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Rheumatic Heart Disease Case Study

CASE 8: Valvular Heart Disease

Gregg S. Hartman

Stephen J. Thomas

A 78-year-old man was admitted with increasing shortness of breath. He had chest pain in the past but was able to continue with normal activities. He had passed out twice in the past year. On physical examination, a loud systolic murmur could be heard at the left sternal border radiating to the neck. His vital signs were: blood pressure 150/90 mm Hg, heart rate 88 beats/minute and irregular. The electrocardiogram (ECG) showed sinus rhythm with atrial premature contractions and left ventricular hypertrophy (LVH) with strain. A transthoracic echocardiogram showed a hypertrophied left ventricle (LV), and Doppler examination demonstrated severe aortic stenosis (AS) with a gradient of 64 mm Hg, mild aortic insufficiency (AI), and moderate mitral regurgitation (MR). He was scheduled for aortic valve replacement (AVR) and possible mitral valve (MV) repair or replacement.

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  1. Medical Disease and Differential Diagnosis
    1. What are the major etiologies of aortic stenosis (AS), aortic insufficiency (AI), mitral stenosis (MS), and mitral regurgitation (MR)?

    2. What are the major changes in the loading conditions of the left ventricle (LV) that result from the four different lesions? Why do they occur? What changes result from them?

    3. What are pressure-volume (P-V) loops? What do the different inflection points represent?

    4. What are representative P-V loops for the four valvular lesions?

    5. Draw the pressure/time curves for the LV, left atrium, pulmonary artery (PA), and aorta for a normal patient and for patients with each of the four valvular lesions.

    6. What are the basic principles of echocardiography? What are M-mode, B-mode, and Doppler color modalities? How do transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) differ?

    7. What are the three TEE vantage points for the comprehensive imaging of the LV? How are pressure gradients measured by echocardiography? How do the pressure gradients derived from Doppler echocardiography differ from those obtained in the catheterization lab by direct pressure measurement?

    8. What are the echocardiographic and cardiac catheterization criteria for the four valvular lesions?



  2. Preoperative Evaluation and Preparation
    1. What are the presenting signs and symptoms of the four valvular lesions listed previously?

    2. What is the New York Heart Association Classification of heart failure?

    3. Discuss the role of premedication for patients with the four different valvular lesions.

    4. How would you premedicate the patient with severe AS and MR?



  3. Intraoperative Management
    1. Outline the hemodynamic management goals for each of the four valvular lesions. What are the anesthetic goals with respect to heart rate and rhythm, preload, afterload, and contractility?

    2. What are the hemodynamic goals for this patient with the combination of severe AS and MR?

    3. How would you monitor this patient with severe AS and MR?

    4. Should the patient have a PA catheter placed before induction?

    5. Is a PA catheter with pacing capabilities indicated?

    6. What anesthetic technique will you employ? Why?

    7. What muscle relaxant would you use for this patient?

    8. What are the usual TEE findings in a patient with AS/AI/MR? How do you grade the severity of AS by TEE? How do you quantify the severity of MR? What is the impact of AS on the severity of MR?

    9. What special considerations particular to cardiopulmonary bypass (CPB) operations do you have for each of the four lesions? Focus on these concerns with respect to the induction and prebypass, bypass, and postbypass periods.

    10. The patient cannot be weaned from bypass following an aortic valve replacement. What are the possible causes?

    11. How would you diagnose right heart failure and pulmonary hypertension? How would you treat it?

    12. What role does an intraaortic balloon pump (IABP) have in this setting?

    13. How does the IABP work to benefit the failing heart?

    14. What role does TEE play in the placement, timing, and demonstration of efficacy of an IABP?

    15. How would you properly time the IABP cycle?

    16. What are the contraindications to the use of an IABP?



  4. Postoperative Management
    1. In the intensive care unit 4 hours later, the patient became hypotensive with a low cardiac output. How could you distinguish between cardiac tamponade and pump failure? How would the TEE images differ?

    2. Would you extubate this patient early in the intensive care unit? Why?

    3. What are the advantages and disadvantages of early extubation?



A. Medical Disease and Differential Diagnosis

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A.1. What are the major etiologies of aortic stenosis (AS), aortic insufficiency (AI), mitral stenosis (MS), and mitral regurgitation (MR)?

Aortic stenosis occurs as a congenital lesion but more commonly as an acquired disease. Stenosis may develop on a previously normal valve following rheumatic fever (RF) or from progressive calcification. Congenitally bicuspid valves are also prone to calcification with eventual stenosis. Calcification of the leaflets can result in incomplete closure of the valve with associated insufficiency.

Aortic insufficiency is usually an acquired disease. The most common causes include bacterial endocarditis and rheumatic heart disease. Annular dilation may result from diseases such as cystic medial necrosis and collagen disorders or following aortic dissections with resultant insufficiency. When occurring as a congenital lesion, AI rarely occurs in the absence of other cardiac abnormalities.

Mitral stenosis is almost always caused by RF, although only half of patients will have a history of an acute febrile illness. The inflammatory process of RF results in thickening of the leaflets and fusion of the commissures. Other rare causes include congenital stenosis and other systemic diseases including systemic lupus erythematosus and carcinoid. Pathophysiology similar to that seen with valvular MS can occur with obstructing left atrial (LA) tumors. MS commonly occurs in conjunction with other valvular heart disease; only 25% of patients present with isolated MS; approximately 40% have combined MS and MR.

Mitral regurgitation can result from defects in the leaflets, the annular ring or the supporting chordae, the papillary muscles, or any combination of these. Primary leaflet dysfunction occurs with RF but can also follow bacterial endocarditis, connective tissue disorders, and congenital malformations. Annular dilation can follow ventricular dysfunction and left ventricular dilation. MV prolapse and/or rupture of papillary muscles results in incomplete leaflet closure or coaptation with resultant MR. Left ventricular ischemia can affect papillary muscle contraction and is the cause of postischemic or postinfarction MR.

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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:727–784.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

A.2. What are the major changes in the loading of the left ventricle (LV) that result from the four different lesions? Why do they occur? What changes result from them?

Aortic stenosis represents a chronic systolic pressure load on the LV. This elevation increases wall tension in accordance with Laplace's law.

The ventricle undergoes parallel duplication of muscle fibers in an attempt to compensate for the increase in tension. This results in increased wall thickness or concentric (common center) hypertrophy and some decrease in radius thereby normalizing wall stress. If the MV remains competent, the major pressure overload occurs in the LV and little change in the other cardiac chambers results.

Aortic insufficiency causes left ventricular diastolic volume overload resulting in eccentric (away from the center) hypertrophy and left ventricular dilation. Compliance, the relationship between volume and pressure is altered only slightly because both end-systolic and end-diastolic volumes increase. Some concentric hypertrophy occurs as well secondary to the increase in wall stress resulting from an increase in left ventricular radius. The diastolic pressure is lower with AI. Remember, the diastolic pressure is the pressure that must be exceeded by the work of the LV to open the aortic valve and result in ventricular ejection. Thus, the increased volume work required to eject the additional blood (which flowed into the LV across the incompetent aortic valve during diastole) is reduced because the work can be performed against a lower outflow impedance (lower diastolic pressure). Stroke volume (SV) and ejection fraction (EF), therefore, may be preserved until late in the disease process. As with AS, the presence of a competent MV confines the changes to the LV. However, the left ventricular dilation that follows chronic AI may result in mitral annular dilation or alteration in chordae tendineae geometry with resultant MR. LA enlargement secondary to MR can, therefore, occur. It may also occur because of LA pressure overload as left ventricular end-diastolic pressures (LVEDPs) rise in the course of AI.

Mitral stenosis results in a chronically underfilled LV because of progressive obstruction to LA emptying. This chronic underloading condition can result in decreased left ventricular thickness and diminished contractile function (a "disuse atrophy" of sort). In addition, if the cause of the MS is rheumatic, myofibril damage may have occurred. Although the LV is pressure and volume underloaded, the left atrium is both pressure and volume overloaded. To maintain flow across the progressively narrowing mitral orifice, the pressure in the left atrium must be correspondingly increasing. Gorlin's equation for pressure gradient follows.

It would predict that the pressure gradient increases by the square of any increase in flow rate or decrease in valve area. The elevations in LA pressure leads to hypertrophy and eventually dilation that predisposes to premature atrial contractions and subsequently atrial fibrillation. The loss of atrial contraction further diminishes forward flow across the stenotic MV. The elevations in LA pressure limit pulmonary venous flow with consequent pulmonary engorgement. The pulmonary vasculature undergoes reactive changes including intimal fibroelastosis inducing irreversible elevations in pulmonary vascular resistance. Right ventricular (RV) failure may develop because this chamber is poorly equipped to deal with the elevations in afterload (e.g., pulmonary hypertension). RV dilation combined with increased RV systolic pressures leads to tricuspid regurgitation.

Mitral regurgitation results in volume overload of the LV. The outflow of the LV is divided between the high-pressure/low-compliance outflow tract of the arterial tree and the low-pressure/high-compliance outflow route across the incompetent MV into the left atrium. Although the volume work of the LV is increased, the high compliance outflow route permits a large portion of this work to be performed at a low pressure; therefore, left ventricular wall tension is minimally increased if increased at all. As with AI, the volume overload results in marked left ventricular dilation and eccentric hypertrophy. In contrast, however, the left atrium is also volume overloaded and undergoes dilation. When the volume overload occurs slowly, the left atrium enlarges and minimal rises in pulmonary pressures result despite large regurgitant volumes. In contrast, the occurrence of acute MR, for example, an acute myocardial infarction with papillary muscle rupture, presents the left atrium with a sudden volume overload. Without the time to dilate, the LA pressure rapidly rises limiting pulmonary drainage with resultant pulmonary engorgement.

