cardiac tamponade(redirected from heart tamponade)
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Causes and symptoms
Causes of acute cardiac tamponade include pericarditis with effusion of serosanguineous fluid into the sac, and either surgical or accidental trauma with leakage of blood into the sac. Occasionally, anticoagulant therapy can lead to extensive bleeding around the heart and cardiac tamponade.
Excessive fluid within the pericardial sac causes pressure against the cardiac structures, interferes with ventricular and atrial filling, and compromises blood supply to the myocardium via the coronary vessels. These conditions occur because of the following events: The compressed atria cannot fill as they normally would and so less blood is available for the ventricles; thus preload (the volume of blood in the ventricles at the end of diastole) is reduced. Ventricular filling is further impaired by compression of the ventricles. As pressure within the ventricles rises because of tamponade, pressure differences between the atria and ventricles are reduced, causing the valves between the two chambers to close before the ventricles have had time to fill completely. Increasing pressure within the heart chambers and in the pericardium impinges on the coronary arteries and veins, reducing blood supply to the myocardium, slowing contractility, and further reducing cardiac output.
Clinical features of cardiac tamponade include increased central venous pressure, falling arterial blood pressure, tachycardia, faint or muffled heart sounds, a narrowing pulse pressure, and an exaggerated inspiratory fall in systolic blood pressure (pulsus paradoxus). Hypoxia of cerebral tissues can produce confusion, restlessness, agitation, panic, and a sense of impending doom. Peripheral hypoxia is signaled by changes in the color, temperature, and excessive sweating.
Diagnosis can be confirmed by echocardiography and other radiologic studies. However, if the situation is acute, these tests cannot be done without endangering the life of the patient; thus diagnosis must be based on clinical findings. Once tamponade is suspected, fluids are administered and a pericardiocentesis is done to remove the compressing fluid.
cardiac tamponadeInterference with the venous return of blood to the heart 2º to accumulation of fluids or blood in pericardium, resulting in ↑ mean right atrial pressure and near-equalization with intrapericardiac pressure, which has a wide range of clinical and hemodynamic effects Etiology 2º to dissecting aneurysm, HTN, post-MI, renal failure, pericarditis, hypothyroidism, autoimmune disease–eg, SLE, chest trauma, CA Diagnosis Echocardiogram Management Pericardiocentesis, ie needle aspiration, pericardial window
car·di·ac tam·pon·ade(kahr'dē-ak tam'pŏ-nād')
cardiac tamponadeAbnormal compression of the heart from outside. This may occur as a result of penetrating injuries or a collection of blood or fluid in the sac surrounding the heart (the PERICARDIUM). Tamponade seriously interferes with heart action and calls for urgent relief.
|Mean LOS:||4 days|
|Description:||MEDICAL: Other Circulatory System Diagnoses With CC|
Acute cardiac tamponade is a sudden accumulation of fluid in the pericardial sac leading to an increase in the intrapericardial pressure. It is a medical emergency whose outcome depends on the speed of diagnosis and treatment as well as the underlying cause. The pericardial sac surrounds the heart and normally contains only 10 to 20 mL of serous fluid. The sudden accumulation of more fluid (as little as 200 mL of fluid or blood) compresses the heart and coronary arteries, compromising diastolic filling and systolic emptying and diminishing oxygen supply. The end result is decreased oxygen delivery and poor tissue perfusion to all organs.
The incidence of cardiac tamponade in the United States is 2 cases per 10,000 individuals, and approximately 2% of penetrating injuries lead to cardiac tamponade. It is a potentially life-threatening condition, needing emergency assessment and immediate interventions. Some patients develop a more slowly accumulating tamponade that collects over weeks and months. If the fibrous pericardium gradually has time to stretch, the pericardial space can accommodate as much as 1 to 2 L of fluid before the patient becomes acutely symptomatic. Three phases of hemodynamic changes occur with acute cardiac tamponade (Table 1). Complications include decreased ventricular filling, decreased cardiac output, cardiogenic shock, and death.
|Phase 1||Accumulation of pericardial fluid leads to increased ventricular stiffness, which requires a higher filling pressure; left and right ventricular filling pressures are higher than the intrapericardial pressure during this phase|
|Phase 2||As fluid accumulates, pericardial pressure increases above the ventricular filling pressure; cardiac output thereby is reduced|
|Phase 3||Decrease in cardiac output continues due to equilibration of pericardial and left ventricular filling pressures|
Cardiac tamponade may have any of a variety of etiologies. It can be caused by both blunt and penetrating traumatic injuries and also iatrogenic injuries, such as those associated with removal of epicardial pacing wires and complications after cardiac catheterization and insertion of central venous or pulmonary artery catheters.
Rupture of the ventricle after an acute myocardial infarction or bleeding after cardiac surgery can also lead to tamponade. Other causes include treatment with anticoagulants, viral infections such as HIV, and disorders that cause pericardial irritation such as pericarditis, neoplasms tuberculosis, or myxedema, as well as collagen diseases such as rheumatoid arthritis or systemic lupus erythematosus.
