Editor's Message
Literature Increases Concerning Concomitant Cardiac and Oncologic Diseases

Brenda Shelton, RN, MS, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

As I approach the eleventh hour and this newsletter is overdue, I find myself stretching every creative brain cell to decide on what to include in this editor’s message, and alas, I find no inspiration. In fact, perhaps I have simply used up all my creative energy pulling together this newsletter. In trying to keep with themed newsletters, Catherine Sargent, RN, MS, AOCN^®, and I planned long ago for this issue to focus on cardiovascular disorders. When we selected this topic, little did we know that others in oncology nursing would be directing their attention to this area of practice. Perhaps the heightened interest in concomitant cardiac and oncologic diseases is related to my soapbox about it all, but then again, perhaps it has more to do with the fact that cardiac health problems have slowly but steadily permeated our specialty practice. For this reason, we have decided to conform to our original plans for this newsletter and will include additional cardiovascular articles in future newsletters as well. Also in a future issue, we will follow up on our SIG-sponsored session at the 2003 Institutes of Learning with summaries of the discussions about management of chest pain and hypertension in patients with cancer.

Last spring, Jo Ann Flounders, MSN, CRNP, OCN^®, CHPN, provided an excellent overview of cardiac tamponade (click here), but we hope this issue of the newsletter will expand on the information she provided. Also in this issue, Catherine reviews a focused article on pulsus paradoxus (see “Article Provides a Comprehensive Review of Pulsus Paradoxus in Cardiac Tamponade"), and I summarized information on the diagnosis and management of cardiac tamponade with references and links to Web sites with real examples (see “Explore These Recent Publications About Pericardial Effusion and Tamponade”). Quite frankly, this concept of adding links to chest x-rays, electrocardiograms, and echocardiograms and locating appropriate illustrations is a new departure for me in writing. I hope you all enjoy the extra information. Also along this theme, the September/October 2003 issue (Vol. 7, No. 5) of the Clinical Journal of Oncology Nursing (click here) published an excellent article titled “Cardiac Toxicity Related to Cancer Treatment” (Loerzel & Dow, 2003) that you may find a good complement to the information in this newsletter.

Reference
Loerzel, V.W., & Dow, K.H. (2003). Cardiac toxicity related to cancer treatment. Clinical Journal of Oncology Nursing, 7, 557–562.

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SIG Welcomes Its New Members


The Acute and Critical Care SIG would like to tip its hat to its newest members. Welcome!

Joleen Begley, RN Jada Beisner, RN, BSN, OCN® Lissa Bekefi, RN, OCN® Diane Bell, RN, BSN Danette Birkhimer, SN, RN, OCN® Leslie Brockelsby, RN, OCN® Rebecca Brooks, RN Jo-Reba Bryson, RN Heesun Chang Anslie Coker, RN Graciela Conde, RN, C, OCN® Sonia Cuchapin, RN, MA, OCN® Gabriela Del Rio, OCN® Linda DiMaggio, RN, OCN® Hannah Donnelly, RN, BSN Juanita D’Souza, RN, BSN, CCRN, OCN® Patricia Emerson, RN, BSN, OCN® Amy Erbeck, RN, BSN Rosemary Farrell, RN, C Jo Ann Fugazzotto Wendy Gill, BSN, RN, OCN® Linda Gilmore, MSN, RNC, OCN® Heather Goes, RN Marguarite Greenspan, RN Rhonda Gunderson, RN Lisa Hammons, RN, OCN® Lisa Hicks, RN Elizabeth Hurter, RN, OCN® Edith Jackson, RN Elizabeth Johnson, RN, MSN Maryann Kolb-Bowman, RN, BSN Melissa Kravitz, RN Debbie Llamas, RN, OCN® Jennifer Lalau, RN, OCN® Tonia Lower, RN Richard Lutzi, RN Susan Lykins, RN, CCM Joyce Martin, RN

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Article Provides a Comprehensive Review of Pulsus Paradoxus in Cardiac Tamponade

Catherine Sargent, RN, MS, AOCN^®
Havertown, PA
sargentc@mlhs.org

Swami and Spodick (2003) provided a comprehensive overview of pulsus paradoxus (PP) during cardiac tamponade, which had not been reviewed in medical journals since 1979. Their review of this disorder was greatly needed.