Back to Quick Links

Braunwald E, Heart disease: a textbook of cardiovascular medicine6th ed. Philadelphia: WB Saunders, 2001.

Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland OH: International Anesthesia Research Society, 1994:141–151.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:727–784.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

A.3. What are pressure-volume (P-V) loops? What do the different inflection points represent?

The P-V loop analysis (Fig. 8.1) depicts the relationship between left ventricular volume and left ventricular pressure during a single cardiac cycle. Opening and closing of the mitral and aortic valves are represented by the inflection points A, B, C, and D, respectively (Fig. 8.1). Moving from points A through D, AB depicts left ventricular filling, BC depicts isovolumetric contraction, CD shows left ventricular ejection, and DA shows isovolumetric relaxation. Point A coincides with opening of the MV and represents left ventricular end-systolic volume and early diastolic pressure. Point B is closure of the MV and the end of diastolic pressure (LVEDP) and volume [left ventricular end-diastolic volume (LVEDV)]. Point C represents the opening of the aortic valve and coincides with systemic, aortic diastolic pressure. Finally, point D is the closure of the aortic valve and represents left ventricular end-systolic pressure and volume, coinciding with the dicrotic notch in the aortic pressure tracing (Fig. 8.1). Left ventricular compliance is the relationship between the change in pressure and change in volume of the chamber and is defined by the slope of the filling phase or segment AB. Preload is the P-V relationship before the onset of contraction (LVEDP). Contractility may be illustrated by the slope of a line called the end-systolic pressure-volume relationship (ESPVR). The ESPVR slope is created by connecting multiple points (D) from multiple P-V loops generated by changing the filling volume to the LV (Fig. 8.2). Increased contractility results in a steeper line whereas diminished contractility results in a flatter relationship. The P-V loop analysis permits illustration of SV and EF. SV is defined as difference in volume from the end of filling to the end of ejection (EDV – ESV), whereas EF is the ratio of SV to total volume in the heart at peak filling (SV/ EDV). Thus, the P-V loop analysis permits illustration of the volume-pressure relationships and their changes with each of the four valvular lesions.

Figure 8.1. Normal pressure-volume loop and valve positions. A, mitral valve (MV) opening; B, MV closure; C, aortic valve (AV) opening; D, AV closure; AB, left ventricular filling; BC, isovolumetric contraction; CD, ejection; DA, isovolumetric relaxation.


Figure 8.2. Contractility. ESPVR, end-systolic pressure-volume relationships.


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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:727–784.

A.4. What are representative P-V loops for the four valvular lesions?

The hallmarks of AS illustrated by the P-V loop analysis framework are a high left ventricular systolic pressure and an upward and counterclockwise rotation in the end-diastolic P-V relationship (AB) indicative of decreased chamber compliance (Fig. 8.3). SV and EF are well preserved, but the ejection phase of the loop occurs at much higher pressures. This is permitted by an increase in contractility of a counterclockwise rotation of the ESPVR line.

Figure 8.3. Pressure-volume loop of aortic stenosis.


The schematic P-V loop for AI depicts the enlarged LV of chronic AI. The minimal change in LVEDP despite the large volume overload is seen by the shift in the diastolic P-V curve to the right (A'B') (Fig. 8.4). Low systemic diastolic pressures result in a brief isovolumetric phase (B'C') and early complete ejection. The isovolumetric relaxation phase is absent as the incompetent valve permits regurgitant filling of the LV from the aorta during diastole even before opening of the MV. When acute AI occurs, the left ventricular compliance is unchanged. Rapid increases in LVEDP from volume overload along the unshifted left ventricular diastolic P-V curve (AB) rapidly lead to increased LA pressure and pulmonary congestion.

Figure 8.4. Pressure-volume loops of acute and chronic aortic insufficiency.


The P-V loop of MS illustrates hypovolemia, the cause of which cannot be determined from the loop alone (Fig. 8.5). Because the predominant impact of MS occurs proximal to the LV, the P-V analysis format is less useful.

Figure 8.5. Pressure-volume loops of mitral stenosis.


In MR, the diastolic P-V relationship (line AB) is shifted to the right, as it is in AI, consistent with a marked increase in compliance (Fig. 8.6). The isovolumetric phase (BC) is nearly absent because the left atrium serves as a low-pressure/high-compliance route for ejection because of the incompetent MV. Decreases in contractility are depicted by a decrease in the slope of the end-systolic-PV line (line through D). Nevertheless SV and EF are maintained because of this low-pressure LA vent.

Figure 8.6. Pressure-volume loop of acute and chronic mitral regurgitation.


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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Sagawa K. Maugan L. Suga H, et al.Cardiac contraction and the pressure-volume relationship New York: Oxford University Press, 1988.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

A.5. Draw the pressure/time curves for the LV, left atrium, pulmonary artery (PA) and aorta for normal patient and patients with each of the four valvular lesions.

Normal curves are shown in Fig. 8.7. The points A, B, C, and D correspond to the same points in the P-V loops.

Figure 8.7. Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in a normal patient.


>Aortic stenosis

The additional systolic pressure work of AS can be seen in the left ventricular pressure tracing (Fig. 8.8). Elevations in LVEDP (point B) can be seen to diminish the perfusion gradient for coronary flow to the LV. The augmentation in left ventricular filling late in diastole secondary to atrial contraction (LA "kick" from sinus rhythm) is highlighted in the inset. Rising left ventricular diastolic pressures secondary to decreased compliance necessitate elevations in LA pressures to permit complete left ventricular volume loading. Atrial systole provides this elevation in LA pressure synchronous with elevations in LVEDP while keeping LA pressures relatively low during the remaining cardiac cycle facilitating pulmonary venous drainage.

Figure 8.8. Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with aortic stenosis.


Aortic insufficiency

The rapid upstroke and rapid decline of arterial pressure indicate absence of aortic valve closure and low end-diastolic aortic pressure (Fig. 8.9). Elevations in the LVEDV and LVEDP are typical of AI. The early increase in LVEDP can result in left ventricular pressures exceeding those of the left atrium during diastole with resultant premature closure of the MV.

Figure 8.9. Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with aortic regurgitation.


Mitral stenosis:

Elevations in pressure are seen in both the LA and PA tracing with MS (Fig. 8.10). The large gradient between LA and left ventricular pressures is highlighted in the inset. Chronic elevation in pulmonary volume induces changes in the luminary vascular bed and leads to pulmonary hypertension.

Figure 8.10. Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with mitral stenosis.


Mitral regurgitation

The hallmark of MR is the marked elevations of LA pressure during systole and the occurrence of a giant "cv" wave and elevated PA pressures (Fig. 8.11).

Figure 8.11. Pressure curves for the left ventricle, left atrium, pulmonary artery, and aorta in patients with mitral regurgitation.


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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:727–784.

A.6. What are the basic principles of echocardiography? What are M-mode, B-mode and Doppler color modalities? How do transthoracic (TTE) and transesophageal (TEE) echocardiography differ?

Echocardiography is the use of sound waves to image structures and blood flow within the heart and great vessels. To image tissue, sound waves are emitted from a transducer at known speeds and constant intervals. The sound packets bounce off structures in their path and the reflected sound waves are received at the point of origin, either by a separate receiving crystal or by the same emitting transducer, which spends a portion of its time in this "listening" mode. The time it takes for the reflected waves to return to the crystal is measured, and because the velocity of sound in tissues is relatively constant, solving for distance can be easily accomplished.

(1/2 because the distance is traversed twice, once to the object and again on returning.)

In this manner, the spatial orientation of cardiac structures can be determined. The strength of the returning signal can be quantified as an amplitude, thus "A" or amplitude mode (Fig. 8.12B). This echo machine codes this amplitude on a black/white scale, thus converting the amplitude to brightness or B-mode scanning (Fig. 8.12C). Fig. 8.12D shows this "ice-pick" view through the LV of the heart. Each change in tissue density results in some sound waves being reflected and hence an interface. In this example, bold lines are seen at the epicardial, the endocardial-chamber, the chamber-endocardial, and the epicardial borders. If these amplitude bars are displayed in a real time, a motion or M-mode display results (Fig. 8.12E). These images were difficult to reliably obtain and interpret because the views represent a linear slice without surrounding structural images for referencing. However, if the probe is rocked back and forth repetitively, multiple M-mode images can be obtained in a given instant and, thus, a two-dimensional image formed. This rapid rocking back and forth of the ultrasound beam is performed electronically in a phased-array transducer. The images derived in this manner appear as a "cine-x-ray" display of myocardial movement. Thus, echocardiography can provide information about the size, shape, location, and movement of myocardial structures.

Figure 8.12. A to E: The process of producing the B-mode and M-mode images. A: A pulse of ultrasound is emitted into the object, and the backscattered echo is received by the same transducer. B: The received acoustic signal is converted to the electric signal (A-mode). C: The amplitude is modulated into brightness (B-mode). D: As subsequent pulses of ultrasound are emitted with the sequentially changing angles and the obtained one-dimensional B-mode images are compounded according to the direction of each ultrasound emission, the first frame of the sector-shaped image is formed. E: When the ultrasound is repeatedly transmitted in one direction, a series of one-dimensional B-mode images is obtained. As these are arranged against time, an M-mode image is obtained. (From Okay Y, Goldiner PL, eds. Transesophageal echocardiography. Philadelphia: JB Lippincott, 1992:12, with permission.)


In addition to determining how long it takes for a given sound wave to return and, thus, deriving the distance from the transducer, contact of the sound wave packet with the reflecting object (tissue, blood cells, air) will alter the wavelength of the sound packet according to the Doppler principle. When the object coming in contact with the sound wave is moving toward the source of the ultrasound, the reflected ultrasound wavelengths are compressed (shorter) or of higher pitch. The opposite occurs when the contacted object is moving away from the sound source. These shifts in frequency are proportional to the velocity of the contacted structure and, thus, the speed and direction of the encountered object (usually of blood flow) can be calculated. This velocity information can be displayed on a color map (Doppler color flow) or on a time/velocity scale (spectral Doppler display). Doppler derived blood flow velocity information can determine laminar and turbulent flow patterns, regurgitant or stenotic lesions, congenital anomalies and can permit quantification of pressure gradients. Using the modified Bernoulli equation, (P = 4 v2), determination of a blood flow velocity permits the estimation of pressure gradients.

