Cardiac resynchronization therapy through biventricular pacing in patients with heart failure and ventricular dyssynchrony

Cardiac resynchronization therapy through biventricular pacing in patients with heart failure and ventricular dyssynchrony

Nancy M. Albert

Department of Thoracic and Cardiovascular Surgery and Heart Failure Disease Management Programs, George M and Linda H. Kaufman Center for Heart Failure at the Cleveland Clinic Foundation, Cleveland, Ohio.

Chronic left ventricular systolic dysfunction, or heart failure, is a common condition, especially in the elderly. It is considered a major public health concern, accounting for 550 000 new cases and contributing to more than 287 000 deaths per year in the United States. (1) A recent report of long-term trends in heart failure incidence and prevalence based on subjects in the Framingham Heart Study showed that the condition stabilized in the last decade and may have declined. (2) However, the number of US citizens who will be aged 65 and older as time progresses is projected to increase toward 2020, as baby-boomers age; thus, heart failure must still be considered an epidemic. (3)

Once diagnosed, recidivism is frequent, quality of life declines, and the prognosis is bleak. In the United States, hospital discharges for diagnosis of heart failure have increased by 155% since 1979 and deaths have increased by 145% during the same period. (1) In 1999, 962 000 patients who were discharged from a hospital were assigned a primary diagnosis of heart failure. (1) These hospitalizations cost Medicare beneficiaries $3.6 billion in 1998. (1)

The burden of heart failure is high, not just for insurers, but also for healthcare providers and patients. For patients under 65 years, 20% of men and 30% of women remain alive after 8 years of diagnosis. (1) In the elderly population over age 65, survival after the first hospitalization for heart failure is even more dismal, with only 25% of patients living beyond 5 years. (4) In a large study that followed men and women for 5 years after their first hospital admission for heart failure, myocardial infarction, and the most frequent types of cancer, only patients with lung cancer had a poorer 5-year survival. (5) In another population study of patients hospitalized with heart failure, median survival rates for men and women who survived more than 30 days were 2.47 and 2.36 years, respectively. (4) In this cohort, the median age was 72 (men) and 78 years (women) and age had the most powerful influence on survival following diagnosis. The case fatality rates over a 10-year period from 1986 to 1995 at 1, 5, and 10 years were 44.5%, 76.5%, and 87.6%, respectively. (4) Long-term heart failure trends evaluated in Framingham Heart Study subjects demonstrated an improvement in survival in both men and women in the last decade (1990-1999) as compared to data from 1950 through 1969. (2) Even so, mortality rates in the most recent decade for men and women aged 65 to 74 years were 28% and 24% at 1 year and 59% and 45% at 5 years, respectively. (2)

These prognostic reports, coupled with an unstable forecast related to incidence and prevalence, reinforce the message that heart failure is a major challenge that requires new treatments to improve survival and quality of life. Healthcare providers must continue to utilize current evidence-based pharmacologic, surgical and self-management principles and approaches, but must also understand and implement newer modalities that can positively impact clinical outcomes and improve the lives of patients and their families. This article discusses a new device-based therapy, cardiac resynchronization (CRT) through biventricular pacing, with goals of promoting greater understanding of the problem of cardiac dyssynchrony, the potential and actual benefits of CRT, nursing implications related to identifying patients who might be candidates for CRT, and caring for patients who have a CRT device in place.


Over time, researchers have studied surrogate markers of mortality and morbidity to better determine the impact of clinical research modalities on heart failure outcomes. As the focus of therapy effectiveness shifted from a target on contractility and hemodynamics to neuroendocrine activation and more recently to ventricular shape and mechanical remodeling, the importance of left bundle branch block and intraventricular and interventricular conduction delays as markers of left ventricular dyssynchrony became apparent.

