antonini-canterin_2013_the_ventricular-arterial_coupling_-_from_basic_pathophysiology_to_clinical.pdf
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- Full Title: antonini-canterin_2013_the_ventricular-arterial_coupling_-_from_basic_pathophysiology_to_clinical.pdf
- Category: #books
Highlights
- ventricular-arterial coupling is commonly calculated by the ratio of effective arterial elastance (EA), a measure of afterload, to LV end-systolic elastance (EES), a relatively load independent measure of LV chamber performance. Both these measures are expressed in mmHg/ml and therefore comparable mathematically. (Page 1)
- Normal invasively determined EEA and EES values in resting subjects are 2.2 ± 0.8 mmHg/ml and 2.3 ± 1.0 mmHg/ml, respectively. As a consequence, when EA/EES ratio is approximately equal to 1.0, LV and arterial system are optimally coupled to produce stroke work, a measure of the efficiency of LV work, corresponding to the product of systolic arterial pressure and stroke volume, and related to O2 consumption.[5] (Page 1)
- [4] However, aortic input impedance is described in the frequency domain, whereas measures of LV contractility are best described in the time domain; consequently direct comparisons between arterial and LV function is difficult. (Page 1)
- In a patient with a failing heart, EES is reduced and EA is increased. In this situation, LV and arterial system are coupled in a suboptimal way resulting in a EA/EES ratio >1.0.[6] An increase in heart rate will further increase EA, worsening the coupling.[7] On the contrary, vasodilator therapy, lowering EA, brings the EA/EES ratio back down toward 1.0, improving the coupling. Similarly, inotropic therapy, increasing EES, improves the coupling.[ (Page 2)
- a rough estimate of ventricular-arterial coupling could be obtained using such a simplified approach: EA = ESP/SV, EES = ESP/ESV where ESP is the end systolic pressure, SV is the stroke volume, and ESV is the end systolic volume. So: EA/EES = (ESP/SV)/(ESP/ESV) and then simplifying, eliminating ESP: EA/EES = ESV/SV The problem with this simplified approach is that the ESV SV ratio is related in mathematical terms to the ejection fraction (1/EF - 1) and therefore it does not add substantial information to the traditional ejection fraction measurement. (Page 2)
- end-systolic pressure can be estimated as 0.9 times the peak brachial systolic pressure. Thus, EA can be easily calculated as 0.9 times the brachial systolic pressure divided by stroke volume, determined at LV outflow tract level by Doppler techniques (Page 2)
antonini-canterin_2013_the_ventricular-arterial_coupling_-_from_basic_pathophysiology_to_clinical.pdf
- Author:
- Full Title: antonini-canterin_2013_the_ventricular-arterial_coupling_-_from_basic_pathophysiology_to_clinical.pdf
- Category: #books
Highlights
- ventricular-arterial coupling is commonly calculated by the ratio of effective arterial elastance (EA), a measure of afterload, to LV end-systolic elastance (EES), a relatively load independent measure of LV chamber performance. Both these measures are expressed in mmHg/ml and therefore comparable mathematically. (Page 1)
- Normal invasively determined EEA and EES values in resting subjects are 2.2 ± 0.8 mmHg/ml and 2.3 ± 1.0 mmHg/ml, respectively. As a consequence, when EA/EES ratio is approximately equal to 1.0, LV and arterial system are optimally coupled to produce stroke work, a measure of the efficiency of LV work, corresponding to the product of systolic arterial pressure and stroke volume, and related to O2 consumption.[5] (Page 1)
- [4] However, aortic input impedance is described in the frequency domain, whereas measures of LV contractility are best described in the time domain; consequently direct comparisons between arterial and LV function is difficult. (Page 1)
- In a patient with a failing heart, EES is reduced and EA is increased. In this situation, LV and arterial system are coupled in a suboptimal way resulting in a EA/EES ratio >1.0.[6] An increase in heart rate will further increase EA, worsening the coupling.[7] On the contrary, vasodilator therapy, lowering EA, brings the EA/EES ratio back down toward 1.0, improving the coupling. Similarly, inotropic therapy, increasing EES, improves the coupling.[ (Page 2)
- a rough estimate of ventricular-arterial coupling could be obtained using such a simplified approach: EA = ESP/SV, EES = ESP/ESV where ESP is the end systolic pressure, SV is the stroke volume, and ESV is the end systolic volume. So: EA/EES = (ESP/SV)/(ESP/ESV) and then simplifying, eliminating ESP: EA/EES = ESV/SV The problem with this simplified approach is that the ESV SV ratio is related in mathematical terms to the ejection fraction (1/EF - 1) and therefore it does not add substantial information to the traditional ejection fraction measurement. (Page 2)
- end-systolic pressure can be estimated as 0.9 times the peak brachial systolic pressure. Thus, EA can be easily calculated as 0.9 times the brachial systolic pressure divided by stroke volume, determined at LV outflow tract level by Doppler techniques (Page 2)