Journal of the Royal Society of Medicine Volume 71 July 1978
501
Clinical experience with transcutaneous aortovelography: preliminary communication' Gillian C Hanson MB MRCP A H Bilton MB BS Whipps Cross Hospital, Leytonstone, London Ell INR
Detailed evaluation ofthe haemodynamic state in the critically ill patient may take time because of difficulty in gaining access to the circulation, and it is not without its dangers. Elaborate systems may be unavailable in certain units because ofexpense or lack of personnel. Monitoring of pulmonary capillary wedge pressure may not reflect left atrial pressure in patients with pulmonary pathology. For these reasons a non-invasive, reproducible and consistent indicator of left ventricular function (Fraser et al. 1976) would be of considerable value in the management of the critically ill. The basic theory of transcutaneous aortovelography (TAV) has been described by Cross & Light (1974). Work by Goldberg (1971) and Huntsman et al. (1975) indicated that it was possible to measure aortic blood flow velocities and accelerations in man by the transcutaneous ultrasonic Doppler method. Clinical evaluation Traces suitable for evaluation could be obtained in approximately 95%o of patients, difficulty being experienced in the elderly patient with emphysema, the restless patient, or the patient with a tracheostomy. In the few patients studied, it would appear that even in those patients with a tracheostomy traces can be obtained after a few days (once the air around the wound has been absorbed) provided there is sufficient room to place the doppler probe between the tracheostome and the suprasternal notch. Our initial clinical evaluation involved hand analysis of the TAV trace (Figure 1) and comparing the extrapolated peak velocity and time averaged velocity (mean aortic velocity) with simple indices of haemodynamic state, such as pulse rate, blood pressure, right atrial pressure, urine output and skin core temperature differential. Clinical situations where the technique proved to be helpful included: the initial evaluation of a shocked patient; and evaluation of the haemodynamic response to a therapeutic manoeuvre. Initial evaluation of a patient in shock: Shock cannot simply be divided into single aetiological components, but in many situations a dominant factor producing the condition can be elicited, which when treated produces haemodynamic improvement. It was shown (Figure 2) that peak velocity and mean aortic velocity were consistently decreased in situations where the dynamic blood volume was low and/or where there was evidence of inadequate left ventricular function. In hypovolaemia the peak velocity and mean aortic velocity rapidly responded, as did the right atrial pressure, to volume replacement (Figures 3, 4). 1
Paper read to Section of Measurement in Medicine, 29 October 1977
0 1 41-0768/78/0071-0501/$O 1.00/0
(C') 1978 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 71 July 1978
502
Glossary to Figures Blood pressure. Systolic pressure. BP SP Mean aortic velocity (see Figure 1) V Central venous pressure or right atrial cvp pressure as measured in the midaxillary line, the patient positioned horizontally. Initial systolic Rate of rise of the initial upstroke of the TAV trace (See Figure 1) acceleration. Extra polated peak velocity, V,
Blood velocity (cm/sec)
A~~~~~~~~~~~~~~~~~~~~~l
_
200 48_______
Z-
108 7-'-
I
0
*V
-... .-
--
.-.
./
. -
Ejection time, tx
0-1se~~~~_
ec
Initial systolic acceleration (cm/sec/sec)
Cardiac cycle period, T Area = 2 * f-V Time - averaged velocity, V =A/T ( mean aortic velocity )
Figure 1. Hand analysis of TAV trace
Shock following myocardial infarction Line around waveform representing aortic systolic flow velocity {
Septic shock (central venous pressure normal)
C
Figure 2. TAV traces on admission of various kinds of shock
.
Journal of the Royal Society of Medicine Volume 71 July 1978 Prior to treatment
Trace
Trc 2
mi
Trace 2
hour 45 min later ~
I
.. ._ . . .. d__ *
a
Trace 3
_.u
. _
~ ~
_
.
~
~
_ ..40
.
.
~
~
~
~
:
I
_. ... _ ~. 0. '_. a
."
a
.
a
a
.
a_ _
0
&
.
6
0
6.
a
5 hours after onset of treatment Total volume of fluid infused 3600 ml
Figure 3. Serial TAV traces during volume replacement for hypovolaemic shock 0
Pulse
(rate/min) 0-
v* BP.SP
20
-------
/
00
-
(mm/Hg) 50 Skin/core differential
10
(OC) 0 25-
(cm/sec)
200 10~~~
A~~~~~~~~~~~ -.0
CVP:-
(cm H20)
A
-
0V
2
.