Prolonged QRS Duration and Cardiac Dyssynchronization

Left bundle branch block is commonly associated with coronary artery disease, hypertension, and cardiomyopathy. About 15% of all patients with heart failure have conduction delays (QRS >120 ms) (6) and approximately 30% of patients with moderate to severe heart failure have prolonged QRS. (7) Researchers found an inverse correlation between QRS duration on the surface electrocardiogram and ejection fraction even when the conduction delay was only mild (QRS duration >130 ins) and this relationship became significant when QRS duration equaled or exceeded 170 ms. (8) Using echocardiographic Doppler measurements, QRS duration ([greater than or equal to]140 ms) was significantly correlated with left ventricular septal-to-posterior wall motion delay (intraventricular delay), but not correlated to interventricular delay (delayed contraction of the left ventricle when compared to the right ventricle) or left ventricular electromechanical delay in stable patients with advanced ischemic and nonischemic heart failure. ( 9) In another study, the combination of prolonged PR interval and intraventricular conduction delay greater than 375 ins was a predictor of poor prognosis in patients with dilated cardiomyopathy. (10)

Ventricular Dyssynchrony and Worsening Left Ventricular Function

Reduced synchronization of ventricular activation can lead to worsening left ventricular function by more than 1 mechanism. In recent years, researchers have used the basal and peak rate of left ventricular pressure increase over time (+[DELTA]P/[DELTA]t) as a marker of left ventricular dysfunction. In studies that assessed left ventricular pressure increase during systole to determine myocardial performance, time course of electrical activation (measured by QRS duration) was found to be an important predictor in the rate of pressure increase in patients with heart failure. (10,11) This finding was independent of other hemodynamic variables and reflected the impact that QRS duration had on isovolumetric contraction, even in the absence of a classic left bundle branch block. (11)

Ventricular Activation Sequence in Dyssynchronous Ventricles

Other researchers assessed causes of QRS widening and left ventricular dyssynchrony in patients with heart failure. They found that ventricular ectopy and the sequence of left ventricular activation are mechanisms that cause conduction delays, thus widening the QRS. (12,13) These delays had mechanical consequences that adversely affected left ventricular performance, leading to global impairment of ventricular function. In one study, reduced synchronization of endocardial activation was secondary to ectopic entry of impulses into the His-Purkinje system and inability of the endocardium to take advantage of the branching structure of the Purkinje network in activating conduction cells. (12)

Cardiac dyssynchrony may also contribute to new ventricular arrhythmias, because mechanical stretch of the left ventricle can trigger calcium release that induces afterdepolarizations (impulse formation during electrical cell repolarization) and arrhythmia. (13)

In another study of ventricular activation sequences in patients with dilated cardiomyopathy, an apex-to-base activation sequence led to increased left and right ventricular activation times and a prolonged global activation time with the base contracting 41 ms after the apex. (14) This is in contrast to normal electrical activation in which the delay in onset of left and right ventricular contraction was approximately 6 ins, and impulses were conducted through antegrade activation by the HisPurkinje system and spread from endocardium to epicardium with activation of the right anterior or inferior base of the heart last (Figure 1). (12,14) Thus, left bundle branch block caused intraventricular and to a lesser extent, interventricular conduction delays.

Mechanical dyssynchrony between the left and right ventricles occurred because conduction abnormalities caused the left ventricle to be activated late, through the septum from the right ventricle with inferoseptal crossing occurring after anteroseptal crossing and the inferior aspect of the left ventricle activated last, remotely from activation of the base. The delay between the onsets of left and right ventricular contraction was 71 ms to 85 ms (Figure 2). (14, 15) In mechanical dyssynchrony, the aortic valve opens and closes significantly later and the mitral valve also opens late; however, timing of right ventricular events remains unchanged. Because the usual sequence of right and left ventricle systole and diastole was reversed, paradoxical ventricular septal wall motion caused interventricular dyssynchrony, and resulted in an abnormal pressure gradient between ventricles. (15, 16)

