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Eur J Cardiothorac Surg 2008;34:1141-1148. doi:10.1016/j.ejcts.2008.05.030
Copyright © 2008, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.
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Right arrow Congestive Heart Failure

Reviews

Recognition of diastolic heart failure in the postoperative heart

Ahmed A. Alsaddique*

King Fahad Cardiac Center, College of Medicine, King Saud University, P.O. Box 7805, Riyadh 11472, Saudi Arabia

Received 11 March 2008; received in revised form 20 May 2008; accepted 21 May 2008.

* Corresponding author. Tel.: +966 1 467 1575; fax: +966 1 468 9493. (Email: alsadd{at}hotmail.com).


   Abstract
Top
 Abstract
1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
 References
 
Diastolic dysfunction is assuming more importance as it is increasingly evident that it can be solely responsible for heart failure. Although many comprehensive studies pertinent to diastolic dysfunction and diastolic heart failure have been recently published, there is a paucity of information on diastolic dysfunction appearing in the postoperative cardiac surgical patient. We sought to look into current literature searching for criteria that could be applied to help diagnose it in this group of patients in the intensive care setting where cardiac surgical patients are usually managed in the immediate postoperative period. Because of the almost similar clinical features it is important to make the distinction between diastolic or systolic heart failure.

Key Words: Diastolic dysfunction in the postoperative heart


   1. Introduction
Top
 Abstract
 1. Introduction
2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
 References
 
Left ventricular (LV) diastolic dysfunction can be defined as the inability of the LV chamber to adequately fill at low atrial pressures unrelated to intrinsic valve disease or pericardial pathology. This dysfunction can result either from an impairment in LV compliance (passive mechanism) or from an alteration in LV relaxation (active process). Relaxation is usually the first to alter in LV diastolic dysfunction and this can occur rather abruptly especially in the context of critical care or anesthesia [1]. The exact prevalence of diastolic heart failure (DHF) is not actually known. It appears however to constitute between 30% and 50% of all hospital admissions for heart failure [2–4]. Diastolic function after cardiac surgery was evaluated by several methods in the past; the clinical impact however has been limited by the technical difficulties of obtaining a serial measurement of the LV diastolic function [5,6]. With improvement and wider use of echocardiography its impact on cardiac surgery has been re-examined. Some of the work in this area has shown that left ventricular diastolic function was severely impaired after cardiopulmonary bypass depending on the myocardial protection used. This was observed in patients with normal preoperative diastolic function who underwent CABG [7,8]. The importance of diastolic dysfunction to the surgeon was further reinforced when it became apparent that it is a predictor of difficult weaning from cardiopulmonary bypass [9]. Salem and associates have demonstrated that diastolic dysfunction on its own is a predictor of mortality in cardiac surgery [10]. Slowly but surely diastolic function that was hitherto ignored by the surgeons started assuming greater importance necessitating a clearer understanding of the pathophysiology involved. Diastolic heart failure in the postoperative setting of cardiac surgery has not to our knowledge been studied before and therefore its true incidence is unknown. It can affect cardiac surgical patients in the postoperative period and should therefore be considered in the differential diagnosis of heart failure. Diastolic heart failure is typically seen in patients with hypertensive or valvular heart disease as well as in hypertrophic or restrictive cardiomyopathy. It is often precipitated by a combination of factors. Diastolic dysfunction has a particularly high incidence in elderly patients and is commonly associated, with low mortality but significant morbidity.

Furthermore, changes in diastolic filling pattern have emerged as a valuable prognostic tool. Left ventricular remodeling following acute myocardial infarction (AMI) is a well-known phenomenon occurring in the earliest post infarction phase and continuing for weeks or months. It has been suggested that a restrictive transmitral filling pattern, which is a marker of diastolic dysfunction, provides significant additional prognostic information in these patients. A short initial deceleration time (DT) < 150 ms obtained as early as 1 day after AMI can identify patients who are likely to undergo LV remodeling in the following year [11]. It is now well documented that remodeling is a precursor of heart failure and a strong predictor of mortality. Therefore an early restrictive filling pattern as evidenced by a short DT identifies patients who are ultimately candidates to progressive LV dilation and dysfunction. Persistence of a restrictive filling pattern is the most powerful independent predictor of severe dilation and late mortality [12,13]


   2. Dynamics of diastole
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
 References
 
Diastole begins at the closure of the aortic valve and lasts until closure of the mitral valve [14]. Broadly speaking, diastole can be looked at as two phases; the first corresponds to LV pressure decline at constant volume, isovolumetric relaxation that lasts from the closure of the aortic valve to opening of the mitral valve. The second phase is auxotonic relaxation corresponding to LV filling lasting until closure of the mitral valve.

