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Feature: CE Connection: Oncology Emergency Series

When cardiac tamponade puts the pressure on

Kaplow, Roberta PhD, APRN-CCNS, AOCNS, CCRN; Iyere, Karen MSN, APRN, AGNP-C, ACCNS-AG

Author Information
doi: 10.1097/01.NURSE.0000511804.75711.a5

In Brief

Figure
Figure

CARDIAC TAMPONADE, a structural oncologic emergency identified by the Oncology Nursing Society, can occur at any time during the cancer trajectory.1 Cardiac tamponade is the compression of the heart due to the abnormal accumulation of fluid in the pericardial space (pericardial effusion), which exceeds normal compensatory mechanisms, impairs cardiac filling, and results in hemodynamic compromise.

This article explains why cardiac tamponade occurs, which patients are at risk, how to recognize the signs and symptoms, and how to care for patients with cancer who experience this life-threatening complication.

Anatomic considerations

The pericardium, which surrounds and protects the heart, normally contains about 30 to 50 mL of fluid, which decreases friction between the visceral and parietal layers during systole and diastole.1 (See An inside look at the normal pericardium.) Besides serous pericardial fluid, blood, pus, gas, or blood clots may accumulate in the pericardial space.

Pericardial effusions may develop slowly (over weeks to months [subacute or chronic pericardial effusions]) or rapidly (over minutes to hours [acute pericardial effusions]), depending on the underlying cause.1 For example, cancer may cause a chronic pericardial effusion whereas chest trauma (such as a cardiac stab wound) will likely cause an acute pericardial effusion due to hemorrhage.

Pericardial effusions can result in impaired cardiac filling, decreased stroke volume (the amount of blood ejected by the left ventricle [LV] with each systole), and cardiac output (CO [the amount of blood ejected by the LV each minute]).2 The hemodynamic effects occur because the heart can't fill and pump effectively.3

Compensatory mechanisms to increase CO include sympathetic nervous system activation, resulting in vasoconstriction and tachycardia. Vasoconstriction increases afterload (the pressure the LV must generate to eject blood into the aorta), which increases myocardial workload. The renin-angiotensin-aldosterone system is also activated, resulting in sodium and water retention, which increases preload (the volume of blood that stretches the ventricle at end-diastole) and additional vasoconstriction.4

The body's ability to compensate for hemodynamic compromise is limited. The more rapidly the pericardial effusion develops, the less likely it is that the body can maintain CO. If compensatory mechanisms fail, the patient can experience shock and cardiac arrest.3,5

Risk factors

Cardiac tamponade is reported to occur in 5% to 50% of patients with a cancer diagnosis.1 The risk factors for cardiac tamponade can be idiopathic, noninfectious, or infectious.5 (See Risk factors for cardiac tamponade.) Because pericardial effusions can cause cardiac tamponade, the risk factors for cardiac tamponade include the causes of pericardial effusion. Patients with metastatic mediastinal tumors are at high risk for developing cardiac tamponade. Cancers likely to metastasize to the heart include chronic myeloid leukemia, Hodgkin and non-Hodgkin lymphomas, melanoma, sarcoma, and those originating in the esophagus, lung, breast, pancreas, liver, thymus, or stomach.3

Some cancer treatments can contribute to the development of cardiac tamponade, including chemotherapy, radiation therapy, biotherapy (such as immunotherapy and gene therapy), and some surgical procedures, such as cardiac surgery valve procedures.1 Patients who've received more than 4,000 centigray (cGy) of radiation to the mediastinum are also at risk for cardiac tamponade, depending on the dose of radiation and length of treatment.1 Similarly, patients who've undergone an extrapleural pneumonectomy (a surgery-based therapy for malignant pleural mesothelioma) and who've received subsequent chemotherapy and radiation therapy are at risk.3,6,7

Iatrogenic causes of cardiac tamponade include CPR, cardiac catheterization, and transvenous pacemaker insertion.8 Acupuncture has also been reported as a cause of cardiac tamponade.3,7

Recognizing cardiac tamponade

Subacute cardiac tamponade (occurring over days to weeks) may be related to a neoplastic pericarditis or a malignant pericardial effusion.8 When pericardial effusions develop slowly, as much as 2 L (2000 mL) may accumulate without hemodynamic compromise.9 Patients with subacute cardiac tamponade may be asymptomatic until the intrapericardial pressure reaches a critical point when signs and symptoms occur.

Acute cardiac tamponade typically occurs with trauma and has a sudden onset. Less than 250 mL can cause hemodynamic compromise when pericardial effusions develop rapidly because the pericardium can't expand quickly enough to compensate.9 The onset of signs and symptoms and the degree of hemodynamic compromise depend on how rapidly the pericardial effusion develops.3 (See Signs and symptoms of cardiac tamponade.)

