Cardiac tamponade

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S Ramyar Ghandriz MD[3]

Cardiac tamponade is a medical emergency condition in which fluid/blood accumulates in the pericardium (the sac in which the heart is enclosed). The elevated pericardial pressure puts significant pressure on the heart, causing a decrease in the diastolic filling of the ventricles, and hence in stroke volume. The end result is ineffective pumping of blood, shock, and potentially death. It is caused mainly by the accumulation of a large or uncontrolled pericardial effusion. 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. Common causes of increased pericardial effusion include hypothyroidism, trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and ventricular rupture. It should be differentiated from tension pneumothorax, hypovolemia and acute congestive heart failure. Patients with cardiac tamponade may present with sudden onset of chest pain, palpitations, breathlessness and lightheadedness. Physical examination may show the classic Beck’s triad (hypotension, muffled heart sound, and elevated jugular venous distension), tachycardia, pulsus paradoxus, and pericardial rub depending on the type, and severity of tamponade. The electrocardiogram in cardiac tamponade usually demonstrates sinus tachycardia, and may sometimes show reduced QRS voltage and electrical alternans. Chest X ray will demonstrate pneumopericardium and cardiac silhouette changes. Echocardiography findings include pericardial effusion, diastolic compression of the RV, diastolic compression of the right atrium (RA), plethora of the inferior vena cava and paradoxical septal motion. Pericardiocentesis can provide a diagnostic sampling of pericardial fluid and can be used as a therapeutic maneuver to evacuate pericardial fluid and lower the pericardial pressure.

Cardiac tamponade is a very common emergent manifestation, which can be caused by traumatic injuries, since the emulation of the disease tracks back to centuries ago. Acknowledgment of existing pericardial is first done by hippocrates, which was continued by Galen to describing what is now known as pericardial effusion.

Cardiac tamponade is an emergency form of cardiac effusion. it is more over classified by the pathological causes. The management of emergent situation is not very differed by the basic cause.

Cardiac tamponade 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 occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml can cause tamponade. However, if the volume of the fluid accumulation is too rapid and or large, then the hemodynamic compromise can occur with a rise in pericardial pressure. This in turn reduces stroke volume, and eventually, cardiac output. If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to a decreased stroke volume.

Cardiac tamponade is caused by the accumulation of a large or uncontrolled pericardial effusion. 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. Common causes of increased pericardial effusion include hypothyroidism, trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and ventricular rupture.

The initial diagnosis of cardiac tamponade can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, hypovolemia and acute congestive heart failure. The differential diagnosis of cardiac tamponade differs based on the type of cardiac tamponade (either acute or subacute).

The cardiac tamponade is most often attributed to the rupture of an acute myocardial infarction or an intrapericardial rupture of a dissecting ascending aortic aneurysm. In developed countries malignancy is the leading cause of cardiac tamponade secondary to pericardial effusion. The incidence of cardiac tamponade based on a giant sample size of about 216 million emergency admissions was about 115,638(0.05%). The incidence of cardiac tamponade increases with age; the mean age was around 61.9. Cardiac temponade mortality rate is significantly different due to its underlying cause.

Most potent risk factors for cardiac tamponade include heart surgeries, cardiac myxomas, myocardial infarction and traumas.

Cardiac tamponade is more of a clinical diagnosis. If the patient clinical manifestation was raising suspicious toward tamponade, CT scan and echocardiogram are diagnostic gold standards for the disease.

Cardiac tamponade is a life-threatening condition requiring urgent intervention to remove the pericardial fluid. Complications include pulmonary edema, cardiac failure, cardiogenic shock and ultimately death.

Cardiac tamponade has a good prognosis if detected early and treated immediately. Short-term survival is mostly dependent on early diagnosis and relief of tamponade. Long-term survival depends upon the prognosis of the underlying cause, irrespective of the mode of treatment.

Cardiac tamponade is more of a clinical diagnosis, but still some diagnostic studies may be helpful.

Patients with cardiac tamponade may present with sudden onset of chest pain, palpitations, breathlessness and lightheadedness. Presentation vary with the cause and acuteness of development of tamponade. An acute cardiac tamponade follows trauma to the chest or rupture of the aorta or heart. A subacute cardiac tamponade occurs in the setting of a neoplasm or renal failure. A low pressure cardiac tamponade occurs in patients who are hypovolemic secondary to hemorrhage or over diuresis.