LV filling depends mainly on the pressure gradient between the LA and LV, which is influenced by compliance of the passive property, active relaxation, and end-diastole by atrial contraction. Traditionally however, diastole is divided into four distinct phases: isovolumic relaxation, early rapid ventricular filling, diastasis and atrial systole. The isovolumic relaxation time is a continuum of systole and is dependent on it. The early rapid ventricular filling phase is dependent on LV relaxation and compliance. Diastasis is dependent on both the heart rate and chamber compliance. The atrial contraction depends on the chamber compliance, left atrial (LA) function and the conduction system of the heart. The major factors that affect diastolic function are ventricular relaxation and compliance. Other factors that influence diastolic function to a lesser degree include systolic function, left atrial pressure, the pericardium and intrathoracic pressure [15]. Ventricular relaxation is an active energy-dependent process that begins in late systole and extends into early or mid disatole [16]. Relaxation can be defined as the time period during which the myocardium loses its ability to generate force, shortens and returns to an unstressed length and force [17]. Peak negative change in the LV pressure over time (dp/dt) and the time constant of relaxation are accepted indices of the rate of relaxation, even though each of these factors has its own limitations [18]. In diastolic dysfunction relaxation abnormalities appear early and the inability of the left ventricle to fill in early diastole significantly affects the rapid filling phase resulting in a compensatory increase in filling with atrial contraction.

The other factor that determines LV filling is chamber compliance, defined as the change in volume over the change in pressure (dV/dP) or the distensibility of the ventricles. It can be derived using the relationship between changes in end diastolic pressure (EDP) and end diastolic volume (EDV) by using the formula [19,20]:


Formula

when ventricular compliance begins to decrease the EDP rises, but the EDV remains unchanged. The increase in EDP reduces the pressure gradient for venous return to the heart leading eventually to a decrease in EDV culminating in decreased cardiac output The effective chamber compliance describes the passive properties of the LV during blood flow across the mitral valve from the LA to LV. Transmitral pressure gradient which is the difference between LA and LV pressures determines the LV filling pattern and is influenced by the rate of LV relaxation and its compliance. Diastolic relaxation is more sensitive to ischemia than systolic contraction, and may lead to subtle relaxation abnormalities without systolic impairment. In coronary artery disease ventricular relaxation as reflected in the early diastolic filling rate may be impaired at rest. In patients with ischemic heart disease impairment of left ventricular diastolic function commonly occurs before systolic dysfunction [21]. The problem in these patients is a decrease in the distensibility of the ventricle during diastole.


   3. Assessment of the diastolic function
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
 References
 
3.1 Echocardiography evaluation
Trans thoracic echocardiography (TTE) plays a major role in the assessment of diastolic function. The combination of several ultrasonic modalities is essential for a proper evaluation. These modalities include:

two-dimensional (2D) echocardiography, pulsed wave Doppler,
color M-mode (CMM) and Doppler tissue imaging (DTI).

The 2D echocardiography can be used to assess the LV systolic function in order to exclude systolic failure during the evaluation of these patients.

Pulsed wave Doppler (PWD) measures the velocity of blood at the Doppler window. This velocity is proportional to the pressure gradient between the LA and LV for the mitral flow evaluation. The mitral blood flow is composed of an E (early) wave for passive diastolic filling followed by an A (atrial) wave for atrial systole. Mitral blood flow is affected by LV relaxation, LV compliance and LA pressure. Normal diastole is characterized by a predominant E wave indicating that most of the LV filling occurs during early diastole [22].

