Share this article on:

Equalization of Intracardiac Pressures in Cardiac Tamponade

Gual-Capllonch, Francisco MD; Escudero, Adrian MD; Buys, Sara MD; Bayes-Genis, Antoni MD, PhD

doi: 10.1213/ANE.0000000000001092
Cardiovascular Anesthesiology: Echo Rounds
Continuing Medical Education

From the Departments of *Cardiology and Anesthesiology, Hospital Germans Trias i Pujol, Badalona, Spain.

Accepted for publication October 4, 2015.

Funding: None.

The authors declare no conflicts of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website.

Reprints will not be available from the authors.

Address correspondence to Francisco Gual-Capllonch, MD, Hospital Germans Trias i Pujol, Crta Canyet s/n, Badalona, Barcelona, Spain. Address e-mail to fgualc@gmail.com.

The patient provided written consent for this publication. A 69-year-old woman with hypertension and paroxysmal atrial fibrillation was scheduled for catheter-based pulmonary vein ablation. The initial transthoracic echocardiogram showed mild left ventricular hypertrophy, normal left ventricular ejection fraction, no valve abnormalities, a severely dilated left atrium, and a pseudonormal left ventricle filling pattern. It also displayed an interatrial septum (IAS) aneurysm with continuous rightward bulging, reflecting left atrial pressure exceeding right atrial pressure (this feature is also seen in transesophageal echocardiogram; Fig. 1 and Supplemental Digital Content 1, Supplemental Video 1, http://links.lww.com/AA/B316). Once in the electrophysiology laboratory, the patient received general anesthesia and positive- pressure ventilation without positive end-expiratory pressure. A transesophageal probe was inserted to exclude left atrial thrombi and to monitor the atrial septal puncture and the procedure itself. Patency of the foramen ovale was assessed with an IV injection of agitated saline along with a simulated Valsalva maneuver, performed with manual inflation of the ventilation bag to achieve an airway pressure of 30 cm H2O for 5 seconds. However, the sensitivity to detect patent foramen ovale was diminished because Valsalva release failed to reverse the IAS curvature. During the pulmonary vein ablation, severe hypotension and a sudden increase in central venous pressure ensued. Transesophageal echocardiogram demonstrated a moderate pericardial effusion (12 mm between pericardial layers behind the right atrium at end diastole) and right atrial systolic free wall inversion (Figs. 2 and 3 and Supplemental Digital Content 2, Supplemental Video 2, http://links.lww.com/AA/B317). The ablation catheter crossing the IAS was immediately removed. In this situation, the IAS lost its permanent rightward bulging and alternated between left and right convexity, revealing equalization of pressures in both atria (Supplemental Digital Content 2, Supplemental Video 2, http://links.lww.com/AA/B317). Pericardiocentesis was successfully performed through a subcostal approach. When a small amount of fluid was removed, her blood pressure normalized, and the IAS curvature returned to baseline (Supplemental Digital Content 3, Supplemental Video 3, http://links.lww.com/AA/B318). A total of 260 mL blood was carefully drained, and the patient was tracheally extubated in stable hemodynamic condition after confirmation that the pericardial effusion had not recurred.

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Cardiac tamponade is a condition characterized by an increased intrapericardial pressure resulting in impaired cardiac filling. An important hemodynamic feature is the equalization of intrapericardial and mean diastolic pressures in cardiac chambers. Consequently, stroke volumes are reduced, and an exaggerated ventricular interdependence occurs as a result of a reduced and fixed intracardiac space. This results in an increase in right heart filling and a decrease in left heart filling during spontaneous inspiration along with the opposite changes during expiration.1 Mild-to-moderate pericardial effusion can cause cardiac tamponade when it rapidly expands in a noncompliant pericardium,1 as occurred in this patient. When using 2-dimensional echocardiography, the grading of pericardial effusion is semiquantitative, based on the size of the echo-free space between the parietal and the visceral pericardium at end diastole.2 Although cardiac tamponade is a clinical and hemodynamic diagnosis, echocardiography is crucial in the detection of pericardial effusion and provides additional functional assessment. The main echocardiographic signs denoting hemodynamic impairment are as follows: (1) free wall chamber inversion or collapse, when the increased intrapericardial pressure exceeds intracavitary pressure, (2) respiratory variations of intracardiac flows, reflecting exaggerated ventricular interdependence, and (3) inferior vena cava plethora, as a result of obstruction to venous return. However, no echocardiographic sign can reveal the equalization of pressures in left and right chambers. In this patient, the IAS basal curvature and its behavior in cardiac tamponade demonstrated this pathophysiologic feature.

The shape and movement of the IAS reflect the interatrial pressure difference, which becomes more apparent when the IAS is aneurysmal. An IAS aneurysm consists of redundant septal atrial tissue bulging at least 10 mm beyond the plane of the IAS.3 In normal conditions, left atrial pressure tends to be slightly higher than right atrial pressure. However, minimal pressure variations because of respiration and physiologic asynchronous atrial contraction regularly cause transient leftward bulging, which can be enhanced by the release of the Valsalva maneuver. Conversely, IAS behavior can mirror the underlying clinical condition. For example, fixed rightward curvature suggests increased pulmonary wedge pressure,4 and leftward IAS bowing can be seen in patients with increased right atrial pressures because of any reason. In the present case, continuous rightward bulging of the IAS despite the Valsalva-like maneuver and the pseudonormal filling pattern suggested a high left atrial pressure because of left ventricular diastolic dysfunction. A minimal atrial septal defect resulting from the transseptal puncture could contribute to the equalization of left and right atrial pressures and explain this IAS behavior. However, the continuous rightward bulging reappeared when pericardial effusion was removed.

