Acute right heart failure: Pathophysiology, recognition, and pharmacological management

REVIEW ARTICLE

Pathophysiology,

Acute Right Heart Failure: Recognition, and Pharmacological

Management

James E. Calvin, Jr, MD, FRCP(C), FACC

F

OR MANY YEARS there had been little interest paid to abnormalities of the right ventricle (RV) largely because of early reports of animal experiments showing little alteration in circulatory homeostasis after the RV had been destroyed.1-3 Interestingly, in all of these studies, the pulmonary resistance was normal and left ventricular (LV) function was not disturbed. However, in the last two decades clinical experience has determined that RV function is quite important in a number of acute clinical situations. A great deal of interest has developed over RV function during pulmonary embolism,4 chronic obstructive pulmonary disease,5-7 adult respiratory distress syndrome,9-‘2 and RV wall infarction.r3 Furthermore, interdependence of RV and LV and interactions between the heart and lungs have further focused attention on RV function.‘4.‘8 The purpose of this paper is to briefly review normal RV function and the pathophysiology of RV failure as it relates to acute critical illness and to outline the variety of clinical situations in which RV function plays an important role in the approach to management. NORMAL

RV ANATOMY

AND FUNCTION

Normally the RV is relatively thin walled compared with the LV and has a “crescent’‘-shaped configuration. For this reason, calculation of RV volume has been difficult in that the assumptions that are made for calculation of LV volume are not valid (ie, the RV is neither a sphere nor an ellipsoid).” Embryologically, the RV has two distinct portions: the inflow tract and the outflow tract. The onset of contraction in the outflow tract is slightly delayed compared with the inflow tract as is its relaxation phase.“” Because of the thin wall structure, the RV is highly compliant and can increase its size significantly without major change in intracavitary filling pressure. The RV’s systolic function has the same three determinants as LV function, ie, preload, afterload, and contractility. In brief, RV stroke volume is proportional to enddiastolic size and is inversely proportional to the vascular load (ie, pulmonary vascular resistance [PVR] or pulmonary artery pressure).” Inotropic agents are capable of shifting these relationships upward.‘8,22,23 The free wall of the RV is supplied by the right coronary artery. However, the intraventricular septum has a dual supply from both the right coronary artery and the left anterior descending artery. The perfusion pressure for blood flow to the RV is throughout the cardiac cycle (the perfusion pressure is the difference between aortic pressure and the RV pressure). This has important implications in Journal of Cardiothoracic and VascularAnesthesia,

that systemic hypotension can lead to RV ischemia, especially if RV pressures (the downstream pressure) are significantly elevated. THE PATHOPHYSIOLOGY

OF ACUTE RIGHT

HEART FAILURE

The established mechanisms for acute right heart failure are shown in Fig 1. As mentioned previously, an inverse relationship between the vascular load and stroke output has been previously demonstrated.*’ Calvin et al demonstrated that RV stroke volume was inversely related to the pulmonary input resistance (a more precise measurement of vascular load; Fig 2). In another recent article, it has been demonstrated that tripling of the pulmonary artery pressure by glass bead embolism is well tolerated by the RV with cardiac output being maintained by both the heart rate (or chronotropic) response and the Frank-Starling mechanism (preload reserve).22.24However, further increases in pulmonary artery pressure sufficient to decrease the cardiac output by 20% result in a disproportionate increase in end-systolic volume compared with end-diastolic volume (ie, stroke volume and ejection fraction decrease as a result). At this particular point, the RV is performing largely pressure work and very little flow work. Adenosine triphosphate and creatinine phosphate levels are normal. These phenomena. represent evidence of an afterload mismatch. LV filling decreases in the face of RV afterload mismatCh.‘7.‘8.22.*4 This has been demonstrated in a number of studies,‘4,‘5 is not necessarily related to either the septal position or presence of the pericardium, and is best described as a “series interaction” between the RV and the LV. As a result of this underfilling of the LV, LV stroke output decreases (because of diminished LV preload) and aortic pressure decreases, which can further aggravate or exacerbate RV coronary perfusion (by reducing RV perfusion pressure).25,26 The pericardium plays a significant role in mediating a direct interaction between the RV and the LV. As the RV dilates within an intact pericardium, RV end-diastolic

From the lJniversi[y of Ottawa Heart Institute, Canada. Address

reprint

requests to James

E.

