Cardiac Tamponade and Management
Cardiac Tamponade and Management
Cardiac Tamponade and Management
Rezwanul Hoque MBBS, MS, FCPS, FRCSG, FRCSEd Associate Professor Department of Cardiac Surgery BSMMU, Dhaka, Bangladesh.
Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. Cardiac tamponade is a medical emergency.
Constrictive pericarditis
scarring and consequent loss of elasticity of the pericardial sac
Effusive-constrictive pericarditis
constrictive physiology with a coexisting pericardial effusion
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The Primary abnormality is rapid or slow compression of all cardiac chambers secondary to increased intrapericardial pressure. The pericardium can stretch over time but at any instant it is inextensible making the heart compete with the increased pericardial contents for the fixed intrapericardial volume. The key elements are the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms. The true filling pressure of the heart is the myocardial transmural pressure which is intracardiac pressure minus pericardial pressure. During inspiration , the right heart increases its filling at the expense of the left heart, so that its transmural pressure transiently improves and then reverts during expiration. Much of the pressure is transmitted to the Right Vent/Atrium (lower pressure systems) which causes bulging of interventricular septum and decreased Lt ventricular compliance and filling.
The amount of pericardial fluid needed to impair the diastolic filling of the heart depends on the rate of fluid accumulation and the compliance of the pericardium. Rapid accumulation of as little as 150 mL of fluid can result in a marked increase in pericardial pressure and can severely impede cardiac output , whereas 1000 mL of fluid may accumulate over a longer period without any significant effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium over time. A more compliant pericardium can allow considerable fluid accumulation over a longer period without hemodynamic insult.
Malignancy HIV infection Infection - Viral, bacterial (tuberculosis), fungal Drugs - Hydralazine, procainamide, isoniazid, minoxidil Postcoronary intervention (ie, coronary dissection and perforation) Trauma Cardiovascular surgery (postoperative pericarditis) Postmyocardial infarction (free wall ventricular rupture, Dressler syndrome) Connective tissue diseases - Systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis Radiation therapy Iatrogenic - After sternal biopsy, transvenous pacemaker lead implantation, pericardiocentesis, or central line insertion Uremia Idiopathic pericarditis Complication of surgery at the esophagogastric junction such as antireflux surgery Pneumopericardium (due to mechanical ventilation or gastropericardial fistula)
The management of postoperative pericardial effusion is a common problem in clinical practice50% to 85% of patients develop effusion after cardiac surgery. Cardiac tamponade, the most feared complication, occurs in approximately 2% of patients and is observed even among those who have a subacute course and are beyond 7 days after surgery. The pathogenesis of postoperative effusions is not completely understood. Early effusions (within 5 to 7 days of surgery) are probably related to pericardial bleeding and perioperative trauma, whereas late effusions are considered the possible consequence of pericarditis. These late effusions often characterize the so-called postpericardiotomy syndrome reported after 10% to 45% of heart surgery cases. Massimo Imazio, Annals of int. med. February 2, 2010vol. 152 no. 3 186-187
The postpericardiotomy syndrome was initially described as a condition that followed surgery for rheumatic mitral stenosis and congenital heart defects. It is an example of the pericardial injury syndrome, a term that includes different pericardial diseases (late postmyocardial infarction pericarditis and posttraumatic and iatrogenic pericarditis) characterized by an initial insult, usually with pericardial bleeding followed 1 to 3 weeks later by pericarditis with effusion. The pathogenesis of the postpericardiotomy syndrome is presumed to be autoimmune, but alternative hypotheses implicate acquired infection. Diagnosis requires the presence of at least 2 of the following: fever lasting beyond the first postoperative week without other causes, pleuritic chest pain, friction rub, pleural effusion, and new or worsening pericardial effusion .
Massimo Imazio, Annals of int. med. February 2, 2010vol. 152 no. 3 186-187
Dyspnea, tachycardia, tachypnea Air hunger, anorexia, fatigue, dysphagia. Cold, clammy extremities Malignancy weight loss, fatigue, anorexia Chest pain pericarditis, MI Joint pain connective tissue Renal failure uremia Medications drug related lupus Recent procedure pacemaker, central line TB night sweats, fever Radiation cancer history
Becks triad
Decreasing arterial pressure, increasing venous pressure and quiet heart
Kussmaul, A, & Stern M. (1873) Pericarditis and the paradox pulse. Berl Klin Woehenscher. 8. Beck, C. (1935) Two cardiac compression triads. JAMA. 104, 714-716.
Elevated JVD
x descent is preserved y descent is decreased or absent
Kussmauls sign
This was described by Adolph Kussmaul as a paradoxical increase in venous distention and pressure during inspiration. This sign is usually observed in patients with constrictive pericarditis but occasionally is observed in patients with effusive-constrictive pericarditis and cardiac tamponade.
>10 mmHg decrease in SBP on inspiration Present in: pulmonary embolism, asthma, COPD Absent in: rapid heart rate, irregular rhythm, ASD, severe AR, regional tamponade, increased LV diastolic pressure
This is an exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure. To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present. The paradox is that while listening to the heart sounds during inspiration, the pulse weakens or may not be palpated with certain heartbeats, while S1is heard with all heartbeats.
Normal RV preload, inspiration LV preload, inspiration RV fills at expense of Pulmonary blood flow or RV free wall
Tamponade LV
Ewart sign
Also known as the Pins sign, this is observed in patients with large pericardial effusions. It is described as an area of dullness, with bronchial breath sounds and bronchophony below the angle of the left scapula.
