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Coupling between the heart and arterial system in heart failure
Coupling Between the Heart and Arterial System in Heart Failure SHIGETAKESASAYAMA, M.D., HIDETSUGUASANOI, M.D., Toyama, Japan
A number of experimental studies have demonstrated the optimal coupling between the ventricle and arterial load, under physiologic and pathologic circumstances, directed to produce maximal stroke work. We investigated matching of the ventricular properties, quantified by the slope of end-systolic pressure-volume relationship, with arterial load properties, expressed by the slope of end-systolic pressurestroke volume relationship. In normal subjects, with ejection fraction of ZOO%, ventricular elastance was nearly twice as large as arterial elastance. This condition affords maximal mechanical efficiency. In patients with moderate heart failure, with ejection fraction of 40-59%, ventricular elastance was almost equal to arterial elastance. This condition affords maximal stroke work from a given end-diastolic volume. In patients with severe heart failure, with ejection fraction of <40%, ventricular elastance was less than half of arterial elastance, which resulted in increased potential energy and decreased work efficiency. Ventriculoarterial coupling is normally set toward higher left ventricular work efficiency, whereas in patients with moderate cardiac dysfunction, ventricular and arterial properties are matched, in order to maximize stroke work at the expense of work efficiency. Neither the stroke work nor work efficiency is near maximum for patients with severe cardiac dysfunction.
A
dequate cardiac output to peripheral tissue can be achieved by means of a unique interaction between the heart and arterial loads, in order to optimize ventricular performance. The ventricle transfers the mechanical energy of contraction to the intracavitary blood, to provide adequate flow to the arterial system [1,2]. The ventricle is generally considered matched to a given load if it allows a maximal amount of external work against that load [3-51.
STROKEVOLUMEPREDICTEDBY VENTRICULAR ARTERIALCOUPLING Sunagawa et al. [6] proposed the framework for coupling of the ventricular arterial loads by modeling the left ventricle as an elastic chamber, which periodically increases its volume elastance (V,) to a value equal to the slope of the linear end-systolic pressure-volume relationship, and the arterial load property as an effective arterial elastance (E,) represented by the slope of the arterial end-systolic pressure-stroke volume relationship. The left ventricular end-systolic pressure (P,,)-left ventricular end-systolic volume (I',,) relationship is approximately linear over a physiologic range, with endsystolic elastance (E,,) and constant volume (V,) axis. The E,, varies in response to changes in ventricular contractility. According to this relationship, the end-systolic pressure varies inversely with stroke volume (SV) for a given end-diastolic volume (V,,):
P,, = E,, We, - SV - Vo> = Ee, Ve, - Vo>
(1)
Arterial system properties can be expressed by a P,, - SV relationship, and SV is calculated analytically, as follows: P,,=E; SV G-3 SV = Wed- V,J/(l + E,/E,,) (3) Assuming that the time-averaged ventricular ejection pressure is close to P,,, ventricular stroke work (SW) can be derived as follows:
SW=SVxP,, = E,, Fe, - Vo>2W-W,,>~U+ W-&,>2l From the Second Department of Internal Medicine, loyama Medical and Pharmaceutlcal University, Toyama, Japan. 2nd Department of Internal Medicine, loyama Medical and Pharmaceutical versity, 2630 Sugitani, Toyama 930-01, Japan.
5514s
May 29, 1991
The American Journal of Medicine
Unl-
(4)
The interaction between the ventricular and arterial P,,-SV relationship is presented in Figure 1. Equation 2 indicates that the greater the SV ejected into the arterial system, the greater is the generated P,,. This relationship can be superim-
Volume 90 (suppl 5B)
SYMPOSIUM
posed on the left ventricular end-systolic pressure/ left ventricular end-systolic volume relationship by reversing the volume axis so that the SV is plotted against some specified end-diastolic volume as a zero reference. The stroke volume that the ventricle can eject from a given Ved can be obtained from the intersection of these two end-systolic pressurevolume relationships. Within the framework of this coupling concept, Sunagawa et al. [6] demonstrated that the ventricle does maximal external work to the arterial load when the ventricular and arterial elastances are equalized, An increase in I’,, induces a rightward shift of the arterial P,,-SV relationship, without a change in the ventricular P,,-V,, relationship, allowing optimal loading to be achieved with the same arterial elastance value. Enhancement of contractility was associated with an increase in the slope of the ventricular P,,--V,, relationship, together with an increase in the arterial elastance by increasing arterial resistance to similar extents. Figure 2 shows the major mechanisms determining SV, under various loading conditions and different inotropic states, with the ratio of the optimal effective arterial elastance to the given ventricular elastance remaining near unity.