Simply, the greater the velocity of blood flow the higher the pressure gradient. Only the component of blood flow parallel to the Doppler beam will be analyzed. The Doppler equation: V = c (FS – FT)/2 FT (cos ), contains the cosine of the angle of incidence between the ultrasound beam and the moving object. Because the cosine of 90 degrees is zero, blood flow that is perpendicular to the ultrasound beam will not have any Doppler shift and, thus, will not be represented in the color display. For this reason, it is important to choose an ultrasound "window" in which the expected blood flow direction is most parallel to the ultrasound.

TTE uses imaging points or "acoustic windows" obtained with the transducer hand held on the chest wall. It is simple and importantly noninvasive. Most standard echocardiograms are obtained from this position. However, during cardiac surgery, the chest wall is in the sterile field and, thus, unavailable. The esophagus lies immediately adjacent to the heart outside of the operative field and, thus, affords an excellent imaging vantage point. In 1976, Yasu Oka from the Albert Einstein College of Medicine developed a practical method of intraoperative imaging. He mounted an ultrasound crystal on the end of a gastroscope and, thus, obtained images of the heart during surgery. This has been refined considerably since. TEE has become the standard of care for heart surgery at many institutions. The close proximity of the probe to the heart affords excellent resolution. The probe is not in the operative field hence surgery is unhindered and sterility is not an issue. Though mildly invasive, the risk of esophageal injury in the anesthetized state is very low.

Intraoperative TEE is beneficial for quantification of cardiac contractility, for determination of the severity of regurgitant and stenotic valvular disease, for the detection of intracardiac shunts and the occurrence of dissections, and as a guide for catheter placement.

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Oka Y, Goldiner PL, Transesphageal echocardiography Philadelphia: JB Lippincott, 1992:9–27.

A.7. What are the three TEE vantage points for the comprehensive imaging of the LV? How are pressure gradients measured by echocardiography? How do the pressure gradients derived from Doppler echocardiography differ from those obtained in the catheterization lab by direct pressure measurement?

The heart has two main axes, the longitudinal axis running from the base to the apex and the short axis perpendicular to that. Because the ultrasound beam can be thought of as a two-dimensional structure, multiple scan planes are required to completely image a three-dimensional structure. The LV may be divided into 16 segments, 6 at the basal level, 6 at the midpapillary level, and 4 at the apical level (Fig. 8.13). By moving the TEE probe in the esophagus and by rotation of the crystal within the transducer tip, the LV can be imaged from three acoustic windows. These are the midesophageal four- chamber, the transgastric short axis, and the transgastric two-chamber view. Normal ventricular motion requires that the wall segment move centrally with systole and similarly undergo thickening along this axis during contraction. Function is usually quantified as normal; mild, moderate, and severe hypokinesis; akinesis; and dyskinesis.

Figure 8.13. Sixteen-segment model of the left ventricle. A: Four-chamber views show the three septal and three lateral segments. B: Two-chamber views show the three anterior and three inferior segments. C: Long-axis views show the two anteroseptal and two posterior segments. D: Mid short-axis views show all six segments at the mid level. E: Basal short-axis views show all six segments at the basal level. (From Shanewise JS, Cheung AT, Aronson S, et al, eds. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. Anesth Analg 89:870–884, 1999, with permission.)


In addition to function, TEE permits the determination of wall thickness and chamber size, important parameters in understanding the pathophysiology of valvular heart disease.

As mentioned previously, pressure gradients are derived via analysis of the Doppler profiles of blood flow. A commonly determined echocardiography gradient is that which is present from the LV to the aorta in the setting of AS. To obtain the change in blood flow velocity across the aortic valve with TEE, the probe is advanced far into the stomach and sharply anteflexed and left deflected to obtain the window from the apex of the heart (deep transgastric long axis) and align the ultrasound beam most parallel to the path of blood flow. From this window, the continuous wave Doppler cursor is directed across the left ventricular outflow tract and aortic valve. An example of such a spectral Doppler display is seen in Fig. 8.14. The large increase in blood flow velocity in this display occurs at the narrowest point along its path, which in this case is the aortic valve. Using the modified Bernoulli equation mentioned previously, a gradient is calculated (100 mm Hg in the example). This represents the maximum instantaneous pressure difference between the LV and the aorta. AS is also quantified at the time of catheterization by measuring the pressures from within the LV and the aorta (Ao) as a rapid response pressure transducer catheter is withdrawn from the LV back to the aorta across the stenotic valve. The standard reported gradient is the difference between the maximum left ventricular and Ao pressures. Fig. 8.15 illustrates that these peaks are not simultaneous events. Thus, Doppler derived AS gradients are usually higher than those derived at the time of left heart catheterization.

Figure 8.14. Continuous wave Doppler across the aortic valve in the deep transgastric apical view from a patient with severaortic stenosis.


Figure 8.15. Pressure gradients in severe aortic stenosis are measured during systole as the difference between aortic and left ventricular pressures displayed using a 0 to 200-mm Hg scale. The peak instantaneous gradient is the maximum gradient noted; the peak-to-peak gradient is the difference between peak left ventricular and aortic pressures. The mean systolic gradient is the average of all systolic pressure gradients noted during systolic ejection (TS). (From Nanda NC, ed. Doppler echocardiography. Philadelphia: Lea & Febiger, 1993:130, with permission.)


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Nanda NC, Doppler echocardiography Philadelphia: Lea & Febiger, 1993:127–138.

Shanewise JS. Cheung AT. Aronson S, et al.ASE/SCA guidelines for performing a comprehensive multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists task force for certification in perioperative transesophageal echocardiography. Anesth Analg89:870–884, 1999.

A.8. What are the echocardiographic and cardiac catheterization criteria for the four valvular lesions?

The TEE severity scales of the various valvular lesions are summarized in Table 8.1.

Aortic stenosis

Echocardiographic criteria for AS include two-dimensional images demonstrating limited aortic valve opening and motion and left ventricular concentric hypertrophy. Doppler examination will reveal a turbulent, high-velocity jet across the aortic valve and color flow Doppler will demonstrate a turbulent, mosaic-appearing color map. The gradient across the aortic valve measured at cardiac catheterization is different from that measured by echocardiography as mentioned previously. Quantification of this Doppler derived pressure gradient again relies on the modified Bernoulli equation.

Because flow is an important determinant of pressure gradients, both these catheterization and Doppler derived values are interpreted along with cardiac output.

Calculations permit the determination of a valve area. Severe AS is present when the gradient exceeds 75 mm Hg and/or the valve area is less than 0.8 cm2.

Aortic insufficiency

Catheterization criteria for AI rely on the qualitative estimation of the regurgitation volume and an estimation of left ventricular size and EF. Similar quantification can be made from Doppler color echocardiography derived data. A commonly used echocardiographic criteria compares the width of the regurgitant jet at the level of the valve to the width of the left ventricular outflow tract. A ratio of greater than 0.66 corresponds with severe AI.

Mitral stenosis

The severity of MS can be obtained by the direct measurement of a diastolic gradient between the left atrium and ventricle at the time of cardiac catheterization. However, this requires a transatrial puncture, a procedure largely replaced by echocardiographic techniques. Echocardiographic diagnosis is based on gradient estimation by Doppler and by measuring the rate of decay in the pressure with the time spent in diastole (pressure half-time). The MV area in cm2 can be derived from an empirical formula wherein the MV area equals 220 divided by this pressure half-time (Hatle constant). Severe MS is present when the end-diastolic gradient exceeds 12 mm Hg corresponding to a valve area of less than 1.0 cm2.

Mitral regurgitation

In the presence of MR, ventriculography will demonstrate the reflux of dye from the LV into the left atrium. Severe MR is diagnosed when dye refluxes into the pulmonary veins. Color Doppler echocardiography permits similar quantification. Estimation relies on an estimation of regurgitant jet volume as compared with the left atrium and via analysis of pulmonary venous flow profiles.

In every case, color Doppler echocardiography is often useful in identifying the cause of the valvular lesion, its extent of involvement within and around the valve, and the associated hemodynamic changes. Thus, for many valvular lesions, it may be sufficient for the diagnosis. Catheterization, however, is often performed to assess the presence of concomitant coronary artery disease, especially in patients of advanced age.

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Braunwald E, Heart disease: a textbook of cardiovascular medicine6th ed. Philadelphia: WB Saunders, 2001.

Perry GJ. Helmcke F. Nanda NC, et al.Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol 1987:9:952–959.

Weyman AE, Principles and practice of echocardiography2nd ed. Philadelphia: Lea & Febiger, 1994:391–574.

B. Preoperative Evaluation and Preparation

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B.1. What are the presenting signs and symptoms of the four valvular lesions listed previously?

See Table 8.2.

Aortic stenosis

The triad of angina, syncope, and congestive heart failure represent the progression of symptoms associated with AS. These symptoms correlate directly with mortality; the 50% survival data for these symptoms are 5, 3, and 2 years from the onset of these symptoms, respectively. Angina results from both increased demand for and a decrease in supply of coronary blood flow. Increased muscle mass from LVH and the high energy requirements to generate increased (high) systolic pressure combine to increase demands for coronary blood flow. In addition, insufficient supply secondary to decreased perfusion gradients and a decrease in coronary vasculature relative to the large amount of myocardium sum to diminish relative myocardial blood supply. Therefore, up to one third of patients with AS can have angina in the absence of significant coronary artery disease.

