Obstructive shock

Last updated
Obstructive Shock
Specialty Critical Care
CausesTension pneumothorax; cardiac tamponade; Budd chiari syndrome; pulmonary embolism; abdominal compartment syndrome; severe aortic stenosis; constrictive pericarditis; SVC syndrome
Diagnostic method Thorough history and physical exam; EKG; echocardiogram; X-ray; CT angiogram
Differential diagnosis Cardiogenic shock; hypovolemic shock; distributive shock
TreatmentDepends on the cause of the obstruction

Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. [1] Obstruction can occur at the level of the great vessels or the heart itself. [2] Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. [3] These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause. [4]

Contents

The physiology of obstructive shock is similar to cardiogenic shock. In both types, the heart's output of blood (cardiac output) is decreased. This causes a back-up of blood into the veins entering the right atrium. [3] Jugular venous distension can be observed in the neck. This finding can be seen in obstructive and cardiogenic shock. With the decrease cardiac output, blood flow to vital tissues is decreased. Poor perfusion to organs leads to shock. Due to these similarities, some sources place obstructive shock under the category of cardiogenic shock. [1] [5]

However, it is important to distinguish between the two types, because treatment is different. [6] In cardiogenic shock, the problem is in the function of the heart itself. In obstructive shock, the underlying problem is not the pump. Rather, the input into the heart (venous return) is decreased or the pressure against which the heart is pumping (afterload) is higher than normal. [7] Treating the underlying cause can reverse the shock. [1] For example, tension pneumothorax needs rapid needle decompression. This decreases the pressure in the chest. Blood flow to and from the heart is restored, and shock resolves. [8]

Signs and Symptoms

As in all types of shock, low blood pressure is a key finding in patients with obstructive shock. [3] [9] In response to low blood pressure, heart rate increases. Shortness of breath, tachypnea, and hypoxia may be present. Because of poor blood flow to the tissues, patients may have cold extremities. Less blood to the kidneys and brain can cause decreased urine output and altered mental status, respectively. [9]

Other signs may be seen depending on the underlying cause. For example, jugular venous distension is a significant finding in evaluating shock. This occurs in cardiogenic and obstructive shock. This is not observed in the other two types of shock, hypovolemic and distributive. [3] Some particular clinical findings are described below.

A classic finding of cardiac tamponade is Beck's triad. The triad includes hypotension, jugular vein distension, and muffled heart sounds. Kussmaul's sign and pulsus paradoxus may also be seen. [10] Low-voltage QRS complexes and electrical alternans are signs on EKG. However, EKG may not show these findings and most often shows tachycardia. [11]

Tension pneumothorax would have decreased breath sounds on the affected side. Tracheal deviation may also be present, shifted away from the affected side. Thus, a lung exam is important. Other findings may include decreased chest mobility and air underneath the skin (subcutaneous emphysema). [12]

Pulmonary embolism similarly presents with shortness of breath and hypoxia. Chest pain worse with inspiration is frequently seen. Chest pain can also be similar to a heart attack. This is due to the right ventricular stress and ischemia that can occur in PE. [13] Other symptoms are syncope and hemoptysis. [14] DVT is a common cause. Thus, symptoms including leg pain, redness, and swelling can be present. [15] The likelihood of pulmonary embolism can be evaluated through various criteria. The Wells score is often calculated. It gives points based on these symptoms and patient risk factors. [13] [14]

Causes

Left-sided tension pneumothorax. Note the area without lung markings which is air in the pleural space. Also note the tracheal and mediastinal shift from the patient's left to right. Pneumothorax CXR.jpg
Left-sided tension pneumothorax. Note the area without lung markings which is air in the pleural space. Also note the tracheal and mediastinal shift from the patient's left to right.

Causes include any obstruction of blood flow to and from the heart. There are multiple, including pulmonary embolism, cardiac tamponade, and tension pneumothorax. Other causes include abdominal compartment syndrome, Hiatal hernia, severe aortic valve stenosis, and disorders of the aorta. Constrictive pericarditis is a rare cause. Masses can grow to press on major blood vessels causing shock. [4] [6]

Tension pneumothorax

A pneumothorax occurs when air collects in the pleural space around the lungs. Normally, this space has negative pressure to allow the lung to fill. Pressure increases as more air enters this space. [7] The lung collapses, impairing normal breathing. Surrounding structures may also shift. When severe enough to cause these shifts and hypotension, it is called a tension pneumothorax. This is life-threatening. The increased pressure inside the chest can compress the heart and lead to a collapse of the blood vessels that drain to the heart. The veins supplying the heart are compressed, in turn decreasing venous return. [7] With the heart unable to fill, cardiac output drops. Hypotension and shock ensue. If not rapidly treated, it can lead to cardiac arrest and death. [8]

Pulmonary embolism

"Saddle" embolism on CT. The filling defect in the pulmonary artery is the clot. Pulmonary Embolism.jpg
"Saddle" embolism on CT. The filling defect in the pulmonary artery is the clot.