Calvin,

Ottawa, MD,

Ontario,

Section

of

of Medicine, Rush Presbyterian St Luke’s Medical Center, 1653 W Congress Pkwy, Chicago, IL 60612. Copyright o 1991 by W. B. Saunders Company IO53-0770/9110505-0018$03.00/0 Cardiology,

Vol5, No 5 (October), 1991:

Department

pp 507-513

507

508

PRESSURE LOAD

t Wall tension

MPENSATION

\ ISCHEMIA

-

\ Volume +

decreased RV out$uJt

(direct)

Increased &icardial Pressure:decreased transseptalpressure

C.P.P.

r,

decreased C.O. 8 BP

(series)

Decreased~ distensibilitv

1

\

.

Decreased Iv preload

/

Fig 1. Schematic diagram of events contributing to the pathophysiology of acute right heart failure.

RV ischemia represents a final end-point in the pa~hclphysiology of acute right heart failure. As RV prcssurc increases and the RV dilates. the demand for oxygen m creases. There is significant evidence to suggest that right coronary blood flow does initially increase to meet this demand24~““.2’(Fig 5). However, because of the inability to increase coronary blood flow further, an imbalance of RV oxygen supply and de mand can develop with resultant ischemia (Fig 6). Finally, RV coronary perfusion pressure decreases during shock states because the downstream pressure (ie, RV end-diastolic pressure) is increasing and the upstream pressure (aortic pressure) is decreasing as a result of LV underfilling.25~2h CLINICAL

pressure increases. The first implication of this observation is that the intrapericardial pressure increases and this external pressure is exerted on the LV and affects its distensibility.‘5~‘7~‘H~*7 This is demonstrated in Fig 3. In an experimental model of acute pulmonary hypertension’produced by ventricular glass bead embolism, it was determined that the LV diastolic pressure:segment length relationship was shifted upward indicating decreased distensibility. This effect was found to be independent of any heart rate change. The second implication of these events is that the transseptal pressure gradient decreases or, in fact, reverses. As a result the septum shifts leftward, further impairing LV filling.= This is demonstrated in Fig 4, which illustrates the two-dimensional echo of a patient with acute pulmonary hypertension. The RV is dilated and septal curvature (normally rightward) is flattened. Kingma et al have clearly demonstrated the inverse relationship between the transseptal pressure gradient and the RV septal-free wall dimension and the direct relationship between the transseptal pressure gradient and the LV septal-free wall dimension.28

CLINICAL

0 L,

0

I

500

I

1000

I

1500

I

2000

I

2500

Input Resistance, Z,

(dyne - s - cm-“) Fig 2. The inverse relationship between RV stroke volume and input resistance in acute pulmonary hypertension in the dog. Acute pulmonary hypertension is modelled by both pulmonary artery constriction and microvascular injury produced by glass bead embolism. (Reprinted with permission.“)

ENTITIES

THAT

CONTRIBUTE

TO RV FAILURE

Clinical entities that contribute to RV failure are shown in Table 1 and can be divided into entities that produce RV pressure or volume overload or depress contractility. It should be noted that LV failure can contribute to RV pressure overload. Acute pulmonary embolism can cause circulatory collapse when more than 50% of the crosssectional area of the pulmonary vascular bed is compromised. It is interesting to note that the RV cannot acutely generate RV systolic pressures greater than 50 mm Hg although in a chronic situation, such as primary pulmonary hypertension, systemic pressures can be observed. Although chronic obstructive pulmonary disease is a wellrecognized cause of car pulmonale, acute vascular injuries of the lungs are taking on increasing importance because of the development of pulmonary hypertension.‘“~“~21.22The USC of positive-pressure ventilation can also affect RV performance in as much as lung hyperinflation can increase pulmonary resistance and RV afterload? A volume overload state of the RV is more commonly observed in congenital cardiac disorders such as atria1 septal defect or ventricular septal defect. Acute tricuspid regurgitation or pulmonary valve insufficiency can occur acutely (secondary to trauma or endocarditis) and cause acute RV volume overload. An acute ventricular septal defect infrequently occurs after myocardial infarction and, indeed, in such cases prognosis is related to the degree of RV dysfunction.” Depressed RV contractility is most commonly observed in RV infarction. Myocardial contusions involving the RV also serve as an important cause of RV dysfunction in the intensive care unit setting.2” RECOGNITION