Aortic insufficiency

Patients with AI have variable clinical presentations, primarily depending on the rapidity with which the left ventricular volume overload develops. When the volume increase occurs gradually as in chronic AI, there is usually a long asymptomatic period. The onset of the symptoms of fatigability and dyspnea signals either reduced cardiac output or increased LVEDP indicative of impairment of left ventricular contractile function. When AI occurs acutely, the ventricular compliance is unchanged; increased left ventricular diastolic volumes from regurgitant flow, therefore, lead to rapid rises in LVEDP and the clinical picture of congestive failure.

Mitral stenosis

MS is a slowly progressive obstruction to flow across the MV with gradual increase in LA pressure and volume. Symptoms of pulmonary congestion result from elevations in LA pressures and not from poor left ventricular systolic function. Atrial fibrillation develops secondary to atrial dilation.

Mitral regurgitation

The time course for the development of MR determines the severity of the symptoms. When the volume of regurgitant flow from the LV to the left atrium increases gradually, the left atrium compensates by gradual dilatation. In contrast, the onset of acute MR can lead to rapid increases in LA pressures and severe pulmonary congestion and congestive heart failure.

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Braunwald E, Heart disease: a textbook of cardiovascular medicine6th ed. Philadelphia: WB Saunders, 2001.

Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

B.2. What is the New York Heart Association classification of heart failure?

The NYHA heart failure classification is based on the amount of symptoms, specifically dyspnea and fatigue. The various classes are listed in the following:

Class I–No symptoms

Class II–Symptoms with ordinary activity

Class III–Symptoms with less than ordinary activity

Class IV–Symptoms at rest

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Criteria Committee of the New York Heart AssociationDiseases of the heart and blood vessels(nomenclature and criteria for diagnosis), 6th ed. Boston: Little, Brown and Company, 1964.

B.3. Discuss the role of premedication for patients with the four different valvular lesions.

The role of premedication is to allay the anxiety of the impending surgical procedure thereby controlling the sympathetic outflow that may accompany the stress response. However, acute changes in heart rate, venous return, and systemic resistance can have particularly profound effects on patients with valvular heart disease.

Patients with AS may benefit from premedication by preventing unnecessary increases in heart rate. Concern however must be taken to ensure adequate venous return and preservation of sinus mechanism (see later).

Patients with AI can similarly benefit from premedication because any increases in afterload, which may accompany sympathetic stimulation, can increase regurgitant volume. Drug doses should be adjusted based on the severity of debilitation and degree of systemic hypoperfusion.

Patients with MS should be premedicated with caution. Elevations in carbon dioxide resulting from narcotic-induced hypoventilation can dramatically elevate pulmonary pressures further compromising right ventricle output. Conversely venodilation may excessively diminish filling pressures.

Patients with MR can respond similarly to those with MS, particularly when pulmonary hypertension is present. However, elevations in systemic pressure from stress can also compromise forward left ventricular output. Proper premedication can be delivered by careful dose selection and the provision of supplemental oxygen.

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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

B.4. How would you premedicate the patient with severe AS and MR?

Premedication of a patient with severe AS and MR must be approached with caution. The patient should receive supplemental oxygen. A light premedication could be provided with small doses of benzodiazepines by mouth. However, I would prefer to titrate in small intravenous doses of sedation while the patient was under the closely monitored situation of the operating room or holding area and with inspired oxygen supplementation. In this setting, incremental doses of midazolam (0.5 mg intravenously) would be administered. It is important to remember that there may be significant delay in the onset of effect of intravenous medications secondary to pooling in the pulmonary and LA systems. Adequate waiting periods must be observed between each aliquot to avoid inadvertent overdose with ensuing respiratory depression, pulmonary hypertension, systemic hypotension, and right heart failure.

C. Intraoperative Management

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C.1. Outline the hemodynamic management goals for each of the four valvular lesions. What are the anesthetic goals with respect to heart rate and rhythm, preload, afterload, and contractility?

Table 8.3 summarizes the hemodynamic goals with respect to heart rate and rhythm, preload, afterload, and contractility.

Aortic stenosis

Patients with AS need the left ventricular filling obtained through a well-timed atrial contraction. Similarly, LVH renders the ventricle stiff and adequate preload is required. Reducing vascular tone will do little to relieve the fixed afterload increases from a stenotic valve but rather lower diastolic coronary perfusion gradients and should be avoided. Patients with AS experiencing angina may require the administration of an -agonist like phenylephrine rather than nitroglycerin to increase coronary perfusion pressure.

Aortic insufficiency

The severity of AI is determined by the size of the regurgitant orifice, the pressure gradient between the aorta and LV during diastole, and the time spent in that phase of the cardiac cycle. Elevated heart rates decrease the time spent in diastole and can lead to a decrease in heart size. Afterload reduction can lessen the regurgitant driving forces but therapeutic maneuvers to accomplish this may be limited by resulting systemic hypotension.

Mitral stenosis

Patients with MS can swiftly deteriorate in the setting of rapid heart rates. The decreased filling time necessitates the marked elevation of LA pressures and pulmonary edema can rapidly ensue. Beta-blockade does result in decreased contractility, which in the setting of decreased cardiac output and blood pressure could be deleterious. However, the loss in contractility is more than offset by the beneficial effects of the reduction of heart rate. Slower heart rates permit adequate time for transfer of blood from the left atrium to the LV across the stenotic MV to occur. In addition, the pressure gradient across the MV is also reduced; thereby lowering LA pressure and diminishing pulmonary congestion. Because there is some variability in the individual response, the use of short-acting -blockers such as esmolol is prudent because an adverse response should be evanescent.

Mitral regurgitation

Patients with MR can rapidly deteriorate with marked increases in systemic blood pressure and afterload. As with other volume overload lesions such as AI, rapid heart rates result in smaller left ventricular volumes. This may lessen any component of MR secondary to annular dilation or chordal malalignment.

C.2. What are the hemodynamic goals for this patient with the combination of severe AS and MR?

In the patient with combined AS and MR, the situation is more complex than when only a singular valvular lesion is present. Careful examination of the hemodynamic goals for each of the two lesions will reveal that therapy beneficial to patients with AS may exacerbate the severity of the MR. Early aggressive intervention is the key to these combined lesions. There usually exists less of a margin for error because minor hemodynamic aberrations can rapidly lead to cardiac collapse. A good rule of thumb is to prioritize the management based on the character of the present symptoms. Patients with AS and MR who present with syncope or angina are best managed for their AS, whereas patients with dyspnea and pulmonary edema are best managed for their congestive symptoms. It is prudent to maintain the patient's own usual hemodynamics and avoid physiologic trespass. TEE evaluation of left ventricular performance can be helpful in separating pulmonary congestion secondary to left heart failure from that secondary to poor diastolic left ventricular compliance.

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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

C.3. How would you monitor this patient?

In addition to the standard American Society of Anesthesiologists (ASA) recommended monitors, the patient would have a radial artery and a pulmonary artery (PA) catheter. Following induction of anesthesia and endotracheal intubation, a TEE probe would be inserted to confirm the valvular pathology and to assess ventricular function. Following valve replacement, the TEE would be used to check for adequacy of valvular function and the absence of paravalvular leaks and to assess post-bypass ventricular function.

C.4. Should the patient have a PA catheter placed before induction?

Volume status may be particularly difficult to assess in patients with valvular heart disease yet of critical importance in the management of these patients. Patients with stenotic lesions depend on adequate filling pressures for diastolic filling of the ventricle. Patients with the volume overload lesions of AI and MR can benefit from the careful reductions in pulmonary pressure guided by the simultaneous assessment of cardiac performance. In these capacities, the PA catheter is useful. Patients with current hemodynamic stability, without severe respiratory distress, can be safely anesthetized before placement of the PA catheter.

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Roizen MF. Berger DL. Gabel RA, et al.Practice guidelines for pulmonary artery catheterization. A report by the American Society of Anesthesiologists task force on pulmonary artery catheterization. Anesthesiology 1993:78:380–394.

C.5. Is a PA catheter with pacing capabilities indicated?

Patients with AS can become severely compromised with the loss of atrial kick or the presence of slow junctional rhythms. Patients with AI or MR can experience left ventricular dilation in the setting of slow heart rates. A PA catheter with atrial and ventricular pacing capacity can be useful in this setting. In patients with intact conduction systems, rate manipulation can often be achieved pharmacologically. Transesophageal atrial pacing is another option; transthoracic pacing elicits a ventricular response only and does not permit atrial stimulation. Transthoracic pacing is indicated when the ability to rapidly open the pericardium and obtain epicardial pacing is limited. This occurs in the setting of reoperations or with patients having a history of inflammatory pericardial disease. Pacing will be limited to capture of the ventricle alone. The loss of atrial contraction can lead to underfilling and hemodynamic compromise in patients dependent on the added volume from atrial systole. One of the other pacing modalities is best in this setting.

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Risk SC. Brandon D. D'Ambra M, et al.Indications for the use of pacing pulmonary artery catheters in cardiac surgery. J Cardiothorac Vasc Anesth 1992:6:275–279.

C.6. What anesthetic technique would you employ? Why?

For the patient undergoing CPB and aortic valve replacement, general anesthesia with endotracheal intubation is the obvious choice. Both narcotics and inhalation anesthetics can be safely administered. When prolonged postoperative ventilation is anticipated, a high-dose narcotic anesthetic has numerous advantages. Recent anesthetic technique for cardiac surgery has focused on the use of techniques permitting earlier extubation, so-called fast-tracking. Anesthetic combinations using smaller total narcotic doses, inhalation anesthetics, and short-acting intravenous sedatives such as propofol are gaining popularity. For uncomplicated valve replacements with good ventricular function, the advantages of early extubation can be safely achieved. In complicated cases with longer bypass periods, poor ventricular function, or post-bypass bleeding, the hemodynamic stability of a high-dose narcotic technique may be advantageous.