Volume infused
(mL)
Time in hours after onset of volume replacement
Figure 4. Sequential indices (in conjunction with TAV traces in Figure 3) taken during volume replacement for hypovolaemic shock
503
Journal of the Royal Society of Medicine Volume 71 July 1978
504
Z-
.
.
.
.
.
.
.
( I ) Before volume replacement
.
.
.
.
.
.
.
.
.
.
.
.
.
(2 ) After volume replacement
T
Z..:-
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
( 3 ) After recovery
Figure 5. Serial TAV traces during the management of patient with severe sepsis 1400 Pulse
*
(rate/min)
120
0
-
100 _
BR SP (mm/Hg)
\
8
......
L
'
30 0/
(cm H20)
(cm/sec2)
\0
-.
,()
2
20
0
*
Initial systolic
acceleration
-
1500 _
U
1000 2000
-
Fluid volume replaced ... ... . (ml) .::1000
6. S Figureplad
dit
~~~~~~~~~~~~~~~~~~~~~~~~~~.....................
te in F Hour.Aftr.reover Minutes........... ~4 fter...........
(M se ma0 e of.patient5with sever
.........................issio
Figure indices (in conjunct.. in. Figure.. 5) during6.Sequential themanagement of patient with io...n.....w..h.T.......a..s severe s
.
.
.
-
I
0
*- *
0
0
0
6
0
0
0
e
I~~~~~~~~~~~~~ I
-w~~
am-=== . *
*
*
*
*
*
*
*
*
*0
*-. 0
*
*~
6 *
0 *
X
d
* 0
(I ) Admission
After isoprenaline infusion forapproximately 2 hours (2) ..... @... .. . s
s
.
me
e. *o
*
~~._
:::.~. r ~c~ _..
.
..
(3) 17 hours after admission recovered
Figure 7. Serial TAV traces in patient with amylobarbitone overdose treated with intravenous isoprenaline
0
0
BP. SP. (mm/Hg)
Pulse
(rate/min)
A
0
CVP
(cm/sec)
(cm H20)
11000 Initial systolic acceleration
(cm/sec-2)
2-0 _ I soprenaline ..
., ., ,:..:.. ..
......
.... ..
200 Minutes after admission
17 hours later
Figure 8. Sequential indices (in conjunction with TAV traces in Figure 7) during management of patient with amylobarbitone overdose. High right atrial pressure, low mean aortic velocity and initial systolic acceleration at time of admission were consistent with diagnosis of impaired myocardial performance. Note rapid improvement with isoprenaline infusion and rapid deterioration when it was temporarily withdrawn (arrowed)
506
Journal of the Royal Society of Medicine Volume 71 July 1978
In shock associated with sepsis, peak velocity and mean aortic velocity were found to be consistently high once the circulating blood volume had been restored. It has been found that the rate of rise of the first part of the upstroke (initial systolic acceleration, Figure 1) is consistently increased in conditions of stress where myocardial function is considered adequate (Figures 5, 6). Evaluation of the haemodynamic response to a therapeutic manoeuvre: TAV was found to be a delicate reflector of change in haemodynamic state following a therapeutic manoeuvre (Figures 7, 8). In such conditions, it is well recognized that the right atrial pressure is only a crude guide to left ventricular performance.
