Chapter 8. Right Heart Valves and Function

• Much as the mitral valve (MV) and aortic valve (AV) direct blood flow into the systemic circulation, the tricuspid valve (TV) and the pulmonic valve (PV) direct flow into the pulmonary circulation. A functioning right ventricle (RV) is critical to effective loading of the left ventricle (LV). Perioperative RV failure can be quite challenging for the anesthesiologist as it often occurs in the setting of pulmonary artery hypertension, which can be difficult to treat.

The TV can develop both stenotic and regurgitant lesions. Tricuspid stenosis (TS) is most often secondary to rheumatic heart disease. Less encountered causes are carcinoid and endomyocardial fibrosis. Obstructing cardiac masses can also occlude the TV.1

Tricuspid regurgitation (TR) occurs secondary to pathologic processes affecting the valve itself or as a consequence of RV dilatation. RV dilatation may occur in the setting of pressure or volume overload. Increased RV systolic pressure develops when the RV must work against an increased resistance. This can occur in clinical situations, which increase pulmonary artery (PA) pressure such as mitral stenosis, severe mitral regurgitation, severe left ventricular dysfunction, pulmonary embolism, primary pulmonary hypertension, or lung disease.

Endocarditis, connective tissue diseases, carcinoid syndrome, anorectic drugs (fenfluramine), Ebstein abnormality (an apically positioned tricuspid valve), pergolide, and chest radiation therapy can likewise result in TR. Ebstein anomaly is due to apical displacement of the tricuspid valve leaflets especially the septal leaflet associated with TR and RV dysfunction.

Patients with TS frequently present with other valvular diseases associated with rheumatic heart disease (eg, mitral stenosis, aortic stenosis). Consequently, their clinical features often represent the impact of these lesions. Long before the patient presents for surgery, echocardiography will have diagnosed any associated lesions.

The patient with TR secondary to pulmonary hypertension is likely to present with signs of right heart failure and systemic venous engorgement. Peripheral edema, hepatic dysfunction, and ascites frequently occur. Systolic pulmonary pressures greater than 55 mm Hg1 will readily produce TR even with normal valve structure. Transvenous pacemaker wires or catheters can both cause a mild degree of TR as well. Additionally, many patients have echocardiographically detected TR without clinical significance.

The right ventricle and the interaction between the right and left heart are critical to maintaining healthy cardiovascular function. Although patients can survive with only a single ventricle devoted to the systemic circulation (eg, Fontan circulation—Chapter 12), a functioning right heart effectively loads the LV so that the stroke volume (SV) is ejected systemically. When the RV fails, the LV may be inadequately loaded reducing SV.

RV failure can develop both acutely and chronically. Acute RV failure can be seen associated with sudden increases in pulmonary vascular resistance (eg, during a protamine reaction) or secondary to myocardial ischemia and infarction. Chronic RV failure presents secondary to progressive increases in pulmonary hypertension (eg, from mitral stenosis, lung diseases, etc) or volume overload as seen in intracardiac left-to-right shunts or primary tricuspid regurgitation.

Both acute and chronic RV failure lead to RV dilatation and TR. Moreover, as the RV dilates the flattening of the intraventricular septum can distort the LV cavity due to interventricular dependence, further impeding LV function. Consequently, failure of the RV reduces LV function leading to decreased cardiac output and hypotension. Acute RV failure during protamine administration for heparin reversal after discontinuation of cardiopulmonary bypass is a dramatic, life-threatening occurrence. As PA pressures increase, the RV distends unable to overcome the pressure load presented to it. The patient develops TR and the LV is severely underloaded. Systemic hypotension can be severe and circulatory collapse imminent. Often, it becomes necessary to reheparinize the patient and institute emergent cardiopulmonary bypass.

Therapy for RV failure is directed at the etiology whether it is restoration of myocardial perfusion in case of myocardial ischemia or decreasing PA pressures during acute increases of pulmonary vascular resistance.

There are no specific inotropic agents that directly target the right ventricle. Milrinone, dobutamine, levosimendan2-5 can all be employed to improve RV contractility. These agents have inotropic effects upon both the left and the right ventricle and will likewise vasodilate both the systemic and pulmonary circulations. Reduction of pulmonary vascular resistance can improve RV function, LV function, and RV-LV interaction. Vasodilators including sodium nitroprusside and nitroglycerin will lower both systemic and pulmonary vascular resistance and can be useful assuming the impact upon systemic pressure does not outweigh any benefit resulting from the diminution of pulmonary vascular resistance.

Nitric oxide (NO) is the molecule by which both nitroprusside and nitroglycerin ultimately produce vasodilatation. NO is present only minimally in the circulation and produces an increase in cGMP in vascular smooth muscle.6-8 Inhaled NO has been available for a number of years and can be delivered to directly dilate the pulmonary vasculature with minimal effects upon the systemic circulation.

Unique right heart cardiomyopathies can also present. Arrhythmogenic right cardiomyopathy9 occurs when the right heart undergoes fatty infiltration. Patients are at risk for sudden death from ventricular dysrhythmias. Often these patients will have been treated with an implantable cardioverter/defibrillator device. Hypertrophic cardiomyopathy (HCM) can likewise present in the right heart although to a far lesser degree than that seen in left heart HCM. A pressure gradient can develop across the right ventricular outflow tract leading to RV failure. These patients too are at risk for sudden cardiac death (SCD).