Hemodynamic Consequences of Cardiac Dyssynchrony

Ventricular conduction delays not only cause ventricular mechanical delays, but also have hemodynamic consequences that worsen ventricular performance and negatively impact the heart failure syndrome. In studies that assessed the hemodynamic outcomes of cardiac dyssynchrony, researchers found decreased performance in septal ejection fraction (-40%), global left ventricular ejection fraction (-10-15%), cardiac output (-20%), mean arterial pressure (-30%), and +[DELTA]P/[DELTA]t (-50%). (15, 16) Other results of abnormal electrical timing were that end-systolic volume and wall stress were increased, ventricular relaxation was delayed and there was a decline in cardiac efficiency. (16) When left sided atrial-ventricular time was delayed, suboptimal chamber filling caused the mitral valve to remain open during late diastole after atrial contraction and contributed to mitral regurgitation during the onset of ventricular systole. (13) In addition, left ventricular dyssynchrony caused alterations in timing of papill ary muscle contraction that led to mitral regurgitation (Figure 2). (17)

Atrioventricular Dyssynchrony

Left atrial-ventricular mechanical delay influences systolic function by modulating preload. In patients with heart failure, optimizing the atrioventricular delay increased left ventricular diastolic filling, thereby increasing stroke volume, and decreased left atrial pressure because presystolic mitral regurgitation was reduced. (17) Using Doppler mitral flow velocity recordings, investigators also found that nonpreload mechanisms, which were not fully understood, dominated in patients with heart failure and influenced aortic pulse pressure and left ventricular [DELTA]P/[DELTA]t maximum. (18) Because pacemakers, including biventricular pacemakers, allow for adjustment of atrioventricular delay time, CRT with an appropriate atrioventricular delay can optimize atrioventricular mechanical timing and intraventricular and interventricular mechanical synchrony.

Prolonged QRS Duration and Mortality

Patients with conduction system delays, indicated by prolonged QRS duration, were also found to have worse clinical outcomes; specifically, increased mortality and sudden cardiac death. (19-22) A QRS width greater than 120 ms increased the risk of mortality by 46% in patients with a history of heart failure and 10 or more premature ventricular contractions per minute. (20) In a study of QRS duration on survival in patients with heart failure, QRS width greater than 140 ms predicted an increased risk of 1-year death by 70% in outpatients followed by cardiologists. (22) Interestingly, when patients in one study were stratified by degree of systolic dysfunction, investigators found that QRS duration was more likely to predict mortality in patients with an ejection fraction >0.30 than in patients with more advanced heart failure (ejection fraction of 0.30 or less). (21) These results provide evidence that intraventricular mechanical dyssynchrony, based on a prolonged QRS duration, identifies patients with moderat e to severe heart failure and ventricular remodeling that may benefit from a therapy that blunts alterations in conduction between the septum and left posterolateral wall.

In summary, prolonged QRS duration due to left bundle branch block causes intraventricular and interventricular conduction delays. Research findings have led to the belief that late contraction of the left posterolateral free wall or inferior ventricular area causes worsening hemodynamic function that can contribute to the development or worsening of ventricular remodeling. Cardiac resynchronization therapy, through atrial synchronized biventricular pacing, simultaneously or sequentially stimulates the right ventricle and the left ventricular free wall. This therapy contributes to modification of intraventricular, interventricular, and atrialventricular activation sequences in patients with ventricular dyssynchrony and may reduce hemodynamic derangements and provide clinical benefits related to reverse remodeling, morbidity, and mortality.


The Present System: Pulse Generator, Leads, Placement, and Electrocardiogram Templates

The device is approximately the same size as a standard device but the pulse generator contains openings for 3 leads the right atrial lead, right ventricular lead, and left ventricular lead. Leads can be unipolar or bipolar shared pacing and sensing leads. If unipolar, the negative poles of each lead are the pace tips and the pacemaker device is the positive pole. Leads may act as a “shared common ring bipolar” in which they pace and sense using the right and left ventricular tip electrode as negative and the right ventricular ring electrode as positive (most common) or be “dual ventricular bipolar” (available in Europe) in which both the right and left ventricular leads have dual bipolar features (tip electrodes are negative and ring electrodes are positive). In the left ventricular position, a steroid eluding lead is used to improve fixation to the vein wall, except in patients for whom a single dose of 1 mg dexamethsone sodium phosphate may be contraindicated.

