CARDIAC TAMPONADE

Dr. Md.Toufiqur Rahman

MBBS, FCPS, MD, FACC, FESC, FRCPE, FSCAI, FAPSC, FAPSIC, FAHA, FCCP, FRCPG

Associate Professor of CardiologyNational Institute of Cardiovascular Diseases(NICVD),

Sher-e-Bangla Nagar, Dhaka-1207

Consultant, Medinova, Malibagh branchHonorary Consultant, Apollo Hospitals, Dhaka and

STS Life Care Centre, Dhanmondi drtoufiq19711@yahoo.com

CRT 2014Washington DC, USA

CARDIAC TAMPONADE

Cardiac tamponade in the decompersated phase of cardiac compression caused by effusion accumulation and the increased intrapericardial pressure.

It is characterized by equal elevation of atrial and pericardial pressure, an exaggerated inspiratory decreased in arterial systolic pressure and arterial hypotension.

Etiology:

Infectious

In systemic autoimmune disease.

In metabolic disorders

Neoplastic

Traumatic

Causes of Pericardial Tamponade

• Malignancy• 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• Iatrogenic - After sternal biopsy, transvenous pacemaker lead implantation,

pericardiocentesis, or central line insertion• Uremia

Pericardial fluid > increase intrapericardial pressure

Intrapericardial pressure equalizes RV diastolic Pressure

Then equalizes LV diastoilic pressureDrop in cardiac output

Pathophysiology

Clinical Features : Short ness of breath, orthopnoea , cough

Chest tightness

Dysphasia

Dizziness, episodes of unconsciousness

In 60% case- cause of pericardial effusion may be a known

medical condition.

Dyspnea, Chest pain, Abdominal pain, Fatigue, Fever, Cough,

Weakness, Palpitation, Maybe in shock, thus not able to elicit

symptoms

S

YMPTOMS

Beck’s TriadS

I

G

N

S

HepatomegalyEvidence of chest wall trauma

Pulsus paradoxsus > 12 mm HgKussmaul sign - paradoxical increase

in venous distention and pressure during inspiration

S

I

G

N

S

Physical Findings :

Depends on severity of cardiac tamponade and the time course of its development.

Elevation of JVP – loss of y descent, X descent present.

Pulsus paradoxus : Pulsus paradoxus is defined as a drop in systolic blood presseur > 10 mmHg during inspiration whereas diastolic blood pressure remains unchanged. It is easily detected by feeling the pulse. During inspiration, the pulse may disappear or its volume diminishes significantly. Clinically significant pulsus paradoxus is apparent when the patient is breathing normally. The magnitude of pulsus paradoxus is evaluated by sphygmomanometry.

Arterial Hypotension

Cardiac pulsation impalpable

Diagnosis :

1) ECG:- Low voltage, BBB

Electrical alternans

Non specific ‘ ST-T’ changes

P-R segment depression.

2) CXR :- Globular cardiomegaly with sharp margins (water

bottle). Epi cardial halo- lucent line within the

cardio pericardial shadow.

3). Echo :

The separation can be detected in echocardiography when the pericardial fluid exceeds 15 –35 ml.

The size of effusion can be graded as

Small (echo free space in diastole < 10 mm)

Moderate (10-20 mm)

Large ( > 20 mm)

Very large > 20 mm and compression of the heart

1). Echo free space:

a)Posterior to LV (Small to moderate)

b)Posterior and anterior (moderate to large)

c)Behind the LA (Large to very large effusion)

2). Decreased movement of posterior pericardium

3). Brisk RV wall movements

4). Swinging heart.

5) Hemopericardium – Clotted blood

6). RV compression – Early diastolic collapse of RV

7). RA free wall indentation (collapse) during late diastole

8 ) LA free wall indentation (when fluid behind LA)

9). LV free wall paradoxic motion.

Doppler :

Generally reduced flows / stroke volume

Exaggerated inspiratory augmentation of right sided and decrease of left sided flows.

Respiratory variation in SVC and IVC flow velocities marked in tamponade.

Hepatic vein expiratory effect – marked atrial reversal.

4). Blood analyses :

a) ESR , CRP, LDH, leukocyes (inflammation markers)

b) Troponin I , CK-MB (Markers of myocardial lesion)

5). Pericardiocentesis and drainage :

PCR and histochemistry for aetiopathogenetic classification

of infection or neoplasia.

6). If previous tests in conclusive

CT

MRI

Pericardioscopy , pericardial biopsy.

low voltage, sinus tach, PR depression, electrical alternans

E

K

G

Enlarge cardiac silhouette, water bottle shaped heart

C

X

R

Pericardial effusion, collapse of the right ventricular, Swinging of the heart in its sac

ECHOCARDIOGRAM

Pericardiocentesis :

Pericardiocentesis is life saving in cardiac tamponade and indicated in effusion > 20 mm in echocardiography (diastole).

But also in smaller effusions for diagnostic purposes.( Pericardial fluid and tissue analysis, pericardioscopy and epicardial / pericardial Biopsy).

Surgical drainage is preferred in traumatic haemopericardium and purulent pericarditis.

Contraindication:

Aortic dissection

Uncorrected coagulopathy

Anticoagulant therapy

Thrombocytopenia < 50000 / mm3

Small posterior and loculated effusion.

Contraindication:

Aortic dissection

Uncorrected coagulopathy

Anticoagulant therapy

Thrombocytopenia < 50000 / mm3

Small posterior and loculated effusion.