VENTRICULAREFFICIENCYPREDICTEDBY A COUPLINGFRAMEWORK
(6)
PVA is the sum of SW and PE and is approximated
by PVA = E,,(V,, - VJ2[(EalE,,)l (1 + &/E,,>21[1 f (E,IE,,)I21 According to the linear relationship between
LEFT VEWTRICLE
,
$
‘I ----
0
;h LW
‘.
‘.
(
0
\
Another criterion for optimal coupling between an energy source and its load is the principle of economical fuel consumption or mechanical efficiency, defined as the ratio of stroke work to myocardial oxygen consumption per beat [7-g]. Burkhoff and Sagawa [7] derived a simple analytic model relating to the properties of the vascular system and the left ventricle to the mechanical work done by the heart and the amount of chemical energy consumed by the heart. Recently Suga and colleagues [lO,ll] have demonstrated that the total mechanical work performed by the ventricle with each cardiac cycle can be estimated by the pressure-volume area (PVA) defined as the sum of the external stroke work and the unexpressed mechanical potential energy (PE) stored in the ventricle at the end of ejection: PE = P,, (V,, - VJ2 (5) Substituting equations 1 and 3 into equation 5, PE can be expressed as PE = E&V,, - Vo)2
KW-G,>2~Wl + -WW2
ON IBOPAMINE / SASAYAMA and ASANOI
(7) PVA
I
)I K.
I
LW
CN
Ved
Figure 1. A schematic illustration of the framework for coupling of the ventricle with the arterial load. Left panel is the left ventricular end-systolic pressure/left ventricular end-systolic volume relationship, and right panel is the arterial end-systolic/ stroke volume relationship. The equilibrium stroke volume can be obtained from the intersections between the two end-systolic pressure-volume relationship lines transformed on the same pressure-volume plane. P,, = end systolic pressure; LVV = left ventricular volume; f, = end systolic volume; SV = stroke volume; V,, = end-diastolic volume. Reprinted with permission from [6].
and myocardial
oxygen consumption (MV02), MV02 = A(PVA) + B (8) Ventricular efficiency (Eff) is, by definition, the ratio between external SW and MV02. Consequently, the following analytic equation is obtained by combining equations 4, 7, and 8: Eff = l/[A(l + E$2E,,)
May 29, 1991
+ BU + &lE,,)2/&Ve, The American Journal of Medicine
- VJ21
Volume 90 (suppl 5B)
(9) 58-15s
SYMPOSIUM
ON IBOPAMINE I SASAYAMA and ASANOI
Figure 2. Effects of changes in end-diastolic volume (Ved), contractility, heart rate, and arterial compliance on ejection fraction (upper panel) and EJE,, ratio. E, = arterial effective elastance; E,, = end-systolic elastance; MID = middle. Reprinted with permission from [6].
Figure 3 shows an example of the predictions of equations 4, 8, and 9, in which SW, MVOz, and efficiency are plotted as a function of effective arterial elastance (E,). With increases in E,, SW initially increases, reaches a plateau, and then decreases. As shown by Sunagawa et al. [6], maximum SW occurs when arterial and ventricular properties are equalized. This matched condition is indicated by the dashed lines at E, = 7 mm Hg/ml (Figure 3). Ventricular efficiency, defined as the ratio between external SW and MVOa, initially rises with increases in E,, reaches a maximum, and then decreases. Optimum efficiency occurs when E, is less than E,, (at E, = 3.4 in this case), as indicated by the dotted lines (Figure 3). Using this model, it was demonstrated that SW is maximum when E, = Ii’,,, but the afterload that results in the greatest efficiency is always less than that which provides the maximum SW: It was suggested that cardiovascular properties are set more toward optimization of ventricular efficiency than stroke work under physiologic conditions.
