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A Man in His 60s With Circulatory Collapse FREE TO VIEW

Yonatan Y. Greenstein, MD; Sameer Khanijo, MD; Mangala Narasimhan, DO, FCCP; Seth Koenig, MD, FCCP
Author and Funding Information

CORRESPONDENCE TO: Yonatan Y. Greenstein, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Hofstra North Shore-LIJ School of Medicine, 410 Lakeville Rd, Ste 107, New Hyde Park, NY 11040


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(1):e11-e16. doi:10.1016/j.chest.2015.11.007
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Published online

A man in his 60s with a medical history of compensated cirrhosis secondary to chronic hepatitis C virus infection and diabetes mellitus presented to the ED complaining of 2 days of shortness of breath and substernal chest pain radiating to his back.

In the ED, the patient had a systolic BP of 60 mm Hg, a heart rate of 110 beats/min, and a respiratory rate of 16 breaths/min; he was afebrile. Results of the rest of the physical examination were normal. His BP improved after receiving 3 L of normal saline. The results of laboratory tests at admission are presented in Table 1. His chest roentgenogram (Fig 1), ECG (Fig 2), and cardiac enzyme test results were unremarkable. A CT angiogram of the chest, abdomen, and pelvis, performed in the ED to evaluate for pulmonary embolism and aortic dissection, demonstrated neither condition. There were scattered areas of bibasilar atelectasis (Fig 3). The patient was subsequently admitted to the inpatient medical ward for further evaluation.

Table Graphic Jump Location
Table 1 Laboratory Results at Admission and 24 h After Admission

ALT = alanine aminotransferase; AST = aspartate aminotransferase.

Figure Jump LinkFigure 3 A-B, Single slice of the patient’s chest CT scan. A, Mediastinal window. B, Lung window.Grahic Jump Location

The following day, the patient again became hypotensive and lethargic, and he was transferred to the medical ICU (MICU) for further care. In the MICU, he was intubated for airway protection, a norepinephrine drip was started, blood and urine culture specimens were obtained, and the patient was given broad-spectrum antibiotics. Results of blood tests revealed worsening leukocytosis, acute kidney injury, transaminitis, and lactic acidosis (Table 1).

A focused, goal-directed ultrasound study was performed to further evaluate the patient’s state of shock and to guide management. Institutional review board approval was not obtained for this case report because all patient data are anonymous and were obtained during routine patient care activities.

Question: Based on the goal-directed ultrasound study findings, what intervention should be considered?

Answer: Pericardiocentesis

This patient presented to the MICU with a rapidly progressive state of shock requiring vasopressor support and mechanical ventilation. Acute myocardial infarction, pulmonary embolism, and an aortic dissection were ruled out on admission. Thoracic ultrasound (Videos 1-4) revealed a normal aeration pattern on the left. The right hemithorax had a diffuse B-line pattern, an alveolar consolidation, and a moderately sized pleural effusion (PLEF). The PLEF was simple without septations, and the alveolar consolidation lacked air bronchograms. Because results of diagnostic studies of the chest had been normal < 24 h earlier, the unilateral pulmonary process was most consistent with pneumonia with a parapneumonic effusion from the patient’s sepsis cascade. The goal-directed echocardiogram revealed a moderately sized pericardial effusion (PEF), which was also absent on the prior CT scan of the chest; this finding raised suspicions that the PEF may be the primary cause of the patient’s worsening state of shock. Pericardial tamponade is a clinical diagnosis made when there is evidence of PEF, shock, or impending cardiovascular collapse and suggestive echocardiographic features, such as right ventricular (RV) diastolic collapse, right atrial (RA) systolic collapse, and a plethoric inferior vena cava (IVC). However, some of these echocardiographic signs may be absent in the face of clinical tamponade when there is underlying cardiopulmonary disease (eg, significant pulmonary hypertension). In such cases, the RV chambers may not compress due to the high RV afterload, despite increased pericardial pressures.

