Pericardial tamponade I31.9

Pericardial tamponade is a serious, acutely life-threatening event that results in obstruction of the filling of all heart cavities (Kühl 2004).

The presence of large amounts of fluid, blood coagulation and/or gas in the pericardial gap leads to an excessive increase in intrapericardial pressure with gradual compression of the right and, in the further course, also of the left heart cavities (Kühl 2004).

With this clinical picture, there is always the risk of sudden circulatory collapse or cardiogenic shock, up to and including pulseless electrical activity (PEA).

In case of a rapid effusion formation, the critical exudate quantity is about 300 - 400 ml (Herold 2018). According to van Aken (2007), even an acute iatrogenic bleeding of only 100 ml can lead to a life-threatening pericardial tamponade.

If the pericardial tamponade develops slowly, the amount of fluid can possibly increase to more than 2000 ml (Kasper 2015).

Pericardial tamponade occurs very rarely (Fritze 2012). According to Erdmann (2009), up to one third of patients with asymptomatic, extensive and chronic pericardial effusion develop pericardial tamponade in the further course of the disease.

Pericardial tamponade can occur in the following diseases:

• Pericarditis (most common cause [Kasper 2015])
• traumatic
• Uremia
• Neoplasia
• Tuberculosis
• other bacterial infections
• Collagenoses
• Vasculitides
• within the framework of a radio station
• acute myocardial infarction (especially under anticoagulation)
• Postpericardiotomy syndrome (heart catheter, myocardial biopsy, pacemaker system, after heart surgery, under anticoagulation, after thrombolysis, etc.)

The obstruction of the filling during diastole leads to a reduced or missing Y-drop in the atrial pressure curve. Equilibration of the diastolic pressure values ultimately leads to premature closure of the AV valves. In early diastole, the intrapericardial pressure briefly exceeds the intracavitary pressure. This mechanism occurs initially only in the right atrium and ventricle, and later also in the left atrium. This leads to a collapse of the thin-walled parts of the heart (atria, right ventricle and the right ventricular outflow tract) (Kühl 2004).

The clinical symptoms of pericardial tamponade are not determined by the size of the effusion, but rather by the restriction of hemodynamics (van Aken 2007).

Three main features of pericardial tamponade are also referred to as the so-called "Beck Triad" ( Kasper 2015). These include:

1. silent to absent heart sounds
2. arterial hypotension
3. increased venous pressure with bulging vessels at the base of the tongue and in the area of the jugular veins (differential diagnosis good to distinguish from volume deficiency shock with collapsed veins).

In addition, may occur (Herold 2018):

• Pulsus paradoxus (inspiratory decrease in blood pressure amplitude by more than 10 mmHg; however, also occurs in patients with tension pneumothorax, armoured heart, pulmonary embolism and severe asthma attack).
• Kussmaul sign (inspiratory pressure increase of the jugular vein; is an indication of epicardial constriction [Schoeneberger 2008])
• Oliguria
• Tachycardia

With slowly developing pericardial tamponade, symptoms more closely resemble heart failure with:

• Orthopnea
• Dyspnea
• Tachypnea
• Liver enlargement possibly with upper abdominal discomfort due to liver capsular tension (Kasper 2015)
• small ascites (Herold 2018)
• Reduced performance
• Dysphagia
• Cough
• Hoarseness
• Singultus
• retrosternal pain, sometimes dependent on position and/or respiration
• load-dependent syncope

In pericardial tamponade, echocardiography shows:

• a so called "swinging heart" with insufficient contractions due to the lack of expansion possibility
• a collapse of the right atrium, later also of the left atrium and the right ventricle
• a pseudoprolapse (van Aken 2007)

The extent of effusion is echocardiographically divided into (Maisch 2008):

• small effusion (the anechoic diastolic separation of peri- and epicardium is < 10 mm)
• moderate effusion (diastolic separation is between 10mm - 20 mm)
• large effusion (diastolic separation is more than 20 mm)
• very large effusion (diastolic separation is more than 20 mm and there are additional signs of compression).

Important clues to the hemodynamic relevance of an effusion can be obtained from the diastolic flow profiles across the mitral and tricuspid valves. Reciprocal respiratory effects typical of tamponade can be demonstrated (Kühl 2004):

• over the mitral valve there is an inspiratory decrease of the maximum velocity of the E wave (abrupt decrease of more than 25% )
• over the tricuspid valve there is an inspiratory increase of the velocity of the E-wave (increase of more than 40%)
• in the expiratory phase exactly the opposite conditions are shown
• during expiration a clear reflux into the hepatic veins is detectable

ECG: In the ECG, the following changes are seen in pericardial tamponade (Kühl 2004):

• the amplitude of the QRS complex decreases (peripheral or central low voltage)
• electrical alternans of P-waves, QRS complexes and T-waves, caused by the anatomical position of the heart changing from beat to beat (Herold 2018)
• Tachycardia
• concave ST segment elevation and PR segment depression (indication of pericarditis)

In the case of an acute pericardial tamponade, the following diseases can be excluded by differential diagnosis:

• acute pulmonary embolism
• acute right heart attack

The ECG and echocardiography provide the decisive indications here.