A 16- or 18-gauge needle, angle of 30-45° to the skin, near the left xiphocostal angle, aiming towards the left shoulder

Mortality rate of approximately 4%, complication rate of 17%

Emergency subxiphoid percutaneous drainage

Complications :

Laceration or perforation of the myocardium and

coronary vessels.

Air Embolism

Pneumothorax

Puncture of the peritoneal cavity or abdominal viscera

Internal mammary artery Fistula

Acute pulmonary odema.

Cardiac Catheterization :

High pressure throughout ventricular diastole.

Near equilibration of Atrial and ventricular diastolic pressure

Atrial traces show absent or amputated Y descent

Arterial and pericardial catheters disclose exaggerated respiratory pressure fluctuations.

Absent coronary diseases

Treatment :

Definite treatment is prompt evacuation of pericardial contents.

1) pericardiocentesis

2). Surgical drainage.

Effective drainage is charecterized by :

1) Disappearance of pulsus paradoxus

2) Frequent relief of dyspnea

3) Disappearance of sign of venous engorgement

4) Reappearance of Y descents

5) Loss of vena cava plethora

6) Loss of diastolic pressure equilibration

7) Prompt loss of electrical alternans

Constrictive Pericarditis :

Constrictive pericarditis is arare but severely disabling consequence of the chronic if flammation of the pericardium in which a thickened, scarred and often pericardium limits diastolic filling of the ventricles and reduced ventricular function.

Tuberculosis

Mediastinal irradiation.

Previous cardiac surgical procedure

Connective tissue diseases.

Clinical Features:

Fatigue

Dysponea

Weight gain

Abdominal discomfort

Nausea

abdominal girth

Ocdema

Physical Finding :

Ascities

Nepato splenomegaly

Ocdema

Severe wasting

Treatment :

Pericardial is the only treatment for permanent constriction. There are two standard approaches

1). Antero lateral thoracotomy ( Fifth inter costal space)

2). Median stenotomy (Faster access to the Aorta and RA)

Complete normalization of cardiac haemodynamics is reported in only 60% of the patients.

Major complication :

1). Acute perioperative cardiac in suffiency

2). Post operative low cardiac output.

Cardiac mortality and morbidity at pericardiectomy is mainly caused by the pre- surgically unre lognised presence of myocardial atrophy or myocardial fibrosis.

Table 3 Diagnosis of cardiac tamponadeClinical presentation

Elevated systemic venous pressurea , hypotensionb, dyspnoea or tachypnoead with clear lungs

Precipiting factors Drugs (cyclosporine, anticoagulants, thrombolytics, etc), recent cardiac surgery, indwelling instrumentation, blunt chest trauma, malignancies, connective tissue disease, renal failure, septicaemiae

ECG Can be normal or non-specifically changed (ST-T wave), electrical alternans (QRS, rarely T), bradycardi (end -stage), Electromechanical dissociation (agonal phase)

Chest X-ray Enlarged cardiac silhouette with clear lungs

M mode / 2D echocardiogram

Diastole collapse of the (1) anterior RV free wall, RA collapse, LA and very rarely LV collapse, increased LV diastolic wall thickness “ pseudohypertrophy”VCI dilatation (on collapse in inspirum) “swinging heart”

Doppler Tricuspid flow flow increases and mitral flow decreases during inspiration (reverse in expiration) systole and diastolic flows are reduced in systemic veins in expirium and reverse flow with atrial contraction is increased.

M-mode Colour Doppler

Large respiratory fluctuations in mitral / tricuspid flows.

Cardiac catheterisation

(1) Confirmation of the diagnosis and quantification of the haemodynamic compromise. RA pressure is elevated (preserved systolic X descent and absent or diminished diastolic Y descent) Intrapericardial pressure is also elevated and virtually identical to RA pressure (both pressure fall in inspiration) RV mid-diastolic pressure elevated and equal to the RA and pericardial pressure ( no-and-plateau configuration) pulmonary artery diastolic pressure is slightly elevated and may correspond to the RV pressure. Pulmonary capillary wedge pressure is also elevated and nearly equal to intrapericardial and right atrial pressure. LV systolic and aortic pressures may be normal or reduced.

(2) Documenting that pericardial aspiration is followed by haemodynamic impronement(3) Detection of the coexisting haemodynamic abnormalities (LV) failure, constriction, pulmonary hypertension (4) Detection of associated cardiovascular diseases (cardiomyopathy, coronary artery disease)

RV /LV angiography

Atrial collapse and small hyperactive chambers.

Coronary angiography

Coronary compression diastole.

Computer topography

No visualisation of subepicardial fat along both ventricles, which show tube-like configuration and anteriorly drawn atrias

Examination of Pericardial Fluid

Basic Tests Hematocrit and cell count Stains: Gram, Ziehl-Nielsen, Special Cultures Viral cultures;identification of appropriate immunoglobulins

Glucose; protein Cytologic examinationImmunocytochemistry

ADDITIONAL TESTS FOR ANTICIPATED DIAGNOSES

Lactate dehydrogenase

Rheumatoid factor;antinuclear antibody

Quantitative complement levels

Cholesterol

Pathologic examination of cell blocks; cytochemical staining

pH

Amylase

Adenosine deaminase

Carcinoembryonic antigen

Inspiration Pleural pressurePulsus Paradoxus

arterial flow and pressure Pericardial pressure

? Pulmonary vascular pooling

Caval flowLV output

RA filling LV transmural pressure LV filling

RV filling pericardial pressure LV compliance

RV volume Left shift of septum

LV compression

Thank Youdrtoufiq19711@yahoo.com

Asia Pacific Congress of Hypertension, 2014, February

Cebu city, Phillipines

Seminar on Management of Hypertension, Gulshan, Dhaka