Future research Research is at present being conducted comparing indices using the TAV technique with those of right ventricular output (thermodilution technique), pulmonary artery pressure and pulmonary capillary wedge pressure. The preliminary results are encouraging. Preliminary investigations suggest that in the absence of any aortic valve or aortic arch deformity this technique will be a reliable non-invasive indicator of left ventricular function. The method is reproducible, consistent, non-invasive and easy to use. References Cross G & Light L H (1974) Biomedical Engineering 9, 464 Fraser C B, Light L H, Shinebourne E A, Buchtal A, Healy M J R & Beardshaw J A (1976) European Journal ofCardiology 4, 181 Goldberg B B (1971) Journal of the American Medical Association 215, 245 Huntsman L L, Gams E, Johnson C C & Fairbanks E (1975) American Heart Journal 89, 605
501
Clinical experience with transcutaneous aortovelography: preliminary communication' Gillian C Hanson MB MRCP A H Bilton MB BS Whipps Cross Hospital, Leytonstone, London Ell INR
Detailed evaluation ofthe haemodynamic state in the critically ill patient may take time because of difficulty in gaining access to the circulation, and it is not without its dangers. Elaborate systems may be unavailable in certain units because ofexpense or lack of personnel. Monitoring of pulmonary capillary wedge pressure may not reflect left atrial pressure in patients with pulmonary pathology. For these reasons a non-invasive, reproducible and consistent indicator of left ventricular function (Fraser et al. 1976) would be of considerable value in the management of the critically ill. The basic theory of transcutaneous aortovelography (TAV) has been described by Cross & Light (1974). Work by Goldberg (1971) and Huntsman et al. (1975) indicated that it was possible to measure aortic blood flow velocities and accelerations in man by the transcutaneous ultrasonic Doppler method. Clinical evaluation Traces suitable for evaluation could be obtained in approximately 95%o of patients, difficulty being experienced in the elderly patient with emphysema, the restless patient, or the patient with a tracheostomy. In the few patients studied, it would appear that even in those patients with a tracheostomy traces can be obtained after a few days (once the air around the wound has been absorbed) provided there is sufficient room to place the doppler probe between the tracheostome and the suprasternal notch. Our initial clinical evaluation involved hand analysis of the TAV trace (Figure 1) and comparing the extrapolated peak velocity and time averaged velocity (mean aortic velocity) with simple indices of haemodynamic state, such as pulse rate, blood pressure, right atrial pressure, urine output and skin core temperature differential. Clinical situations where the technique proved to be helpful included: the initial evaluation of a shocked patient; and evaluation of the haemodynamic response to a therapeutic manoeuvre. Initial evaluation of a patient in shock: Shock cannot simply be divided into single aetiological components, but in many situations a dominant factor producing the condition can be elicited, which when treated produces haemodynamic improvement. It was shown (Figure 2) that peak velocity and mean aortic velocity were consistently decreased in situations where the dynamic blood volume was low and/or where there was evidence of inadequate left ventricular function. In hypovolaemia the peak velocity and mean aortic velocity rapidly responded, as did the right atrial pressure, to volume replacement (Figures 3, 4). 1
Paper read to Section of Measurement in Medicine, 29 October 1977
0 1 41-0768/78/0071-0501/$O 1.00/0
(C') 1978 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 71 July 1978
502
Glossary to Figures Blood pressure. Systolic pressure. BP SP Mean aortic velocity (see Figure 1) V Central venous pressure or right atrial cvp pressure as measured in the midaxillary line, the patient positioned horizontally. Initial systolic Rate of rise of the initial upstroke of the TAV trace (See Figure 1) acceleration. Extra polated peak velocity, V,
Blood velocity (cm/sec)
A~~~~~~~~~~~~~~~~~~~~~l
_
200 48_______
Z-
108 7-'-
I
0
*V
-... .-
--
.-.
./
. -
Ejection time, tx
0-1se~~~~_
ec
Initial systolic acceleration (cm/sec/sec)
Cardiac cycle period, T Area = 2 * f-V Time - averaged velocity, V =A/T ( mean aortic velocity )
Figure 1. Hand analysis of TAV trace
Shock following myocardial infarction Line around waveform representing aortic systolic flow velocity {
Septic shock (central venous pressure normal)
C
Figure 2. TAV traces on admission of various kinds of shock
.
Journal of the Royal Society of Medicine Volume 71 July 1978 Prior to treatment
Trace
Trc 2
mi
Trace 2
hour 45 min later ~
I
.. ._ . . .. d__ *
a
Trace 3
_.u
. _
~ ~
_
.
~
~
_ ..40
.
.
~
~
~
~
:
I
_. ... _ ~. 0. '_. a
."
a
.
a
a
.
a_ _
0
&
.
6
0
6.
a
5 hours after onset of treatment Total volume of fluid infused 3600 ml
Figure 3. Serial TAV traces during volume replacement for hypovolaemic shock 0
Pulse
(rate/min) 0-
v* BP.SP
20
-------
/
00
-
(mm/Hg) 50 Skin/core differential
10
(OC) 0 25-
(cm/sec)
200 10~~~
A~~~~~~~~~~~ -.0
CVP:-
(cm H20)
A
-
0V
2
.