General anesthesia and mechanical ventilation may hamper the assessment of cardiac tamponade, because pressure ventilation reverses the respiratory effect of intracardiac flows, interfering with some of the typical echo Doppler findings (Table 1). In this state, respiratory variation in mitral inflow is markedly attenuated as cardiac tamponade develops.5 Moreover, inferior vena cava dilatation is expected in this situation, and its inspiratory collapsibility, a better predictor of right atrial pressure than vena cava size itself, is abolished as negative intrathoracic pressure does not occur.

Table 1

Table 1

A limitation in this study is the lack of electrocardiograph tracing in the figures and videos depicted. This should be recorded routinely in all echocardiographic examinations.

In summary, this is an illustrative observation of a pathophysiologic characteristic of cardiac tamponade. IAS curvature provides qualitative information about interatrial pressure relation, which can be useful in some clinical scenarios. Different echocardiographic Doppler variables are required to assess the hemodynamic relevance of a pericardial effusion, each one with its own limitations (Table 1). In this case, IAS behavior revealed the equalization of pressures in cardiac chambers, a central feature of cardiac tamponade.

Back to Top | Article Outline

Clinician’s Key Teaching Points

By Kent H. Rehfeldt, MD, Kimberly Howard-Quijano, MD, and Martin J. London, MD

  • Cardiac tamponade results when increased intrapericardial pressure limits cardiac filling and impairs cardiac output. Under these conditions, the intrapericardial pressure and mean diastolic pressure in the cardiac chambers equalize, exaggerating ventricular interdependence and reducing stroke volume. Tamponade can occur even when a small-to-moderate pericardial effusion develops quickly in a patient with a noncompliant pericardium.
  • Echocardiographic features consistent with tamponade include inversion of cardiac chamber free walls, leftward shift of the ventricular septum during spontaneous inspiration, inferior vena cava dilation, and increased respiratory variation in intracardiac blood flow. For example, the normal decline in early mitral inflow velocity during spontaneous inspiration is magnified and may exceed 30%. However, transesophageal echocardiography assessment of tamponade during mechanical ventilation becomes more difficult as respiratory-related changes may be attenuated or abolished.
  • In this case, a patient undergoing a catheter-based ablation procedure developed hypotension with a new pericardial effusion. The interatrial septum, which had consistently bowed rightward because of increased left heart pressures in the setting of diastolic dysfunction, began to oscillate between the right atrium and left atrium indicative of an equalization of pressure between the atria. Once the tamponade was relieved, the septum again bowed consistently rightward, suggesting reduction in intrapericardial pressures.
  • Although numerous echocardiographic findings may point to the diagnosis of cardiac tamponade, in most cases, equalization of intracardiac pressures is difficult to directly visualize. Observation of interatrial septal position may enhance the assessment of the relative pressures in the atria. Echocardiographic features of tamponade that rely on respiratory-related flow changes are attenuated by mechanical ventilation and may not be apparent during intraoperative transesophageal echocardiography examinations.
Back to Top | Article Outline

DISCLOSURES

Name: Francisco Gual-Capllonch, MD.

Contribution: This author helped design the study, conduct the study, and write the manuscript.

Attestation: Francisco Gual-Capllonch approved the final manuscript.

Name: Adrian Escudero, MD.

Contribution: This author helped design the study and write the manuscript.

Attestation: Adrian Escudero approved the final manuscript.

Name: Sara Buys, MD.

Contribution: This author helped write the manuscript.

Attestation: Sara Buys approved the final manuscript.

Name: Antoni Bayes-Genis, MD, PhD.

Contribution: This author helped conduct the study and write the manuscript.

Attestation: Antoni Bayes-Genis approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.

Back to Top | Article Outline

REFERENCES

1. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684–90
2. Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, Hung J, Garcia MJ, Kronzon I, Oh JK, Rodriguez ER, Schaff HV, Schoenhagen P, Tan CD, White RD. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr. 2013;26:965–1012.e15
3. Mügge A, Daniel WG, Angermann C, Spes C, Khandheria BK, Kronzon I, Freedberg RS, Keren A, Denning K, Engberding R, Sutherland GR, Vered Z, Erbel R, Visser CA, Lindert O, Hausmann D, Wenzlaff P. Atrial septal aneurysm in adult patients. A multicenter study using transthoracic and transesophageal echocardiography. Circulation. 1995;91:2785–92
4. Royse CF, Royse AG, Soeding PF, Blake DW. Shape and movement of the interatrial septum predicts change in pulmonary capillary wedge pressure. Ann Thorac Cardiovasc Surg. 2001;7:79–83
5. Faehnrich JA, Noone RB Jr, White WD, Leone BJ, Hilton AK, Sreeram GM, Mark JB. Effects of positive-pressure ventilation, pericardial effusion, and cardiac tamponade on respiratory variation in transmitral flow velocities. J Cardiothorac Vasc Anesth. 2003;17:45–50
6. Reydel B, Spodick DH. Frequency and significance of chamber collapses during cardiac tamponade. Am Heart J. 1990;119:1160–3
    7. Sagristà-Sauleda J, Angel J, Sambola A, Alguersuari J, Permanyer-Miralda G, Soler-Soler J. Low-pressure cardiac tamponade: clinical and hemodynamic profile. Circulation. 2006;114:945–52

      Supplemental Digital Content

      Back to Top | Article Outline
      © 2016 International Anesthesia Research Society