VENTRICULOARTERIAL COUPLINGIN NORMAL SUBJECTSAND PATIENTSWITH HEART FAILURE The concept of ventriculoarterial interaction has been extended for the first time to human studies, and physiologic matching of cardiac performance with arterial load has been evaluated in terms of the above-mentioned ventricular and arterial volume elastance [X2]. Eight normal subjects with no signs and symptoms of cardiac disease, four patients with atypical chest pain, and 16 patients with cardiac dysfunction constituted the study group. All patients had supporting clinical, chest radiographic, and echocardiographic evidence of impaired left ventricular func5C16S
May 29, 1991
The American Journal of Medicine
tion. Severity of cardiac disease ranged from class II to class III. Subjects were divided into three groups based on their resting left ventricular ejection fraction (EF), which was determined by echocardiography. Group A consisted of 12 subjects with left ventricular EF of 160%. Group B consisted of seven patients with mild left ventricular dysfunction in whom EF was 40-59%. Group C consisted of nine patients with greater left ventricular dysfunction, in whom EF was <40%. A 19-gauge cannula was inserted percutaneously into a brachial artery and was connected to a straingauge manometer. After eontrol recordings at rest, the systolic pressure was charged by about 40 mm Hg by intravenous infusion of phenylephrine and nitroprusside. Two-dimensional targeted M-mode echocardiograms of the left ventricular cavity were recorded simultaneously with arterial pressure. Left ventricular volume was determined using the Teichholz et al formula [13]. Left ventricular endsystolic pressure was approximated from the arterial dicrotic pressure, which was considered to have been caused by aortic valve closure. Left ventricular contractile properties were defined by the slope of the left ventricular endsystolic pressure/left ventricular end-systolic volume relationship (E,, and V,) and arterial system properties by E,. SW was calculated as P&V,, V,,,). P,, and V,, are graphically determined data points at which the two left ventricular end-systolic pressure/left ventricular end-systolic volume relationship lines intersect. The ratio of SW to the systolic PVA, which has been defined as the total mechanical energy of the ejecting contraction, was determined. Figure 4 shows a representative ventricular P,,V,, relationship and arterial P,, - SV relationships
Volume 90 (suppl 5B)
SYMPOSIUMON IBOPAMINEISASAYAMAand ASANOI
(mmHg)
I
-Ea
Ees
ESP 0
b
3
9 6 Ea (mmHg/ml)
12
15
ul r( .
IB
vo
ESV
Ved
(ml)
Figure 4. Schematic representation of ventr~culoarterial coupling on the pressure-
0
I 0
volume plane. The shaded area represents the stroke work (SW) and the triangular area shows end-systolic potential energy (PE). Maximal SW (SW max) for a given end-diastolic volume (V,,) can be determined when E,, is assumed to be equal to E,. E, = arterial effective elastance; E,, = end-systolic elastance; ESP = end-systolic pressure; V, = volume; ESV = end-systolic volume; V,, = end-diastolic volume. Reprinted with permission from [12]
I I 1 3
6
9
12
1s
Ea (mmHg/ml)
I 0
50
Left
150
100
Ventricular
Volume
200
(ml/m’)
Figure 5. Representatrve
0 Figure stroke values dotted
3
6 9 Ea (mmHg/ml
12
15
3. Relationship between f,, the quantifier of afterload impedance, and work (SW), myocardial O2 consumption (MVOP), and ventricular efficiency. E, at greatest SW and greatest efficiency have been indicated by dashed and knes, respectively. Reprinted with permission from [A.