PP initially was described by Kussmaul in 1873 after he noticed that the radial pulse disappeared on inspiration in patients with cardiac compression by pericardial contents. He considered this disappearance paradoxic because the cardiac apex continued to beat. Swami and Spodick (2003) described PP as a pathophysiologic continuum—on one end, a cyclic respiratory cardiac response is normal and the systolic blood pressure falls (> 10 mm Hg) during inspiration from its higher expiratory level. At the other end of the continuum, as in cardiac tamponade, the systolic and diastolic blood pressures fall (sBP > dBP).

During normal respiration at the beginning of the continuum, an interaction occurs between respiration and circulation caused by changes in pleural pressure. For example, pleural pressure decreases during inspiration, lowering intrathoracic pressure but not extrathoracic venous pressure. With almost a vacuum or convection method, this, in turn, increases blood return to the thorax and causes the right heart to fill. The cycle of inspiration and expiration during normal breathing causes the alternating filling of the right and left heart. This filling affects stroke volume, left ventricular and right ventricular stroke volumes, preload, and afterload.

Alternately, PP in cardiac tamponade is the “end” of the continuum. In their article, Swami and Spodick (2003) listed other conditions that can lead to PP such as pulmonary embolism, right ventricular infarction, severe obstructive pulmonary disease (which signifies serious disease), bilateral pleural effusion, tension pneumothorax, constrictive pericarditis (in some cases), circulatory shock (which is mostly hemorrhagic), restrictive cardiomyopathy, extraneous cardiac compression, and tracheal compression. The authors stated that the appearance of PP typically indicated critical cardiac compression by pericardial contents, which causes a significant reduction in intracavitary volume and systolic pressures.

In a patient with PP, inspiration causes a significant increase in right heart filling and a decrease in left heart filling. Clinically, this causes a decrease in the systolic blood pressure. Additionally, during cardiac tamponade, both the left and right heart compete for a fixed intrapericardial volume, thus leading to inspiratory right heart filling at the expense of the left heart. In cardiac tamponade, the filling volume of all chambers is decreased; however, the increase during inspiration over expiration is proportionally much higher than normal.

In summary, the inspiratory sequences of PP are as follows.

1. Inspiration leads to a decrease in pleural pressure.
2. Pulmonary wedge and left atrial pressures fall below pericardial pressure.
3. Decreased left ventricle output and decreased left ventricle filling take place.
4. Left ventricle compression occurs.
5. The decreased pericardial pressure simultaneously causes increased caval flow, increased right atrial filling, and increased right ventricle volume.
6. Left shift of the intraventricular septum occurs, which leads to left ventricular compression.
7. Increased pericardial pressure can lead to decreased left ventricular transmural pressure and/or left ventricle compression.

Focus on the Facts of Pulsus Paradoxus

Brenda Shelton, RN, MS, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

Definition

• Pulsus paradoxus is a drop in systolic blood pressure of more than 10 mm Hg during inspiration; in hypotension, 5 mm may be considered significant.
  
• Kussmaul originally described this symptom in 1873.

Web Site Offers Practical Information for Cardiovascular Nurses

Brenda Shelton, RN, MS, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

Nurse-Beat.com is a nurse-dedicated site that is developed and maintained by a single nurse (Deborah W. Kumar) and pharmacist editor (Linda Monteleone). The site originated in 1997 and shows evidence of updating as recently as summer 2003. Nurse-Beat.com has a few unique and helpful features and a number of links to other sites that would interest cardiovascular nurses, although the home page is unclear about which features are unique and which are simply lists of links (note: not all of the links worked). The basic subheads within the Web site home page include the following.

