Cardiac tamponade

Cardiac tamponade. It occurs in approximately 2 out of 10,000 people, it must be treated promptly and adequately, on which the life of the patient depends.


Clinical syndrome secondary to the accumulation of fluid in the pericardial cavity, generating an exaggerated increase in intrapericardial pressure, progressive limitation of diastolic filling and reduction of systolic volume and cardiac output.

Aspects of Pericardial Physiology

  • The pericardium normally contains 15 to 50 cc of pericardial fluid.
  • It tolerates the addition of 80 to 200 cc of liquid quickly.
  • The addition of more than 150-200 cc quickly increases markedly the intrapericardial pressure.
  • The slow accumulation of fluid allows the pericardium to distend without raising intrapericardial pressures.
  • Intrapericardial pressure is 0 or negative. Transmural distension pressure = Intracardiac pressure – Pericardial pressure.
  • The pericardium also contributes to ventricular interdependence: diastolic coupling of both ventricles.
  • The increase in intrapericardial pressure depends on several factors:

-Absolute volume of spill

-Speed ​​of liquid accumulation

-Physical characteristics of the pericardium



In tamponade as a consequence of increased intrapericardial pressure, there is an increase and equalization of diastolic pressures, with collapse of the cardiac chambers and restriction of filling flows. As compensatory mechanisms, there will be an adrenergic hyperstimulation and the RAAS system (renin-angiotensin-aldosterone). The clinical manifestations will occur as a consequence of low cardiac output and increased peripheral vascular resistance (RVP).


  • All the causes of Pericarditis and pericardial effusion can produce cardiac tamponade, the most frequent are:
  • Neoplasms
  • Viral or idiopathic pericarditis
  • Acute myocardial infarction
  • Uremic pericarditis
  • Cardiac perforation
  • Purulent pericarditis
  • Aortic dissection
  • Myxedema
  • Uremia

Risk factor’s

These factors increase the probability of developing this condition.

Clinical manifestations

  • The Beck triad is characteristic when there is an abrupt increase in intrapericardial pressure above 20 mmHg due to cardiac rupture.
  • In the rest, patients present:
  • Anxiety, restlessness
  • Chest pain: radiating to the sharp, throbbing neck, shoulders, back or abdomen, worsened by deep breathing or coughing
  • Breathing difficulty
  • Discomfort, sometimes relieved by sitting upright and leaning forward
  • Syncope , dizziness
  • Pale, grayish, or bluish skin
  • Palpitations
  • Accelerated breathing
  • Inflammation of the abdomen or other areas

Other symptoms that can occur with this disease are:

  • Vertigo
  • Drowsiness
  • Arterial hypotension
  • Weak or absent pulse

Physical exam

  • High venous pressure
  • Paradoxical pulse
  • Tachypnea
  • Tachycardia
  • Arterial hypotension
  • Still heart
  • Pericardial rub

Complementary exams

  • Chest x-ray: There are no radiographic data to validate the diagnosis of cardiac tamponade. It may be normal due to acute hemopericardium, there may be an increase in the cardiac silhouette due to pericardial effusion, but it does not indicate any typical hemodynamic involvement at this time.
  • ECG: It is neither sensitive nor specific. Pericarditis and effusion abnormalities can be seen. Electrical alternation with changes in the morphology of the QRS and the P wave, which is due to wobbles of the heart that approaches it and moves it away from the chest wall, has greater value in extreme cardiac tamponade.
  • Echocardiogram:

1. Verify the pericardial effusion.

2. It allows us the differential diagnosis with: Acute myocardial infarction of the right ventricle, constrictive pericarditis.

3. Diastolic collapse of the right atrium and right ventricle.

4. Inspiration shows an increase in the dimensions of the right ventricle and a decrease in those of the left ventricle. This is shown with the Doppler system: Increased transtricuspid flow rates and decreased transmitral (> 15%). Sometimes the decrease in transmitral flow is so great that the aortic valve closes prematurely. These variations in respiratory flow are not predictive of the hemodynamic severity of cardiac tamponade. Other findings are: Plethora of inferior cava, Pseudo hypertrophy of the left ventricle and oscillating heart.

  • Cardiac catheterization

1-It is of great value to establish the hemodynamic repercussion of cardiac tamponade.

2-Allows confirmation of cardiac tamponade.

3-Guide the pericardiocentesis.

4-Detect coexisting problems.

Other findings are:

1-Elevation of pressure in the right atrium.

2-Sine x relevant.

3-Sinus and small or absent.

4-Equality of pressures in the right atrium, right ventricle and intrapericardially. On inspiration, the intrapericardial pressure falls slightly more compared to that of the right atrium.

5-Absence of sign of the square root in the pressure curve of the right ventricle.

6-During expiration the pressure in the right atrium is somewhat higher than the intrapericardial pressure, producing a gradient that promotes filling of the right ventricle.

Differential diagnosis

  • Other causes of the classic triad (hypotension, jugular engorgement and paradoxical pulse): Pulmonary thromboembolism , tension pneumothorax, acute myocardial infarction of the right ventricle.
  • With other causes of low cardiac output or “shock” situations: septic shock, hemorrhagic shock in recent postoperative period.

– Specific signs of tamponade:

  • Diastolic collapse of the right atrium.
  • Diastolic collapse of the right ventricle.
  • Diastolic collapse of left cavities.
  • Abnormal inspiratory increase in tricuspid flow.
  • Pseudohypertrophy of the left ventricle.
  • Pendulum heart.
  • Inspiratory reduction of the E wave in the transmitral flow

Expectations (prognosis)

Tamponade is life threatening if left untreated. Results are usually good if the condition is treated promptly, but keep in mind that recurrences of this condition may occur. Complications

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