Similar to patients with standard pacemakers, the device is implanted in a pectoral pocket of the upper left or right chest. Patients with CRT should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation, electrosurgical cautery, lithotripsy, and radiofrequency ablation. In addition, external defibrillation paddles or pads should not be placed directly over the device.

All leads are placed via a transvenous approach. Right atrial and right ventricular leads are placed in the same fashion as traditional pacemaker leads. The left ventricular lead is specifically designed to be placed in a left ventricular cardiac vein after being threaded through the coronary sinus (Figure 3A). A venogram of the coronary vein anatomy should be obtained to provide a road map of the venous anatomy. The venogram image will determine what veins are present, the location of veins along the left lateral wall, and the size, tortuosity, and angulation of the left lateral veins. Ultimately, it is the venogram image that assists in determining the left ventricular lead choice and positioning of the lead. This is important because cardiac vein anatomy varies considerably among patients. One goal in lead placement is to cannulate a left lateral or posterolateral cardiac vein that provides the greatest physical separation from the lead in the right ventricle apex (Figure 3B). Cardiac resynchronization the rapy at left ventricular free wall sites, rather than at anterior wall sites, produced significantly better left ventricular systolic performance (larger +[DELTA]P/[DELTA]t and pulse pressure), demonstrated by hemodynamic values obtained after implantation. (23)

The change in electrocardiogram template after CRT will be dependent on the patient’s interventricular or intraventricular conduction delay before implantation, presence of premature ventricular contractions or fusion beats, and ventricular output controls of the device. Regardless of the preimplant rhythm, as the device delivers increasingly higher output (in volts) and pulse width (in milliseconds) to capture both the right and left ventricular chambers, the QRS configuration will reflect the altered electrical conduction vector. Generally, the QRS, ST segment, and T wave may become smaller in size with a narrower width and the pacer spike becomes larger as the amplitude of the output is increased (Figure 4).


Cardiac resynchronization therapy is currently approved by the Food and Drug Administration and indicated for the reduction of symptoms of moderate to severe heart failure (New York Heart Association functional class III or IV). Patients must be symptomatic despite being on a stable optimal medical regime (ie, 2 months on core therapies) (Table 1), have an ejection fraction of 0.35 or less and a QRS duration equal to or greater than 130 ins. For patients with known ischemic cardiomyopathy due to a history of myocardial infarction and an ejection fraction less than or equal to 0.30, a combination implantable cardioverter defibrillator/CRT device may be used. (24)

Results of Recent Outcomes Studies

To date, there have been many small, single center studies and large, multicenter, long-term studies that have found specific indices of benefit when CRT was applied to patients with moderate to advanced heart failure, based for the most part on the indications outlined previously. In studies with a control group, all patients received the device and were randomized to control versus treatment by having the device initially turned on or off for a specified period before all patients had their devices turned on for further follow-up. Some studies were crossover studies in which devices initially turned on were then turned off after a specific period (ie, 12 weeks) and vice versa. In both research designs, patients were not told if their device was on or off during the study period.