Physical examination may vary depending on the type of cardiac tamponade. Physical examination may show the classic Beck’s triad (hypotension, muffled heart sound, and elevated jugular venous distension), tachycardia, pulsus paradoxus, and pericardial rub depending on the type, and severity of tamponade. Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure.

Non-specific markers of inflammation are generally elevated in pericarditis. This include the CBC, elevated C-reactive protein, ESR. The cardiac troponin is elevated if there is injury to the underlying myocardium, a condition termed myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.

The electrocardiogram in cardiac tamponade usually demonstrates sinus tachycardia, and may sometimes show reduced QRS voltage and electrical alternans.

Cardiac tamponade is a clinical diagnosis, however chest X ray can be helpful sometimes. It will demonstrate pneumopericardium and cardiac silhouette changes.

The role of echocardiography in the evaluation of the patient with pericarditis is to characterize the presence, size, location and hemodynamic impact of a pericardial effusion. Tamponade is characterized by pericardial effusion, diastolic compression of the RV, diastolic compression of the right atrium (RA), plethora of the inferior vena cava and paradoxical septal motion.

A CT scan is not commonly used for the diagnosis of cardiac tamponade as it is effectively diagnosed based on clinical features and echocardiography. Findings on CT include [Superior vena cava]] andInferior vena cava enlargement, Hepatic and renal vein enlargment, periportal edema, reflux of contrast material, collapse of the right atrium, Pericardial thickening.

Cardiovascular MRI is not commonly used for the diagnosis of cardiac tamponade as it is effectively diagnosed based on clinical features and echocardiography. Findings include Pericardial effusion, distension of the vena cavae and hepatic vein, collapse of the right sided cardiac chambers, interventricular septum shifts towards the left, paradoxical septal motion.

There are no other imaging findings associated with cardiac tamponade.

There are no other diagnostic studies associated with cardiac tampnoade.

If the patient is symptomatic, and if there are signs of cardiac tamponade, urgent pericardiocentesis should be performed. Additional supportive therapy includes the administration of oxygen, fluid repletion, echocardiographic monitoring, treatment of underlying pathology, reversal of anticoagulation and monitoring.

Percutaneous pericardiocentesis is a procedure where fluid is aspirated from the pericardium (the sac enveloping the heart) using a needle via a percutaneous approach. Pericardiocentesis can provide a diagnostic sampling of pericardial fluid and can be used as a therapeutic maneuver to evacuate pericardial fluid and lower the pericardial pressure.

There are no established measures for the primary prevention of cardiac tamponade.

There are no established measures for the secondary prevention of cardiac tamponade.

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Template:Infobox Anatomy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The pericardium is a double-walled sac that contains the heart and the roots of the great vessels.

There are two layers to the pericardial sac: the fibrous pericardium and the serous pericardium. The serous pericardium, in turn, is divided into two layers, the parietal pericardium, which is fused to and inseparable from the fibrous pericardium, and the visceral pericardium, which is in fact the epicardium, or the outer surface of the heart.

In between the parietal and visceral pericardial layers there is a potential space called the pericardial cavity. It is normally lubricated by a film of pericardial fluid. Too much fluid in the cavity (such as in a pericardial effusion) can result in pericardial tamponade, which refers to compression of the heart within the pericardial sac.

There are two small chambers or sinuses are located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.

The pericardial sinuses are:

• Oblique pericardial sinus
• Transverse pericardial sinus

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• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

Template:WikiDoc Sources CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S. Ramyar Ghandriz MD[3]

Cardiac tamponade 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 occurs rapidly (as may occur after trauma or myocardial rupture) as little as 100 ml can cause tamponade. However, if the volume of the fluid accumulation is too rapid and or large, then the hemodynamic compromise can occur with a rise in pericardial pressure. This in turn reduces stroke volume, and eventually, cardiac output. If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to a decreased stroke volume.

• The pericardium is made up of two layers^[1][2][3][4]
  • Fibrous pericardium
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno-pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.

• There are two small chambers or sinuses located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.^[5][6][7]

• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal mesocardium rupture embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon the normal collapse of the thorax

• The outer pericardium is made of fibrous tissue which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase. This causes obstructive shock to develop, and if left untreated, cardiac arrest may occur (in which case the presenting rhythm is likely to be Pulseless electrical activity). ^[8][9][10].