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DiNardo JA. Anesthesia for cardiac surgery2nd ed. Stamford, CT: Appleton & Lang, 1998:109–140.

Howie MB. Black HA. Romanelli VA, et al.A comparison of isoflurane versus fentanyl as primary anesthetics for mitral surgery. Anesth Analg 1996:83:941–948.

Tuman KJ. McCarthy RJ. Spiess BD, et al.Comparison of anesthetic techniques in patients undergoing heart valve replacement. J Cardiothoracic Anesth 1990:4:159–167.

C.7. What muscle relaxant would you use for this patient?

Muscle relaxants can alter hemodynamics both from the effects of histamine release including vasodilatation and bronchospasm and through effects on rhythm. Although slowing of heart rates usually benefits the patient with angina, it may have severe consequences in patients with valvular heart disease. The typical high-dose narcotic anesthesia usually results in bradycardia secondary to the vagotonic actions. Pancuronium-mediated increases in heart rate usually offset these actions and result in a stable heart rate.

Certainly the newly released long-duration relaxants doxacurium and pipe-curonium have the potential for minimal effects on hemodynamics. However, as outlined previously, the potential side effect of one agent may be rationally used to counter the adverse effect of another. Hemodynamically "neutral" relaxants such as vecuronium, rocuronium, or cis-atracurium could be used but their intermediate duration of action offers little if any advantage in this setting.

Therefore, it is important to choose that combination of agents that will promote hemodynamic stability in a particular patient with his or her unique hemodynamic presentation. In this patient, I would use pancuronium in conjunction with the high-dose narcotic anesthetic.

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Fleming N. Con: the choice of muscle relaxants is not important in cardiac surgery. J Cardiothorac Vasc Anesth 1995:9:768–771.

Hudson RJ. Thomson IR. Pro: the choice of muscle relaxants is important in cardiac surgery. J Cardiothorac Vasc Anesth 1995:9:768–771.

C.8. What are the usual TEE findings in a patient with AS/AI/MR? How do you grade the severity of AS by TEE? How do you quantify the severity of MR? What is the impact of AS on the severity of MR?

The severity of AS is usually stated in terms of aortic valve area (AVA). Normal AVA is 2.5 to 3.5 cm2. Moderate stenosis is when the AVA is within the range of 0.8 to 1.2 cm2 and severe stenosis when the AVA is less than 0.8 cm2. A patient with a large peak pressure gradient (usually more than 75 mm Hg) in the absence of excessively high cardiac output is usually considered to have severe AS as well. In the setting of low cardiac outputs, the pressure gradient may not be that great (20 to 30 mm Hg), and determination of AVA is required. This can be accomplished with echocardiography.

MR is graded by the amount of blood regurgitated backward into the left atrium during systole. Doppler color flow permits quantification of this flow. Common methods for MR quantification include the depth of MR jet extent into the left atrium (25% mild MR, 25% to 75% moderate MR, and more than 75% severe MR). Other methods of quantification include calculation of the area of the regurgitant jet by planimetry, by comparison of the MR jet area to the area of the left atrium, and by analysis of pulmonary vein flow profiles. It is important to remember that the amount of regurgitant blood flow in the setting of MR is determined by the amount of time spent in systole, the size of the defect in the MV, and the pressure gradient across the defect. Thus, MR severity by Doppler color flow is load dependent. The lower pressure of the anesthetic state can often mask more severe degrees of MR seen when the patient is under his or her usual hemodynamic conditions.

The left ventricular pressures are increased in the setting of AS. Therefore, the gradient across the MV is increased often leading to more severe MR. Following replacement of the stenotic aortic valve and elimination of the outflow tract obstruction, left ventricular pressures are markedly reduced. Moderate levels of MR without major structural defects in the MV apparatus usually revert to minimal or certainly less severe levels following reduction in the left ventricular outflow obstruction.

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Spain MG. Smith MD. Grayburn PA, et al.Quantitative assessment of mitral regurgitation by Doppler color flow imaging. Angiographic and hemodynamic correlations. JACC 1989:13:585–590.

C.9. What special considerations particular to cardiopulmonary bypass (CPB) operations do you have for each of the four lesions? Focus on these concerns with respect to the induction and prebypass, bypass, and postbypass periods.

Aortic stenosis

Critical to the management of a patient with AS is the avoidance of hypotension. Low blood pressure can initiate a cascade of events leading to cardiac arrest. Hypotension decreases the gradient for coronary perfusion with resultant ischemia. Ischemia leads to diminished cardiac output and decreased blood pressure further compromising coronary perfusion. The occurrence of cardiac arrest in a patient with AS is particularly catastrophic because closed chest cardiac massage will provide little gradient for blood flow across a stenotic aortic valve.

Patients with AS are particularly dependent on their atrial kick for adequate ventricular filling volume and can rapidly become hypotensive and ischemic following the onset of an supraventricular tachycardia (SVT) or atrial fibrillation. These rhythms are not uncommon during atrial cannulation. Therefore, it is of particular importance that every preparation for the initiation of CPB be made before atrial manipulation. Increased muscle mass of LVH can be more difficult to adequately protect with cardioplegia. Careful attention to surface cooling, myocardial temperature measurement, and/or the use of retrograde cardioplegia can be helpful. Following aortic valve replacement, hypertension from left ventricular output now unopposed by any valvular lesion can result in stress on suture lines and excessive bleeding. It is important to remember that the compliance of the LV is unchanged by surgery and still critically dependent on adequate preload and sinus rhythm.

Aortic insufficiency

Patients undergoing AVR for AI can often present difficult management decisions. The usual treatment measures for hypotension (-agonist) may have deleterious effects by increasing regurgitant volume. The use of combined - and -agonists, (ephedrine, epinephrine, or infusions of dopamine or dobutamine) may be required. Although it would serve to lessen regurgitant volume, afterload reduction is beneficial in only a subset of patients with AI. Those patients with elevated LVEDP, reduced EFs, diminished cardiac output, and systemic hypertension usually benefit from afterload reduction. In contrast, those patients without the previously mentioned constellation may experience a decrease in forward cardiac output secondary to diminished preload from reduced venous return. Systemic hypotension usually limits the utility in the acute setting. The presence of AI makes initiation of CPB a critical period. Periods of bradycardia or ventricular fibrillation can lead to rapid volume overload of the LV through the incompetent aortic valve. Pacing, electrical defibrillation, and/or cross clamping should be performed to prevent ventricular distention. Similarly, myocardial protection is compromised by AI. Generation of adequate root pressures is usually not obtainable; hence delivery of cardioplegia requires aortotomy and cannulation of the coronary ostia. Use of retrograde cardioplegia is advantageous. Following AVR, the ventricle no longer has the lower pressure/impedance outflow afforded by the low aortic diastolic pressure. Inotropic support is often required. As with AS, the presence of an aortic suture line necessitates rapid response to hypertension to avoid bleeding and dissection.

Mitral stenosis

Patients undergoing MV replacement for MS are particularly challenging. Marked elevations in pulmonary vascular resistance can be present with associated right heart failure. Stasis in the left atrium necessitates the careful echocardiographic examination for the presence of atrial thrombi. Manipulation of the heart before cross-clamping should be avoided. Following replacement, the chronically under filled, under worked LV may be unable to handle the new volume load. Inotropic support is usually required. Afterload reduction and improved systemic perfusion via an IABP may be beneficial.

Mitral regurgitation:

Similarly, patients with MR may have pulmonary hypertension and right heart failure. In contrast to AI, almost all patients with MR can be greatly benefited by afterload reduction, both pharmacologically and/or via an IABP. Diminution of left ventricular systolic pressure via afterload reduction decreases the pressure gradient from the LV to the left atrium during systole with resultant decreased regurgitant volume.

Prebypass assessment can be misleading. Preserved EFs and elevated SVs may mask marked left ventricular systolic dysfunction. It should be remembered that much of the left ventricular volume is ejected into the low-pressure/impedance outflow path of the left atrium. This route is no longer available after valve replacement. Following MV replacement, dysfunctional ventricles may be unable to provide adequate forward flow into the systemic circuit with its elevated vascular resistance and usually necessitate the use of inotropic support.

Patients previously in atrial fibrillation without marked atrial enlargement often revert to or can be converted to sinus rhythm following valve replacement. The capacity of maintaining a person in sinus rhythm dramatically decreases when the diameter of the atrium is more than 5 cm.

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Hartman GS. Management of patients with valvular heart disease1994 IARS Review Course Lectures Cleveland, OH: International Anesthesia Research Society, 1994:141–151.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed.. Philadelphia: WB Saunders, 1999:727–784.

C.10. The patient cannot be weaned from bypass following an aortic and mitral valve (MV) replacement. What are the possible causes?

The adequacy of myocardial preservation should be considered. LVH without or with accompanying coronary artery disease increases myocardial oxygen demands. Prolonged cross-clamp time necessitated by dual valve replacement can lead to inadequate and/or nonhomogeneous myocardial protection. In addition, there may be residual cardioplegia present within the myocardium. Therefore, some degree of postbypass left ventricular dysfunction can be anticipated. Inotropic support may be required. It is important to remember that although the obstruction to left ventricular ejection is acutely relieved by replacement of the stenotic valve, left ventricular compliance is largely unchanged. Adequate preload still depends on sinus rhythm and sufficient left ventricular filling pressures [pulmonary capillary wedge pressure (PCWP) or LVEDP]. Elevations in pulmonary vascular resistance may render estimation of LA pressure via the PA catheter inaccurate. In this setting, placement of an LA catheter is indicated. TEE may prove invaluable in identifying surgically correctable causes for inability to wean from CPB. Evaluation of left ventricular filling and contractility can help resolve the situation of low cardiac output and high filling pressures. A small under-filled LV with hyperdynamic contractility and a dilated, overfilled, hypokinetic LV can both give the same hemodynamic parameters but obviously require different pharmacologic interventions. Abnormal valve seating may compromise flow into the coronary ostia and return to bypass with valve repositioning and/or coronary artery bypass grafting may be indicated. Similarly, perivalvular leaks or aortic dissections can be readily identified.