A pulmonary embolism (PE) is an obstruction of the pulmonary arteries. [13] Deaths from PE have been estimated at ~100,000 per year in the United States. However, this may be higher in recent years. [16] Most often, the obstruction is a blood clot that traveled from elsewhere in the body. Most commonly, this is from a deep vein thrombosis (DVT) in the legs or pelvis. [13] Risk factors are conditions that increase the risk of clotting. This includes genetic (factor V Leiden) and acquired conditions (cancer). [17] Trauma, surgery, and prolonged bed-rest are common risks. Covid-19 is a recent risk factor. [18]

This obstruction increases the pulmonary vascular resistance. If large enough, the clot increases the load on the right side of the heart. The right ventricle must work harder to pump blood to the lungs. With back-up of blood, the right ventricle can begin to dilate. Right heart failure can ensue, leading to shock and death. [18]

A PE is considered "massive" when it causes hypotension or shock. A submassive PE causes right heart dysfunction without hypotension. [18]

Cardiac tamponade

Echocardiogram of cardiac tamponade. Fluid surrounding the heart impairs proper filling. This swinging of the heart causes electrical alternans seen on EKG. Pericardial effusion with tamponade.gif
Echocardiogram of cardiac tamponade. Fluid surrounding the heart impairs proper filling. This swinging of the heart causes electrical alternans seen on EKG.

A pericardial effusion is fluid in the pericardial sac. When large enough, the pressure compresses the heart. This causes shock by preventing the heart from filling with blood. This is called cardiac tamponade. The chambers of the heart can collapse from this pressure. The right heart has thinner walls and collapses more easily. With less venous return, cardiac output decreases. The lack of blood flow to vital organs can cause death. [19]

Various conditions can cause a pericardial effusion. Inflammation of the pericardium is called pericarditis. [20] This is caused by infection, [21] renal failure [22] or autoimmune disease. [23] Trauma can cause blood to fill the pericardium. Cancer can also cause effusions. [24] [25] [26] [27] Whether an effusion causes tamponade depends on the amount of fluid and how long it took to accumulate. When fluid collects slowly, the pericardium can stretch. Thus, a chronic effusion can be as large as 1 liter. [27] Acute effusions can cause tamponade when small because the tissue does not have time to stretch. [28]

Hiatal hernia

Abdominal organs particularly the stomach can escape into the thoracic cavity. Transient conditions have been known to exist. As with other causes of Obstructive shock the herniated organ can prevent the proper filling of ventricles or even atria. The Japanese documented a woman suffering from distressful cardiac symptoms that occurred sporadically, it wasn't until imaging was performed and she was allowed to actually eat food during the procedure that the staff documented a transient sliding hiatal hernia which resulted in the compression on the heart.

Diagnosis

Rapid evaluation of shock is essential given its life-threatening nature. Diagnosis requires a thorough history, physical exam, and additional tests. One must also consider the possibility of multiple types of shock being present. For example, a trauma patient may be hypovolemic from blood loss. This patient could also have tension pneumothorax due to trauma to the chest. [29]

Vital signs in obstructive shock may show hypotension, tachycardia, and/or hypoxia. A physical exam include be thorough, including jugular vein exam, cardiac and lung exams, and assessing skin tone and temperature. [29] Response to fluids may aid in diagnosis. [3] Labs including a metabolic panel can assess electrolytes and kidney and liver function. Lactic acid rises due to poor tissue perfusion. This may even be an initial sign of shock and rise before blood pressure decreases. [1] Lactic acid should lower with appropriate treatment of shock. [29] EKG should also be performed. Tachycardia is often present, but other specific findings may be present based on the underlying cause. [10] [30]

