Assessment of diastolic dysfunction and anesthetic considerations in diastolic

dysfunction

By: Dr.Gopan. G Date: 19-01-2015

Moderator: Dr. Satyen Parida

Definition Inability of ventricle to fill at low atrial pressures.

Impaired relaxation impaired compliance

( Active process) ( passive process)

(Lusitrophy)

Duration of diastole

Mechanical point of view starts with closure of aortic valve

ends with closure of mitral valve

Molecular level

Dissociation of actin-myosin cross bridges

Ref: Gillebert TC, Leite-Moreira AF, De Hert SG. Relaxation-systolic pressure relation. A load-independent assessment of left ventricular contractility. Circulation 1997; 95: 745–52

Early phase of LV Ejection

Diastole – an active process

4 phases of Diastole Isovolumetric relaxation from closure of semi-lunar valves

till opening of AV valves

Rapid filling Trans valvular pressure gradient

Diastasis Low flow

Late rapid filling Atrial kick

Diastolic dysfunction- mechanisms

Slow/ incomplete myocardial relaxation- MI, LVH

Impaired peak LV filling rate

Altered elasticity- fibrosis

Pericardial constriction

LVEDP LVEDV

Clinical manifestations

Diagnosis

Gold standard Direct measurement of LV pressure & volume.

Micromanometer & conduction catheters.

Echocardiography

ECHO Trans-mitral flow velocity

Trans-mitral flow Preferred view- ME 4 chamber

Modality- PWD

Sample volume: 1-3 mm @ mitral leaflets

Trans-mitral flow

Peak E wave velocity: 70 – 100 cm/sec.

Peak A wave velocity: 45 – 70 cm/sec.

E deceleration time (DT): 160 – 240 msec.

Iso- Vol. Relaxation Time- 65± 20 ms.

The deceleration time (DT) shows the pressure decay of early

filling. The shorter the DT, the higher the filling pressure.

1) Impaired relaxation pattern

E/A <1 DT ↑ ( >240 ms) IVRT > 90 ms.

2) Pseudo- normal pattern

3) Restrictive pattern

E/A > 1.5

DT ↓ (<160 ms)

IVRT < 70 ms.

Trans-mitral flow

Limitations

Affected by age, rate, rhythm, loading conditions, LV systolic function,

Atrial function & mitral valve disease.

Cannot be used in isolation to predict Diastolic dysfunction

Limitations

Affected by age, rate, rhythm, loading conditions, LV systolic function,

Atrial function & mitral valve disease.

Cannot be used in isolation to predict Diastolic dysfunction

Pulmonary venous inflow

Preferred view- ME 4C view

for LUPV

Modality- PWD

Sample volume 2-3mm, 1-2

cm into PV

Pulsatile PVF pattern is generated by the ‘x’ and ‘y’ descents of the LAP tracing

Normal pulmonary venous flow

Peak S wave velocity: 60 ± 15 cm/sec.

Peak D wave velocity: 40 ± 15 cm/sec.

Peak S / Peak D ratio: 1.3 – 1.5 ( ± 0.3).

Peak Ar wave velocity: -32 cm/sec.

Ar duration: 137 + 31 msec.

Pulmonary venous flow

Limiting factors

Technical difficulties in

getting arterial waveforms

Load dependence

LA wall artifacts

Effects of arrhythmias

Ar velocity > 35 cm/s and (Ar- Adur) > 30 msec is highly predictive of LVEDP > 15 mm Hg.Ref: Rossvol et al JACC; 1999 21: 1687

Trans-mitral Color M-Mode–Derived Early Propagation Velocity

Early diastolic LV filling

Wave front of propagation from LV base to apex

Preferred view- ME 4C view

Modality- CFD and M mode

Colour flow sector- on LV cavity with parallel M-mode alignment

Trans- mitral velocity profile (Vp) ≈ LV suction in early diastole

Less affected by preload than TMF and PVF.

Trans-mitral Color M-Mode–Derived Early Propagation Velocity

Trans-mitral Color M-Mode–Derived Early Propagation Velocity

Method described by Garcia et al., in which the slope of the first aliasing

velocity (the outermost velocity) is measured, is considered the most

reliable and reproducible method.

A Vp value of <0.50 m/s is consistent with impaired relaxation.

Trans-mitral Color M-Mode–Derived Early Propagation Velocity

Limitations

may not be possible to measure Vp because the slope of flow

propagation is sometimes curvilinear and does not “travel” a

sufficient distance (<4 cm) into the LV cavity or is difficult to

appreciate.

merely diagnoses the presence of abnormal relaxation, and not

necessarily its severity.