Like all other heart valves the pulmonic valve can develop both stenotic and regurgitant lesions; however, it is least likely to be affected by acquired heart disease.1 Pulmonary stenosis (PS) may be congenital or acquired as seen in carcinoid syndrome. PS results in RV failure and underloading of the LV. Pulmonary regurgitation is also unusual but may occur due to annular dilatation as a result of pulmonary hypertension or following balloon valvuloplasty of a stenotic pulmonary valve. Additionally, patients following tetrology of Fallot repair frequently developed pulmonary regurgitation.

Right heart structures are located anteriorly and therefore away from the transesophageal echocardiography (TEE) probe. Consequently, they are less well visualized than those of the left ventricle. Nonetheless, TEE can assist in the perioperative discernment of both RV function and valvular integrity. The basic views of the right heart and its structures were discussed in the introduction to TEE.

RV function is not as easy to characterize on TEE as is that of the LV. Video 8–1 reveals a normally contracting RV. In contrast, Video 8–2 presents a dilated, dysfunctional RV. In this instance, the RV has dilated to overcome the increased resistance presented to it by chronic pulmonary hypertension eventually resulting in RV dilation and leftward movement of the intraventricular septum into the LV (Figures 8–1 and 8–2).

Acute, perioperative RV failure can be identified through the use of TEE. Pulmonary emboli can be seen in the PA (Video 8–3). During an acute protamine reaction, the RV dilates acutely while the LV is underloaded resulting in hemodynamic collapse.

TR is found frequently during TEE examination perioperatively. Most frequently, TR is associated with dilatation of the RV. However, as mentioned above other disease states can produce TR. The severity of TR is generally judged based upon the area of the regurgitant jet, vena contracta of the regurgitant jet, or proximal isovelocity surface area. Also it is possible to use pulsed wave Doppler to interrogate the hepatic veins. Systolic reversal of hepatic vein flow in a manner similar to that of systolic reversal of pulmonary vein flow in mitral regurgitation is associated with severe TR.

TS is a rare lesion. Its severity can be determined by measuring flow velocity over the stenotic valve and using the Bernoulli equation to calculate a pressure gradient. A pressure gradient higher than 5 mm Hg is considered significant.

Examination of the PV is difficult using TEE (Video 8–4). Figure 8–3 demonstrates a pulmonary artery catheter passing through the pulmonic valve. Using the midesophageal ascending aorta short axis view, the main PA can be identified as it divides into left and right pulmonary arteries (Figure 8–4). Usually the left pulmonary artery is difficult to visualize due to the interposition of the left main bronchus.

TR often occurs secondary to pulmonary hypertension associated with other cardiac lesions. Consequently TR is frequently surgically addressed in combination with other interventions (eg, mitral valve repair/replacement).9,10 Ring annuloplasty is performed to restore integrity to the valve assuming leaflet structure is normal. Valve replacement is employed when the tricuspid leaflets no longer permit repair. Pulmonic valve surgery is relatively rare and is directed at restoring competency of the PV. The Ross procedure for correction of AV disease involves harvest of the patient's pulmonic valve for placement into the aortic position and subsequent use of a homograft to replace the pulmonic valve. Otherwise, operations on the PV in the adult patient are unusual.

RV failure may occur acutely during any cardiac surgical procedure. Classic protamine reactions will readily produce pulmonary hypertension and RV dysfunction. Should they occur management is directed at restoration of RV function. Inotropic agents such as epinephrine, dobutamine, and milrinone, can be used to increase RV contractility and produce vasodilatation. NO, if available can be employed to dilate the pulmonary vasculature. If necessary the patient can be reheparinized and placed on emergent CPB.

In patients with chronic pulmonary disease and long-standing pulmonary hypertension, RV function may be worsened with the institution of positive pressure ventilation. PA pressures might also increase in the setting of light anesthesia, hypoxemia, or hypercarbia. Perioperative volume overload can readily distend a poorly compliant RV. When weaning from cardiopulmonary bypass the anesthesiologist directly sees the RV from the head of the table allowing immediate visualization of a distended failing RV.

In patients with right-sided valvular lesions it might not be possible or prudent to place pulmonary arterial catheters. If considered desirable, the PA catheter can be placed in the venous circulation and then advanced by the surgeon after completion of the surgical repair.

The Patient with Endocarditis

Endocarditis should be suspected whenever a patient presents with a new-onset heart murmur, positive blood cultures, fever, and splinter hemorrhages.1 Patients can present with endocarditis with negative blood cultures. Echocardiographic visualization of the vegetation is critical in identification of the valves affected and the hemodynamic consequence of the infection. Antibiotic therapy can be used when the lesions are without hemodynamic consequence; however, should patients develop hemodynamic compromise, surgery is indicated. Likewise, recurrent embolism from valvular vegetations or infected prosthetic valves may need to be addressed surgically.

Case Questions

A 33-year-old IV drug abuser presents for surgery. Video 8–5 reveals the presence of vegetation on which valve/s?

An aortic valve vegetation is demonstrated.

The patient is taken for surgery and the valve replaced. Following administration of protamine the patient's systemic blood pressure is 60/40 mm Hg, his PA pressure is 60/40 mm Hg. What is the most likely diagnosis?

Patient is experiencing a protamine reaction. His right heart has dilated and his LV is underloaded.

What are the treatment options at this time?

The patient is treated with inotropic support and the RV becomes more contractile, systemic blood pressure is restored to 90/70 mm Hg, and PA pressure is now 45/20 mm Hg. The remaining protamine is administered slowly and his ACT is corrected.

Had he not responded to inotropic therapy what other options are available to the anesthesia and surgery team?

The patient can be reheparinized and placed on cardiopulmonary bypass. Inhaled NO therapy can be started to lower PA pressures and decrease RV afterload.