At the bedside, point-of-care echocardiography should be used. [29] This is non-invasive and can help diagnose the four types of shock. [31] Echocardiography can look for ventricular dysfunction, effusions, or valve dysfunction. [3] [32] Measurement of the vena cava during the breathing cycle can help assess volume status. [29] [31] A point-of-care echocardiogram can also assess for causes of obstructive shock. The vena cava would be dilated due to the obstruction. In pulmonary embolism, the right ventricle will be dilated. Other findings include paradoxical septal motion or clots in the right heart or pulmonary artery. Echocardiography can assess for pericardial effusion. In tamponade, collapse of the right atrium and ventricle would be seen due to pressure in the pericardial sac. [31]

A chest X-ray can rapidly identify a pneumothorax, seen as absence of lung markings. Ultrasound can show the lack of lung sliding. However, imaging should not delay treatment. [8] CT angiography is the standard of diagnosis of pulmonary embolism. Clots appear in the vasculature as filling defects. [18]

Treatment

In any type of shock, rapid treatment is essential. Delays in therapy increase the risk of mortality. This is often done as diagnostic assessment is still occurring. [29] Resuscitation addresses the ABC's - airway, breathing, and circulation. Supplemental oxygen is given, and intubation is performed if indicated. Intravenous fluids can increase blood pressure and maintain blood flow to organs. [1]

However, fluids should be given with caution. Too much fluid can cause overload and pulmonary edema. [29] In some cases, fluids may be beneficial. Fluids can improve venous return. [7] For example, tamponade prevents normal cardiac filling due to pressure compressing the heart. In this case, giving fluids can improve right heart filling. [19] [33] However, in other causes of obstructive shock, too much fluid can worsen cardiac output. Thus, fluid therapy should be monitored closely. [3]

After these stabilizing measures, further treatment depends on the cause. Treatment of the underlying condition can quickly resolve the shock. For tension pneumothorax, needle decompression should be done immediately. A chest tube is also inserted. [3] [8] Cardiac tamponade is treated through needle or surgical decompression. [3] Needle pericardiocentesis can be done at the bedside. This is often the preferred therapy. A catheter may be placed for continued drainage. [34] If these methods are not effective, surgery may be needed. Pericardial window is a surgery that is particularly in cases of cancer. [10] [35]

Massive pulmonary embolism requires thrombolysis or embolectomy. Thrombolysis can be systemic via IV alteplase (tPA) or catheter-directed. tPA works to break up the clot. A major risk of tPA is bleeding. Thus, patients must be assessed for their risk of bleeding and contraindications. Catheter-directed therapy involves giving tPA locally in the pulmonary artery. It can also fragment and remove the clot itself (embolectomy). This local therapy has a lower risk of bleeding. Surgical embolectomy is a more invasive treatment, associated with 10-20% surgical mortality risk. [18]

Related Research Articles

<span class="mw-page-title-main">Pericardium</span> Double-walled sac containing the heart and roots of the great vessels

The pericardium, also called pericardial sac, is a double-walled sac containing the heart and the roots of the great vessels. It has two layers, an outer layer made of strong inelastic connective tissue, and an inner layer made of serous membrane. It encloses the pericardial cavity, which contains pericardial fluid, and defines the middle mediastinum. It separates the heart from interference of other structures, protects it against infection and blunt trauma, and lubricates the heart's movements.

<span class="mw-page-title-main">Cardiac tamponade</span> Buildup of fluid around the heart

Cardiac tamponade, also known as pericardial tamponade, is a compression of the heart due to pericardial effusion. Onset may be rapid or gradual. Symptoms typically include those of obstructive shock including shortness of breath, weakness, lightheadedness, and cough. Other symptoms may relate to the underlying cause.

<span class="mw-page-title-main">Pleurisy</span> Disease of the lungs

Pleurisy, also known as pleuritis, is inflammation of the membranes that surround the lungs and line the chest cavity (pleurae). This can result in a sharp chest pain while breathing. Occasionally the pain may be a constant dull ache. Other symptoms may include shortness of breath, cough, fever, or weight loss, depending on the underlying cause. Pleurisy can be caused by a variety of conditions, including viral or bacterial infections, autoimmune disorders, and pulmonary embolism.