at baseline (solid line) and after pressure manipulation (dashed line) for patients in Groups A, B, and C. Linear relationships between corresponding end-systolic pressure and volume have been ob-
ventricular end-systolrc pressure-volume and arterr end-systolic pressure-stroke volume relationships for patients in Groups A, 8, and C, at baseline (solid lines) and after pressure manipulations (dashed lines).
served in these patients. E,, was 4.5 mm Hg/ml/m’ in group A and this value decreased substantially as the heart failed (2.5 mm Hg/ml/m2 in group B and 1.5 mm Hg/mllm2 in group C). With a reduction of EF, Ved and V,, were progressively augmented and E, tended to increase. In group A, E,IE,, was 0.50, and E, tended to increase, with E,, being nearly twice as much as E,. In group B, E,IE,, was 0.97,
May 29, 1991
The American Journal of Medicine
Volume 90 (suppl 56)
5517s
SYMPOSIUM
ON BOPAMINE / SASAYAMA and ASANOI
Ea
Ea/Ees
mmHg/mQ/m’ 4.or
4.0r
A
0
0
A
B
C
A
B
C
*p
Figure 6. Arterial effective elastance (E,) (left panel) and its ratio to the ventricular volume elastance (E,,) (right panel) for patients in Groups A, 6, and C.
EW/PVA
EW/EWmax
with the ventricle providing maximal transfer of mechanical energy of contraction to the arterial system. Thus the normal coupling condition in Group A is surprisingly similar to the data of Burkhoff and Sagawa [71, and cardiovascular interaction in normal subjects was set to optimize left ventricular work efficiency in the resting state (Figure 6). Moderately depressed hearts maximize SW as demonstrated by Sunagawa [6] but they generate a greater potential energy with consequent reduction in work efficiency (Figure 7). Severely depressed hearts were no longer capable of maintaining SW or work efficiency properly. In summary, analysis of ventriculoarterial coupling delineated the distinction between normal and variably failing hearts. The coupling concept is considered to have great potential usefulness toward gaining insight into the relevance of adaptational changes and therapeutic responses in congestive heart failure.
REFERENCES 1. Piene H, Sund T: Does normal pulmonary impedance constitute the optimal load for the right ventricle? Am J Physlol 1982; 242: H154-60.
0
2. Yamakoshi K: Interaction between heart as a pump and artery as a load. Jpn Circ J 1985; 49: 195-205. 3. Sunagawa K, Maughan WL, Burkhoff D, Sagawa K: Left ventricular interaction with arterial load studied in isolated canine heart Am J Physiol 1983; 245: Hn380.
A
B
C * p
Figure 7. Left panel: The left ventricular pump efficiency indicated by the ratio of external work to pressure volume area (EWIPVA). Right panel: The ratio of EW to its maximum value attainable.
with E,, being nearly equal to E,. In group C, E,/ E,, increased to 2.29, with E,, being far less than E,. Figure 5 shows the left ventricular pump efficiency, indicated by the ratio of external work (EW) to PVA and the ratio of EW to its maximum value attained. Pump efficiency was highest in Group A (82% + 5%) and progressively fell with a reduction of EF (to 69% i 5% in Group B and 50% ? 10% in Group C). EW was near its maximum in Group B patients with moderate cardiac failure,
5518s
May 29, 1991
The American Journal of Medicine
4. Piene H, Sund T: Flow and power output of right ventricle facing load with variable input impedance. Am J Physiol 1979; 237: H125-30. 5. Van den Horn GJ, Westerhof N, Elzinga G: Optimal power generation by ihe left ventricle: A study in the anesthetized open thorax cat. Circ Res 1985; 56: 252-61. 6. Sunagawa K, Maughan WL, Sagawa K: Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle. Circ Res 1985; 56: 586-95. 7. Burkhoff D, Sagawa K: Ventricular efficiency predicted by an analytical model. Am J Physiol 1986; 250: R1021-7. 8. Suga H, lgarashi Y, Yamada 0, Goto Y: Mechanical efficiency of the left ventricle as a function of preload, afterload, and contractility. Heart Vessels 1985; 1: 3-8. 9. Elzinga G, Westerhof N: Pump function of the felme left heart: changes with heart rate and its bearing on the energy balance. Cardiovasc Res 1980; 14: 81-92. 10. Suga H: Total mechanical energy of a ventricle model and cardiac oxygen consumption. Am J Physiol 1979; 236: H498-505. 11. Suga H, Hayashi T, Shirahata M, Ninomiya I: Critical evaluation of left ventricular systolic pressure volume area as predictor of oxygen consumption rate. Jpn J Physiol 1980; 30: 907-19. 12. Asanoi H, Sasayama S, Kameyama T: Ventriculoarterial coupling in normal and failing heart in humans. Circ Res 1989; 65: 483-93. 13. Teichholz LE, Kreulen T, Herman MV, Gorlin R: Problems in echocardlographicangiographic correlations in the presence of absence of synergy Am J Cardiol 1976; 37 (I): 7-11.