PWD is used to assess transmitral flow velocity recording and pulmonary veins flow velocity variables in the evaluation of diastolic dysfunction [23,24]. The four useful variables from mitral flow are: peak early diastolic transmitral flow velocity (E), peak late diastolic transmitral flow velocity (A), early filling deceleration time (DT) and A wave duration (A dur) [25,26] A normal E / A ratio is considered to be between 0.75 and 1.5. Early filling DT reflects LV compliance in early diastole. The normal DT is usually less than 220 ms [27].

Pulmonary venous (PV) flow is composed of two waves, one systolic and the other one is diastolic. The pattern of the flow is used for the assessment of diastolic dysfunction. These variables include: peak systolic pulmonary flow velocity, peak diastolic pulmonary flow velocity, pulmonary venous atrial reversal flow velocity (AR) and AR duration (ARdur).

The major problem with the use of PV flow variables is the difficulty in obtaining adequate measurement. The other equally important point is that these Doppler flow parameters are influenced by a variety of factors, among them being the loading conditions, besides they cannot differentiate between systolic and diastolic heart failure [28,29]. Therefore the results from these measurements are inconsistent and accordingly inconclusive. They cannot therefore be recommended for use in the fresh postoperative cardiac surgical patient.

Color M-mode (CMM) Doppler flow propagation velocity (V p) is a reliable diastolic index. It displays velocity information along a line that extends from the mitral valve to the LV apex, providing superior temporal resolution (5 ms), spatial resolution (1 mm) and velocity resolution (5 cm/s). The commonly used variable for CMM Doppler is the V p into the LV, which is the velocity at which the blood travels from the mitral valve to the LV apex. In sinus rhythm CMM is characterized by two distinct waves, one corresponds to the E wave and the second one to the A wave.

V p relates well to LV relaxation and appears to be load independent. A V p value of less than 45 cm/s is consistent with diastolic dysfunction in patients older than 30 years of age <55 cm/s in patients less than 30 years of age [30,31].

Doppler tissue imaging (DTI) is an ultrasound imaging modality that directly measures myocardial velocity during the cardiac cycle and allows wall movement to be directly analyzed [32,33]. The myocardial portion commonly studied is above the mitral annulus. Three waveforms are described; peak systolic wave, early diastolic wave (E a) and the end diastolic wave related to the atrial contraction. The E a wave is independent of loading state and is used to assess LV relaxation, a cut off of 8 cm/s for E a measurement is now widely accepted as a sign of diastolic dysfunction [34].

These two new modalities M-mode (CMM) and Doppler tissue imaging (DTI) have emerged as the ones that are least affected by loading conditions and thus provide a strong complimentary role in the assessment of diastolic function. When measuring DTI Khouri and associates measure only early diastolic myocardial velocity (E a) at the lateral corner of the mitral annulus, because it has been noted that the lateral annular velocity is more reproducible than the septal annular velocity [35].

Transthoracic echocardiography (TTE) is sometimes unsuccessful in the postoperative heart suspected of DHF. This is because of the hemodynamic instability, the close proximity to a fresh surgical wound, presence of drains and dressings or due to the inability to optimally position the patient. In addition mechanical ventilation with high positive end-expiratory pressure, pacing wires, or ECG leads, further add to the obstacles for the desired examination window resulting in a poor image quality.

3.2 Use of transesophageal echocardiography (TEE)
TEE has a well-established role in cardiac surgery as it has proved to be a valuable tool for intraoperative decisions particularly in valve surgery [36]. In addition it has also proved to be useful in the field of intensive care for the assessment of hemodynamics and to track its variations after therapeutic interventions. Repeated measurements of left ventricular end-diastolic dimension are recommended to accurately allow tracking the hemodynamic changes, as a single determination is not felt to be reliable. TEE can adequately assess right ventricular function and left ventricular filling pressure using combined Doppler modalities [37]. The same parameters that are described for assessing diastolic function utilizing TTE can be achieved using TEE [38,39].