<span class="mw-page-title-main">Pericarditis</span> Medical condition

Pericarditis is inflammation of the pericardium, the fibrous sac surrounding the heart. Symptoms typically include sudden onset of sharp chest pain, which may also be felt in the shoulders, neck, or back. The pain is typically less severe when sitting up and more severe when lying down or breathing deeply. Other symptoms of pericarditis can include fever, weakness, palpitations, and shortness of breath. The onset of symptoms can occasionally be gradual rather than sudden.

<span class="mw-page-title-main">Pericardiocentesis</span> Procedure where fluid is aspirated from the pericardium

Pericardiocentesis (PCC), also called pericardial tap, is a medical procedure where fluid is aspirated from the pericardium.

Kussmaul's sign is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart dysfunction.

Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium. It consists of fever, pleuritic pain, pericarditis and/or pericardial effusion.

<span class="mw-page-title-main">Beck's triad (cardiology)</span> Medical condition

Beck's triad is a collection of three medical signs associated with acute cardiac tamponade, a medical emergency when excessive fluid accumulates in the pericardial sac around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

<span class="mw-page-title-main">Hemothorax</span> Blood accumulation in the pleural cavity

A hemothorax is an accumulation of blood within the pleural cavity. The symptoms of a hemothorax may include chest pain and difficulty breathing, while the clinical signs may include reduced breath sounds on the affected side and a rapid heart rate. Hemothoraces are usually caused by an injury, but they may occur spontaneously due to cancer invading the pleural cavity, as a result of a blood clotting disorder, as an unusual manifestation of endometriosis, in response to Pneumothorax, or rarely in association with other conditions.

Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. Pulsus paradoxus is not related to pulse rate or heart rate, and it is not a paradoxical rise in systolic pressure. Normally, blood pressure drops less precipitously than 10 mmHg during inhalation. Pulsus paradoxus is a sign that is indicative of several conditions most commonly pericardial effusion.

<span class="mw-page-title-main">Pericardial effusion</span> Medical condition

A pericardial effusion is an abnormal accumulation of fluid in the pericardial cavity. The pericardium is a two-part membrane surrounding the heart: the outer fibrous connective membrane and an inner two-layered serous membrane. The two layers of the serous membrane enclose the pericardial cavity between them. This pericardial space contains a small amount of pericardial fluid, normally 15-50 mL in volume. The pericardium, specifically the pericardial fluid provides lubrication, maintains the anatomic position of the heart in the chest, and also serves as a barrier to protect the heart from infection and inflammation in adjacent tissues and organs.

Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

<span class="mw-page-title-main">Acute pericarditis</span> Medical condition

Acute pericarditis is a type of pericarditis usually lasting less than 6 weeks. It is the most common condition affecting the pericardium.

Pleural disease occurs in the pleural space, which is the thin fluid-filled area in between the two pulmonary pleurae in the human body. There are several disorders and complications that can occur within the pleural area, and the surrounding tissues in the lung.

<span class="mw-page-title-main">Hemopericardium</span> Medical condition

Hemopericardium refers to blood in the pericardial sac of the heart. It is clinically similar to a pericardial effusion, and, depending on the volume and rapidity with which it develops, may cause cardiac tamponade.

Right atrial pressure (RAP) is the blood pressure in the right atrium of the heart. RAP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system. RAP is often nearly identical to central venous pressure (CVP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when venous tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

The Hs and Ts is a mnemonic used to aid in remembering the possible reversible causes of cardiac arrest. A variety of disease processes can lead to a cardiac arrest; however, they usually boil down to one or more of the "Hs and Ts".

<span class="mw-page-title-main">Postpericardiotomy syndrome</span> Medical condition

Postpericardiotomy syndrome (PPS) is a medical syndrome referring to an immune phenomenon that occurs days to months after surgical incision of the pericardium. PPS can also be caused after a trauma, a puncture of the cardiac or pleural structures, after percutaneous coronary intervention, or due to pacemaker or pacemaker wire placement.

<span class="mw-page-title-main">Purulent pericarditis</span> Inflammation of the sac surrounding the heart due to bacterial infection.

Purulent pericarditis refers to localized inflammation in the setting of infection of the pericardial sac surrounding the heart. In contrast to other causes of pericarditis which may have a viral etiology, purulent pericarditis refers specifically to bacterial or fungal infection of the pericardial sac. Clinical etiologies of purulent pericarditis may include recent surgery, adjacent infection, trauma, or even primary infection. The onset of purulent pericarditis is usually acute, with most individuals presenting to a medical facility approximately 3 days following the onset of symptoms.