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Thomas SJ, Kramer JL, Manual of cardiac anesthesia2nd ed. New York: Churchill Livingstone, 1993:81–127.

C.11. How would you diagnose right heart failure and pulmonary hypertension? How would you treat it?

Right heart failure is diagnosed by the elevations in right-sided filling pressures, specifically central venous pressure (CVP). Careful examination is required to rule out tricuspid insufficiency as the cause of the CVP elevation. A high CVP indicates the inability of the right heart to adequately propel the venous return volume into the pulmonary circulation. Elevation in the PA pressures is indicative of pulmonary hypertension. The combination of high CVP and high PA pressures indicates severe right heart failure. This scenario can be difficult to manage. Attempts to elevate systemic perfusion pressure with -agonists can worsen pulmonary hypertension. Administration of vasodilators to lower pulmonary pressures results in systemic hypotension. In this setting, it is often prudent to return to CPB, relieve ventricular distention, and improve myocardial perfusion. During this "rest period," adjustments in inotropic therapy, ventilation, and cardiac rhythm can be instituted. Optimization of acid-base status and hemoglobin concentration should also be performed. Separation from bypass can then be reattempted.

Typical inotropic agents effective in this setting are those with high degrees of -adrenergic potency. Commonly employed agents include dobutamine, epinephrine, and/or the phosphodiesterase-III inhibitors (PDI-III) amrinone and milrinone. It is not uncommon to require the administration of -agonists to counteract the systemic vasodilating effects of prostaglandin E1 and the PDI-III agents. Some selective pulmonary vasodilating action and systemic vasoconstricting effects can often be achieved by administration of pulmonary vasodilating agents such as prostaglandin E1 via the right-sided access (CVP or PA catheter) and infusion of the -agonists via the LA line. Thus, the vasoconstriction of the pulmonary arterial bed can be minimized.

Nitric oxide (NO) is a potent, inhaled pulmonary vasodilator. Its half-life in the systemic circulation is extremely short permitting its administration to the pulmonary vasculature with minimal systemic hypotensive effects. NO can selectively and effectively dilate the pulmonary vasculature. The exact method of delivery, scavenging of waste gases, and high cost remain as obstacles to its clinical application.

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Body SC. Hartigan PM. Shernan SK, et al.Nitric oxide: delivery, measurement, and clinical application. J Cardiothorac Vasc Anesth 1995:9:748–763.

Kieler-Jensen N. Houltz E. Ricksten SE. A comparison of prostacyclin and sodium nitroprusside for the treatment of heart failure after cardiac surgery. J Cardiothor Vasc Anesth 1995:9:641–646.

C.12. What role does an intraaortic balloon pump (IABP) have in this setting?

An IABP may be useful, because unlike any pharmacologic maneuver it is capable of increasing mean pressure during diastole critical for coronary perfusion while lowering afterload to systolic left ventricular ejection. Myocardial dysfunction secondary to inadequate protection during bypass can be reduced by decreased afterload and augmentation of diastolic pressures through IABP counterpulsation.

C.13. How does the IABP work to benefit the failing heart?

An IABP is a catheter with a large balloon (40 to 60 cc) at its tip. It is positioned in the thoracic aorta distal to the left subclavian artery origin and proximal to the take-off of the renal vessels. It is timed to inflate during diastole to increase diastolic perfusion pressure to the coronary arteries, great vessels, and major abdominal organs and to deflate just before systole to decrease afterload thereby increasing forward cardiac output. It is the unique modality, which can improve coronary perfusion pressures while reducing myocardial oxygen demand.

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Cheung AT. Savino JS. Weiss SJ. Beat-to-beat augmentation of left ventricular function by intraaortic counterpulsation. Anesthesiology 1996:84:545–554.

C.14. What role does TEE play in the placement, timing, and demonstration of efficacy of an IABP?

The thoracic aorta and aortic arch can be clearly imaged by TEE. Imaging of the take-off of the left subclavian artery facilitates optimal postioning of the IABP. In addition, before insertion the aorta can be evaluated for dissection or the presence of severe atheromatous disease, both contraindications to IABP insertion. TEE can demonstrate the efficacy of an IABP by showing enhanced ventricular emptying during systole and filling during diastole.

C.15. How would you properly time its cycle?

Inflation should occur just following the dicrotic notch and deflation before the upstroke in the aortic pressure curve. Augmentation in diastolic and mean pressures with a reduction in systolic pressure should follow its proper function.

C.16. What are the contraindications to the use of an IABP?

The most common contraindications are AI and severe aortic disease, atheromatous, aneurysmal, or a dissection. Although often listed as absolute contraindications, there are reports of the effective use of IABP in these settings.

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Sanfelippo PM. Baker NH. Ewy HG, et al.Experience with intraaortic balloon counterpulsation. Ann Thorac Surg 1986:41:36–41.

D. Postoperative Management

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A 41-year-old female sought medical care due to severe dyspnea. The patient had had acute rheumatic disease in childhood. During evolution, she developed mitral stenosis. The symptoms became incapacitating and she underwent mitral commissurotomy at 36 years. She progressed well for a few years until dyspnea recurred and she was once again submitted to surgery, at 41 years, when she underwent mitral valve plasty (03/16/2005).

After the last surgery, she had dyspnea on great exertion for about three months, when it progressed and started to be triggered by middle, and finally by mild exertion, and at three days before hospitalization (10/10/2005), it had become present even at rest. The patient attributed the recent worsening to current medication discontinuation: captopril 25 mg, furosemide 80 mg, 0.25 mg digoxin and warfarin 2.5 mg daily.

Physical examination (10/10/2005) showed the patient was in good general health, dyspneic, with a marked increase in jugular venous pressure, pulse rate of 92 bpm, blood pressure of 100/60 mmHg. Lung examination was normal. Cardiac auscultation showed irregular rhythm without additional heart sounds. Systolic murmur +/4+ was diagnosed in the mitral valve area. There were no alterations at the abdominal examination, but slight edema of the lower limbs.

Laboratory tests (10/10/2005) showed hemoglobin 11.7 g/dL, hematocrit 35%, WBC, 3,900/ mm3, platelets, 12.9000 /mm3, creatinine 1.3 mg / dL, urea 31 mg / dL, sodium 135 mEq/L, potassium 3.6 mEq/L, INR 1.19 and activated partial thromboplastin time (patient / control) 1.09.

The electrocardiogram (10/10/2005) showed frequency of 90 bpm, atrial fibrillation, low voltage QRS complex, undetermined QRS axis in the frontal plane and presence of intraventricular stimulus conduction disturbance, of the right branch type and decreased left ventricular potential, suggesting right ventricular overload (Figure 1).

Figure 1

Atrial Fibrillation, low voltage QRS complexes, right bundle branch block, low voltage of left QRS complexes, right ventricle hypertrophy

The patient was admitted for treatment. She remained in the emergency unit for five days and was admitted (on October 15, 2005). She received furosemide 120 mg intravenously, 40 mg of enalapril, 0.25 mg of digoxin, 50 mg of hydrochlorothiazide and 120 mg of enoxaparin daily by subcutaneous route, as well as dobutamine 10 µg/kg.min intravenously.

At hospitalization she had hypotension, increased edema and creatinine elevation (Table 1). After three days, the patient developed anuria, anasarca and finally shock with hypotension with 60 mmHg despite the use of 15 µg/kg.min of dobutamine.

The laboratory tests (10/20/2005) showed creatinine 3.2 mg/dL and then 5.9 mg / dL, Urea 75 mg / dL and, during evolution, 115 mg / dL (Table 1).

At physical examination (10/20/2005) the patient was in poor general condition, with blood pressure of 80/50 mmHg, heart rate 90 bpm, crackles in both lungs, arrhythmic heart sounds (atrial fibrillation), systolic murmur + / 4 + in the mitral area, ascites and edema ++++ / 4+.

The electrocardiogram (20/10/2005) showed atrial fibrillation, heart rate of 100 bpm, low QRS voltage, intraventricular conduction disturbance of the right bundle branch block type stimulus, decreased left ventricular strength (Figure 2).

Figure 2

Atrial Fibrillation, low voltage QRS complexes, right bundle branch block, low voltage of left QRS complexes in horizontal plane, right ventricle hypertrophy.

The echocardiogram (on October 21) showed normal left ventricle, dilated and hypokinetic right ventricle, mitral valve calcification, commissural fusion, moderate stenosis and moderate tricuspid regurgitation (Table 2). Transesophageal echocardiogram (on October 21) showed pulmonary artery dilation with a large thrombus image (10 × 5.0 cm) extending to its left branch and the presence of autocontrast in the left atrium.

The diagnosis of pulmonary thromboembolism was made and 100 mg of r-TPA was administered intravenously in two hours. The patient went into shock, which required vasoactive drugs. Intravenous norepinephrine was administered, associated with ceftriaxone and metronidazole, as well as vancomycin for empiric treatment of the systemic infection. Mechanical ventilation was initiated with tracheal intubation for ventilatory support.

Pulmonary arteriography (on October 24) showed pulmonary artery pressures of 30/15/22 (systolic/diastolic/mean) mmHg. No images suggestive of pulmonary thromboembolism were identified.

The patient had an abundant epistaxis episode, which required transfusion of fresh plasma.

CT scan of the skull (on October 24) showed a hypoattenuating nodular area in the caudate nucleus head to the left, with no other alterations.