The three classic signs of cardiac tamponade, hypotension, muffled heart sounds, and distended neck veins, are called Beck's triad and occur only in a minority of patients with acute cardiac tamponade.5,8 Increased intrapericardial pressure and decreased CO cause hypotension. The pericardial effusion muffles heart sounds. Impaired venous return to the heart secondary to increased intrapericardial pressure causes neck vein distension.3,10

A key diagnostic sign of cardiac tamponade in patients with moderate-to-severe cardiac tamponade is pulsus paradoxus, or a large inspiratory decrease in systolic BP (greater than 10 mm Hg) during normal breathing.11 (See Effects of respiration and cardiac tamponade on ventricular filling and CO.)5 Pulsus paradoxus should also be suspected if the intensity of the patient's pulse decreases during inspiration.3,12

Diagnosing cardiac tamponade

Prompt recognition of cardiac tamponade's signs and symptoms and its rapid diagnosis are essential because delays in treatment can result in further hemodynamic compromise, possibly leading to end-organ damage and cardiac arrest.

Table
Table:
Risk factors for cardiac tamponade3,8,15,20
Table
Table:
Signs and symptoms of cardiac tamponade8

Although cardiac tamponade is a clinical diagnosis based on the patient's health history and physical assessment findings, two-dimensional and Doppler echocardiography are important in identifying the size and location of pericardial effusion and in assessing its hemodynamic significance.8,11 Transthoracic echocardiography, which is noninvasive, may be performed at the bedside.

ECG findings in a patient with cardiac tamponade frequently include sinus tachycardia and low QRS voltages.8,13 Electrical alternans (beat-to-beat alterations in the QRS complex) may also be present.8,13 (See Electrical alternans.)

Although a chest X-ray may be performed to help diagnose cardiac tamponade, at least 200 mL of pericardial fluid must be present before the cardiac silhouette enlarges.8 Computed tomography and cardiovascular magnetic resonance may also be used to help diagnose cardiac tamponade, but these studies take longer to perform than a transthoracic echocardiogram, and are more costly.3,14

Although rarely used, cardiac catheterization may be performed to diagnose cardiac tamponade. If it's used and cardiac tamponade is present, equalization of diastolic pressures will be noted. In addition, increased right-sided heart pressures and concomitant decreases in left-sided heart pressures will be revealed. A pulsus paradoxus is attributed to the latter physiologic change.8,11

Lab findings

Once the diagnosis has been made, lab tests may help identify the underlying cause of cardiac tamponade. These include a complete blood cell count, comprehensive metabolic panel, erythrocyte sedimentation rate, and thyroid panel.1 Cultures of the pericardial fluid may be performed to help determine whether an infectious source is present. The pericardial fluid may also be sent for cytology to assess for malignant cells.3,5

Management strategies

Treatment for most patients with cardiac tamponade is primarily focused on either percutaneous or surgical drainage of the pericardial effusion to relieve the elevated intrapericardial pressure and restore hemodynamic stability.8,14 Treatment options vary depending on the severity and cause of cardiac tamponade.

Percutaneous drainage

Percutaneous catheter drainage, or pericardiocentesis, with echocardiographic or fluoroscopic guidance, is indicated for severely hemodynamically unstable patients.11,15 A catheter is inserted into the pericardial space to drain the pericardial effusion. This may be followed by continuous catheter drainage.3

Preprocedure nursing care of the patient undergoing pericardiocentesis includes explaining the procedure to the patient, ensuring the patient has a patent venous access device, obtaining baseline vital signs, placing the patient in semi-Fowler position to promote fluid moving to a dependent position, and administering sedation and analgesia as prescribed.3,16

During the procedure, the nurse monitors the patient's vital signs and clinical status to assess for signs and symptoms of complications such as dysrhythmias, pneumothorax, coronary artery laceration, pulmonary laceration, right ventricular puncture, or cardiac arrest.3,16 Following pericardiocentesis, ensure that a 12-lead ECG and chest X-ray are performed. Continue to monitor vital signs and hemodynamic status until drainage is negligible (<25 mL over 24 hours), at which point the catheter is removed. Evaluate the patient's response to treatment to ensure that signs and symptoms of cardiac tamponade have resolved. Assess the catheter insertion site for signs of infection, including erythema, edema, increased warmth, pain, or purulent drainage.3,16

  • Balloon pericardiotomy. This intervention is considered for a recurrent malignant pericardial effusion. An inflatable balloon-tipped catheter is used to develop a pathway for drainage of the pericardial effusion into the mediastinum, reducing pericardial effusion recurrence.3,17,18 Nursing care of a patient undergoing balloon pericardiotomy is the same as that described for patients undergoing a pericardiocentesis.
  • Sclerotherapy. Instillation of sclerosing agents into the pericardial space after pericardiocentesis can effectively prevent recurrent pericardial effusions, but it can be very painful for patients. Instillation of sclerosing agents, such as bleomycin and doxycycline, causes scar formation, leaving no room for pericardial effusions to develop.3,14,16

Nursing care for patients undergoing sclerotherapy is the same as that described for patients undergoing pericardiocentesis. Because administration of sclerotherapy can be painful, administer sedation and analgesia as prescribed.