• Feature articles: These basic articles would interest cardiovascular nurses, but they are extremely limited in scope and depth of content.
• Strip show: This section features some real patient strips of specific cardiac rhythms and conditions. The ones presented look good, but many do not have samples. Oncology nurses should really check this out just to see the hyperkalemia tracings.
• Cardiac pharmacology: These short, easy-to-read profiles highlight a few cardiac drugs and include a rapid synopsis.
• Cardiac anatomy and physiology: Great pictures and tutorials are available here.
• Cardiac surgery
• Electrocardiogram and arrhythmias: This is a good, basic review of rhythms and would make a good teaching adjunct for nurses who are just learning rhythms.
• Hemodynamics
• News
• Patient education
• Books
• Continuing education: The site provides links to many sites with cardiovascular nursing continuing education—some with fees and some without. The links do not provide identifying information, and I found it time consuming to constantly click and never find any free continuing education.
• Fun sites
• Jobs
• Newsgroups
• Personal sites by nurses
• Advanced cardiac life support and CPR: This was a great feature and rapidly linked me to several good simulation sites.
• Cardiac cases and conditions: The options are limited, but they are well researched.
• Chat rooms and support groups
• Government sites
• Journal and references: Too many of these links required previous access registration and subscription.
• Nursing organizations
• Pharmacology
• Alternative medicine
• Cardiac catheterization: This link did not work.
• Echocardiography: This feature has a good listing of links with actual echocardiograms.
• Heart and lung sounds: This quick reference lists some good heart and lung sound simulation sites.
• List serves
• Nursing schools
• Research: This section has links to several evidence-based practice sites, especially those with cardiovascular topics profiled.

Explore These Recent Publications About Pericardial Effusion and Tamponade
Brenda Shelton, RN, MS, CCRN, AOCN^®
Finksburg, MD
sheltbr@jhmi.edu

In this issue of the newsletter, Catherine Sargent, RN, MS, AOCN^®, carefully evaluated a recently published article describing the clinical significance and development of pulsus paradoxus (see “Article Provides a Comprehensive Review of Pulsus Paradoxus in Cardiac Tamponade”). This unique and key symptom of progressive and clinically significant pericardial effusion is rapidly becoming difficult to assess because of our dependence upon automated blood pressure devices in patient blood pressure monitoring. In addition, although it is a classic presentation in cardiac tamponade, pulsus paradoxus also may be present in patients with chronic obstructive lung disease or mechanical ventilatory support and may be absent in patients with severe shock, in acute myocardial infarction with pericardial adhesions, or with right ventricular hypertrophy (Spodick, 2003). For these reasons, I summarized some additional information and included a bibliography of recently published information about pericardial effusion and tamponade.

Risk Factors
Patients with cancer at greatest risk for development of pericardial effusion are those with tumors within the chest. Chest tumors may cause venous or lymphatic obstruction that affects pericardial fluid dynamics or, in rare cases, actually metastasizes to the pericardium. The most common malignant association with pericardial effusion is lung cancer, followed by breast cancer and malignant lymphomas. Excess capillary permeability as seen with congestive heart failure, hypothyroidism, systemic lupus erythematosus, uremia, leukemia, or certain antineoplastic agents (e.g., cytosine arabinoside, interleukin-2) also may cause excess fluid in the pericardial sac (Flounders, 2003). Infectious or hemorrhagic etiologies are uncommon but may occur in the myelosuppressed patient (Atar, Chiu, Forrester, & Siegel, 1999; Flounders). HIV disease has been associated with a significant risk for pericardial effusion, particularly related to infection (Gowda et al., 2003). Patients with effusions related to therapy rather than the malignancy itself have a better prognosis for long-term survival (Lindenberger, Kjellberg, Karlsson, & Wranne, 2003). Even with treatment, survival is estimated at 89 days for patients with malignant effusions; however, 95% of patients experience symptomatic relief of symptoms with aggressive treatment (Lindenberger et al.).

Clinical Presentation
Many patients with cancer do not exhibit pericarditis and, instead, only develop progressive pericardial effusion that can lead to cardiac tamponade if untreated. The accumulation of fluid in the pericardial sac leads to more positive intrapericardial pressures that impede the return of the lower pressure venous blood. When venous return is compromised slowly over a long period of time, the primary clinical feature is right heart failure. This is the most common presentation for patients with cancer. Venous congestion manifested as dyspnea, edema, or elevated jugular venous pressure, and hepatosplenomegaly is the typical clinical picture. Other common findings include muffled heart sounds, a lateral shift in the point of maximal impulse, and tachycardia. If more rapidly developing or in its late stages of effusion leading to tamponade, arterial hypotension and frank perfusion deficits exist and patients present with cyanosis, hypoxemia, cool and clammy extremities, oliguria, and mental status changes. If pericardial effusion becomes so severe that it prevents all venous return of blood and causes cardiac arrest, it often presents as an electrocardiogram (ECG) rhythm without a pulse termed “pulseless electrical activity.” This occurs because the myocardial pump fails rather than the conduction pathway. This results in normal electrical conduction with presence of an ECG waveform but absence of contraction and cardiac output evidenced by the lack of a pulse.