• Aortic dissection
• Pneumothorax

other causes for a state of shock (Schönenberger 2008):

• pericarditis
• Pleuritis

In the case of a chronic pericardial tamponade, the following diseases can be excluded by differential diagnosis:

• different causes of right heart failure (pulmonary hypertension, e.g. due to an obstructive ventilation disorder)
• restrictive cardiomyopathies
• ischaemic heart failure
• Pulmonary venous occlusive diseases (PVOD)
• intracardiac tumors

Here, imaging diagnostics are of greater importance (Kühl 2004).

In any unclear state of shock, pericardial tamponade should be excluded (Kühl 2004). Pericardial tamponade is an absolute indication for emergency or urgent ultrasound-guided pericardiocentesis. In special cases surgical drainage (EG-D) may also be necessary (Schoenenberger 2008).

In ultrasound-guided pericardiocentesis, the optimal puncture site should be determined beforehand by echocardiography. By injecting echo contrast medium into the puncture needle, its correct position in the pleural gap can be checked before inserting the drainage catheter. In most cases, access to the pericardium through a subxiphoidal puncture is chosen, since the greatest possible safety and success rate can then be expected. The puncture needle should be guided flat below the thoracic wall at an angle of 15 degrees towards the left shoulder or along the left sternal margin.

Even the relief of small amounts of fluid in acute pericardial tamponade often leads to a significant clinical improvement for the patient. With large effusion volumes (> 1,000 ml), however, relief should only be gradual, otherwise there is a risk of acute right ventricular dilatation (Schoenenberger 2008).

Indications for surgical intervention e.g. pericardiotomy, pericardial windowing (Schoenenberger 2008):

• secured tamponade from which no fluid can be aspirated (e.g. in the case of a localised effusion)
• after aspiration there is no clinical improvement
• traumatic or iatrogenic tamponades (e.g. after myocardial biopsy, pacemaker electrode insertion, etc.)
• in case of a relapse with rapid refilling
• postoperative tamponade
• purulent pericarditis
• Tamponade for aortic dissection or myocardial rupture

For further diagnostics, the removed puncture should be examined in the laboratory chemically, immunologically, molecularly, microbiologically and cytologically for the cause of the tamponade (Maisch 2008).

Contraindication (van Aken 2007):

• Aortic dissection (absolute contraindication; there is a risk of secondary lethal rupture)
• The presence of coagulopathy is a relative contraindication and must be decided on a case-by-case basis in this life-threatening clinical picture

Complications (Kühl 2004):

• Perforation of the right ventricle
• Malfunction of the inferior vena cava or liver veins
• Laceration of a vein or artery of the coronary vessels
• Tension Pneumopericardium
• Tension pneumothorax
• in up to 5%, life-threatening complications occur despite optimal conditions and implementation (Erdmann 2009)

Monitoring: When monitoring the patient after the intervention in the intensive care unit, measurements of heart rate, blood pressure and clinical signs of tamponade should be controlled or monitored for at least 24 hours. In the first period after the procedure, regular control chocardiographies are recommended.

The intrapericardial catheter can be left in situ for several days for repeated aspirations or instillation of drugs (Schoenenberger 2008)

Drug therapy: In the literature, the drug supply with positive inotropic substances in patients with pericardial tamponade who show considerable hypotension is controversially discussed. Volume administration for hypotension is generally indicated. However, there is also the danger of an acceleration or reinforcement of the existing tamponade (Marx 2015).

The prognosis of pericardial tamponade depends on the duration and severity of hemodynamic compromise. In case of early discharge, the prognosis is generally good with regard to the consequences of this compromise; otherwise the underlying disease influences the further prognosis (Marx 20015). An aortic dissection or a rupture in myocardial infarction as the cause of pericardial tamponade usually ends lethally very quickly (Schoenenberger 2008).

In non-malignant effusions, a recurrence is to be expected in up to 25% - 30% of cases. Close echocardiographic monitoring is therefore recommended (Marx 2015).

1. van Aken H et al (2007) Intensive Care Medicine. Georg Thieme Publisher SS 190-193
2. Angstwurm M et al. (2014) Mediscript StaR: The state exam revision course for the Hammer exam. Elsevier Urban and Fischer publishing house. 92
3. Erdmann E (2009) Clinical Cardiology: Diseases of the heart, the circulation and the vessels near the heart. Springer Publishing House SS 363-365
4. Fritze J et al. (2012) The medical review: legal issues, functional tests, assessments. Springer Publishing House SS 371-376
5. Gerabek W E et al (2007) Encyclopedia of the History of Medicine. Volume 1 Walter de Gruyter Publisher S 583
6. Herold G et al (2018) Internal Medicine. Herold Publisher S 235
7. Kühl H P et al (2004) Acute and chronic constrictive pericarditis. The internist 45: 573-586
8. Maisch B et al (2008) New possibilities for the diagnosis and therapy of pericarditis. The internist 49: 18-25
9. Marx G et al (2015) Intensive care medicine. Springer Publishing House SS 660-667
10. Schoenenberger R A et al. (2008) Internistic emergencies: Safe through the acute situation and the following 48 hours. Thieme Publishing House SS 77-79
11. Zerkowski H R et al (2006) HerzAkutMedizin: A manual for the cardiological, anaesthesiological and internal medicine practice. Steinkopff Publishing House Darmstadt S 49