Videos 5 through 9 show the patient’s echocardiographic examination. Video 5 is the parasternal long-axis view and shows a circumferential anechoic space surrounding the heart, which represents the PEF. When the PEF is predominately posterior, it may be confused for a PLEF. PEFs will climb anterior to the descending thoracic aorta, whereas a PLEF will dive deep to the descending aorta. Although not well visualized in this video, the RV outflow track may reveal early diastolic collapse in tamponade. The RV outflow tract is the more compressible area of the right ventricle and tends to collapse earlier than the body of the right ventricle. Video 6 is the parasternal short-axis view demonstrating normal left ventricular function with a circumferential PEF. The interventricular septum demonstrates mild flattening throughout the cardiac cycle, suggesting possible RV volume and/or pressure overload. In the context of the rapidly progressive PEF, we believed that the mild flattening was an unlikely cause for the patient’s shock state. Video 7 is the apical four-chamber view. Due to the patient’s body habitus and respiratory status, a good on-axis view was impossible. However, lateral to the left ventricle, the PEF was more echogenic, with a plankton-like appearance likely representing an inflammatory or infectious process. It was not possible from this view to determine if there was a collapse of the right-sided chambers throughout the cardiac cycle, indicative of tamponade physiology. Video 8 displays the subcostal view, which provides excellent visualization of the changes in the right atrium and ventricle when pericardial pressures exceed intracardiac pressures. Our patient’s subcostal view reveals the circumferential nature of the effusion and plankton sign, as seen in the apical four-chamber view. The right ventricle appears to be collapsed throughout the cardiac cycle. There is no evidence of RA systolic collapse. A real-time ECG tracing is helpful in determining which part of the cardiac cycle chambers are being compressed. Due to the urgency in this case, this procedure was not performed. Video 9 is an M-mode image of the IVC in the longitudinal axis just before it empties into the right atrium. It is 2.51 cm in diameter and does not vary in size with respiration. A distended IVC without variation is a universal finding in cardiac tamponade. Although it is extremely sensitive for tamponade, it is not very specific because patients may not be volume responsive, they may have preexisting pulmonary hypertension, or they may be receiving mechanical ventilation; all of these factors increase the diameter of the IVC and cause a reduction in the magnitude of respiratory variation.

Cardiac tamponade is a clinical diagnosis whereby patients classically have hypotension, tachycardia, elevated jugular venous pulsations, and a pulsus paradoxus. Tamponade physiology occurs when the pressure in the pericardium approaches or exceeds the pressure in the cardiac chambers, causing impaired cardiac filling. This outcome is best seen during the phase of the cardiac cycle in which the pressure in that chamber is lowest (ie, RA collapse during late diastole and early systole, RV collapse during diastole). RA systolic collapse is the most sensitive (70%-100%) feature of cardiac tamponade on echocardiography, and its specificity increases if it is present for more than one-third of systole. RV diastolic collapse is specific (85%-100%) but insensitive (60%-90%) for tamponade. In addition to two-dimensional echocardiography, more advanced Doppler-based measurements help quantify the visual changes that occur during goal-directed echocardiography when increased pericardial pressures are present. However, it must be stressed that a diagnosis of cardiac tamponade should not rely on any one specific two-dimensional or Doppler-derived echocardiographic finding. A distended IVC with < 50% inspiratory reduction in diameter is seen, with a sensitivity of 97% and a specificity of 40%.

The size of a PEF is classified based on distance between the visceral and the parietal pericardium during diastole: minimal, < 0.5 cm; small, 0.5 to 1.0 cm; moderate, 1.0 to 2 cm; and large, > 2 cm. Hemodynamic compromise is usually not observed until at least a moderate to large PEF is present. However, a localized PEF, as can be seen after cardiac surgery, or a rapidly expanding PEF may not follow these guidelines. Video 10 is an off-axis apical four-chamber view that demonstrates a significant amount of pericardial fluid located posteriorly.

The patient was in shock with tachycardia, evidence of RV collapse throughout the cardiac cycle, and a distended IVC. There was no evidence of RA collapse, and a pulsus paradoxus was not present. Lack of a pulsus paradoxus does not rule out cardiac tamponade because a number of conditions can lead to its absence. Given the absence of the PEF on the chest CT scan the day prior to the patient’s rapid decompensation and signs of septic shock, an ultrasound-guided pericardiocentesis was performed at the bedside by the MICU team to rule out cardiac tamponade and to sample the pericardial space. Each of the views normally obtained during the routine goal-directed echocardiogram are reviewed for the best trajectory to insert the needle. We have found that a PEF diameter > 1 cm throughout the cardiac cycle is a safe site for insertion. We do not use real-time guidance but prefer to measure the depth until penetration of the parietal pericardium and the angle of trajectory. A guidewire is inserted followed by a pericardiocentesis catheter. Agitated saline is injected to confirm placement within the pericardium. Video 11 shows the agitated saline being flushed through the intrapericardial catheter. Ultrasound-guided pericardiocentesis, which has a very low complication rate, is the procedure of choice in the MICU. A total of 800 mL of purulent fluid was removed from the pericardial space (Fig 4). Results of pericardial fluid analysis are shown in Table 2. Despite removal of the pericardial fluid, the patient’s hemodynamics did not improve, and he progressed to multiorgan failure from a disseminated staphylococcal infection. The patient died on hospital day 5.