Surgical drainage

• Pericardiectomy involves surgical removal of the entire pericardium or a portion of it (pericardial window) via a median sternotomy or thoracotomy.15 Performed less frequently than pericardiocentesis, this procedure relieves pressure around the heart, allowing it to contract and relax more freely. A pericardiectomy is a treatment option for patients with recurrent malignant pericardial effusions and cardiac tamponade.19

Additional therapies

  • Volume repletion, or volume expansion, with agents such as blood, plasma, dextran, or saline may be needed in patients with cardiac tamponade until therapeutic pericardial effusion drainage can be performed.8
  • Inotropic agents such as dobutamine, with or without vasodilators, may be used in some patients with cardiac tamponade to help reverse hypotension.8
  • Sedation, such as midazolam, and analgesics, such as fentanyl, may be prescribed, depending on the patient's hemodynamic status.14

Nursing interventions

When signs and symptoms related to cardiac tamponade are present, call a rapid response, immediately notify the patient's healthcare provider, and prepare the patient for diagnostic testing and therapeutic interventions. Nurses have a primary role in monitoring patients for any deterioration in clinical status. Keep patients with cardiac tamponade who are hypotensive on bed rest with their legs elevated above heart level to increase venous blood return to the heart.16 Patients who aren't hypotensive should be maintained on bed rest in semi-Fowler position or leaning forward.16 Assess for respiratory distress and prepare to administer supplemental oxygen as needed. Place the patient on continuous cardiac monitoring to assess for dysrhythmias.16 Anticipate preparing the patient for emergent pericardiocentesis with echocardiographic guidance. Prepare for volume repletion with isotonic solutions such as 0.9% sodium chloride solution, or inotropic support with agents such as I.V. dobutamine, depending on the patient's hemodynamic status. Monitor intake and output closely, especially hourly urine outputs.

If the patient undergoes percutaneous pericardiocentesis, monitor and document the amount and characteristics of the drainage and obtain specimens for lab analysis as prescribed. Monitor the catheter insertion site for signs and symptoms of infection.

Patient education

After assessing patients' readiness and ability to learn, teach them the signs and symptoms (such as shortness of breath) that might indicate recurrent pericardial effusion, and whom to notify.

Patients and their families will require emotional support and education about diagnostic and therapeutic procedures. Catheter site or surgical wound care instructions should be provided, as indicated.3 Patients should be encouraged to maintain adequate hydration and nutrition and to implement strategies to promote relaxation and decrease anxiety.16

Patients also need to be instructed about when to follow up with their primary care provider or oncologist. Similarly, if a surgical procedure was performed, follow-up with the surgeon should be included.

Stay on alert

Cardiac tamponade is a potentially life-threatening complication of cancer, cancer treatment, or both. High levels of clinical suspicion are needed to identify patients at risk, recognize signs and symptoms early, and provide therapeutic interventions and supportive therapies for optimal patient outcomes.

An inside look at the normal pericardium

The pericardium forms a fibrous covering around the heart, holding it in a fixed position in the thorax and providing physical protection and a barrier to infection. The pericardium consists of a tough outer fibrous layer and a thin inner serous layer. The outer fibrous layer is attached to the great vessels that enter and leave the heart, the sternum, and the diaphragm. The fibrous pericardium is highly resistant to distension; it prevents acute dilation of the heart chambers and exerts a restraining effect on the left ventricle. The inner serous layer consists of a visceral layer and a parietal layer. The visceral layer, also known as the visceral pericardium or epicardium, covers the entire heart and great vessels and then folds over to form the parietal layer that lines the fibrous pericardium. Between the visceral and parietal layers is the pericardial cavity, a potential space that contains 30 to 50 mL of serous fluid. This fluid acts as a lubricant to minimize friction between the two layers as the heart contracts and relaxes.

Figure
Figure

Effects of respiration and cardiac tamponade on ventricular filling and CO

During inspiration, venous flow into the right heart increases, causing the interventricular septum to bulge into the left ventricle. This produces a decrease in left ventricular volume, with a subsequent decrease in stroke volume. In cardiac tamponade, the fluid in the pericardial space produces further compression of the left ventricle, causing an exaggeration of the normal inspiratory decrease in stroke volume and systolic BP.

Figure
Figure

Electrical alternans

The arrows point to each QRS complex. Note the alternating amplitude of the QRS complexes. Every other QRS complex has reduced amplitude alternating with increased amplitude. The most frequent cause of electrical alternans is a pericardial effusion.

Figure
Figure

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