Diagnostic Confirmation
When pericardial effusion is suspected, the gold standard for diagnosis is an echocardiogram. This shows fluid within the pericardial sac, hypotonic wall motion, and decreased ventricular filling. This is illustrated in Spodick’s (2003) recent article, as well as at the E-chocardiography Journal’s Web site (www2.umdnj.edu/~shindler/abc.html). While awaiting the specialists who can obtain an echocardiogram, other rapid bedside diagnostic tests such as a chest x-ray and a 12-lead ECG can be obtained and may show distinctive abnormalities indicating possible pericardial effusion. These changes are depicted in articles by Lau, Civitello, Hernandez, and Coulter (2002) and Gentlesk and McCabe (2001). The chest x-ray often shows an enlarged cardiac silhouette (usually greater than half the chest width) and a widened mediastinum (described as the water bottle silhouette) when more than 250 ml is present in the pericardial sac (Goyle & Walling, 2002). See the eMedicine.com site to review a typical chest x-ray finding with pericardial effusion (click here). The 12-lead ECG may show low-voltage or consistent ST elevation across all leads (see the photographs in Gentlesk and McCabe’s article). The PR segment is depressed, and the ST segment elevation shows an upward concave appearance nicknamed the “smiling face” ST (Goyle & Walling). Unlike myocardial infarction, the ECG lacks T wave inversions or reciprocal changes (Goyle & Walling). In their article, Goyle and Walling included pictures of these ECG changes. Another less frequent but more specific observation is the presence of “electrical alternans” where Q waves alternate upward and downward deflection. This occurs because the heart “floats” in relation to the leads recording its electricity (Goyle & Walling), which can be seen at ECG Library’s Web site (www.ecglibrary.com/ecghome.html).

Management Strategies
A pericardial effusion may be asymptomatic or result in cardiac arrest. For patients with small or asymptomatic effusions, symptomatic support and correction of the etiology of effusion are priorities. This may involve implementation of antineoplastic therapies or correction of congestive or capillary permeability conditions. Nursing goals include alleviation of pain or dyspnea and reduction of oxygen demands. If possible, patients should be on a cardiac monitor that includes ST segment monitoring. In addition, they should be on complete bedrest and receive oxygen therapy to maximize their oxygen saturation.

For patients with clinically significant pericardial effusion and impending cardiac tamponade, emergent removal of fluid from the pericardium is necessary. This can be accomplished by needle pericardiocentesis, balloon pericardiotomy, pericardial catheter drainage, or performance of a surgical pericardial window. Until the appropriate technology is available to remove pericardial fluid, massive volumes of IV fluids are administered rapidly in an attempt to raise the venous pressure above the pericardial pressure so that some returning blood can enter the heart and be pumped out into the arterial circulation. This excess fluid can be diuresed easily from the vascular space after definitive pericardial drainage is performed. The urgency of the patient’s clinical symptoms, the presence of other treatable disorders (e.g., concomitant pleural effusions), and physician preference may guide the treatment decision. Key nursing care for these management strategies are included in Table 1. The pericardial catheter is a unique management strategy used most commonly by patients with cancer. It resembles a nephrostomy tube but is made of a less flexible material. The tip is curled in the classic pigtail to help hold it in place because it is difficult to suture (see Figure 1). Few references are available to guide nurses in the care of these catheters. A summary of the clinical protocol used at Johns Hopkins Hospital is included within Table 1 to outline nursing care of patients having pericardial drainage interventions.

References
Atar, S., Chiu, J., Forrester, J.S., & Siegel, R.J. (1999). Bloody pericardial effusion in patients with cardiac tamponade. Is the cause cancerous, tuberculous, or iatrogenic in the 1990s? Chest, 116, 1564–1569.