The y descent
The y descent is abolished in the jugular venous or right atrial waveform. This is due to an increase in intrapericardial pressure, preventing diastolic filling of the ventricles.
CVS
Tachycardia Hypotension (occasionally hypertensive) Cool extremities Pericardial rub (30%) Muffled heart sounds
Other
Tachypnea with clear lung sounds Hepatomegally
Suggested diagnostic algorithm for evaluation of patients suspected to have cardiac tamponade.
Overview of the diagnosis and management of cardiac tamponade. E = early diastolic filling; ECG = electrocardiography; IVC = inferior vena cava; IVRT = isovolumic relaxation time; JVP = jugular venous pressure; LA = left atrium; RA = right atrium; RV = right ventricle.
Mayo Clin Proc. 2010 June; 85(6): 572593. doi: 10.4065/mcp.2010. 0046
Sinus Tachycardia
Low Voltage
Electrical alternans
Diffuse upsloping ST segment elevations leads II, III, AVF, and V3 to V6 ST concave upwards PR segment elevation in AVR and PR segment depression in other limb leads, V5 and V6
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Echocardiography
Pericardial effusion Collapse of right atrium and right ventricle during diastole Left atrial collapse in 25% patients Dilatation of IVC and < 50% decrease in diameter during inspiration Respiratory variation of mitral/ tricuspid velocities and RV/ LV volumes.
Swinging of the Heart with a Large Pericardial Effusion (PE), Causing Electrical Alternation and Consequent Tamponade
Swinging of the Heart with a Large Pericardial Effusion (PE), Causing Electrical Alternation and Consequent Tamponade. In Panel A, the heart swings to the right, and lead II shows a small QRS complex. In Panel B, the heart swings to the left, and the QRS complex is larger. P denotes pericardium, and LV left ventricle
Cardiac tamponade secondary to tuberculosis in a 32-year-old man with acquired immunodeficiency syndrome.
Cardiac tamponade in a newborn with respiratory distress syndrome who developed pneumopericardium associated with barotrauma from mechanical ventilation.
Pneumopericardium with cardiac tamponade in an adult patient with blunt thoracic trauma.
Monitor ABP invasively Have surgeon scrub Prep & drape patient before induction Maintain preload Maintain spontaneous ventilation Epinephrine / Dobutamine available Maintain tachycardia Avoid dramatic increase in afterload
Local General
Mask LMA ETT
SV
Awake fiberoptic Asleep blind nasal
DL f/b PPV
Oxygen Volume expansion with blood, plasma, or saline to maintain adequate intravascular volume Bed rest with leg elevation
This may help increase venous return.
1. Pericardiocentesis: Blindly in the case of an emergency With ECHO, fluoroscopy or CT guidance 2. Pericardiotomy: If the heart cannot be reached by a needle/catheter. Indicated in patients with intrapericardial bleeding, clotted hemopericardium. 3. Positive airway pressure should be avoided as it decreases cardiac output.
Pericardial window
Recurrent effusion
involves the surgical opening of a communication between the pericardial space and the intrapleural space or to the exterior. This is usually a subxiphoid approach with resection of xiphoid. Recently, a left paraxiphoidian approach with preservation of xiphoid has been described.]Open thoracotomy and/or pericardiotomy may be required in some cases.
Pericardial-peritoneal shunt Pericardiodesis - corticosteroids, tetracycline, or antineoplastic drugs can be instilled into the pericardial space sclerosing the pericardium Pericardiectomy: Resection of the pericardium (pericardiectomy) through a median sternotomy or left thoracotomy is rarely required to prevent recurrent pericardial effusion and tamponade.
Gross anatomic features of relapsing pericarditis. Left, Anterior view of fibrinous pericardium in a patient with recurrent pericarditis. Right, Thickened fibrinous pericardium after surgical pericardiectomy.
Photograph courtesy of William D. Edwards, MD. Mayo Clin Proc. 2010 June; 85(6): 572593. doi: 10.4065/mcp.2010.0046
Overview of the management of relapsing pericarditis. CMR = cardiac magnetic resonance imaging; CRP = C-reactive protein; CT = computed tomography; ESR = erythrocyte sedimentation rate; NSAID = nonsteroidal anti-inflammatory drug; WBC = white blood cell count. *Corticosteroids should not be routinely used initially unless there is a rheumatologic etiology or NSAIDs and colchicine are contraindicated.
Mayo Clin Proc. 2010 June; 85(6): 572593. doi: 10.4065/mcp.2010.0046
Intraoperative aspect.
After pericardiocentesis, leave the intrapericardial catheter in place after securing it to the skin using sterile procedure and attaching it to a closed drainage system via a 3-way stopcock. Periodically check for reaccumulation of fluid, and drain as needed. The catheter can be left in place for 1-2 days and can be used for pericardiocentesis. Serial fluid cell counts can be useful for helping discover an impending bacterial catheter infection, which could be catastrophic. If the WBC count rises significantly, the pericardial catheter must be removed immediately.
A Swan-Ganz catheter can be left in place for continuous monitoring of hemodynamics and to assess the effect of reaccumulation of pericardial fluid.
A repeat echocardiogram should be performed within 24 hours. A repeat chest radiograph should be performed within 24 hours.
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