References

  1. 1 2 3 4 5 Doerschug KC, Schmidt GA (2016). "Shock: Diagnosis and Management.". In Oropello JM, Pastores SM, Kvetan V (eds.). Critical Care. McGraw Hill. ISBN   978-0-07-182081-3.
  2. Weil MH (May 2007). "Shock: Shock and Fluid Resuscitation". Merck Manual Professional. Archived from the original on 12 February 2010.
  3. 1 2 3 4 5 6 7 8 9 Walley KR (2014). "Shock". In Hall JB, Schmidt GA, Kress JP (eds.). Principles of Critical Care (4th ed.). McGraw Hill. ISBN   978-0-07-173881-1.
  4. 1 2 Haseer Koya M, Paul M (2021). "Shock". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30285387 . Retrieved 2021-10-28.
  5. Cotran RS, Kumar V, Fausto N, Robbins SL, Abbas AK (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 141. ISBN   978-0-7216-0187-8.
  6. 1 2 Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W (November 2018). "The Nomenclature, Definition and Distinction of Types of Shock". Deutsches Ärzteblatt International. 115 (45): 757–768. doi:10.3238/arztebl.2018.0757. PMC   6323133 . PMID   30573009.
  7. 1 2 3 4 Funk DJ, Jacobsohn E, Kumar A (February 2013). "Role of the venous return in critical illness and shock: part II-shock and mechanical ventilation". Critical Care Medicine. 41 (2): 573–579. doi:10.1097/CCM.0b013e31827bfc25. PMID   23263572. S2CID   23603180.
  8. 1 2 3 4 Jalota R, Sayad E (2021). "Tension Pneumothorax". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   32644516 . Retrieved 2021-10-26.
  9. 1 2 Massaro AF (2018). "Approach to the Patient with Shock.". In Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J (eds.). Harrison's Principles of Internal Medicine (20th ed.). McGraw Hill. ISBN   978-1-259-64401-6.
  10. 1 2 3 Stashko E, Meer JM (2021). "Cardiac Tamponade". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   28613742 . Retrieved 2021-10-28.
  11. Chen LL (May 2019). "Under pressure: Acute cardiac tamponade". Nursing Critical Care. 14 (3): 35–37. doi: 10.1097/01.CCN.0000553086.79399.f0 . ISSN   1558-447X. S2CID   109167732.
  12. Roberts DJ, Leigh-Smith S, Faris PD, Blackmore C, Ball CG, Robertson HL, et al. (June 2015). "Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review". Annals of Surgery. 261 (6): 1068–1078. doi: 10.1097/SLA.0000000000001073 . PMID   25563887. S2CID   1472242.
  13. 1 2 3 4 Vyas V, Goyal A (2021). Acute Pulmonary Embolism. Treasure Island (FL): StatPearls Publishing. PMID   32809386 . Retrieved 2021-10-27.{{cite book}}: |work= ignored (help)
  14. 1 2 Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, et al. (January 2020). "2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS)". European Heart Journal. 41 (4): 543–603. doi: 10.1093/eurheartj/ehz405 . PMID   31504429.
  15. Waheed SM, Kudaravalli P, Hotwagner DT (2021). "Deep Vein Thrombosis". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   29939530 . Retrieved 2021-11-08.
  16. Martin KA, Molsberry R, Cuttica MJ, Desai KR, Schimmel DR, Khan SS (September 2020). "Time Trends in Pulmonary Embolism Mortality Rates in the United States, 1999 to 2018". Journal of the American Heart Association. 9 (17): e016784. doi:10.1161/JAHA.120.016784. PMC   7660782 . PMID   32809909.
  17. Sista AK, Kuo WT, Schiebler M, Madoff DC (July 2017). "Stratification, Imaging, and Management of Acute Massive and Submassive Pulmonary Embolism". Radiology. 284 (1): 5–24. doi:10.1148/radiol.2017151978. PMID   28628412.
  18. 1 2 3 4 5 Sakr Y, Giovini M, Leone M, Pizzilli G, Kortgen A, Bauer M, et al. (2020-09-16). "Pulmonary embolism in patients with coronavirus disease-2019 (COVID-19) pneumonia: a narrative review". Annals of Intensive Care. 10 (1): 124. doi: 10.1186/s13613-020-00741-0 . PMC   7492788 . PMID   32953201.