Volume 90 (suppl 56)
A number of experimental studies have demonstrated the optimal coupling between the ventricle and arterial load, under physiologic and pathologic circumstances, directed to produce maximal stroke work. We investigated matching of the ventricular properties, quantified by the slope of end-systolic pressure-volume relationship, with arterial load properties, expressed by the slope of end-systolic pressurestroke volume relationship. In normal subjects, with ejection fraction of ZOO%, ventricular elastance was nearly twice as large as arterial elastance. This condition affords maximal mechanical efficiency. In patients with moderate heart failure, with ejection fraction of 40-59%, ventricular elastance was almost equal to arterial elastance. This condition affords maximal stroke work from a given end-diastolic volume. In patients with severe heart failure, with ejection fraction of <40%, ventricular elastance was less than half of arterial elastance, which resulted in increased potential energy and decreased work efficiency. Ventriculoarterial coupling is normally set toward higher left ventricular work efficiency, whereas in patients with moderate cardiac dysfunction, ventricular and arterial properties are matched, in order to maximize stroke work at the expense of work efficiency. Neither the stroke work nor work efficiency is near maximum for patients with severe cardiac dysfunction.
A
dequate cardiac output to peripheral tissue can be achieved by means of a unique interaction between the heart and arterial loads, in order to optimize ventricular performance. The ventricle transfers the mechanical energy of contraction to the intracavitary blood, to provide adequate flow to the arterial system [1,2]. The ventricle is generally considered matched to a given load if it allows a maximal amount of external work against that load [3-51.
STROKEVOLUMEPREDICTEDBY VENTRICULAR ARTERIALCOUPLING Sunagawa et al. [6] proposed the framework for coupling of the ventricular arterial loads by modeling the left ventricle as an elastic chamber, which periodically increases its volume elastance (V,) to a value equal to the slope of the linear end-systolic pressure-volume relationship, and the arterial load property as an effective arterial elastance (E,) represented by the slope of the arterial end-systolic pressure-stroke volume relationship. The left ventricular end-systolic pressure (P,,)-left ventricular end-systolic volume (I',,) relationship is approximately linear over a physiologic range, with endsystolic elastance (E,,) and constant volume (V,) axis. The E,, varies in response to changes in ventricular contractility. According to this relationship, the end-systolic pressure varies inversely with stroke volume (SV) for a given end-diastolic volume (V,,):
P,, = E,, We, - SV - Vo> = Ee, Ve, - Vo>
(1)
Arterial system properties can be expressed by a P,, - SV relationship, and SV is calculated analytically, as follows: P,,=E; SV G-3 SV = Wed- V,J/(l + E,/E,,) (3) Assuming that the time-averaged ventricular ejection pressure is close to P,,, ventricular stroke work (SW) can be derived as follows:
SW=SVxP,, = E,, Fe, - Vo>2W-W,,>~U+ W-&,>2l From the Second Department of Internal Medicine, loyama Medical and Pharmaceutlcal University, Toyama, Japan. 2nd Department of Internal Medicine, loyama Medical and Pharmaceutical versity, 2630 Sugitani, Toyama 930-01, Japan.