3.3 Natriuretic peptides
BNP is a marker of systolic left ventricular dysfunction and heart failure. It however increases in subjects with diastolic dysfunction (mean 20.3 ± 4.7 pg/ml vs control 9.6 ± 0.5 pg/ml, p < 0.001). A normal BNP level virtually excludes the presence of diastolic dysfunction and concomitant LVH. Increased BNP concentrations in subjects with diastolic dysfunction are strongly related to LVH [40]. In patients with normal systolic function, elevated BNP levels and diastolic filling abnormalities might help to reinforce the diagnosis diastolic dysfunction [41,42] A-type atrial, natriuretic peptide (ANP) is secreted from the atria in response to dilatation. Brain-type (B-type) natriuretic peptide (BNP) is a neurohormone that is released by the cardiac myocytes when left ventricular wall stress increases. After secretion the pro-hormone is cleaved to the biologically active hormone (BNP) and an inactive N-terminal fragment (N-BNP). Plasma levels of BNP increase in direct relation to increase in ventricular EDV and EDP of both right and left side [43]. A rise in BNP produces vasodilatation and an increase in renal sodium excretion [44]. Atrial natriuretic peptide and brain natriuretic peptide are known to be indices for heart failure. Postoperative ANP plateaus on the third postoperative day and decreases gradually down to the preoperative level by one month. Postoperative BNP plateaus, show a very slow decrease and it never reaches down to the preoperative level [45,46]. This pattern of changes in the BNP and ANP levels after cardiac surgery makes it rather impractical to use them as markers for heart failure in the immediate postoperative setting of these patients.

3.4 Cardiac catheterization
The characteristic finding of DHF is an elevated left ventricular end diastolic pressure (LVEDP) over 16 mmHg in the presence of a normal LV chamber size [47,48] Vasan and Levy recommended cardiac catheterization as a prerequisite for making the diagnosis of a definite DHF [49]. In the postoperative setting of open-heart surgery with heart failure cardiac catheterization is probably not warranted and the diagnosis can be made by less invasive methods.

3.5 Multidetector CT (MDCT) of the heart
Cardiac MDCT is most commonly performed for the purpose of noninvasive cardiac angiography. Image data are acquired continuously during a single breath-hold scan, typically 10–15 s in duration. Contrast is required for angiography and for endocardial border definition, with typical doses in the range of 60–80 ml per scan, quite comparable to a diagnostic cardiac catheterization. Patients with cardiomyopathies of all etiologies represent a large and growing population that stands to benefit from advanced imaging techniques [50]. Electron-beam computed tomography (EBCT) has been shown to be a reliable tool for the assessment of ventricular diastolic function and to detect constrictive filling pattern [51,52]. These tools cannot be utilized in the assessment of the postoperative heart for logistical reasons.

3.6 Cardiac magnetic resonance
Cardiac magnetic resonance (CMR) is the latest addition to the diagnostic tools. The specific advantage of CMR over echocardiography is the possibility to acquire images in any selected plane or along any selected axis.

A routine CMR examination in the setting of heart failure will acquire short access images covering the entire heart from base to apex in addition to the long access slices. It can also provide a range of LV filling parameters almost similar to those obtained by echocardiography [53,54]. CMR is considered as a valid alternative for echocardiography when an adequate echocardiographic assessment cannot be obtained. It is the diagnostic modality of choice for assessing small changes in LA or LV volumes and in LV mass [55]. Clinical use of CMR is expanding and starting to address diastolic LV dysfunction. It is not of course practical to obtain CMR in the fresh postoperative cardiac surgical patient suspected to have DHF.


   4. Overview of the relevant predisposing factors
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
5. Diagnosis of diastolic...
 6. Conclusions
 References
 
Primary diastolic failure is typically seen in patients with hypertensive or valvular heart disease as well as in hypertrophic or restrictive cardiomyopathy but can also occur in a variety of other clinical situations. The main risk factors for this form of heart failure are advancing age, hypertension and diabetes mellitus [56]. There is a high incidence of diastolic dysfunction among normotensive patients with diabetes [57]. Increased matrix collagen, interstitial fibrosis, myocardial microangiopathy, and myocytes hypertrophy are common findings in the diabetic heart that can lead to diastolic dysfunction. Tight glycemic control decreases the risk of heart failure in patients with diabetes [58,59].

