If necessary, concomittant myectomy should be considered. After surgery on ICU, I recommend fluid and PDE3-Inhibitor administration. Avoid Beta adrenergics. Later prescribe beta blockers and aldosterone antagonists.

Thanks, Sebastian

But we can face the problem of fluid loading in severe stiffness of the left ventricular wall. In severe diastolic dysfunction fluid  load may cause lung edema, whereas a normal left atrial pressure usually is not sufficient to ensure adequate filling of the left ventricle.

If possible, please describe how you spend more fluid load at a small left ventricular cavity, and there are no  with the LVOT?

What doses  of  milrinone are optimal  in  yuor  opinion?

Do  You  use  circulatory  support  and,  if You  use it,  what kind of circulatory support  do You  prefer in  such  cases?

We determine left atrial pressure the first 10 hours after surgery.

This facillitates optimal filling without the risk of pulmonary edema.

We Start Enoximone at end of bypass at 5 to 10 mg/h and reduce dosage down to 2.5 to 5 mg/h on ICU. We usually discontinue Enoximone the next morning.

What about enoximone induced periferic vasodilatation and reduced preload? What do you think about Heart rate control and how do you do it?

Thank You,  Sebastian.

What is the maximum value of left atrial pressure you use for optimal filling of the left ventricle?

And  what  about  circulatory support during severe  diastolic disfunction?

Excellent question!

We faced a similar situation in the OR and I can briefly state our experience. However I must add that the problem was compounded by the presence and worsening of mitral regurgitation; we were forced to go back on cardiopulmonary bypass(CPB) and repair the Mitral valve by placing an annuloplasty band; we came off CPB with the help of Milrinone. 

So the key issues are judicious use of inodilators; monitor PA pressures and MVO2; ideally we should use atrial wires to avail of A-pacing should the need arise especially in the setting of LVH and as mentioned earlier MR of greater than 2+ may need surgical attention.

Excellent reply of Suresh Keshavmurthy. Milnirone and PA monitoring might be a good alternative to LAP and Enoximone. However, LAP has the advantage of not beeing biased by pulmonary issues. Of course, concomittant valvular pathologies have to be fixed when of hemodynamic relevance. In reply to Evtushenko: We fill the patient until rapid increment of LAP in correlation to volume offering occurs. It is less a question of absolute LAP values, it is more of the patient´s hemodynamic associated to Echo and LAP control. 

Controled volume infusion with LAP and Beta Block to reduce the heart rate.

Rather than answer directly, I would ask this question:  why did you have LV depression?  It was presumably not present preoperatively.  After more than 25 years in the practice of cardiac surgery, I finally concluded that poor ventricular function postoperatively that was not there (to the same extent) preoperatively meant that I was not protecting the LV adequately. For the next 13 years, until I retired a few months ago, I altered my myocardial protection technique to one using pure blood cardioplegia (cold) with added potassium and magnesium providing the ability to give large volumes of cardioplegia with minimal crystalloid administration, e.g., one liter of blood cardioplegia contained only about 5 ml of crystalloid.  By giving a large volume of cardoplegia frequently (every 10 minutes, 500 ml cardioplegia) I essentially eliminated LV dysfunction coming off bypass, including in patients with tight AS and hypertrophied ventricles. And, with minimal amounts of crystalloid, edema and lung dysfunction does not occur.

There is a downside, however.  I found that I spent about ⅓ of my cross clamp time giving cardioplegia and thereby considerably extended my cross clamp times.  On the other hand, the payoff in patient results and ease of postoperative care rendered the extra time rather trivial.

Dear Vander Salm. The question is not about systolic dysfunction, but about diastolic dysfunction and small left ventricle.

The question was indeed about diastolic dysfunction; I apologize if my answer seemed to address systolic dysfunction only.  I found, however, that diastolic function is similarly preserved by adequate myocardial protection, even in the face of sudden resistance unloading of the hypertrophic LV as is the case with AVR and AS.

In case the typical measures do not succeed to alleviate your patients symptoms, you may want to think about a carotid baroreceptor stimulator! In the clinical trials this form of treatment has shown most convincing results in various forms of diastolic heart failure! We have had the opportunity to observe this in our own patients primarily treated for hypertension but also those specifically treated for diastolic heart failure! The effect may be as dramatic as relieving the patients of symptoms within 2 weeks of activation of the device. (Rheos, CVRx Inc., USA)

I thank everyone involved in the discussion. Once again, let me clarify the problem. The question concerned the postoperative state of the decompensated diastolic dysfunction in patients with significant left ventricular hypertrophy and initially low values of left ventricular end-diastolic volume. These small values of left ventricular volume on the background (for example, critical aortic stenosis) are influenced by a increased afterload, which enhances end-diastolic pressure, and supports left ventricular volume. Instantaneous reduction of afterload immediately after surgical correction  reduce the end-diastolic pressure of the left ventricle, and as a result, reduce the volume of the left ventricular cavity and its stroke volume.

In such condition (in our observation) volume loading dosage is low-effective. We tried to maintain the pressure in the left atrium at higher values, but not higher than 20-22 mmHg. Sometimes we use pulmonary monitoring, but only in  cases where there is no express transpulmonary gradient. Also, we use  beta-blockers, but dosage  of which can be limited by the hypotension due to low cardiac output. We absolutely do not use beta-mimetics, and to maintain blood pressure assign alpha-mimetics (norepinephrine).

Application of any techniques circulatory support in cases of  decompensated diastolic dysfunction and low left ventricular cavity did not show any significant their clinical effectiveness. Therefore, the question remains open.

Dear Thomas James Vander Salm!

I absolutely agree with the fact that diastolic dysfunction may be exacerbated due to inadequate myocardial protection.Therefore, for myocardial protection we always use the combined method of the  cardioplegic (CP) solution infusion: initiation of the CP we perform  by  antegrade infusion, and then to achieve adequate perfusion of subendocardial layers of the myocardium in hypertrophic heart - about 50% of the dose cardioplegic solution, we introduce into the coronary sinus. However, inadequate myocardial protection  not only worsening diastolic dysfunction, but also the reduction of contractility of the left ventricle. Here we are talking about only those patients with adequate myocardial protection.  Thank You  very much for  estimable  comments.

Dear Maximilian!

Thank you for your very important comment. I know a way of  a carotid baroreceptor stimulation for the reduction of blood pressure in patients with resistant  arterial hypertension. However, the remark about the effectiveness of this method for the treatment of diastolic dysfunction in postoperative patients, I ‘d never note before. Furthermore, I believe that the pathogenesis of the diastolic dysfunction in patients with arterial  hypertension and in patients after correction of left ventricular output pathology is different. Therefore, if you allow me, I would like to ask a few questions:

1. What is your experience of using this method in postoperative patients?

2. Which parameters of stimulation (for example the impulse amplitude, duration, impulse shape, duration of stimulation, etc.) of the of a carotid baroreceptor stimulation you use in postoperative patients and whether they differ from those in patients with hypertension?

3. Do you use in the early postoperative period implantable system? And if so, whether there are any special techniques of its implantation after sternotomy or ministernotomy?

4. Do You use stimulation technique  alone or in combination with the other methods of intensive medical therapy?

Dear Giuseppe!

You are certainly right, but there is technology and external (non-invasive) stimulation of the carotid baroreceptors

And thank You, Giuseppe, for the  information about ranolazine