Remarkably, published studies showed many similar benefits of CRT based on quality of life and clinical improvement. In the MIRACLE (Multisite InSync Randomized Clinical Evaluation) and other smaller studies, patients assigned to CRT had significantly improved distance walked in 6 minutes, quality of life, peak oxygen consumption, exercise time on the treadmill, symptoms, New York Heart Association functional class, and ejection fraction (Table 2). (25-30) Cardiac resynchronization led to decreased hospitalization rates and less need for intravenous medications for the treatment of heart failure. (25)

Some studies assessed metabolic and ventilation parameters to determine exercise performance and tolerance with CRT. In these, peak oxygen consumption improved significantly (26,28,31) and oxygen consumption at anaerobic threshold also increased. (26) In addition, heart rate at rest decreased significantly and maximum achieved heart rate increased significantly, indicating improved heart rate adaptation throughout exercise. (31)

A reduction in left ventricular diameters and volumes signifies reversal of ventricular remodeling, an important goal of heart failure management. Investigators compared changes in left ventricular diameters and function with CRT by obtaining detailed echocardiographic data. Left ventricular end-diastolic diameter decreased, interventricular mechanical delay decreased, mitral regurgitation decreased, and left ventricular filling time increased. (29) In patients who had tissue Doppler imaging before and after implantation, in addition to improvements noted above, patients also had reductions in left ventricular end-systolic and diastolic volumes and improved longitudinal systolic shortening. (32) Researchers in the PATH-CHF (Pacing Therapies for Congestive Heart Failure) study used echocardiography to determine the underlying mechanisms of dyssynchrony that, when reversed with CRT, led to the greatest hemodynamic benefits. Patients with greater than 25[degrees] delayed inward movement of the lateral wall in re lation to septal motion (intraventricular dyssynchrony) were most likely to have increased peak positive left ventricular pressure (+[DELTA]P/[DELTA]t) improvements coupled with synchronous wall motion after CRT initiation. (33) These findings have clinical implications in screening patients with heart failure for CRT. This noninvasive method of determining dyssynchrony may help establish patients who are most likely to benefit from therapy.

Other improvements have been found that reflect an improved heart failure status. Cardiac resynchronization therapy improved blood pressure and decreased sympathetic nervous system activity, (34,35) decreased episodes of ventricular tachycardia in a patient with refractory ventricular ectopy to drug therapy and conventional dual chamber pacing, (36) and improved interventricular contractile synchrony (from 27.5 to 14.1 degrees). (37) In patients with heart failure, permanent atrial fibrillation, and chronic right ventricular pacing, adding a third lead for CRT led to improved ejection fraction, quality of life scores, New York Heart Association functional class, and peak oxygen consumption during a 6-minute walk, and decreased left ventricular diastolic and end-systolic diameters, mitral regurgitation, and hospitalizations. (38-40)

Preliminary mortality results in patients randomized to CRT or control demonstrated that CRT trended toward improved short-term (3 month) survival, (41) and led to a statistically significant improvement in death or hospitalization over a 6-month period (25) however, neither study was designed to detect differences in survival between groups. These results were encouraging and provided evidence of initial therapy efficacy.

Preliminary results of the Comparing Medical Therapy, Pacing and Defibrillation in Chronic Heart Failure study (COMPANION) were presented at the Annual Scientific Sessions of the American College of Cardiology on March 31, 2003, in Chicago, Ill. Researchers reported a significant reduction in the combined endpoints of death, hospitalization, or intravenous emergency care treatment greater than 4 hours (risk reduction of 18.9%) and death or heart failure hospitalization (risk reduction of 35.8%). One-year all cause mortality in the optimally treated medical group was 19%. Patients who received optimal medical therapy plus cardiac resynchronization had a nonsignificant 23.9% reduction in mortality. Compared to the optimal medical therapy group, patients who received cardiac resynchronization plus an implantable defibrillator had a 43.4% reduction (P = .002). These results confirm the earlier reports of reduced morbidity and provide further evidence of mortality benefits.