Volume infused
(mL)
Time in hours after onset of volume replacement
Figure 4. Sequential indices (in conjunction with TAV traces in Figure 3) taken during volume replacement for hypovolaemic shock
503
Journal of the Royal Society of Medicine Volume 71 July 1978
504
Z-
.
.
.
.
.
.
.
( I ) Before volume replacement
.
.
.
.
.
.
.
.
.
.
.
.
.
(2 ) After volume replacement
T
Z..:-
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
( 3 ) After recovery
Figure 5. Serial TAV traces during the management of patient with severe sepsis 1400 Pulse
*
(rate/min)
120
0
-
100 _
BR SP (mm/Hg)
\
8
......
L
'
30 0/
(cm H20)
(cm/sec2)
\0
-.
,()
2
20
0
*
Initial systolic
acceleration
-
1500 _
U
1000 2000
-
Fluid volume replaced ... ... . (ml) .::1000
6. S Figureplad
dit
~~~~~~~~~~~~~~~~~~~~~~~~~~.....................
te in F Hour.Aftr.reover Minutes........... ~4 fter...........
(M se ma0 e of.patient5with sever
.........................issio
Figure indices (in conjunct.. in. Figure.. 5) during6.Sequential themanagement of patient with io...n.....w..h.T.......a..s severe s
.
.
.
-
I
0
*- *
0
0
0
6
0
0
0
e
I~~~~~~~~~~~~~ I
-w~~
am-=== . *
*
*
*
*
*
*
*
*
*0
*-. 0
*
*~
6 *
0 *
X
d
* 0
(I ) Admission
After isoprenaline infusion forapproximately 2 hours (2) ..... @... .. . s
s
.
me
e. *o
*
~~._
:::.~. r ~c~ _..
.
..
(3) 17 hours after admission recovered
Figure 7. Serial TAV traces in patient with amylobarbitone overdose treated with intravenous isoprenaline
0
0
BP. SP. (mm/Hg)
Pulse
(rate/min)
A
0
CVP
(cm/sec)
(cm H20)
11000 Initial systolic acceleration
(cm/sec-2)
2-0 _ I soprenaline ..
., ., ,:..:.. ..
......
.... ..
200 Minutes after admission
17 hours later
Figure 8. Sequential indices (in conjunction with TAV traces in Figure 7) during management of patient with amylobarbitone overdose. High right atrial pressure, low mean aortic velocity and initial systolic acceleration at time of admission were consistent with diagnosis of impaired myocardial performance. Note rapid improvement with isoprenaline infusion and rapid deterioration when it was temporarily withdrawn (arrowed)
506
Journal of the Royal Society of Medicine Volume 71 July 1978
In shock associated with sepsis, peak velocity and mean aortic velocity were found to be consistently high once the circulating blood volume had been restored. It has been found that the rate of rise of the first part of the upstroke (initial systolic acceleration, Figure 1) is consistently increased in conditions of stress where myocardial function is considered adequate (Figures 5, 6). Evaluation of the haemodynamic response to a therapeutic manoeuvre: TAV was found to be a delicate reflector of change in haemodynamic state following a therapeutic manoeuvre (Figures 7, 8). In such conditions, it is well recognized that the right atrial pressure is only a crude guide to left ventricular performance.
Future research Research is at present being conducted comparing indices using the TAV technique with those of right ventricular output (thermodilution technique), pulmonary artery pressure and pulmonary capillary wedge pressure. The preliminary results are encouraging. Preliminary investigations suggest that in the absence of any aortic valve or aortic arch deformity this technique will be a reliable non-invasive indicator of left ventricular function. The method is reproducible, consistent, non-invasive and easy to use. References Cross G & Light L H (1974) Biomedical Engineering 9, 464 Fraser C B, Light L H, Shinebourne E A, Buchtal A, Healy M J R & Beardshaw J A (1976) European Journal ofCardiology 4, 181 Goldberg B B (1971) Journal of the American Medical Association 215, 245 Huntsman L L, Gams E, Johnson C C & Fairbanks E (1975) American Heart Journal 89, 605