  19. 1 2 Kearns MJ, Walley KR (May 2018). "Tamponade: Hemodynamic and Echocardiographic Diagnosis". Chest. 153 (5): 1266–1275. doi:10.1016/j.chest.2017.11.003. PMID   29137910. S2CID   23963678.
  20. Dababneh E, Siddique MS (2021). "Pericarditis". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   28613734 . Retrieved 2021-11-08.
  21. Chang SA (November 2017). "Tuberculous and Infectious Pericarditis". Cardiology Clinics. Pericardial Diseases. 35 (4): 615–622. doi:10.1016/j.ccl.2017.07.013. PMID   29025551.
  22. Nesheiwat Z, Lee JJ (2021). "Uremic Pericarditis". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30725605 . Retrieved 2021-11-08.
  23. García-Carrasco M, Pinto CM, Poblano JC, Morales IE, Cervera R, Anaya JM (2013-07-18). "Systemic lupus erythematosus". In Anaya JM, Shoenfeld Y, Rojas-Villarraga A, Levy RA, Cervera R (eds.). Autoimmunity: From Bench to Bedside. Bogota (Colombia): El Rosario University Press.
  24. Vakamudi S, Ho N, Cremer PC (2017-01-01). "Pericardial Effusions: Causes, Diagnosis, and Management". Progress in Cardiovascular Diseases. A New Renaissance in Pericardial Diseases. 59 (4): 380–388. doi:10.1016/j.pcad.2016.12.009. PMID   28062268.
  25. Sharma NK, Waymack JR (2021). "Acute Cardiac Tamponade". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30521227 . Retrieved 2021-10-27.
  26. Imazio M, Gaita F, LeWinter M (October 2015). "Evaluation and Treatment of Pericarditis: A Systematic Review". JAMA. 314 (14): 1498–1506. doi:10.1001/jama.2015.12763. hdl: 2318/1576078 . PMID   26461998.
  27. 1 2 Ewer MS, Benjamin RS, Yeh ET (2003). "Metastatic involvement of cardiac structures". Holland-Frei Cancer Medicine (6th ed.). BC Decker.
  28. Pérez-Casares A, Cesar S, Brunet-Garcia L, Sanchez-de-Toledo J (2017-04-24). "Echocardiographic Evaluation of Pericardial Effusion and Cardiac Tamponade". Frontiers in Pediatrics. 5: 79. doi: 10.3389/fped.2017.00079 . PMC   5401877 . PMID   28484689.
  29. 1 2 3 4 5 6 7 Vincent JL, De Backer D (October 2013). "Circulatory shock". New England Journal of Medicine. 369 (18): 1726–34. doi: 10.1056/nejmra1208943 . PMID   24171518. S2CID   6900105.
  30. Chiabrando JG, Bonaventura A, Vecchié A, Wohlford GF, Mauro AG, Jordan JH, et al. (January 2020). "Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 75 (1): 76–92. doi: 10.1016/j.jacc.2019.11.021 . PMID   31918837. S2CID   210132213.
  31. 1 2 3 McLean AS (August 2016). "Echocardiography in shock management". Critical Care. 20 (1): 275. doi: 10.1186/s13054-016-1401-7 . PMC   4992302 . PMID   27543137.
  32. Ivens EL, Munt BI, Moss RR (August 2007). "Pericardial disease: what the general cardiologist needs to know". Heart. 93 (8): 993–1000. doi:10.1136/hrt.2005.086587. PMC   1994428 . PMID   17639117.
  33. Marik PE, Weinmann M (June 2019). "Optimizing fluid therapy in shock". Current Opinion in Critical Care. 25 (3): 246–251. doi:10.1097/MCC.0000000000000604. PMID   31022087. S2CID   133607214.
  34. Sagristà-Sauleda J, Mercé AS, Soler-Soler J (May 2011). "Diagnosis and management of pericardial effusion". World Journal of Cardiology. 3 (5): 135–143. doi: 10.4330/wjc.v3.i5.135 . PMC   3110902 . PMID   21666814.
  35. Adler Y, Charron P, Imazio M, Badano L, Baron-Esquivias G, Bogaert J, et al. (November 2015). "European Society of C 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the task force for the diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) endorsed by: the European Association for CardioThoracic Surgery (EACTS)". European Heart Journal. 36 (42): 2921–64. doi: 10.1093/eurheartj/ehv318 . PMC   7539677 . PMID   26320112.