Many of the benefits listed above were pacer dependent. When CRT was withheld, loss of cardiac improvements was found. (26,42) In addition, various interventricular delay times (known as sequential CRT; one ventricle is preactivated [or electrically stimulated] on purpose before the other) have been studied before and after CRT placement to enhance optimization of left ventricular systolic and diastolic dysfunction. In 20 consecutive patients with left bundle branch block, Sogaard and colleagues (43) examined tissue Doppler images of ii different interventricular delays, including simultaneous CRT (both the right and left ventricles are electrically activated at the same time). Compared to simultaneous CRT, sequential CRT caused a further reduction in delayed contraction. Left ventricular ejection fraction and diastolic filling time increased immediately, and this occurred without further atrioventricular delay optimization. After 3 months of CRT, ejection fraction improved even further. Interestingly, preact ivation of the left ventricular lead was superior in 9 patients (all but one had dilated cardiomyopathy with delayed contraction in the lateral and posterior left ventricular walls before CRT) and preactivation of the right ventricular lead was superior in the remaining ii patients (all but one had ischemic cardiomyopathy with left ventricular septal and inferior wall dyssynchrony pre CRT). (43)

These results emphasized that even though patients had similar QRS morphology, the location of mechanical dyssynchrony differed and was related to the underlying etiology of heart failure. Preimplantation evaluation of the mechanical dyssynchrony to determine the location of the delayed contractile segments and thus the best location of the left ventricular pacing lead can improve left ventricular performance. This and other research results provide a reminder that there are still questions that need to be answered; however, generalized improvements in cardiac function, ventricular remodeling and clinical status provide evidence of the need to incorporate CRT in patients who meet therapy indications.

Large-scale studies to assess the long-term effect of CRT on mortality and hospitalization, as well as healthcare costs have recently been completed or are nearing the end of enrollment. (44,45) Other areas of research that warrant further exploration are use of CRT in specific subgroups, such as patients with large territories of transmural scar post myocardial infarction; device placement and therapy initiation timing (mild, moderate, or advanced heart failure and elderly who may also be frail or have life-limiting secondary diagnoses); location of left ventricular lead (epicardial or endocardial and posterior, lateral or other wall) and device delays (atrioventricular, interventricular, and refractory periods). In addition, device companies are upgrading implant tools and delivery systems, leads, hardware, and computer programming to decrease placement issues (especially placement of the left ventricular lead), minimize complications associated with insertion and to determine if there is a “best” electrica l configuration.


Patient Education

Before CRT is initiated, patients must understand that it does not replace standard medical therapies and that they still must follow their pre-CRT pharmacologic and nonpharmacologic plan of care. After implantation and before discharge, patients must receive standard pacemaker education on care of their incision and instructions on how to provide data telephonically to their healthcare provider at predetermined follow-up intervals (usually every 3-6 months). Similar to the need to adhere to pharmacologic therapies, the device must pace both ventricles 100% of the time for the benefits to be realized. Patients need to understand that their device may need to be reprogrammed to optimize heart function and that they will be followed regularly over time at a center that utilizes equipment from their device manufacturer. Battery life with 100% biventricular pacing and 10% atrial pacing is approximately 6 to 7 years.

Nurse Initiatives

Nurses have the opportunity to impact patient outcomes related to heart failure care strategies. Because heart failure is now recognized as a high volume, high-risk condition related to morbidity, mortality, and cost, the Joint Commission for Accreditation of Hospital Organizations implemented core measures to assure quality hospital care. Nurses implement many of these core measures, especially those associated with patient education. Many managed care organizations, hospital teams, and cardiology group practices reported benefits after developing and implementing disease management programs that promoted optimization of consensus recommendations in heart failure management. (46 47) Again, these programs were often initiated and implemented by nurses to promote the use of the right therapies at the right time and at the right level based on individual patient etiology and severity of condition. As nurses take on more of a leadership role in collaborating with physicians to determine the timing of therapies, especially when the patient enters the healthcare system with worsening condition, the full spectrum of therapies must be available, including CRT.

Patients admitted to a hospital are a “captive audience” because healthcare professionals have the opportunity to optimize therapies that improve length and quality of life; therefore, the acute hospital period is a point in time when strategies must be set in motion or initiated, even if the intent is to provide the full service after discharge when the patient’s condition has stabilized. Nurses need to actively participate on multidisciplinary teams responsible for developing programs that will ultimately promote actions consistent with national consensus recommendations and large research trials.

