Cardiac Tamponade and Management

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Cardiac tamponade and management Dr. Md. Rezwanul Hoque MBBS, MS, FCPS, FRCSG, FRCSEd Associate Professor Department of Cardiac Surgery BSMMU, Dhaka, Bangladesh.

Transcript of Cardiac Tamponade and Management

Page 1: Cardiac Tamponade and Management

Cardiac tamponade and management

Dr. Md. Rezwanul HoqueMBBS, MS, FCPS, FRCSG, FRCSEd

Associate ProfessorDepartment of Cardiac SurgeryBSMMU, Dhaka, Bangladesh.

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Definition

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.

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Cardiac Tamponade

Pericardial compression syndromes- 3 causesCardiac tamponade

accumulation of pericardial fluid under pressure and may be acute or subacute

Constrictive pericarditisscarring and consequent loss of elasticity of the pericardial sac

Effusive-constrictive pericarditisconstrictive physiology with a coexisting pericardial effusion

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Pathophysiology

1. The Primary abnormality is rapid or slow compression of all cardiac chambers secondary to increased intrapericardial pressure.

2. 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.

3. The key elements are the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms.

4. The true filling pressure of the heart is the myocardial “transmural pressure” which is intracardiac pressure minus pericardial pressure.

5. 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.

6. 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.

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Slow vs. rapid fluid accumulationThe 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.

Spodick, D. H. N Engl J Med 2003;349:684-690

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Acute vs. Chronic

Pericardium-relatively stiff

Reserve Volume 10-20cc

Compromise volume 150cc

Slow accumulation - pericardial stretch

Volumes to 2 liters reported in chronic disease

Spodick, D. (1985) Threshold of pericardial constraint. J Am Coll Cardiol. 6, 296-297.

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Causes of Pericardial Tamponade 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)

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Postoperative pericardial effusionThe management of postoperative pericardial effusion is a common problem in clinical practice—50% 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

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Postperiocardiotomy syndromeThe 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 post–myocardial 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

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SymptomsDyspnea, tachycardia, tachypneaAir hunger, anorexia, fatigue, dysphagia.Cold, clammy extremitiesMalignancy – weight loss, fatigue, anorexiaChest pain – pericarditis, MIJoint pain – connective tissueRenal failure – uremiaMedications – drug related lupus Recent procedure – pacemaker, central lineTB – night sweats, feverRadiation – cancer history

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Cardiac Tamponade

1873 Dr. KussmaulKussmaul sign-inspiratory jugular venous distentionPulsus Paradoxus- “pulse simultaneously slight and irregular, disappearing during inspiration and reappearing upon expiration

Beck’s triadDecreasing 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.

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Elevated JVDx descent is preservedy descent is decreased or absent

Kussmaul’s 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.

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Pulsus Paradoxus

>10 mmHg decrease in SBP on inspirationPresent in: pulmonary embolism, asthma, COPDAbsent in: rapid heart rate, irregular rhythm, ASD, severe AR, regional tamponade, increased LV diastolic pressure

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Pulsus paradoxus or paradoxical pulse

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.

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Tamponade physiology

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Pulsus Paradoxus

Normal Tamponade

RV preload, inspiration

LV preload, inspiration or

RV fills at expense of RV free wall

LV

Pulmonary blood flow

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Ewart signAlso 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 descentThe 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.

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CVSTachycardiaHypotension (occasionally hypertensive)Cool extremitiesPericardial rub (30%)Muffled heart sounds

OtherTachypnea with clear lung soundsHepatomegally

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  Suggested diagnostic algorithm for evaluation of patients suspected to have cardiac tamponade.

Restrepo C S et al. Radiographics 2007;27:1595-1610

©2007 by Radiological Society of North America

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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): 572–593. doi: 10.4065/mcp.2010.0046

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World J Cardiol. 2011 May 26;3(5):135-43

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ECG

Sinus Tachycardia

Low Voltage

Electrical alternans

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Pericarditis

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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Chest X Ray

www.clinic-clinic.com

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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.

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Echocardiogram (tamponade is clinical diagnosis)

Pericardial effusionEarly diastolic collapse of the right ventricular free wallLate diastolic compression/collapse of the right atriumSwinging of the heart in its sacLV pseudohypertrophy

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Spodick, D. H. N Engl J Med 2003;349:684-690

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

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  Cardiac tamponade secondary to tuberculosis in a 32-year-old man with acquired immunodeficiency syndrome.

Restrepo C S et al. Radiographics 2007;27:1595-1610

©2007 by Radiological Society of North America

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 Cardiac tamponade in a newborn with respiratory distress syndrome who developed pneumopericardium associated with barotrauma from mechanical ventilation.

Restrepo C S et al. Radiographics 2007;27:1595-1610

©2007 by Radiological Society of North America

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  Pneumopericardium with cardiac tamponade in an adult patient with blunt thoracic trauma.

Restrepo C S et al. Radiographics 2007;27:1595-1610

©2007 by Radiological Society of North America

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Right Heart CatheterizationIf patient is stable and diagnosis is in doubt can perform a Right heart catheterization to measure Right sided pressuresIn tamponade, near equalization (within 5 mm Hg) of the right atrial, right ventricular diastolic, pulmonary arterial diastolic, pulmonary capillary wedge pressure and LV diastolic pressure( LV catheterization).Right atrial pressure tracings show abolished systolic y descent

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Anesthetic goals for tamponade

Monitor ABP invasivelyHave surgeon scrubPrep & drape patient before inductionMaintain preloadMaintain spontaneous ventilationEpinephrine / Dobutamine availableMaintain tachycardiaAvoid dramatic increase in afterload

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Anesthetic options

LocalGeneral

MaskLMAETT

SVAwake fiberopticAsleep blind nasal

DL f/b PPV

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Treatment

Oxygen Volume expansion with blood, plasma, or saline to maintain adequate intravascular volume Bed rest with leg elevation

This may help increase venous return. Inotropic drugs (i.e. dobutamine)

Choose inotropes that do not increase systemic vascular resistance while increasing cardiac output.

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Treatment

1. Pericardiocentesis: • Blindly in the case of an emergency• With ECHO, fluoroscopy or CT guidance2. 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.

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Treatment

Pericardial windowinvolves 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.

Recurrent effusion

Pericardial-peritoneal shuntPericardiodesis - corticosteroids, tetracycline, or antineoplastic drugs

can be instilled into the pericardial space sclerosing the pericardiumPericardiectomy: Resection of the pericardium (pericardiectomy)

through a median sternotomy or left thoracotomy is rarely required to prevent recurrent pericardial effusion and tamponade.

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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): 572–593. doi: 10.4065/mcp.2010.0046

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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): 572–593. doi: 10.4065/mcp.2010.0046

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Spodick, D. H. N Engl J Med 2003;349:684-690

Paraxiphoid:The needle is inserted between the xiphoid process and left costal margin.It is inserted at an angle of 15 degrees to bypass the costal margin.The hub is depressed so that it is pointed towards the left shoulder.The needle is advanced slowly until the pericardium is pierced and fluid is aspirated.A 16-18 guage sheathed needle is used to leave the sheath in the pericardial space.For prolonged drainage a pigtail angiographic catheter is placed in the pericardial space.Follow up Doppler to assess reaccumulation of fluid.

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Intraoperative aspect.

Motas C et al. Interact CardioVasc Thorac Surg 2010;10:4-5

Published by European Association for Cardio-Thoracic Surgery. All rights reserved.

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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.

After care