Blood cultures (10/25/2005) showed the presence of A. baumannii (sensitive only to imipenem). Hemodialysis (on October 26) was not tolerated by the patient, due to hypotension, and could not be performed.

The patient developed shock and died (10/26/2005).

Clinical aspects

This is 41-year-old patient with a history of rheumatic disease who developed mitral stenosis and underwent mitral commissurotomy at age 36 due to the presence of incapacitating symptoms. In our country, the combination of mitral stenosis with rheumatic disease is quite common1. About 25% of all patients with rheumatic disease have isolated mitral stenosis; 40% have double mitral dysfunction2. The mean time interval between the initial acute onset and the appearance of symptoms can vary from a few to more than 20 years.

The presence of symptoms of heart failure (classes III and IV of the New York Heart Association), together with echocardiographic data that confirm significant anatomic lesion, is crucial for intervention indication: balloon valvuloplasty or surgery (commissurotomy or valve replacement). Whenever possible, there is an attempt to correct the valve defect, keeping the patient’s valve system, postponing prosthesis implantation. In this case, commissurotomy was performed, which maintained the patient well for approximately five years, when she started to present symptoms again, when mitral valve repair was performed. This evolution in the rheumatic patient can occur due to repeated episodes of valvulitis, hence the need to maintain secondary prophylaxis with benzathine penicillin in patients with cardiac involvement, preferably throughout life or up to the fifth decade, when it is not possible1.

After the last surgical intervention, the patient remained asymptomatic for a short time, with dyspnea recurrence that developed into striking symptoms in about three months. The deterioration was attributed to drug discontinuation which, in our country, is a common cause of heart failure decompensation, regardless of the etiology.

On admission, the patient had respiratory distress with clean lungs, irregular heartbeat without incidental heart sounds, minor systolic murmur in the mitral area and mild lower-limb edema. These findings point to a syndromic diagnosis of right heart failure. The normal pulmonary symptomatology and the absence of additional heart sounds do not indicate left ventricular dysfunction the cause of decompensation. The irregular rhythm suggests uns atrial rhythm, which may be atrial fibrillation, a common association with mitral valve disease together with large atriums.

The patient’s initial laboratory tests did not exhibit significant alterations. The electrocardiogram (ECG) confirmed the presence of atrial fibrillation and alterations compatible with right ventricular overload, corroborating the aforementioned physical examination. Moreover, it showed low voltage complexes. The so-called dielectric effect is defined by the presence of QRS complexes with an amplitude < 0.5 mV in the frontal plane leads and < 1 mV in the precordial plane. The etiology is varied, including extracardiac factors (obesity, chronic obstructive pulmonary disease, hypothyroidism), pericardial diseases (pericardial effusion, constrictive pericarditis) and intrinsic myocardial diseases (rheumatic myocarditis, restrictive cardiac syndromes, arrhythmogenic right ventricular dysplasia).

The patient’s initial treatment was directed to heart failure due to systolic dysfunction, consisting of angiotensin-converting enzyme (ACE) inhibitors, diuretics, digitalis and full heparinization due to atrial fibrillation, considering the risk for thromboembolic events. After hospitalization, the patient developed low cardiac output syndrome with hypotension, convergent blood pressure and worsening of renal function, despite the use of inotropic agents (dobutamine). Moreover, there was worsening of the congestive symptoms, with worsening of edema and crackles in both lung. Given this clinical picture, the differential diagnosis includes diseases that present with predominantly right heart failure, leading to shock.

The most likely hypothesis is pulmonary thromboembolism (PTE). In the case of PTE, it would be possible to explain the clinical, electrocardiographic and evolution alterations (“shock with clean lungs”). It should be noted that the patient had risk factors for PTE, with heart failure, atrial fibrillation and valvular heart disease, plus the fact that this disease is responsible for approximately 15% of decompensated heart failure.

Echocardiography was crucial for the patient’s diagnosis. The valvular dysfunction with an area of 1.4 cm2 would hardly justify the patient’s clinical picture alone, or her evolution, considering the undertaken measures. The clear signs of right ventricular dysfunction, with evidence of large thrombus in the pulmonary artery, corroborate the clinical picture, pointing to the diagnosis of PTE. The pulmonary hypertension in this case can be a consequence of mitral valve disease as well as the PTE.

The differential diagnosis for the image of a large thrombus located in the pulmonary artery is the pulmonary artery sarcoma, or metastatic squamous cell tumor. Of these, the most frequent diagnostic error of pulmonary embolism is the pulmonary artery sarcoma. It is a rare tumor of the cardiovascular system, originated from the dorsal area of the pulmonary artery trunk or the right or left pulmonary arteries. Due to the insidious growth and the rarity of presentation, it is often inappropriately treated as PTE3. However, this possibility becomes unlikely in this clinical case, due to failure in identifying the lesion on the pulmonary arteriography.

Another differential diagnosis, when evaluating the presence of atrial fibrillation with thromboembolic phenomena associated with the dielectric effect on ECG, is cardiac amyloidosis. However, it has low clinical suspicion when one analyzes the history of the disease, as well as the echocardiographic results and subsequent clinical course.

The use of thrombolytic therapy has consensual indication in this case, considering the clinical signs of thromboembolic event. It is classified as massive PTE when there is hemodynamic instability. The therapy rationale is the thrombus dissolution, decreasing the right ventricular overload and the pulmonary artery pressure levels. There are reports in the literature on the acute resolution of large thrombi, decreasing the mechanical obstruction of the right ventricle2. However, the migration of thrombus fragments distally can impair the success of thrombolysis and the expected outcome in relation to clinical evolution might not be attained. In fact, although indicated, there is no evidence of reduction in mortality with the use of thrombolytic agents in cases of massive PTE4.

The patient’s unfavorable evolution, although the arteriography did not disclose a thrombus in the pulmonary artery system, leads us to reflect on what else contributed to the poor outcome. Here we face some relevant points.

The first is the fact that the patient developed coagulopathy followed by evident bleeding. The normal coagulation at admission leads us to a diagnosis of acquired coagulopathy. The thrombolysis carried out in the PTE treatment certainly played a role in the etiology of the coagulation disorder. Moreover, as we will see below, the patient developed bacterial infection and there may have been disseminated intravascular coagulation secondary to sepsis. There are no reports of other documented bleeding, in addition to epistaxis, but the sharp decrease in hemoglobin levels associated with the incoagulable activated partial thromboplastin time (APTT) suggests active bleeding. Thus, hemorrhagic shock together with the clinical picture is among the possibilities and it might be related, in addition to the epistaxis, to the vascular access complication.

The second point is related to infection confirmed by blood cultures positive for Acinetobacter baumannii. A mixed shock (cardiogenic and septic) justifies the patient’s poor prognosis and her refractoriness to the measures that were undertaken. In recent years, there has been an increase in the resistance of Acinetobacter baumannii to broad-spectrum antibiotics. This has coincided with the increased incidence of sepsis by this agent5. Risk factors associated with sepsis by Acinetobacter are: prior use of broad-spectrum antibiotics, use of urinary catheters, mechanical ventilation and previous surgery. The mortality in these cases is around 38%.

The main factors of poor prognosis related to sepsis by Acinetobacter are the use of inadequate antibiotics and mechanical ventilation5. This patient had both factors.

The third point that draws attention to this case is the worsening of left ventricular function, as demonstrated in the patient’s last echocardiogram. Some possibilities can be suggested: myocardial depression in sepsis, rheumatic myocarditis and coronary thromboembolism. Rheumatic myocarditis results from an immune cellular process and therefore may occur without humoral manifestations, such as arthritis and chorea. It is usually associated with valvulitis and has a transitory character. It can be observed, in this case, that there is rheumatic disease activity, considering the early post-valvuloplasty dysfunction. Interleukin-4 appears to play a critical role in modulating local immune response due to its anti-inflammatory properties1.

Myocardial depression in sepsis can be found in approximately 40% of septic patients due to several factors, including reduction of coronary flow, myocardial edema, direct action of cytokines (IL-1, TNF-alpha) and of nitric oxide, leading to reduced levels of intracellular calcium6. Both myocarditis and myocardial depression in sepsis usually involve the myocardium as a whole, not focusing on specific territories. There are cases, however, when these conditions may mimic myocardial infarction. This patient had diffuse left ventricular hypokinesis, but more pronounced in the anterior and septal regions.

Based on this information, one can consider myocardial ischemia as a possible diagnosis. Coronary lesions, even non‑obstructive ones, may lead to myocardial ischemia due to hypoperfusion secondary to shock, sometimes culminating in myocardial infarction (currently classified as myocardial infarction type 2)7. Another possibility is coronary embolism as a result of systemic thromboembolic phenomenon secondary to atrial fibrillation.

In fact, there have been reports of this kind in the literature, involving both the right coronary artery as well as the anterior descending artery. It is noteworthy that, despite evidence of spontaneous contrast in the left atrium, the presence of thrombus in the left atrium was not demonstrated. However, this fact does not exclude the hypothesis. Another possibility is coronary embolism resulting from paradoxical embolism. The present of patent foramen ovale is frequent, being estimated at about 15-20% of normal individuals. Thrombus in the venous system, right-left shunt, increased pressure in the right system and systemic embolism are conditions that make the diagnosis likely8. The patient had at least three such conditions. The fact that the echocardiogram did not identify the presence of patent foramen ovale can be a result of low sensitivity to identify this condition. However, this patient had already undergone two heart surgeries with valve manipulation, making this diagnosis unlikely.

As a last point, we have kidney failure, which progressed during patient evolution, with hemodialysis being indicated. This clinical picture can be easily explained by the mixed shock. However, one cannot rule out a possible thromboembolic etiology.