There are many ways that acute and critical care nurses can promote the use of heart failure therapies known to benefit patients across the continuum of care. Written standards of care that include CRT must be made available to healthcare providers who can influence practice. They must be widely visible if the intent is to trigger optimization of therapies. This can be achieved by written guidelines developed into laminated pocket cards or wall posters, physician admitting order sheets, preprinted progress notes or care pathways, and checklists and discharge instruction forms. Written algorithms or protocols provide specific directions related to indications and timing of various pharmacologic, device, and other therapies and are especially beneficial in promoting a more aggressive and consistent approach when care is provided by teams that rotate to different services or when care is provided by noncardiology physicians and nurses.

Algorithms and protocols can be set up to be physician-initiated and nurse-mediated. In this way, the bedside nurse or advanced practice nurse can set in motion specific actions once it has been determined that a patient meets criteria for treatment. In the emergency care setting, an electrophysiology consult can be planned at follow-up if a patient meets CRT indications (before the acute decompensation episode). This might be especially important in those patients with a high recidivism rate. In the acute or critical care setting, nurses might provide patients with anticipatory information about the potential need for CRT if their condition deteriorates or fails to improve after discharge. This information might promote patient adherence with follow-up monitoring and will facilitate discussions of the plan of care and need for changes to improve outcomes. In addition, if an echocardiogram is necessary to determine heart failure etiology, it can be performed with an eye towards determining CRT eligibility by assessing for the presence and degree of left ventricular dyssynchrony in addition to determining ejection fraction and valve status.


Cardiac resynchronization therapy provides a new adjunct in the armamentarium of therapies available to patients who remain symptomatic despite optimized standard therapies. It does not cure heart failure; patients must maintain evidence-based therapies promoted by the American Heart Association and American College of Cardiology. 48 Therapy benefits can be influenced by lead placement and device programming, so it is essential that qualified personnel are consulted to initiate and monitor therapy. While we await final analysis of COMPANION and other studies that definitively answer the question of mortality benefits, substantial data support CRT in reversing left ventricular remodeling, providing hemodynamic benefits, and most importantly, imparting clinical benefits related to functional status, symptoms, quality of life, and morbidity. Acute and critical care nurses can take an active role in promoting this intervention for patients with wide QRS and cardiac dyssynchrony who are likely to benefit through i mprovement in cardiac function and efficiency.

Table 1

Optimal medical management for patients with advanced left ventricular

systolic dysfunction

“Core” oral pharmacologic therapies

* Angiotensin-converting enzyme inhibitor at target dose **

Rationale: Suppresses activation of the renin-angiotensin-aldosterone

system (RAAS) by decreasing production of angiotensin II. Also,

suppresses degradation of bradykinin, thus stimulating nitric oxide

production. Leads to arterial and venous dilatation, decreasing

afterload and preload; ultimately, improves survival, ejection

fraction, morbidity, and exercise tolerance.

* Beta-blocker at target dose

Rationale: slows heart rate (thereby improving diastolic function) and

modulates activation of norepinephrine by the sympathetic nervous

system (SNS). Improves survival ejection fraction, exercise tolerance,

and morbidity.

* Digoxin at low dose

Rationale: Modulates the neuroendocrine axis (RAAS and SNS), increases

inotropy, and slows the heart rate through negative chronotropic

actions. Improves exercise tolerance and morbidity.

* Spironolactone at low dose

Rationale: Competes with aldosterone in the distal tubule, promoting

excretion of sodium and water. Improves survival and morbidity in

patients with advanced heart failure.

* Loop diuretic at dose to maintain euvolemia

Rationale: Reduces sodium and water retention, thereby relieving

symptoms of heart failure.