Doppler Tissue Imaging Measures tissue velocities and motion.

Preferred view- ME 4C

Modality- PWD optimized for tissue motion

Sample volume- 5- 10 mm within 1 cm of mitral leaflet insertion

Doppler Tissue Imaging

Reduced E’ velocity for age

is considered diagnostic of

abnormal LV relaxation.

E’- Early diastolic waveA’ – Late diastolic waveS’ – Systolic wave

Doppler Tissue Imaging

E/ E’ ratio < 8 identifies patients with normal LVEDP

E/ E’ ratio > 15 identifies patients with LVEDP > 12 mm Hg

Ref: Nagueh et al. JACC 1997. 30: 1527

Doppler Tissue Imaging

Average E’ velocity may not accurately represent global LV

diastolic function in the presence of basal lateral and septal

wall motion abnormalities.

E’ wave represents only the relaxation (early) phase of

diastole and does not provide any information about LV

compliance.

Prognosis

Diastolic dysfunction develops early in most cardiac diseases.

Clinical studies have shown the association of short mitral DT with heart-failure and death.

Pulmonary venous velocities was less frequently examined but were still predictive of clinical events.

Several studies have shown that E/E´ is highly predictive of adverse events. It is the most reproducible echocardiographic parameters to estimate PCWP and is the preferredprognostic parameter in many cardiac conditions.

Anesthetic considerations in diastolic dysfunction

Effect of inhalational anaesthetics on diastolic function

Halothane and sevoflurane do not cause prolongation of the IVRT.

In preexisting diastolic dysfunction, sevoflurane causes a slight improvement in early LV relaxation assessed with E’ velocity.

Isoflurane did not exacerbate preexistent diastolic dysfunction and had no lusitropic effects.

Effect of IV anaesthetics on diastolic function

Propofol prolongs the IVRT in patients with no history of cardiac disease, but does not cause worsening of preexisting diastolic dysfunction.

Barbiturates and ketamine exert similar effects by inhibition of sarcolemmal transport of calcium ions.

The impact of etomidate on LV diastolic function has not been studied

Anaesthetic considerations

Detailed Pre-operative evaluation

Assessment of functional status & exercise tolerance

Optimizing the patient

Perioperative drugs

Diuretics

Beta blockers, calcium channel blockers

ACEI & ARBs

Statins

Antiplatlets

Monitoring - Major surgeries

Standard monitoring tools

Invasive arterial pressures

Monitoring volume status is important

Central venous pressures or Pulmonary artery catheter or TEE

GA or Regional

No definite recommendation either way

Epidural vs. spinal ?

Epidural wins

General anesthesia

Good induction practices

Consideration for age

Titrate to effect

Hpoxia, hypercarbia worsens PHT

General anesthesia

IV induction & maintained with volatile agents ,

opioids & muscle relaxants.

Greater hemodynamic instability

Drug combination for hemodynamics Low dose nitroglycerin and titrated phenylephrine

Either agent alone can worsen the hemodynamics

Nitroglycerine + Titrated phenylephrine

1. Preserves vascular distensibility

2. Avoids reduction in preload

3. Maintains coronary perfusion pressure

4. Maintains stroke volume with minimal cardiac work

Management of hypertensive crisis

Sound anesthetic practices

Plan for post-op analgesia

Intravenous calcium channel blocker

IV nitroglycerin

Post-op diastolic heart failure

Optimise preload

Diuretics

Use of nitrates

CPAP

As contractile function is preserved, the role of sympathomimetic

inotropes is limited.

Specific drugs for diastole Milrinone

o Phosphodiesterase III inhibitor

o Inotropic, vasodilatory with minimal chronotropy

o Increases calcium ion uptake to SR

o Lusitropic effect more evident in heart failure

o Bolus dose of 50µgm/Kg over 60 minutes

o Infusion of 0.375 to 0.75µgm/Kg/min

Specific drugs for diastole Levosimendan

o Sensitizes the contractile elements to calcium and a has

positive inotropic effect, by modulating the interaction

between troponin and calcium.

o combines a vasodilator effect, by opening ATP-sensitive

potassium channels.

o Improves both systolic and diastolic function

Conclusion

The prognostic significance of diastolic dysfunction in

cardiac patients cannot be understated.

A simplified approach will allow assessment of severity of

diastolic function in nearly all cases and allow tailoring of

management.

Practical approach to diastolic dysfunction

Ref: Nagueh et al European Journal of Echocardiography (2009) 10, 165–193

Thank you