LV systole

IVCT

  • Mitral valve closure (MVC) to aortic valve opening (AVO)

  • Isovolumic contraction — LA contraction is finished, LA/LV pressures are almost equal, the MV closes. The LV pressure rises above the LAP, the MV is closed; the pressure is not yet high enough for AV opening ➜ isovolumic contraction phase (part of systole but no output)

Systole

  • AVO to aortic valve closure (AVC)

  • Systolic ejection — LV-pressure > AV-pressure ➜ maximum pressure at mid-systole. Peak contraction & deformation happen in end-systole

  • The AV closes after the peak systole, with the LV pressures declining

Auswurf

  • Mitralklappenschluss bis Aortenklappenöffnung

  • Systolischer Auswurf — LV Druck > AV Druck ➜ maximaler Druck in der Mid-Systole. Peak Kontraktion & Deformation passiert in der Endsystole

  • Die AV schließt sich nach der Peaksystole mit einem Druckabfall des LV

IVCT happening before S’

IVCT happening before S’

LVOT signal

LVOT signal

Nakatani S, 2011

LV diastole

IVRT

  • AVC to MV-opening (MVO)

  • Isovolumic relaxation — compression & torsion lead to energy of the elastic elements of the cardiomyocytes & extracellular matrix in end-systole ➜ recoil & untwist in early diastole due to relaxed state“ + active myocyte relaxation ➜ LV-volume ↑ & LV-pressure ↓ = measurable

  • At the beginning of diastole, LV pressures are just below AV pressures; the LV pressures are just above the LAP ➜ the IVRT is a short time interval of expansion of the LV without volume change ➜ AV & MV are closed = isovulmetric relaxation time (around 40ms)

Lateral TDI for time intervals

Lateral TDI for time intervals

Early filling (E-Wave)

  • Due to untwisting & relaxation, the LV pressure drops, LAP is higher than the LV pressure, the suction opens the MV ➜ end of the IVRT & beginning of the E-wave. A short (30-40ms) period lowers the LV pressure even though the LV volume expands ➜ a gradient from LA to LV ➜ flow acceleration

  • 80-90% of the blood volume is sucked into the LV during this time (duration around 140ms)

Diastasis

  • The LV is in a relaxed state, LV pressures rise mildly, there is almost no pressure difference between the LA & the LV

  • The MV is semi-open“

  • Heart rate dependent — bradycardia, long diastasis; tachycardia, almost no diastasis

Short diastasis

Short diastasis

Long diastasis

Long diastasis

Atrial contraction (A-wave)

  • LA contraction elevates LV pressures ➜ MV opens again, LV fills with blood again

  • In normal filling pressures, almost no counterpressure“ from the LV, a little bit of blood flows back to the PV, 10-20% of the blood is transported with <5mmHg of pressure

  • The LVEDP, LAP, PV, and pulmonary pressures are low

Bradycardia in ACS, restriction

Bradycardia in ACS, restriction

Nakatani S, 2011

The contents of the website, including the videos, were created without influence from third parties.

The contents of the website, including the videos, were created without influence from third parties.

The Strain Book

Represented by Dr. Martin Altersberger

Contact: heart.lungs.ultrasound@gmail.com

The Strain Book

Represented by Dr. Martin Altersberger

Contact: heart.lungs.ultrasound@gmail.com

© 2026 The Strain Book by Dr. Martin Altersberger. All rights reserved.

© 2026 The Strain Book by Dr. Martin Altersberger. All rights reserved.

© 2026 The Strain Book by Dr. Martin Altersberger. All rights reserved.