Nonpharmacologic therapies

* 2000-mg sodium diet

* Daily weight monitoring

* Daily activity and exercise

* Fluid restriction (if persistent hypervolemia and hyponatremia)

Surgical therapies (eg, coronary artery revascularization, repair of

mitral regurgitation, replacement of aortic valve) as indicated

** May use angiotensin II receptor blocker or hydralazine/nitrate

combination when patients have contraindications to angiotensin-

converting enzyme inhibitors.

Table 2

Clinical benefits of cardiac resynchronization therapy indicates better

quality of life

Study group improvement

beyond control group


Clinical parameter At 6-month follow-up

Distance walked in 6 minutes + 29 m *

Quality of life + -9 points *

Peak oxygen consumption + 0.9 mL/kg/min *

Total exercise time + 62 seconds *

Ejection fraction + 4.6 percentage points *

Study group improvement

beyond control group


Clinical parameter At 3-month follow-up

Distance walked in 6 minutes + 73 m *

Quality of life + – 13 points *

Peak oxygen consumption + 1.2 mL/kg/min *

Total exercise time

Ejection fraction

* P [greater than or equal to] .001.

+ Scale: Minnesota Living with Heart Failure Questionnaire. A higher

score indicates worse quality of life.


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This article has been designated for CE credit. A close-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Describe the proposed mechanisms and outcomes of ventricular dyssynchrony

2. Identify the goals of cardiac resynchronization therapy in heart failure and ventricular dyssynchrony

3. Discuss nursing care and nursing implications of cardiac resynchronization therapy

CE Test Questions

Cardiac Resynchronization Therapy Through Biventricular Pacing in Patients With Heart Failure and Ventricular Dyssynchrony

1. For patients under age 65, what percentage of men remain alive after 8 years of diagnosis of chronic left ventricular systolic dysfunction?

a. 10%

b. 20%

c. 30%

d. 40%

2. For patients under age 65, what percentage of women remain alive after 8 years of diagnosis of chronic left ventricular systolic dysfunction?

a. 10%

b. 20%

c. 30%

d. 40%

3. What percentage of patients with heart failure have conduction delays (QRS > 120 ins)?

a. 10%

b. 15%

c. 25%

d. 50%

4. Which one of the following terms relate to the delayed contraction of the left ventricle when compared to the right ventricular?

a. Intraventricular delay

b. Interventricular delay

c. Electromechanical delay

d. Ventricular dyssynchrony

5. Which one of the following is not a hemodynamic consequence of cardiac dyssynchrony?

a. Decreased ejection fraction

b. Delayed ventricular relaxation

c. Mitral regurgitation

d. Decreased end-systolic volume

6. In patients with a history of heart failure, a QRS width of greater than 140 ms increases the risk of 1-year death by what percent?

a. 10%

b. 30%

c. 50%

d. 70%

7. During cardiac resynchronization therapy, which site produces significantly better left ventricular systolic performance?

a. Left ventricular anterior wall

b. Right atrial wall

c. Left atrial wall

d. Left ventricular free wall

8. Which one of the following is not an indication for cardiac resynchronization therapy in heart failure?

a. Ejection fraction of 0.35 or greater

b. QRS duration> 130 ms

c. Optimal medical therapy for at least 2 months

d. New York Heart Association functional class III or TV

9. Battery life with 100% biventricular pacing and 10% atrial pacing is approximately how many years?

a. 3 to 4 years

b. 4 to 5 years

c. 6 to 7 years

d. 8 to 9 years

10. Patients with cardiac resynchronization therapy should avoid all except which of the following?

a. Magnetic resonance imaging

b. Electrosurgical cautery

c. Lithotripsy

d. Microwave radiation


The author is on the speaker’s bureau for Medtronic. Inc. She is not an employee nor does she have a consulting relationship with any of the pacemaker/device companies.

COPYRIGHT 2003 American Association of Critical-Care Nurses

COPYRIGHT 2003 Gale Group