Cardiac tamponade is typically not heritable, but it is more common among patients with Marfan’s syndrome or others with heritable connective tissue disease.
Gender, ethnic/racial, and life span considerations
Although a patient of any age can develop a cardiac tamponade, the very young and the elderly have fewer reserves available to cope with such a severe condition. Because trauma is the leading cause of death for individuals in the first four decades of life, traumatic tamponade is more common in that age group, whereas the older adult is more likely to have an iatrogenic tamponade. Males have higher rates of unintentional injury than do females; in children, cardiac tamponade is more common in boys than in girls with a male-to-female ratio of 7:3. Cardiac tamponade related to HIV infection is more common in young adults, whereas cardiac tamponade due to malignancy or renal failure is more often seen in elderly patients. Ethnicity and race have no known effect on the risk of cardiac tamponade, but more males than females develop pericarditis.
Global health considerations
Traumatic injury resulting in pericardial bleeding or tuberculosis resulting in pericardial effusions are the most common causes of cardiac tamponade in developing nations. Pericardial effusions most commonly result from malignancies in developed nations, but motor vehicle crashes and myocardial rupture also contribute to the prevalence.
The patient’s history may include surgery, trauma, cardiac biopsy, viral infection, insertion of a transvenous pacing wire or catheter, or myocardial infarction. Elicit a medication history to determine if the patient is taking anticoagulants or any medication that could cause tamponade as a drug reaction (procainamide, hydralazine, minoxidil, isoniazid, penicillin, methysergide, or daunorubicin). Ask if the patient has renal failure, which can lead to pericarditis and bleeding. Cardiac tamponade may be acute or accumulate over time, as in the case of myxedema, collagen diseases, and neoplasm. The patient may have a history of dyspnea and chest pain that ranges from mild to severe and increases on inspiration. There may be no symptoms at all before severe hemodynamic compromise.
The primary symptoms are related to shock: dyspnea, tachycardia, tachypnea, pallor, and cold extremities. The patient who has acute, rapid bleeding with cardiac tamponade appears critically ill and in shock. Assess airway, breathing, and circulation (ABCs), and intervene simultaneously. The patient is acutely hypovolemic (because of blood loss into the pericardial sac) and in cardiogenic shock and should be assessed and treated for those conditions as an emergency situation.
If the patient is more stable, when you auscultate the heart, you may hear a pericardial friction rub as a result of the two inflamed layers of the pericardium rubbing against each other. The heart sounds may be muffled because of the accumulation of fluid around the heart. If a central venous or pulmonary artery catheter is present, the right atrial mean pressure (RAP) rises to greater than 12 mm Hg, and the pulmonary capillary wedge pressure equalizes with the RAP. Systolic blood pressure decreases as the pressure on the ventricles reduces diastolic filling and cardiac output. Pulsus paradoxus (> 10 mm Hg fall in systolic blood pressure during inspiration) is an important finding in cardiac tamponade and is probably related to blood pooling in the pulmonary veins during inspiration. Other signs that may be present are related to the decreased cardiac output and poor tissue perfusion. Confusion and agitation, cyanosis, tachycardia, and decreased urine output may all occur as cardiac output is compromised and tissue perfusion becomes impaired.
Assessment of cardiovascular function should be performed hourly; check mental status, skin color, temperature and moisture, capillary refill, heart sounds, heart rate, arterial blood pressure, and jugular venous distention. Maintain the patient on continuous cardiac monitoring, and monitor for ST-wave and T-wave changes.
Acute cardiac tamponade can be sudden, unexpected, and life-threatening, causing the patient to experience fear and anxiety. Assess the patient’s degree of fear and anxiety, as well as her or his ability to cope with a sudden illness and threat to self. The patient’s family or significant other(s) should be included in the assessment and plan of care. Half of all patients with traumatic injuries have either alcohol or other drugs present in their systems at the time of injury. Ask about the patient’s drinking patterns and any substance use and abuse. Assess the risk for withdrawal from alcohol or other drugs during the hospitalization.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Echocardiogram||Normal size, shape, position, thickness, and movement of structures||Echo-free zone anterior to right ventricular wall and posterior to the left ventricular wall; there may also be a decrease in right ventricular chamber size and a right-to-left septal shift during inspiration||Records echoes created by deflection of short pulses of ultrasonic beam off cardiac structures; may also be done as a transesophageal procedure with transmitter inserted into esophagus (transesophageal echocardiogram)|
Other Tests: Prolonged coagulation studies and/or a decreased hemoglobin and hematocrit if the patient has lost sufficient blood into the pericardium; electrocardiogram and chest x-ray; computed tomography; arterial blood gases; creatine kinase and isoenzymes; HIV testing
Primary nursing diagnosis
DiagnosisDecreased cardiac output related to decreased preload and contractility.