Flounders, J.A. (2003). Cardiovascular emergencies: Pericardial effusion and cardiac tamponade. Oncology Nursing Forum, 30(2). Retrieved December 20, 2003, from http://www.ons.org

Gentlesk, P.J., & McCabe, J. (2001). Pericarditis, acute. E-medicine Journal, 2(11). Retrieved January 4, 2004, from http://www.emedicine.com/med/topic1781.htm

Gowda, R.M., Khan, I.A., Mehta, N.J., Gowda, M.R., Sacchi, T.J., & Vasavada, B.C. (2003). Cardiac tamponade in patients with human immunodeficiency virus disease. Angiology, 54, 469–474.

Goyle, K.K., & Walling, A.D. (2002). Diagnosing pericarditis. American Family Physician, 66, 1695–1702.

Johns Hopkins Hospital. (2001). Johns Hopkins nursing practice manual: Pericardial catheter. Baltimore, MD: Author.

Lau, T.K., Civitello, A.B., Hernandez, A., & Coulter, S.A. (2002). Cardiac tamponade and electrical alternans. Texas Heart Institute Journal, 29(1). Retrieved January 1, 2004, from http://www.texasheartinstitute.org/lau291.html

Lindenberger, M., Kjellberg, M., Karlsson, E., & Wranne, B. (2003). Pericardiocentesis guided by 2-D echocardiography: The method of choice for treatment of pericardial effusion. Journal of Internal Medicine, 253, 411–417.

Spodick, D.H. (2003). Acute cardiac tamponade. New England Journal of Medicine, 349, 684–689.

Bibliography
Brown, D.V. (2002). Dicrotic pulse in pericardial tamponade. Journal of Cardiothoracic and Vascular Anesthesia, 16, 742–745.

Campione, A., Cacchiarelli, M., Ghiribelli, C., Caloni, V., D’Agata, A., & Gotti, G. (2002). Which treatment in pericardial effusion? Journal of Cardiovascular Surgery, 43, 735–739.

Dosios, T., Theakos, N., Angouras, D., & Asimacopoulos, P. (2003). Risk factors affecting survival of patients with pericardial effusion submitted to subxiphoid pericardiostomy. Chest, 124, 242–246.

Hawley, J., Dreher, H.M., & Vasso, M. (2003). Under pressure: Treating cardiac tamponade. Identify this potentially fatal complication early and intervene appropriately. Nursing Management, 34(2), 44D, 44F, 44H.

Hsu, L., Scavee, C., Jais, P., Hocini, M., & Haissaguerre, M. (2003). Transcardiac pericardiocentesis: An emergency life-saving technique for cardiac tamponade. Journal of Cardiovascular Electrophysiology, 14, 1001–1003.

Kirsner, K. (2003). Cancer: New therapies and new approaches to recurring problems. AANA Journal, 71(1), 55–62.

Knoop, T., & Willenberg, K. (1999). Cardiac tamponade. Seminars in Oncology Nursing, 15, 168–173.

Retter, A.S. (2002). Pericardial disease in the oncology patient. Heart Disease, 4(6), 387–391.

Shelton, B.K. (in press). Neoplastic cardiac tamponade. In C. Ziegfeld, B.K. Shelton, & M. Olsen (Eds.), Manual of oncology nursing (2nd ed.). Philadelphia: Lippincott Williams & Wilkins.

Spodick, D.H. (2003). Acute pericarditis. JAMA, 289, 1150–1158.

Strimel, W.J., & Noe, S. (2002). Pericardial effusion. E-Medicine Journal, 3(10). Retrieved January 4, 2004, from http://www.emedicine.com/med/topic1786.htm

Swami, A., & Spodick, D. (2003). Pulsus paradoxus in cardiac tamponade: A pathophysiologic continuum. Clinical Cardiology, 26, 215–217.

van Steijn, J.H., Sleijfer, D.T., van der Graaf, W.T., van der Sluis, A., & Nieboer, P. (2002). How to diagnose cardiac tamponade. Netherlands Journal of Medicine, 60, 334–338.

Yarlagadden, C., & Hout, W.M. (2002). Cardiac tamponade. E-Medicine Journal, 3(9). Retrieved January 1, 2004, from http://www.emedicine.com/med/topic283.htm

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