The defect in DHF is a combination of impaired ventricular relaxation and a decrease in passive ventricular distensibility [1,60]. The low cardiac output associated with DHF is due to inadequate ventricular filling, not impaired systolic contraction, an important point to remember when managing these patients. LV filling depends mainly on the pressure gradient between the LA and LV, which is influenced by compliance, active relaxation and end diastole by atrial contraction [28]. There are a number of predisposing factors that can contribute to DHF in the postoperative cardiac surgical patient. The mechanisms by which these factors exert their effect are briefly explained.

Atrial fibrillation is a fairly common occurrence in the postoperative period. It causes loss of atrial contraction that results in impaired diastolic filling.

Myocardial hypertrophy is another predisposing factor found in some of the valvular lesions and in hypertensive patients. Its presence interferes with the passive late phase of diastolic filling of the LV contributing to diastolic dysfunction.

Myocardial ischemia in the postoperative cardiac surgical patient significantly slows active myocardial relaxation during early diastole. It may also lead to rhythm disturbances that will further aggravate LV diastolic dysfunction.

Tachyarrhythmias impair LV filling by shortening diastolic phase of the cardiac cycle resulting in impaired LV filling [17,61].

The effect of positive pressure ventilation on cardiac performance to which virtually all of open heart surgery patients are subjected to postoperatively is a complex one involving changes in preload and afterload for both right and left ventricles. Positive pressure ventilation can lower ventricular filling thereby reducing preload and it usually reduces afterload enhancing ventricular emptying during systole. The effect on cardiac output depends on whether the effect on preload or afterload predominates. If the patient is normovolemic and intrathoracic pressure is within normal the effect on afterload reduction predominates resulting in an increase in the cardiac output. The increase in stroke volume leads to increase in systolic blood pressure during lung inflation and results in a phenomenon known as reverse pulses paradoxus. The beneficial effects of positive pressure ventilation on cardiac output are reversed by hypovolemia leading to decreased cardiac output and hypotension [62,63].

Pericardial constriction or tamponade that causes increased resistance to diastolic filling of part or all of the heart could become a contributing factor. Renal insufficiency results in volume overload that leads to a slowing of myocardial relaxation potentially contributing to DHF [64].

Chronic anemia is usually accompanied by an increase in cardiac mass due to volume overload. In the animal model chronic anemia resulted in increased left ventricular end-diastolic pressure and decreased functional reserve, which in turn can lead to diastolic dysfunction. It can also lead to tachycardia that it turn shortens diastole resulting in diastolic dysfunction. The anemia that is seen in the postoperative period due to excessive postoperative blood loss is transient acute and is usually rapidly corrected in these patients leading to very little if any effect on the diastolic function [65].

Chronically uncontrolled hypertension is by far the most common predisposing factor in diastolic heart failure. It can lead to DHF through a number of ways; one of them is by causing LV hypertrophy that can result in a delayed LV relaxation with all its attendant effects on diastolic filling. The other mechanism is related to a reduced arterial compliance that can also contribute to diastolic dysfunction [66]. Hypertension that is seen at times in the postoperative period is usually transient, is quickly managed and therefore does not pose the same risk of the more common form of hypertension. At times one may need to pace the heart in the postoperative period; as most pacing wires placed at surgery are ventricular, pacing under these circumstances would affect diastolic filling bringing about diastolic dysfunction or could even trigger DHF in some instances. This is largely due to the loss of the atrial contribution to LV filling. It is therefore better to keep this possibility in mind and make the extra effort of placing both atrial and ventricular wires for sequential pacing if the need ever arises.

There seems to be some evidence that nitric oxide (NO) metabolism plays a role in acute diastolic dysfunction following episodes of ischemia and reperfusion. It is thought that NO could have a beneficial role as pretreatment with cGMP donors or with NO donors protects myocytes from relaxation failure in animal models [67–69].

It is worthwhile to mention that for DHF to develop it requires the interplay of more than one predisposing factor. This is an important fact to remember in management of these patients (Table 1 ).


