A very large hemorrhagic pericardial effusion due to malignancy as seen on ultrasound which was causing tamponade. closed arrow: the heart, open arrow: the effusion
|Classification and external resources|
|Patient UK||Cardiac tamponade|
Cardiac tamponade, also known as pericardial tamponade, is a type of pericardial effusion in which fluid, pus, blood, clots, or gas accumulates in the pericardium (the sac in which the heart is enclosed), resulting in slow or rapid compression of the heart.
Cardiac tamponade is pressure on the heart muscle which occurs when the pericardial space fills up with fluid faster than the pericardial sac can stretch. If the amount of fluid increases slowly (such as in hypothyroidism) the pericardial sac can expand to contain a liter or more of fluid prior to tamponade occurring. If the fluid effusion occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 mL can cause tamponade.
Myocardial rupture is a somewhat uncommon cause of pericardial tamponade. It typically happens in the subacute setting after a heart attack, in which the infarcted muscle of the heart thins out and tears. Myocardial rupture is more likely to happen in elderly individuals without any previous cardiac history who suffer from their first heart attack and are not revascularized either with thrombolytic therapy or with percutaneous coronary intervention or with coronary artery bypass graft surgery.
One of the most common settings for cardiac tamponade is in the first 24 to 48 hours after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade. Nurses will frequently clear clots from the tubes, but even with these efforts chest tubes can become clogged.
Cardiac tamponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium. This commonly occurs as a result of chest trauma (both blunt and penetrating), but can also be caused by myocardial rupture, cancer, uremia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissection, or whilst the patient is taking anticoagulant therapy. The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances.
Causes of increased pericardial effusion include hypothyroidism, physical trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and myocardial rupture. One of the most common causes is heart surgery, when post operative bleeding fails to be cleared by clogged chest tubes.
If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. Eventually, increasing pressure on the heart forces the septum to bend in towards the left ventricle, leading to a decrease in stroke volume. This causes the development of obstructive shock, which if left untreated may lead to cardiac arrest (often presenting as pulseless electrical activity).
Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure. In a trauma patient presenting with PEA (pulseless electrical activity) in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade.
Signs of classical cardiac tamponade include three signs, known as Beck's triad. Low blood pressure occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid buildup inside the pericardium.
Other signs of tamponade include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs and symptoms of shock (such as fast heart rate, shortness of breath and decreasing level of consciousness). However, some of these signs may not be present in certain cases. A fast heart rate, although expected, may be absent in people with uremia and hypothyroidism.
In addition to the diagnostic complications afforded by the wide-ranging differential diagnosis for chest pain, diagnosis can be additionally complicated by the fact that patients will often be weak or faint at presentation. For instance, a fast rate of breathing and difficulty breathing on exertion that progresses to air hunger at rest can be a key diagnostic symptom, but it may not be possible to obtain such information from patients who are unconscious or who have convulsions at presentation.
Tamponade can often be diagnosed radiographically. Echocardiography, which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. A large cardiac tamponade will show as an enlarged globular-shaped heart on chest x-ray. During inspiration, the negative pressure in the thoracic cavity will cause increased pressure into the right ventricle. This increased pressure in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. At the same time, right ventricle volume is markedly diminished and sometimes it can collapse.
Initial treatment given will usually be supportive in nature, for example administration of oxygen, and monitoring. There is little care that can be provided pre-hospital other than general treatment for shock. A number of the Helicopter Emergency Medical Services (HEMS) in the UK, which have doctor/paramedic teams, have performed an emergency thoracotomy to release clotting in the pericardium caused by a penetrating chest injury.
Prompt diagnosis and treatment is the key to survival with tamponade. Some pre-hospital providers will have facilities to provide pericardiocentesis, which can be life-saving. If the patient has already suffered a cardiac arrest, pericardiocentesis alone cannot ensure survival, and so rapid evacuation to a hospital is usually the more appropriate course of action.
Initial management in hospital is by pericardiocentesis. This involves the insertion of a needle through the skin and into the pericardium and aspirating fluid under ultrasound guidance preferably. This can be done laterally through the intercostal spaces, usually the fifth, or as a subxiphoid approach. A left parasternal approach begins 3 to 5 cm left of the sternum to avoid the left internal mammary artery, in the 5th intercostal space. Often, a cannula is left in place during resuscitation following initial drainage so that the procedure can be performed again if the need arises. If facilities are available, an emergency pericardial window may be performed instead, during which the pericardium is cut open to allow fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.
In heart surgery patients post op, the nurses monitor the amount of chest tube drainage. If the drainage volume drops off, and the blood pressure goes down, this can suggest tamponade due to chest tube clogging. In that case, the patient is taken back to the operating room for an emergency reoperation.
If aggressive treatment is offered immediately and no complications arise (shock, AMI or arrhythmia, heart failure, aneurysm, carditis, embolism, or rupture), or they are dealt with quickly and fully contained, then adequate survival is still a distinct possibility.
- Spodick, DH (Aug 14, 2003). "Acute cardiac tamponade.". The New England Journal of Medicine 349 (7): 684–90. doi:10.1056/NEJMra022643. PMID 12917306.
- Forauer AR, Dasika NL, Gemmete JJ, Theoharis C (Feb 2003). "Pericardial tamponade complicating central venous interventions". J Vasc Interv Radiol. 14 (2 Pt 1): 255–9. doi:10.1097/01.RVI.0000058329.82956.5c. PMID 12582195.
- Meniconi, A; C H ATTENHOFER JOST; R JENNI (Nov 2000). "How to survive myocardial rupture after myocardial infarction". Heart 84 (5): 552–552. doi:10.1136/heart.84.5.552. PMC 1729480. PMID 11040020.
- Porth, Carol; Carol Mattson Porth (2005). Pathophysiology: concepts of altered health states (7th ed.). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-4988-3.
- Gwinnutt CL, Driscoll PA (2003). Trauma Resuscitation: The Team Approach (2nd ed.). Oxford: BIOS. ISBN 1-85996-009-X.
- Isselbacher EM, Cigarroa JE, Eagle KA (Nov 1994). "Cardiac tamponade complicating proximal (retrograde) aortic dissection. Is pericardiocentesis harmful?". Circulation 90 (5): 2375–8. doi:10.1161/01.CIR.90.5.2375. PMID 7955196.
- Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan (2004). Oxford handbook of clinical medicine (6th ed.). Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-852558-3.
- Patton KT, Thibodeau GA (2003). Anatomy & physiology (5th ed.). St. Louis: Mosby. ISBN 0-323-01628-6.
- American College of Surgeons Committee on Trauma (2007). Advanced Trauma Life Support for Doctors, 7th Edition. Chicago: American College of Surgeons
- Holt L, Dolan B (2000). Accident and emergency: theory into practice. London: Baillière Tindall. ISBN 0-7020-2239-X.
- Shlamovitz, Gil (4 August 2011). "Pericardiocentesis". Medscape. Retrieved 16 August 2011.
- Yarlagadda, Chakri (11 August 2011). "Cardiac Tamponade Treatment & Management". Medscape. Retrieved 16 August 2011.
- Synovitz C.K., Brown E.J. (2011). Chapter 37. Pericardiocentesis. In Tintinalli J.E., Stapczynski J, Ma O, Cline D.M., Cydulka R.K., Meckler G.D., T (Eds), Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e. Retrieved September 19, 2014 from http://accessmedicine.mhmedical.com/content.aspx?bookid=348&Sectionid=40381499.