OutcomesCirculation status; Cardiac pump effectiveness; Tissue perfusion: Abdominal organs and peripheral; Vital signs status; Fluid balance
InterventionsCardiac care: Acute, Fluid/electrolyte management, Fluid monitoring; Shock management: Volume, Medication administration, Circulatory care
Planning and implementation
The highest priority is to make sure the patient has adequate ABCs. If the patient suffers hypoxia as a result of decreased cardiac output and poor tissue perfusion, oxygen, intubation, and mechanical ventilation may be required. If the symptoms are progressing rapidly, the physician may elect to perform a pericardiocentesis to normalize pericardial pressure, allowing the heart and coronary arteries to fill normally so that cardiac output and tissue perfusion are restored. Assist by elevating the head of the bed to a 60-degree angle to allow gravity to pull the fluid to the apex of the heart. Emergency equipment should be nearby because ventricular tachycardia, ventricular fibrillation, or laceration of a coronary artery or myocardium can cause shock and death. Pericardiocentesis usually causes a dramatic improvement in hemodynamic status. However, if the patient has had rapid bleeding into the pericardial space, clots may have formed that block the needle aspiration. A false-negative pericardiocentesis is therefore possible and needs to be considered if symptoms continue.
The patient must be taken to surgery after this procedure to explore the pericardium and stop further bleeding. If the patient has developed sudden bradycardia (heart rate < 50 beats per minute), severe hypotension (systolic blood pressure < 70 mm Hg), or asystole, an emergency thoracotomy may be performed at the bedside to evacuate the pericardial sac, control the hemorrhage, and perform internal cardiac massage if needed. The patient may also require fluid resuscitation agents to enhance cardiac output.
|Medication or Drug Class||Dosage||Description||Rationale|
|Sympathomimetics such as dopamine hydrochloride||Varies by drug||Stimulates adrenergic receptors to increase myocardial contractility and peripheral resistance||Supports blood pressure and cardiac output in emergencies until bleeding is brought under control; only used if fluid resuscitation is initiated|
The highest nursing priority is to maintain the patient’s ABCs. Emergency equipment should be readily available in case the patient requires intubation and mechanical ventilation. Be prepared to administer fluids, including blood products, colloids or crystalloids, and pressor agents, through a large-bore catheter. Pressure and rapid-volume warmer infusors should be used for patients who require massive fluid resuscitation. A number of nursing strategies increase the rate of fluid replacement. Fluid resuscitation is most efficient through a short, large-bore peripheral intravenous (IV) catheter in a large peripheral vein. The IV should have a short length of tubing from the bag or bottle to the IV site. If pressure is applied to the bag, fluid resuscitation occurs more rapidly.
Emotional support of the patient and family is also a key nursing intervention. If the patient is awake as you implement strategies to manage the ABCs, provide a running explanation of the procedures. If blood component therapy is essential, answer the patient’s and family’s questions about the risks of hepatitis and transmission of HIV.
Evidence-Based Practice and Health Policy
Mahon, L., Bena, J.F., Morrison, S.M., & Albert, N.M. (2012). Cardiac tamponade after removal of temporary pacer wires. American Journal of Critical Care, 21(6), 432–440.
- Intensive monitoring for the first 3 hours following removal of temporary pacer wires, which are routinely placed following cardiac surgery, is recommended by the American Association of Critical-Care Nurses to identify complications, such as cardiac tamponade.
- A cross-sectional review of 23,717 medical records of patients who underwent cardiac surgery at the Cleveland Clinic in northeast Ohio revealed that reoperation for cardiac tamponade occurred in less than 1% of the sample population (9.7 cases per 10,000). In the total sample, 73% had hypertension, 47% had peripheral artery disease, 44% had a history of myocardial infarction, 10% had atrial fibrillation or flutter, and 10% had a ventricular dysrhythmia.
- Among patients who underwent reoperation for cardiac tamponade, 80% were smokers compared to 60% of those who did not have a reoperation (p = 0.06), and 48% had a history of heart failure compared to 29% of those who did not have a reoperation (p = 0.08).
- Symptoms of cardiac tamponade following removal of the temporary pacer wires in this sample included dyspnea within 4 hours of removal, hypotension, tachycardia, bleeding into the chest tube or pleural drain, and cardiac arrest. Blood pressure changes were the single most common sign, occurring in 52% of patients who required reoperation for cardiac tamponade.
- Physical findings of cardiovascular and neurological systems
- Adequacy of ABCs, mental status, skin color, vital signs, moisture of mucous membranes, capillary refill, heart sounds, presence of pulsus paradoxus or jugular venous distention, hemodynamic parameters, intake and output
- Response to interventions
- Fluid resuscitation, inotropic agents, pericardiocentesis, surgery
- Presence of complications
- Asystole, ventricular tachycardia, ventricular fibrillation; recurrence of tamponade; infection; ongoing hemorrhage