Diastolic dysfunction (DD)


Occurs between closure of the aortic valve to closure of the MV.
Relaxation begins when maximal shortening and LV pressure has been reached, shortly before ejection has finished, but clinically it begins with AV closure.
Early diastolic relaxation (lusitropy) is energy dependent (requires ATP for sequestration of calcium and actin-myosin dissociation).
Compliance is the volume/pressure relationship and is an intrinsic property of the heart.

4 phases of flow:

  • Isovolumetric relaxation - no flow
  • Early rapid filling down transmitral pressure gradient
  • Diatasis – low flow in mid diastole
  • Late rapid filling – atrial contraction - contributes about 30% of LV filling.
These can more simply be considered as 2 components - active relaxation (early diastole) and passive compliance (mid and late diastole).
The normal LV can accommodate a wide range of venous return without elevation of filling pressures.
Dysfunction results from both impaired active relaxation and reduced passive compliance.
Just like there are RWMAs in systolic failure, diastolic failure also demonstrates regional variations.
The overall effect is impaired LV filling and a higher LVEDP for a given LVEDV which leads to pulmonary venous congestion.


Impaired relaxation – common in IHD (reduced ATP) and made even worse by hypertrophy.
Impaired peak LV filling rate – inadequate transmitral pressure gradient due to raised LVP or inability to generate negative LVP (suction) – the latter is achieved by titin (a protein) which is compressed in systole and forcefully re-expands in early diastole like a spring.
Stiffness of LV – fibrosis and hypertrophy.
Constriction – pericardial or compression from dilated RV

By disease:

Restrictive cardiomyopathy
  • Hypertension
  • AS
  • Hypertrophic cardiomyopathy

Symptoms are the same as for LVSD
40% of those with symptoms of HF have preserved EF.
All patients with systolic dysfunction due to heart disease will have diastolic dysfunction.

Exacerbating factors

DD made worse by:
Afib – Atrial contribution to filling more important as LVP rises but Afib very common as atrial dilatation results from elevated LVP.
Tachycardia – reduces time for the compromised diastolic filling.
Hypertension – increased LV wall tension (afterload) impairs relaxation.


Diagnosed by symptoms of HF or raised BNP with preserved EF (>50%).
LV catheterisation is gold standard but ECHO much more practical.

Echo and mitral inflow

Detailed explanations and implication of diastolic dysfunction in intensive care can be found in


Underlying pathology - hypertension control, IHD, Afib.
ACEi, A2s and CA blockers can all reduce hypertension and reverse LVH.
Restore SR if possible. Often not due to dilated LA so rate control then important. Digoxin not useful like in systolic D as increased inotropy is not required and calcium uptake is impaired.
Treatment of IHD will provide increase O2 supply, improving active relaxation and reducing LVEDP and remodelling.
Activation of RAS (in an effort to increase LAP) cause progression of cardiomyopathy and remodelling. Treatments to prevent this (eg ACEi should be used cautiously as the LV is very preload dependent).
Exercise will reduce resting HR and improve Ca uptake.


Better than systolic dysfunction but become equivalent >70 yrs.


Diastolic dysfunction. CEACCP
Haemodynamic monitoring using echocardiography in the critically ill