• Ordinarily, drainage from the pericardium occurs via the thoracic duct and the right lymphatic duct into the right pleural space. In the absence of disease, the normal pericardium contains only 20-50 cc of serous fluid due to ultrafiltration from the blood. Up to about 75 cc can accumulate acutely in the pericardium without hemodynamic compromise. Much greater amounts of fluid can accumulate chronically over a prolonged period of time as the pericardial sac stretches slowly to accommodate the fluid without hemodynamic compromise. However, if the volume of the fluid accumulation is too rapid and or large, then the hemodynamic compromise can occur with a rise in pericardial pressure. This in turn reduces stroke volume, and eventually, cardiac output.

• If fluid continues to accumulate, then with each successive diastole, less and less blood enters the ventricles, as the increasing pressure presses on the heart and forces the septum to bend into the left ventricle, leading to a decreased stroke volume.

Below is a video demonstrating hemorrhagic effusion leading to cardiac tamponade. {{#ev:youtube|QwgfuDegC5Y}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.

Cardiac tamponade is caused by the accumulation of a large or uncontrolled pericardial effusion. 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. Common causes of increased pericardial effusion include hypothyroidism, trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and ventricular rupture.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Any cause of pericardial effusion capable of compromising the hemodynamic status of a patient is potentially life threatening.^[1][2]

The most common cause of cardiac tamponade include the following^{[3][4][5][6][7][8][9]}

• Ascending aortic dissection
• Collagen vascular diseases
• Iatrogenic – central line insertion, pacemaker insertion, coronary interventions, myocardial biopsy
• Idiopathic
• Malignancy – breast cancer, Kaposi’s sarcoma, lung cancer, lymphomas
• Penetrating trauma
• Pericarditis

Bacteria – pneumococcus, streptococcus, staphylococcus

Fungus – blastomyces, cryptococcus, histoplasma, pneumocystis carinii

Tuberculous

Virus – coxsackie virus, echovirus, CMV

• Post myocardial infarction treatment – heparin, thrombolytics
• Radiation
• Uremia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.D. [2]Ramyar Ghandriz MD[3]

The initial diagnosis of cardiac tamponade can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, hypovolemia and acute congestive heart failure. The differential diagnosis of cardiac tamponade differs based on the type of cardiac tamponade (either acute or subacute).

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.^[1] Other acute disorders that cardiac tamponade must be distinguished from include:

• Aortic dissection
• Congestive heart failure
• Hypovolemia
• Pulmonary embolus
• Right ventricular myocardial infarction
• Tension pneumothorax

• Constrictive pericarditis
• Congestive heart failure
• Cirrhosis

Signs of classical cardiac tamponade include three signs, known as Beck’s triad. Hypotension occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid inside the pericardium.^[2]

Other signs of tamponade include pulsus paradoxus (a drop of at least 10mmHg in arterial blood pressure on inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs & symptoms of shock (such as tachycardia, breathlessness and decreasing level of consciousness).

Echocardiography, which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. Tamponade can often be diagnosed radiographically, if time allows and the chest x-ray may show a large, globular heart if the pericardial effusion is large.

The following table outlines the major differential diagnoses of Shock on the basis of clinical manifestations..^{[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40]}

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]

The cardiac tamponade is most often attributed to the rupture of an acute myocardial infarction or an intrapericardial rupture of a dissecting ascending aortic aneurysm. In developed countries malignancy is the leading cause of cardiac tamponade secondary to pericardial effusion.The incidence of cardiac tamponade based on a giant sample size of about 216 million emergency admissions was about 115,638(0.05%). The incidence of cardiac tamponade increases with age; the mean age was around 61.9. Cardiac temponade mortality rate is significantly different due to its underlying cause.

• The incidence of cardiac tamponade based on a giant sample size of about 216 million emergency admissions was about 115,638(0.05%)^[1][2][3][4]

• Cardiac temponade mortality rate is significantly different due to its underlying cause.^[5][1][6]
• Overall, hospitalized mortality rate is around 14.3% and sub groups with higher mortality are :
  1. Sepsis (odds ratio:3.17)
  2. Chest trauma (odds ratio:2.15)
  3. Metastatic cancer:(odds ratio:1.90)
  4. Acute kidney injury(odds ratio:1.91)
  5. Idiopathic pericarditis (odds ratio: 0.21, least cause of mortality)

• The incidence of cardiac tamponade increases with age; the mean age was around 61.9.^[1][7]

• There is no racial predilection to cardiac tamponade.