OF RIGHT

HEART

FAILURE

When acute RV pressure overload is present, the major symptoms are related to dyspnea and chest pain, the latter being an angina1 equivalent. These are present in the majority of cases. Cough, hemoptysis, and syncope are less common. On examination tachypnea is observed in more than 80% of cases, whereas the incidence of tachycardia is more variable. The neck veins are usually distended and either dominant “a” or “v” waves can occur. The a wave is largely on the basis of reduced RV compliance and the v wave

509

ACUTE RIGHT HEART FAILURE

20l8Mh

-Embolism

0)

e

14-.

E z u

12-

i

lo-

E

8-

?i 8Fig 3. LV diastolic pressure segment length relationships before and after the production of pulmonary hypertension from pulmonary artery glass bead embolism. Pulmonary hypertension shifts the relationship upward and to the left. (Reprinted with permission.‘*)

42-

0 12.5

I 13.5

manifests itself as tricuspid regurgitation develops. A prominent “y” descent can be observed with an associated decrease in RV distensibility, most commonly being observed in RV infarction. RV lifts may be palpated during acute RV volume overload states. An accentuated second heart sound in the face of pulmonary hypertension is common and murmurs of tricuspid regurgitation can be heard. The diastolic murmur of pulmonary regurgitation is less common acutely.

14.5 LV

15.5 SEGMENT

16.5

LENGTH

17. 5

1 18.5

(mm)

The electrocardiogram (ECG) can be helpful in acute RV disorders. For instance, if concomitant ST segment elevation is observed in leads V,R or V,R, in association with either prominent R waves in leads V, and V, or the presence of Q waves in leads II, III, and AVF, RV wall infarction is highly suspected.” Whereas chronic RV hypertrophy can be diagnosed by specific adult criteria such as QRS axis > llo”, R/S ratio in V, > 1, or an R/S ratio in V, < 1, the ECG lindings of acute RV pressure overload are rather nonspecific.” The best source of information comes from patients with acute pulmonary embolism (Table 2). Rhythm disturbances, QRS abnormalities, and ST segment abnormalities were found to be present in a majority of cases (90%). The presence of atria1 and ventricRATIO

1.5

1.5

1

1

0.5

0.5

0

0 MPAC

CQNTFIOL

-

Fig 4. Cross-sectional, two-dimensional echo of patient with acute pulmonary hypertension. The RV is dilated and the septal (arrow) configuration is flattened.

RV BLOOD FLOW

SPAC

m

SPAC +incr AP

ENDO/EPI

Fig 5. Total RV blood flow and the RV endocardial:epicardial blood flow ratio during control, moderate pulmonary artery constriction (MPAC), a severe pulmonary artery constriction producing shock (SPAC), and after increasing eortic pressure (AP). RV blood flow initially increases while endocardial:epicardial blood flow ratlo remains unchanged during MPAC. Both decrease with SPAC and then increase after AP is increased. (Data from Gold and Bathe.“)

510

WTTI a,--

(ml/minliOO ~~~

g mmhg)

Table 2. ECG Abnormalities

in 131 Patients With

Pulmonary Embolism

Rhythm disturbances ??

Premature beats

I?

