CARDIAC TAMPONADEPrepared By:

Sharmin Susiwala

“Cardiac tamponade, also known as pericardial tamponade, is an acute type of pericardial effusion in which fluid accumulates in the pericardium leads to pressure on the heart muscle which occurs when the pericardial space fills up with fluid faster than the pericardial sac can stretch.” 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.

The condition is a medical emergency

INTRODUCTION

For all patients, malignant diseases are the most common cause of pericardial tamponade

Malignant diseases - 30-60% of cases Tamponade can occur as a result of any type of

pericarditis. Pericarditis can result from the following:Human immunodeficiency virus (HIV) infection Infection - Viral, bacterial (tuberculosis), fungal

ETIOLOGY

Other causes are:Trauma to the chest(either penetrating trauma involving

the pericardium or blunt chest trauma)Drugs - Hydralazine, procainamide, isoniazid, minoxidilPostcoronary intervention - Ie, coronary dissection and

perforationAcupuncturePostcardiac percutaneous procedures – Including mitral valvuloplasty atrial septal defect (ASD) closure left atrial appendage occlusion

Cardiovascular surgery - Postoperative pericarditis Postmyocardial infarction - Free wall ventricular rupture,

Dressler syndrome Connective tissue diseases - Systemic lupus

erythematosus, rheumatoid arthritis, dermatomyositis Radiation therapy to the chest Iatrogenic – - After sternal biopsy- transvenous pacemaker lead implantation- pericardiocentesis- central line insertion- In 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.

Anticoagulation treatment Idiopathic pericarditis Complication of surgery at the esophagogastric junction

- Eg, antireflux surgery Pneumopericardium - Due to mechanical ventilation or

gastropericardial fistula Hypothyroidism Still disease Duchenne muscular dystrophy Type A aortic dissection

The outer layer of the heart is made of fibrous tissue which does not easily stretch, and so once fluid begins to enter the pericardial space, pressure starts to increase.

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

This causes obstructive shock to develop, and if left untreated then cardiac arrest may occur

PATHOPHYSIOLOGY

Dyspnea,Tachycardia,Tachypnea Dizziness, drowsiness, or palpitations Cold, clammy extremities H/0 Malignancy – weight loss, fatigue, anorexia Chest pain – pericarditis, MI MS pain – Fever , connective tissue disorder Renal failure – uremia Medications – drug related lupus Recent cardiovascular surgery, coronary

intervention, or trauma Recent procedure – pacemaker, central line TB – night sweats, fever Radiation – cancer history

SYMPTOMS

Beck triad Described in 1935, this complex of physical

findings, also called the acute compression triad. Refers to increased jugular venous pressure,

hypotension, and diminished heart sounds. These findings result from a rapid accumulation

of pericardial fluid. This classic triad is usually observed in patients

with acute cardiac tamponade.

PHYSICAL EXAMINATION

Tachycardia Distant or muffled heart sounds Hepatomegaly Evidence of chest wall trauma Pulsus paradoxsus > 12 mm Hg Pulsus paradoxus (or paradoxical pulse) is an

exaggeration (>12 mm Hg or 9%) of the normal inspiratory decrease in systemic blood pressure.

Kussmaul sign - paradoxical increase in venous distention and pressure during inspiration

Abolished y descent

Chest radiography Chest radiography findings may show cardiomegaly, a water

bottle–shaped heart, pericardial calcifications, or evidence of chest wall trauma.

DIAGNOSIS

CT scanning Reveals compression of the coronary sinus an earlier marker for

cardiac tamponade in 46% of patients.

Echocardiogram (diagnostic test of choice) Pericardial effusion Early diastolic collapse of the right ventricular free wall Late diastolic compression/collapse of the right atrium Swinging of the heart in its sac LV pseudohypertrophy

ECG ST segment changes on the ECG which may also show low voltage

QRS complexes Sinus tachycardia, PR depression,

Pulse Oximetry Respiratory variability in pulse-oximetry waveform

is noted in patients with pulsus paradoxus.

Lab Studies

Pre-hospital care Initial treatment given will usually be supportive in nature. 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.

TREATMENT

Hospital management• 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.

• 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.

Cardiogenic shock AMI Arrhythmia Heart failure Aneurysm Carditis Embolism Rupture

COMPLICATIONS