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  		Table 1 Common predisposing conditions for postoperative DHF and their mechanisms
 

   5. Diagnosis of diastolic heart failure in postoperative cardiac surgical patients
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
6. Conclusions
 References
 
This description applies to postoperative cardiac surgical patients in the intensive care environment. The diagnostic criteria are therefore based on invasive hemodynamic measurements and not the usual clinical symptoms and physical signs. As ventricular compliance begins to decrease, the EDP rises but the EDV remains unchanged. The increase in EDP reduces the pressure gradient necessary for ventricular filling and this eventually leads to a lower EDV resulting in a decrease in cardiac output via the Frank–Sterling mechanism.

The usual method of assessing cardiac failure by the relationship between ventricular filling pressure and stroke volume does not distinguish between systolic and diastolic heart failure. The EDP is elevated in both types of heart failure. The EDV is increased in systolic heart failure and is decreased in diastolic heart failure, thus it is the parameter that will distinguish systolic from diastolic heart failure [70]. The measurement that is most often utilized to distinguish between diastolic and systolic heart failure is the ejection fraction (EF). The EF is normal or near normal in patients with DHF and is reduced in systolic heart failure.

Pulmonary artery catheter with a fast response thermistor can measure the EF of the right ventricle. These catheters are able to register the temperature (T) changes during each cardiac cycle. The change in temperature is due to dilution of the indicator fluid by venous blood that fills the ventricle during diastole. The amount of blood that fills the ventricle during diastole is equal to the stroke volume, the temperature differences between each plateau on the curve (T 1 – T 2) is the thermal equivalent of the stroke volume (SV) (Fig. 1 ). Temperature T 1 is the thermal marker for EDV. The EF becomes equivalent to the ratio (T 1 – T 2)/T 1 or (SV/EDV) [71,72]. Once the EF is measured the stroke volume can be calculated by dividing the cardiac output by heart rate. The EDV can be determined by rearranging the EF formula EDV = SV/EF. The normal RV right ventricular (RV) EF using thermodilution method is 0.45–0.50 which is about 10% lower than the EF measured by radionuclide imaging [73]. The accepted norm for RVEDV is [80–140 ml/m2] [74].


Figure 1
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  		Fig. 1. Thermodilution ejection fraction for the right ventricle. T B baseline blood temperature. T 1, T 2 and T 3 are successive temperature plateaux (adapted with permission from the publisher Springer).

 
The chief points to help in the diagnosis of diastolic heart failure in the postoperative heart are: (1) hemodynamic evidence of heart failure; (2) mean pulmonary capillary wedge pressure >12 mmHg [75]; (3) adequate cardiac index; (4) echocardiographic evidence of raised left atrial pressure (LAP) as evidenced by a distended LA with the interatrial septum displaying a fixed curvature towards the right atrium [76,77]; (5) echocardiographic evidence of a small LV in the absence of hypovolemia and valvular heart disease; (6) low EDV as determined by the pulmonary artery catheter; and (7) EF better or similar to the preoperative one (Table 2 ). Indeed according to the European criteria, a normal cardiac index in the face of pulmonary edema suggests diastolic heart failure [75]. Echocardiography is a useful tool to diagnose diastolic heart failure. In the postoperative heart suspected to have DHF it is not always possible to get an adequate assessment. In addition, air trapped within the postoperative mediastinum creates poor acoustic windows through which ultrasounds waves cannot pass. An echocardiography study that would simply establish that the left ventricular function has not deteriorated compared to the preoperative one and rules out the presence of cardiac tamponade or significant pericardial effusion can usually be done and would probably suffice under the circumstances. If the hemodynamics allow one can probably use TEE to diagnose DHF, it remains however an invasive procedure that should only be carried out by an experienced operator. Published guidelines for performance of TEE should be followed [78–80]. The information gained by TEE should be integrated with the rest of the hemodynamic parameters (pulmonary artery occlusion pressures or pulmonary artery end-diastolic pressures), LA dimensions, and conventional Doppler imaging of mitral inflow in conjunction with DTI of the lateral mitral annular wall.