The patient died due to refractory shock, not tolerating dialysis. Considering what was discussed, we suppose that the patient did not adequately carry out the secondary prophylaxis of rheumatic fever, since the evolution of post-valvuloplasty. She had decompensated heart failure, related to medication discontinuation and pulmonary thromboembolism. She had an episode of massive PTE during hospitalization, which, despite adequate therapy, developed unfavorably. This evolution is due to sepsis by Acinetobacter and myocardial dysfunction, which may be related to sepsis and / or possibly acute myocardial infarction by coronary thromboembolism (Dr. Eduardo Gomes Lima, Dr. Ricardo D’Oliveira Vieira, Dr. Paula Bombonati).

Diagnostic hypothesis: Chronic rheumatic mitral valve disease, post-valvuloplasty mitral dysfunction, pulmonary thromboembolism and mixed shock (cardiogenic, septic) (Dr. Eduardo Gomes Lima, Dr. Ricardo D’Oliveira Vieira, Dr. Paula Bombonati)

Necropsy

The heart weighed 630 g (normal weight for women is between 250-300 g), with mild hypertrophy and moderate left atrium dilation, with marked thickening of the endocardium (Figure 3). Seen from the atrial side, the mitral valve had the “fish mouth” aspect with reduced opening, commissural fusion and severe thickening of the cusps (Figure 3). There was also mild multifocal calcification and evidence of previous valve surgery as shown by the presence of surgical stitches in almost the entire valve circumference, largely included in the valve tissue and surroundings (signs consistent with prior valvuloplasty - Figure 3). From the ventricular side, the valve apparatus showed marked deformity and shortening, represented by cords exhibiting severe thickening, fusion and retraction (Figure 4).

Figure 3

Photograph of the opened left atrium (LA), showing mild hypertrophy and moderate dilation. Note the endocardial thickening characterized by its whitish color (asterisk). The mitral valve (Mi), with double lesion, shows commissural fusion, characteristic...

Figure 4

Photograph of the open heart through the left ventricular outflow tract (LVOT). Note the thickened anterior cusp of the mitral valve (Mi), with intense fusion and cord retraction, quite characteristic of rheumatic disease. At the top, the aortic valve...

At handling and maneuvering with water flow, valve mobility and cusp coaptation were significantly impaired, suggesting double valve lesion with stenosis greater than regurgitation as functional alterations. In the aortic valve, the semilunar showed diffuse thickening and mild collapse, indicating valve insufficiency. The left ventricle was moderately dilated and hypertrophied, showing an area of fibrous scar in the median septum and endocardial tip (Figure 4). The sections showed septal wall thinning with transmural replacement of heart muscle by fibrotic scarring (Figure 5), affecting approximately 10% of the left ventricular muscle mass. On the right chamber side, there was marked atrial dilation and in the ventricle, mild hypertrophy and moderate dilation (Figure 6).

Figure 5

Photograph of the open heart cut transversally at the median height of the interventricular septum (between the dotted lines in red). Note, in A, the thinning of the wall (between arrows) with substitution by off-white fibrous tissue. B. Histology of...

Figure 6

Photograph of the open heart through the right ventricle (RV) inflow tract. Note in A, dilation of the cavities of the right atrium (RA) and right ventricle (RV), the latter also showing hypertrophy. The tricuspid valve (Tri) shows intrinsic insufficiency...

The tricuspid valve suggested intense insufficiency, secondary to mild thickening of the cusps with discrete fusion and retraction of the cords, as well as annulus dilation (Figure 6). Macroscopic and microscopic examination revealed no obstructive coronary lesions, but only mild intimal thickening (Figure 7). The central pulmonary arteries and trunk showed no macroscopic alterations.

Figure 7

Histology of the major epicardial coronary arteries: right coronary (RC2), circumflex branch (CX2) and anterior descending branch (AD2) of the left coronary in the second centimeters, and posterior descending branch (PD1) of the right coronary artery,...

Upon examination of the other organs, we detected alterations of chronic passive congestion in the lungs (already showing passive pulmonary hypertension) and liver, as morphological substrate of overall congestive heart failure associated with valvular heart disease. The right lung showed extensive lobar area with hardening and hemorrhage, macroscopically indicating a heart attack or “red-gray hepatization”, with lobar pneumonia being subsequently characterized through histology. This infectious picture was also associated with the presence of acute pyelonephritis, represented by multiple cylinders of polymorphonuclear neutrophils in renal pyramids, which also infiltrated the interstitium. The spleen was enlarged (250 g, normal weight is approximately 150 g) at the expense of the red pulp, showing an acute splenitis pattern (Figure 8). Morphological changes related to shock, such as acute renal tubular necrosis, hepatic centrilobular necrosis and cerebral edema with herniation of the cerebellar tonsils were also observed and thus, septic shock was considered as the immediate cause of death. (Dr. Jussara Bianchi Castelli)

Figure 8

Histology of infectious alterations and secondary to septic shock observed in major organs. A. Lobar pneumonia characterized by dense alveolar filling with neutrophilic infiltration (asterisk). B. Detail of A at higher magnifications: Note the cellular...

Anatomopathological diagnoses: Chronic rheumatic mitral-aortic-tricuspid valve disease; valvular heart disease with overall congestive heart failure; healed transmural septal myocardial infarction; lobar pneumonia; acute pyelonephritis; septic shock. (Dr. Jussara Bianchi Castelli)

Comment

This case shows typical aspects of valvular heart disease by chronic rheumatic heart disease, due to the age and macroscopic and microscopic aspects of the heart. What seems unusual is the presence of myocardial infarction associated with rheumatic disease.

In chronic rheumatic valvular heart disease, imposing a situation of increased myocardial work and therefore, greater oxygen consumption, it is unlikely that significant coronary disease would remain asymptomatic. In this case, the coronary artery lesions were very mild, with only fibrous intimal thickening without plaque or occlusive lesions or lesions recognized as being a risk for rupture and thrombosis. Therefore, it was considered unlikely that the detected healed infarction was related to atherosclerotic arterial disease and such events. In fact, the prevalence of chronic arterial disease is low among patients with rheumatic valvular heart disease and this is not a protective effect. This is associated with clinical and demographic differences and risk factors of these diseases, which has been shown in several studies, some discussed below.

A Brazilian study showed that the prevalence of coronary artery disease was lower among patients with rheumatic heart disease (4%) and high among patients with valvular heart disease of non-rheumatic etiology (33%)9. In another study of 77 necropsies of patients who died after surgery for valve dysfunction treatment in rheumatic disease, a rate of 13% of significant coronary artery disease was observed and that was more common after the age of 40, also in those patients with isolated aortic or mitral-aortic lesions, rather than with isolated mitral valve lesion10.

Therefore, for these reasons, the cause suggested for the occurrence of myocardial infarction was a previous perioperative event. Epidemiological data record myocardial infarction as a complication of cardiac surgery in less than 1% (34 cases in 11,210) and point to a statistically significant association with mitral, aortic or double valve procedure. Only 33.3% of the 34 cases studied showed coronaries free of obstruction at the necropsy11.

Apart from the handling and the trauma of the heart, in addition to surgical technical difficulties, for these cases without significant coronary disease, some other etiopathological mechanisms are considered as a cause of perioperative infarctions in cardiac surgery for valve replacement, such as coronary embolization (personal communication: e.g., we observed once, in a necropsy, calcium emboli to the coronaries in a case of mitral valve replacement that presented with severe dystrophic calcification), coronary gas embolism, coronary vasospasm, topic hypothermia or inappropriate cardioplegia, among others. The prognosis of perioperative myocardial infarction is not necessarily bad, but its occurrence should warrant appropriate measures and prevention in surgical valve replacement6,12. (Dr. Jussara Bianchi Castelli)

Editor da Seção: Alfredo José Mansur (rb.psu.rocni@rusnamja)

Editores Associados: Desidério Favarato (rb.psu.rocni@otaravaflcd)

Vera Demarchi Aiello (rb.psu.rocni@arevpna)

References

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3. Matto A, Fedullo PF, Kapelanski D, Iiowate JS. Pulmonary artery sarcoma: a case report of surgical cure and 5-year follow-up. Chest. 2002;122(2):745–747.[PubMed]

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5. Gomez J, Simarro E, Baños V, Requena L, Ruiz J, Garcia F, et al. Six year prospective study of risk and prognostic factors in patients with nosocomial sepsis caused by Acinetobacter baumannii. Eur J Clin Microbiol Infect Dis. 1999;18(5):358–361.[PubMed]

6. Okamura Y, Takeuchi Y, Gomi A, Nagashima M, Mori H, Hattori J. Clinical evaluation of perioperative myocardial infarction as a complication of valve replacement. Kyobu Geka. 1989;42(12):1012–1015.[PubMed]

7. Thygesen K, Alpert JS, White HD, Jaffe AS, Apple FS, Galvani M, et al. Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Circulation. 2007;116(22):2634–2653.[PubMed]

8. Ward R, Jones D, Haponik EF. Paradoxical embolism: an underrecognized problem. Chest. 1995;108(2):549–558.[PubMed]

9. Kruczan DD, Silva NA, Pereira BB, Romão VA, Correa WB, Filho, Morales FE. Coronary artery disease in patients with rheumatic and non-rheumatic valvular heart disease treated at a public hospital in Rio de Janeiro. Arq Bras Cardiol. 2008;90(3):197–203.[PubMed]

10. Coleman EH, Soloff LA. Incidence of significant coronary artery disease in rheumatic valvular heart disease. Am J Cardiol. 1970;25(4):401–404.[PubMed]

11. Rotberg T, Macías R, Correa-Suárez R, Luna P, Malo R. Trans and postoperative myocardial infarct in heart surgery. Arch Inst Cardiol Mex. 1976;46(1):82–97.[PubMed]

12. Laurindo FR, Grinberg M, Campos de Assis RV, Jatene AD, Pileggi F. Perioperative acute myocardial infarction after valve replacement. Am J Cardiol. 1987;59(6):639–642.[PubMed]

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