5514s
May 29, 1991
The American Journal of Medicine
Unl-
(4)
The interaction between the ventricular and arterial P,,-SV relationship is presented in Figure 1. Equation 2 indicates that the greater the SV ejected into the arterial system, the greater is the generated P,,. This relationship can be superim-
Volume 90 (suppl 5B)
SYMPOSIUM
posed on the left ventricular end-systolic pressure/ left ventricular end-systolic volume relationship by reversing the volume axis so that the SV is plotted against some specified end-diastolic volume as a zero reference. The stroke volume that the ventricle can eject from a given Ved can be obtained from the intersection of these two end-systolic pressurevolume relationships. Within the framework of this coupling concept, Sunagawa et al. [6] demonstrated that the ventricle does maximal external work to the arterial load when the ventricular and arterial elastances are equalized, An increase in I’,, induces a rightward shift of the arterial P,,-SV relationship, without a change in the ventricular P,,-V,, relationship, allowing optimal loading to be achieved with the same arterial elastance value. Enhancement of contractility was associated with an increase in the slope of the ventricular P,,--V,, relationship, together with an increase in the arterial elastance by increasing arterial resistance to similar extents. Figure 2 shows the major mechanisms determining SV, under various loading conditions and different inotropic states, with the ratio of the optimal effective arterial elastance to the given ventricular elastance remaining near unity.
VENTRICULAREFFICIENCYPREDICTEDBY A COUPLINGFRAMEWORK
(6)
PVA is the sum of SW and PE and is approximated
by PVA = E,,(V,, - VJ2[(EalE,,)l (1 + &/E,,>21[1 f (E,IE,,)I21 According to the linear relationship between
LEFT VEWTRICLE
,
$
‘I ----
0
;h LW
‘.
‘.
(
0
\
Another criterion for optimal coupling between an energy source and its load is the principle of economical fuel consumption or mechanical efficiency, defined as the ratio of stroke work to myocardial oxygen consumption per beat [7-g]. Burkhoff and Sagawa [7] derived a simple analytic model relating to the properties of the vascular system and the left ventricle to the mechanical work done by the heart and the amount of chemical energy consumed by the heart. Recently Suga and colleagues [lO,ll] have demonstrated that the total mechanical work performed by the ventricle with each cardiac cycle can be estimated by the pressure-volume area (PVA) defined as the sum of the external stroke work and the unexpressed mechanical potential energy (PE) stored in the ventricle at the end of ejection: PE = P,, (V,, - VJ2 (5) Substituting equations 1 and 3 into equation 5, PE can be expressed as PE = E&V,, - Vo)2
KW-G,>2~Wl + -WW2
ON IBOPAMINE / SASAYAMA and ASANOI
(7) PVA
I
)I K.
I
LW
CN
Ved
Figure 1. A schematic illustration of the framework for coupling of the ventricle with the arterial load. Left panel is the left ventricular end-systolic pressure/left ventricular end-systolic volume relationship, and right panel is the arterial end-systolic/ stroke volume relationship. The equilibrium stroke volume can be obtained from the intersections between the two end-systolic pressure-volume relationship lines transformed on the same pressure-volume plane. P,, = end systolic pressure; LVV = left ventricular volume; f, = end systolic volume; SV = stroke volume; V,, = end-diastolic volume. Reprinted with permission from [6].
and myocardial
oxygen consumption (MV02), MV02 = A(PVA) + B (8) Ventricular efficiency (Eff) is, by definition, the ratio between external SW and MV02. Consequently, the following analytic equation is obtained by combining equations 4, 7, and 8: Eff = l/[A(l + E$2E,,)
May 29, 1991
+ BU + &lE,,)2/&Ve, The American Journal of Medicine
- VJ21
Volume 90 (suppl 5B)
(9) 58-15s
SYMPOSIUM
ON IBOPAMINE I SASAYAMA and ASANOI
Figure 2. Effects of changes in end-diastolic volume (Ved), contractility, heart rate, and arterial compliance on ejection fraction (upper panel) and EJE,, ratio. E, = arterial effective elastance; E,, = end-systolic elastance; MID = middle. Reprinted with permission from [6].