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  		Table 2 Features that would suggest DHF in a postoperative heart
 
As it has been determined that objective measurement of LV diastolic function serves to confirm rather than establish the diagnosis of diastolic heart failure, the diagnosis of diastolic heart failure can be assumed without the measurement of the various parameters that reflect LV diastolic function in the presence of acute pulmonary edema associated with indirect signs of elevated left atrial pressure [56].

5.1 Role of substernal epicardial echocardiography imaging technology (SEE IT)
Because of the limitation of the conventional echocardiography in the postoperative heart a novel approach has been described. It is an echocardiographic window, utilizing a modified mediastinal drainage tube incorporating a sleeve for the insertion of a transesophageal echocardiography probe. There are major probe manipulations within the sheath in order to get all the eleven SEE views. Images obtained with SEE were compared with those obtained by TEE. Right ventricle and anterior structures were better visualized by SEE and the limitations of examination relate to posterior structures including the distal and descending aorta [77,81,82]. The examination can be repeated as frequently as needed in order to better monitor the response. There are currently no studies that examined the diastolic function using the SEE IT modality but it remains an area of great potential. It is interesting to note that substernal images are not parallel to the blood flow and the alignment is poor.

The management of DHF should be directed at

A. reduction of pulmonary congestion,
B. correction of the predisposing factors.

Pulmonary congestion can be tackled by improving LV filling. A small decrease in LVEDV leads to reduction of LVEDP thereby improving LV filling by helping to restore the gradient between the LA and the LV.

Diuresis should be used with great caution in this setting as the high filling pressures are helping to maintain the cardiac output. Positive inotropic agents have no role in the management. Vasodilators are useful such as nitroglycerine and milrinone; they have lusitropic action that helps ventricular relaxation and are considered the drugs of choice [83]. Correctable factors should be addressed like cardiac tamponade or significant pericardial effusion. The effect of volume overload and positive pressure ventilation should not be overlooked as it can contribute to DHF in the presence of other factors. Myocardial ischemia is one of the main reasons of diastolic dysfunction in the early postoperative period. Acute graft malfunction leading to myocardial ischemia should be suspected in the early postoperative period in the event of unexplained signs of DHF even in the absence of electrocardiographic changes suggestive of ischemia. Several other factors including pain-induced tachycardia and hypertension may have an additive effect. It is perhaps wise to insert a left atrial line at surgery in patients with a high probability of developing DHF in the postoperative period in order to directly monitor the LA pressure and guide therapy when the need arises much more accurately.


   6. Conclusions
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
References
 
It is time for surgeons to be diastole conscious. Patients should be preoperatively assessed for any factors that could precipitate DHF in the postoperative period. Particular attention should be paid to a history of DHF in the past, evidence of LV hypertrophy and atrial dysrhythmias that can affect LV filling. Age over 70 years, female gender, chronically uncontrolled hypertension and diabetes mellitus should raise the alarm level. Patients identified to be prone to develop DHF, hypovolemia and tachyarrhythmias are to be avoided. Diastolic heart failure is an underestimated entity with a high risk of acute decompensation during the perioperative period. The possibility of DHF should be entertained in the differential diagnosis of cardiac failure in the postoperative setting.

In patients with a high likelihood of postoperative diastolic failure a baseline BNP is probably indicated, because BNP levels are potentially useful when a baseline concentration is known for the patient. The increase in the BNP level is proportional to the severity of heart failure [84].


   Acknowledgments
 
The author thanks William H. Gaasch, MD, Professor of Medicine, University of Massachusetts Medical School and Tufts University School of Medicine for his critique of the manuscript. The author is grateful for his unique approach that reflects the depth of his knowledge.


   References
Top
 Abstract
 1. Introduction
 2. Dynamics of diastole
 3. Assessment of the...
 4. Overview of the...
 5. Diagnosis of diastolic...
 6. Conclusions
 References
 

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A. A. Alsaddique, A. G. Royse, C. F. Royse, and M. A. Fouda
Management of diastolic heart failure following cardiac surgery
Eur. J. Cardiothorac. Surg., February 1, 2009; 35(2): 241 - 249.
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