Atrial

3

Ventricular

9

Atrial fibrillation

3

QRS abnormalities

65

Right axis

5

Left axis

12

Incomplete right bundle branch block Complete right bundle branch block PO

RVF

Fig 6. RV myocardial supply/demand ratio in a canine model of acute pulmonary hypertension produced by glass bead embolism. Ratio is calculated by dividing the RV blood flow measured by microsphere technique (a) by RV tension time index (‘ITI) measured by planimetry. An imbalance appears after the pulmonary artery pressure is tripled (PO). *P < 0.05 v baseline. (Data from Calvin and Guinn.‘*)

5 11

RV hypertrophy

5

S,S,S, pattern

9

S,Q,T, pattern

11

ST-T abnormalities

64

T-wave inversion

40

ST-T segment depression

33

ST-T segment elevation

11

Reprinted with permission of the American Heart Association, lncx2

ular premature beats is not common. Both right and left axis abnormalities can be detected and right bundle branch block can be observed in some cases. The characteristic S,S,S, and S,Q,T, patterns are observed in approximately 10% of cases (Fig 7). T wave inversion and nonspecific ST segment depression can also occur in over one third of the cases. The ECG of RV contusion is also nonspecific.30 ASSESSMENT

OF RV FUNCTION

Invasive Means

Noninvasive Means Both scintigraphic used to determine

fractions have been widely used to estimate RV function. The normal RV ejection fraction is approximately 55%.’ ‘.I’ Echo-Doppler represents a major advance.i4.‘5 This test allows a look at RV size, the configuration of the intravcntricular septum, and contractility. Doppler assessment allows the estimation of the pulmonary artery pressure with a great deal of accuracy.

and echocardiographic studies can be RV function. First-pass RV ejection

Table 1. Clinical Entities That May Contribute to RV Failure Increased pressure load Pulmonary embolism Pulmonary disease (hypoxic pulmonary vasoconstriction; destruction of pulmonary vascular bed) Chronic airflow obstruction (emphysema, chronic bronchitis) Interstitial lung disease Neuromuscular chest wall restriction Primary pulmonary hypertension Elevated pulmonary venous pressure LV failure Mitral stenosis and insufficiency Adult respiratory distress syndrome Positive-pressure ventilation Pulmonic valve stenosis Increased volume load Atrial septal defect Ventricular septal defect Tricuspid valve insufficiency Decreased contractility

Contrast ventriculography can be performed? However, the geometry of the RV makes it difficult to compute volume.‘” It is rarely used now and replaced by the noninvasive techniques. However, hemodynamic monitoring does remain the mainstay of managing the acutely ill patient with RV decompensation. The use of a pulmonary artery catheter allows the determination of right atrial, RV, and pulmonary artery pressures. Right heart pressure can confirm the elevated right atria1 pressures, prominence of either a or v waves, and y descents. The RV pressure tracing may show a square root sign in its diastolic portion. Cardiac output can also be measured. Recently, the thermodilution technique has been refined, allowing for the determination of RV ejection fraction and volumes. This advance is based on the recent manufacture of a rapid-response thermistor allowing for beat-to-beat temperature variations.” Although this is an exciting advance, the influence of a concomitant tricuspid regurgitation on the estimation of ejection fraction and volume still remains to be determined. Interpretation of the results should be made with caution.

lschemia Right coronary artery occlusion Systemic hypotension (poor right coronary perfusion) RV contusion (chest trauma) Mediastinal radiation p-Blockade

MANAGEMENT

OF PATIENTS WITH RIGHT HEART FAILURE

The principles of management are listed in Table 3. Most authorities believe that RV preload must be optimized. The best example of this approach has been the use of volume

511

ACUTE RIGHT HEART FAILURE

III

aVF

v3

V6

Fig 7. An ECG from a patient with acute pulmonary hypertension. Note the right axis deviation, S,QT, pattern and qR configuration in V,.