Figure 3 shows an example of the predictions of equations 4, 8, and 9, in which SW, MVOz, and efficiency are plotted as a function of effective arterial elastance (E,). With increases in E,, SW initially increases, reaches a plateau, and then decreases. As shown by Sunagawa et al. [6], maximum SW occurs when arterial and ventricular properties are equalized. This matched condition is indicated by the dashed lines at E, = 7 mm Hg/ml (Figure 3). Ventricular efficiency, defined as the ratio between external SW and MVOa, initially rises with increases in E,, reaches a maximum, and then decreases. Optimum efficiency occurs when E, is less than E,, (at E, = 3.4 in this case), as indicated by the dotted lines (Figure 3). Using this model, it was demonstrated that SW is maximum when E, = Ii’,,, but the afterload that results in the greatest efficiency is always less than that which provides the maximum SW: It was suggested that cardiovascular properties are set more toward optimization of ventricular efficiency than stroke work under physiologic conditions.
VENTRICULOARTERIAL COUPLINGIN NORMAL SUBJECTSAND PATIENTSWITH HEART FAILURE The concept of ventriculoarterial interaction has been extended for the first time to human studies, and physiologic matching of cardiac performance with arterial load has been evaluated in terms of the above-mentioned ventricular and arterial volume elastance [X2]. Eight normal subjects with no signs and symptoms of cardiac disease, four patients with atypical chest pain, and 16 patients with cardiac dysfunction constituted the study group. All patients had supporting clinical, chest radiographic, and echocardiographic evidence of impaired left ventricular func5C16S
May 29, 1991
The American Journal of Medicine
tion. Severity of cardiac disease ranged from class II to class III. Subjects were divided into three groups based on their resting left ventricular ejection fraction (EF), which was determined by echocardiography. Group A consisted of 12 subjects with left ventricular EF of 160%. Group B consisted of seven patients with mild left ventricular dysfunction in whom EF was 40-59%. Group C consisted of nine patients with greater left ventricular dysfunction, in whom EF was <40%. A 19-gauge cannula was inserted percutaneously into a brachial artery and was connected to a straingauge manometer. After eontrol recordings at rest, the systolic pressure was charged by about 40 mm Hg by intravenous infusion of phenylephrine and nitroprusside. Two-dimensional targeted M-mode echocardiograms of the left ventricular cavity were recorded simultaneously with arterial pressure. Left ventricular volume was determined using the Teichholz et al formula [13]. Left ventricular endsystolic pressure was approximated from the arterial dicrotic pressure, which was considered to have been caused by aortic valve closure. Left ventricular contractile properties were defined by the slope of the left ventricular endsystolic pressure/left ventricular end-systolic volume relationship (E,, and V,) and arterial system properties by E,. SW was calculated as P&V,, V,,,). P,, and V,, are graphically determined data points at which the two left ventricular end-systolic pressure/left ventricular end-systolic volume relationship lines intersect. The ratio of SW to the systolic PVA, which has been defined as the total mechanical energy of the ejecting contraction, was determined. Figure 4 shows a representative ventricular P,,V,, relationship and arterial P,, - SV relationships
Volume 90 (suppl 5B)
SYMPOSIUMON IBOPAMINEISASAYAMAand ASANOI
(mmHg)
I
-Ea
Ees
ESP 0
b
3
9 6 Ea (mmHg/ml)
12
15
ul r( .