• Cardiac tamponade affects men and women equally.
• There is no study suggesting a meaningful sex difference among diagnosed patients.

• It needs around 12 days of hospitalization and a mean cost of $160,397.

• The leading cause of developing tamponade in developed countries is cancer.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]

Cardiac tamponade is a life-threatening condition requiring urgent intervention to remove the pericardial fluid. Complications include pulmonary edema, cardiac failure, cardiogenic shock and ultimately death.

Cardiac tamponade has a good prognosis if detected early and treated immediately. Short-term survival is mostly dependent on early diagnosis and relief of tamponade. Long-term survival depends upon the prognosis of the underlying cause, irrespective of the mode of treatment.

• Because of restrictive manners of cardiac tamponade , it causes acute heart failure and increase in blood hydro-static pressure.^[1]
• In severe forms, increase in hydro-static pressure and decompensated left and right heart failure causes pulmonary edema, low blood pressure,low brain blood supply and eventually death.

Cardiac tamponade is a life-threatening condition requiring urgent intervention to remove the fluid from the pericardial cavity. If untreated, the patient may develop the following complications^[2]:

• Pulmonary edema due to decreased forward flow of blood from the left ventricle and increased pressures within the pulmonary vasculature.
• Cardiac failure secondary to inadequate ventricular filling and cardiac output.
• Cardiogenic shock
• Pulseless electrical activity
• Death

• The prognosis of cardiac tamponade depends upon tow factors:

1. The underlying condition
2. duration of diagnosis and treatment

• The prognosis of a cardiac tamponade is typically good with early recognition and management of the condition and the underlying causes of the tamponade. 3.2% of the total deaths over a 10-year period were attributable to cardiac tamponade in a postmortem study of 14,368 patients in County of Cornwall, UK between 1995 and 2004.^[3]
• Cardiac tamponade caused by central venous catheters had a mortality rate of 77% before 1980 and 47% between 1980-1989^[4].
• Patients with underlying malignancy has the highest rate of mortality^[5]. Short-term survival is mostly dependent on early diagnosis and relief of tamponade. Long-term survival depends upon the prognosis of the underlying cause, irrespective of the mode of treatment^[2].

• Tamponade secondary to idiopathic effusion and penetrating chest wounds has been shown to be associated with better outcomes with emergent removal of pericardial fluid.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.

If the patient is symptomatic, and if there are signs of cardiac tamponade, urgent pericardiocentesis should be performed. Additional supportive therapy includes the administration of oxygen, fluid repletion, echocardiographic monitoring, treatment of underlying pathology, reversal of anticoagulation and monitoring.

• There is not much pre-hospital care that can be provided other than general treatment for shock which includes intravenous fluids.
• Some pre-hospital providers will have facilities to provide pericardiocentesis, but this is generally futile if the patient has already suffered a cardiac arrest before arrival of the healthcare professional. ^[1]Rapid evacuation to a hospital equiped to perform invasive procedures is usually the more appropriate course of action.

Tamponade presents as a spectrum of illness. There is not much debate about the course of management in the treatment of the very sick or the asymptomatic patient with a large effusion who has no signs or symptoms of cardiac tamponade. The course of treatment is often debated in those patients with echocardiographic evidence of tamponade but no clinical findings. A prudent strategy in these cases is to observe the progression of the disease process and intervene at the onset of any evidence of compromise. Volume repletion, serial echocardiographic and clinical assessment is warranted in these cases.

• Watchful monitoring of a patient’s clinical status
• Serial echocardiography
• Volume repletion (saline, plasma, or blood)
• Treatment of underlying etiology and reversal of anticoagulation
• The role of ionotropic agents is unclear

If the patient is symptomatic and has signs of cardiac tamponade the initial management in the hospital setting is by urgent pericardiocentesis. ^[2] This involves aspirating the fluid by inserting a needle through the skin and into the pericardium. Often, a cannula is left in place during resuscitation following initial drainage so that additional fluid can continue to drain. If there is distortion of anatomy, a small effusion, or if the effusion is loculated or located posteriorly, an emergency pericardial window may be performed instead. ^[3] This procedure involves cutting the pericardium open to allow the fluid to drain. Following stabilization of the patient, surgery is provided to seal the source of the bleed and mend the pericardium.

Nitroglycerin

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