loading as the mainstay of treating patients with RV wall infarction. Interestingly, clinical studies of RV wall infarction have shown that response to volume loading is blunted when the right-sided filling pressures exceed 10 mm Hg?7,38 However, when low filling pressures (below 10 mm Hg) are encountered, volume loading appears to be warranted. The optimal range of right-sided filling pressures in acute RV pressure overload is not known and treatment should be individualized. Work by Prewitt and Ghignone39 has suggested that volume loading can be deleterious. In this study, pulmonary hypertension in dogs was induced by glass bead embolism. Volume loading sufficient to increase the RV and LV end-diastolic pressures above 10 mm Hg resulted in a decrease in cardiac output. This observation is probably explained by the fact that if RV contractility is markedly depressed, the Frank-Starling curve is relatively flat. Increasing RV filling pressure in this situation will not increase stroke output but will increase RV end-diastolic pressure and intrapericardial pressure and will reverse the transseptal pressure gradient. These changes exacerbate the pericardial and transseptal interactions alluded to previously. The best guide is to manage each patient individually. Volume loading when the central venous pressure is less than 10 mm Hg should be initiated and the cardiac output should be followed closely. Further volume loading should be avoided when the right atria1 pressure increases more than 3 mm Hg without an appreciable change in cardiac output. The maintenance of aortic pressure is an important issue in managing such patients.25,39 Agents that increase aortic pressure have been shown to reverse RV ischemia and Table 3. Principles of Managing Right Heart Failure Optimize RV preload Maintain aortic pressure RV afterload reduction 02 Vasodilators Increase RV contractility Digoxin Dobutamine/dopamine/amrinone

actually improve RV function.= Vasodilators are commonly used to treat the elevated PVR observed in acute RV pressure overload. However, their effects on the systemic circulation to lower aortic pressure can actually precipitate RV ischemia and shock. It is advisable to keep a close eye on the aortic diastolic pressure and pressor agents should be added to keep it from falling significantly. RV afterload reduction can be used but with caution. Oxygen is a useful and safe vasodilator and relieves the pulmonary hypoxic vasoconstriction in chronic obstructive pulmonary disease40 and acute vascular injuries in the lungs. It is also useful in primary pulmonary hypertension (unpublished data). It is has very little effect on systemic blood pressure. A good pulmonary vasodilator is still to be found. There are a number of reports attesting to the utility of calcium blocker$’ hydralazine,38s4’~43 and arachidonic acid metabo1iteY in chronic pulmonary hypertensive disorders. Although hydralazine can be used in such patients, it does have a potent effect on the systemic circulation and must be used with a great deal of caution. There appears to be little role for the use of calcium blockers in patients with acute RV pressure overload, although in chronic primary pulmonary hypertension they have been shown to be of benefit.4’ The use of nitroglycerin and nitroprusside has not been demonstrated to have consistent beneficial effect in an experimental model of canine oleic acid pulmonary edema; indeed, hydralazine appeared to be superior to nitroprusside.3”.42Prostaglandin E, (PGE,) has been used in a number of clinical situations with varying success. Initial enthusiasm was based on a clinical study by Holcroft et a1,45 which suggested reduced mortality in patients with acute lung injury treatecl with PGE,. A recent clinical trial with PGE,46 confirmed its ability to reduce PVR but showed no effect on mortality in patients with acute lung injury. Other studies in experimental models have shown minimal success with PGE, as a vasodilator.47-49 In the patient with acute massive pulmonary embolism, the use of thrombolytic agents and/or embolectomy is the most direct approach to reduce RV afterload and should be

512

initiated

along with concomitant

therapy

to manage

RV

The

USC of inotropic

still remains rine,

agents

an important

dopamine,

and

to increase

tool.

ot its intropic

dobutamine

all

vasodilator

properues and partially properties.“’

bccausu

:H

RV contractility

Isoproterenol, can

SUMMARY

norepinephincrease

RV

In an experimental model of glass bead embolism, dopamine, norepinephrine,3H and dobutaminelxz4 have enhanced RV function and can be used in the clinical setting to manage such patients. Amrinone has also been shown to be of benefit partially

ventricular

because

its pulmonary

dysfunction.

contractility.

Acute RV failure is an increasingly more common clinical entity and problem. ,4 good understanding of the pathophysiology is required to develop a treatment strategy. Principles of treatment outlined include optimizing RV preload, cautiously reducing RV afterload, and enhancing RV contractility.

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function

car pulmo-

Effect of increased treatment on right failure (ARF). Am

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MT: Pulmonary hypertension in severe N Engl J Med 296:476-480, 1977

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S, Garneys

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interaction

in

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ACUTE RIGHT HEART FAILURE

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