IB
vo
ESV
Ved
(ml)
Figure 4. Schematic representation of ventr~culoarterial coupling on the pressure-
0
I 0
volume plane. The shaded area represents the stroke work (SW) and the triangular area shows end-systolic potential energy (PE). Maximal SW (SW max) for a given end-diastolic volume (V,,) can be determined when E,, is assumed to be equal to E,. E, = arterial effective elastance; E,, = end-systolic elastance; ESP = end-systolic pressure; V, = volume; ESV = end-systolic volume; V,, = end-diastolic volume. Reprinted with permission from [12]
I I 1 3
6
9
12
1s
Ea (mmHg/ml)
I 0
50
Left
150
100
Ventricular
Volume
200
(ml/m’)
Figure 5. Representatrve
0 Figure stroke values dotted
3
6 9 Ea (mmHg/ml
12
15
3. Relationship between f,, the quantifier of afterload impedance, and work (SW), myocardial O2 consumption (MVOP), and ventricular efficiency. E, at greatest SW and greatest efficiency have been indicated by dashed and knes, respectively. Reprinted with permission from [A.
at baseline (solid line) and after pressure manipulation (dashed line) for patients in Groups A, B, and C. Linear relationships between corresponding end-systolic pressure and volume have been ob-
ventricular end-systolrc pressure-volume and arterr end-systolic pressure-stroke volume relationships for patients in Groups A, 8, and C, at baseline (solid lines) and after pressure manipulations (dashed lines).
served in these patients. E,, was 4.5 mm Hg/ml/m’ in group A and this value decreased substantially as the heart failed (2.5 mm Hg/ml/m2 in group B and 1.5 mm Hg/mllm2 in group C). With a reduction of EF, Ved and V,, were progressively augmented and E, tended to increase. In group A, E,IE,, was 0.50, and E, tended to increase, with E,, being nearly twice as much as E,. In group B, E,IE,, was 0.97,
May 29, 1991
The American Journal of Medicine
Volume 90 (suppl 56)
5517s
SYMPOSIUM
ON BOPAMINE / SASAYAMA and ASANOI
Ea
Ea/Ees
mmHg/mQ/m’ 4.or
4.0r
A
0
0
A
B
C
A
B
C
*p
Figure 6. Arterial effective elastance (E,) (left panel) and its ratio to the ventricular volume elastance (E,,) (right panel) for patients in Groups A, 6, and C.
EW/PVA
EW/EWmax
with the ventricle providing maximal transfer of mechanical energy of contraction to the arterial system. Thus the normal coupling condition in Group A is surprisingly similar to the data of Burkhoff and Sagawa [71, and cardiovascular interaction in normal subjects was set to optimize left ventricular work efficiency in the resting state (Figure 6). Moderately depressed hearts maximize SW as demonstrated by Sunagawa [6] but they generate a greater potential energy with consequent reduction in work efficiency (Figure 7). Severely depressed hearts were no longer capable of maintaining SW or work efficiency properly. In summary, analysis of ventriculoarterial coupling delineated the distinction between normal and variably failing hearts. The coupling concept is considered to have great potential usefulness toward gaining insight into the relevance of adaptational changes and therapeutic responses in congestive heart failure.
REFERENCES 1. Piene H, Sund T: Does normal pulmonary impedance constitute the optimal load for the right ventricle? Am J Physlol 1982; 242: H154-60.
0
2. Yamakoshi K: Interaction between heart as a pump and artery as a load. Jpn Circ J 1985; 49: 195-205. 3. Sunagawa K, Maughan WL, Burkhoff D, Sagawa K: Left ventricular interaction with arterial load studied in isolated canine heart Am J Physiol 1983; 245: Hn380.
A
B
C * p
Figure 7. Left panel: The left ventricular pump efficiency indicated by the ratio of external work to pressure volume area (EWIPVA). Right panel: The ratio of EW to its maximum value attainable.
with E,, being nearly equal to E,. In group C, E,/ E,, increased to 2.29, with E,, being far less than E,. Figure 5 shows the left ventricular pump efficiency, indicated by the ratio of external work (EW) to PVA and the ratio of EW to its maximum value attained. Pump efficiency was highest in Group A (82% + 5%) and progressively fell with a reduction of EF (to 69% i 5% in Group B and 50% ? 10% in Group C). EW was near its maximum in Group B patients with moderate cardiac failure,
5518s
May 29, 1991
The American Journal of Medicine
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Volume 90 (suppl 56)