 13 mm. Marked as (1), the highest velocities were likely found in a segment with maximal narrowing; (2) shows elevated velocities in another segment with less narrowing; (3) hyperemic signals likely in a proximal vessel; and (4) branch signals.

The differential diagnosis includes the presence of a mirror artifact and hyperemia.

This is a complex recording obtained in a patient with subarachnoid hemorrhage who developed a severe MCA vasospasm. The use of a large (13-mm) sample volume may produce simultaneous display of waveforms detected at different arterial segments (i.e. terminal ICA, proximal Ml, mid-Mi MCA or neighboring segments with different patency). Although the highest velocities in waveform (1) are likely attributable to the site of maximum vasospasm (the mean flow velocity of 295 cm/s), the presence of mirror artifact [18] and hyperemia (as a potential cause of it being a bright reflector) should be excluded using the Lindegaard ratio [19]. The signal-to-noise ratio appears to be optimized, i.e. no noise in the background. This patient was on hypertension-hemodilution-hypervolemia (triple H) therapy and hyperemia was mostly ruled out by the Lindegaard ratio of 10 (see also Chapter 6).

Severe stenosis, acute thrombosis and occlusions

Case history. A 65-year-old man with an acute stroke and carotid thrombosis unilateral to the site of insonation (Figure 5.17).

Interpretation. This tracing displays a loud bidirectional bruit with a turbulent high-velocity signal of a stenotic origin. Minimal aliasing is present. The envelope above baseline indicates weak peak systolic tracings that lead to underestimation of the velocity increase.

Similar waveforms can be found at a severe stenosis with turbulent flow when a sample volume is positioned slightly off the vessel segment that has the highest-velocity jet. Remember that the highest-velocity jet can usually be found at the exit of a focal stenosis. By itself, this waveform is already diagnostic, showing that some flow velocities were lost to turbulence and the peak velocity values may be decreasing as disease progresses towards near-occlusion. Velocities taken from such waveforms usually underestimate the highest velocity and this may affect grading the severity of a lesion.

Transcranial Doppler Interpretation
Figure 5.16 Increased velocities, multiple waveforms and severe vasospasm.

Figure 5.17 Turbulence, bruits and velocity underestimation.

Figure 5.18 Continuous bruit and delayed systolic flow acceleration.

Figure 5.19 A weak signal.

Case history. A 76-year-old man with a recent TIA (Figure 5.18).

Interpretation. This tracing displays a turbulent signal of variable intensity with bidirectional bruits. This waveform can be found in a poststenotic segment. The peak systolic complex is not clearly visualized since a laminar flow profile is not re-established yet [ 1 ].

This waveform that contains bruits of variable intensity and incomplete spectral velocity tracing should alert the sonographer to expand the search for the highest-velocity jet and to suspect a subtotal stenosis with bruits of prolonged duration.

Case history. A 71-year-old woman with an ACA territory stroke and a proximal moderate carotid stenosis (Figure 5.19).

Interpretation. This tracing shows a bidirectional signal with a low-resistance waveform above baseline that is optimized and has a slighdy delayed systolic upstroke. A high-velocity weak signal below baseline (marked as *) is not optimized since overgaining does not change the signal-to-noise ratio and measurements are erroneous.

This recording shows a weak signal suspicious of a focal velocity increase in a branching vessel (below baseline). If a stenosis is located deep in the intracranial vasculature (i.e. depths of insonation 65 mm or more), sound attenuation and limited pulse repetition frequency may preclude its definition and measurement. Increasing gain may help to visualize the waveform but may be insufficient (as in this case) for automated tracings since the signal-to-noise ratio in a

Figure 5.17 Turbulence, bruits and velocity underestimation.

Transcranial Ultrasound WaveformHow Reduce Noise Occulation Viray

Figure 5.20 A branch occlusion.

Figure 5.20 A branch occlusion.

Transcranial Doppler Interpretation

weak stenotic signal is low and remains unaffected. Reducing the sample volume to focus on this specific signal may also reduce sensitivity of Doppler if burst pressure is reduced. If waveforms presented in this case are detected, use manual measurements to quantify velocity increase. The use of power M-mode-guided TCD spectral assessment may lead to the sites of disturbed signals [20], and the use of contrast-enhanced ultrasound agents [21] may help to avoid this technical problem.

Case history. A 75-year-old man with an M2 MCA occlusion and ICA occlusion (Figure 5.20).

Interpretation. A low-resistance waveform above baseline has a short systolic upstroke and flattened systolic complex. Comparison with a non-affected vessel will help to determine whether this is a blunted or dampened signal (see flow grading criteria in Chapter 10). A high resistance minimal signal below the baseline has no end-diastolic flow.

This recording shows a complex signal that can be obtained in the intracranial vessels at the site of or just proximal to an arterial occlusion, affecting for example the M1-M2 MCA bifurcation. An arterial occlusion can produce a variety of residual flow signals [22] (see Chapter 10 & Part V). These waveforms can

Figure 5.21 A minimal signal (systolic spike).

be recognized by abnormal appearances of the systolic complex and end-diastolic flow compared to the unaffected side, including absent end-diastolic flow. Nevertheless, changes in flow pulsatility and velocity are often accompanied by signs of flow diversion or compensatory velocity increase, and these findings point to hemodynamic significance of suspected arterial obstruction.

Case history. A 62-year-old woman with an Ml MCA occlusion (Figure 5.21).

Interpretation. This is a minimal bidirectional signal with no end-diastolic flow. This waveform can be representative of a residual flow signal around MCA clot if collaborated by additional findings indicating occlusion at this location. Bruits and vessel intercepting at a nearly 90° angle should be considered as a possible explanation.

This recording shows a systolic spike (or a minimal residual flow signal) obtained at the site of an acute MCA occlusion. In this case, systolic spikes with low velocities and bruit-like appearance are seen followed by periods with no diastolic flow indicating very high resistance to flow and abolishment of brain perfusion, at least during diastole. Generally, flow signals obtained at near-90° angles have some recognizable

Figure 5.22 An oscillating or reverberating flow signal.

Systolic Spikes Brain Death

waveform components and the waveforms extending into diastole can be slightly improved by reangulation of a transducer.

Circulatory arrest

Case history. A 41-year-old woman with TBI and clinical progression to brain death (Figure 5.22).

Interpretation. Both waveforms represent an extremely high resistance to flow. Marked as (1), flow signals above baseline represent sharp spikes with abrupt flow deceleration to zero at the time of closure of the aortic valve and no positive end-diastolic flow. Marked as (2), the same blood pool reverses its direction during entire diastole producing the sign of flow reverberation or oscillation.

In this case, an extremely high resistance to flow precludes brain perfusion [15,23-25]. This waveform was observed in a patient who developed massive brain swelling with progression into cerebral circulatory arrest. If reverberating flow is found in both proximal MCAs and the basilar artery, it predicts the absence of brain perfusion that can be demonstrated by nuclear cerebral blood flow studies. Hemodynam-ically, this waveform indicates that all blood that passed through the sample volume towards the brain in systole was pushed out of the distal vasculature in diastole resulting in no flow passage to brain parenchyma.

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