Figure 4
Figure Jump LinkFigure 4 Purulent fluid drained from the pericardial space.Grahic Jump Location
Table Graphic Jump Location
Table 2 Results of Pericardial Fluid Analysis

Purulent pericarditis may complicate an underlying primary infection (in this case, rapidly progressive pneumonia). At autopsy, purulent pericarditis has been found in up to 13% of patients admitted to the ICU with a diagnosis of sepsis. It should be included in the differential diagnosis of patients with a PEF and undifferentiated shock with or without echocardiographic signs of tamponade physiology. These PEFs may progress rapidly to cardiac tamponade because fluid can quickly accumulate. Repeated focused echocardiograms should be performed and consideration of drainage if the PEF continues to enlarge. Similar to that seen in the present case, the presenting symptom is often fever with substernal chest pain radiating to the upper back (the phrenic nerve passes through the anterior pericardium and innervates the trapezius muscles).

  • 1.

    Echocardiography is the procedure of choice to diagnose a PEF; it allows detection and qualitative volume assessment and may shows signs of tamponade physiology.

  • 2.

    Two-dimensional echocardiographic signs of cardiac tamponade include RA systolic collapse, RV diastolic collapse, and a distended IVC.

  • 3.

    Ultrasound-guided pericardiocentesis is the procedure of choice to sample pericardial fluid.

  • 4.

    Purulent pericarditis should be included in the differential diagnosis of patients with undifferentiated shock with a PEF.

Author contributions: Y. Y. G. was responsible for data collection, primary authorship, and composition of the manuscript. S. K. was responsible for the secondary authorship and editing. M. N. and S. K. contributed to the study concept, crucial reviews, and editing. Y. Y. G. takes full responsibility for the integrity and accuracy of the data. All authors reviewed the final manuscript prior to submission.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Additional information: To analyze this case with the videos, see the online version of this article.

Cosio F.G. .Martínez J.P. .Serrano C.M. .de la Calada C.S. .Alcaine C.C. . Abnormal septal motion on cardiac tamponade with pulsus paradoxus: echocardiographic and hemodynamic observations. Chest. 1977;71:787-789 [PubMed]journal. [CrossRef] [PubMed]
 
Levitov A. .Mayo P.H. .Slonim A.D. . Echocardiographic diagnosis of cardiac tamponade.Loeb M.S..Davis K.J.. Critical Care Ultrasonography.  :135-141 [PubMed]journal
 
Otto C.M. . Pericardial disease. Textbook of Clinical Echocardiography.  :254-270 [PubMed]journal
 
Spodick D.H. . Acute cardiac tamponade. N Engl J Med. 2003;349:684-690 [PubMed]journal. [CrossRef] [PubMed]
 
Salem K. .Mulji A. .Lonn E. . Echocardiographically guided pericardiocentesis—the gold standard for the management of pericardial effusion and cardiac tamponade. Can J Cardiol. 1999;15:1251-1255 [PubMed]journal. [PubMed]
 
Arsura E.L. . Purulent pericarditis misdiagnosed as septic shock. South Med J. 1999;92:285-288 [PubMed]journal. [CrossRef] [PubMed]
 
Shiber J. . Purulent pericarditis: acute infections and chronic complications. Hosp Phys. 2008;44:9-17 [PubMed]journal
 

Figures

Figure Jump LinkFigure 3 A-B, Single slice of the patient’s chest CT scan. A, Mediastinal window. B, Lung window.Grahic Jump Location
Figure Jump LinkFigure 4 Purulent fluid drained from the pericardial space.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Laboratory Results at Admission and 24 h After Admission

ALT = alanine aminotransferase; AST = aspartate aminotransferase.

Table Graphic Jump Location
Table 2 Results of Pericardial Fluid Analysis

References

Cosio F.G. .Martínez J.P. .Serrano C.M. .de la Calada C.S. .Alcaine C.C. . Abnormal septal motion on cardiac tamponade with pulsus paradoxus: echocardiographic and hemodynamic observations. Chest. 1977;71:787-789 [PubMed]journal. [CrossRef] [PubMed]
 
Levitov A. .Mayo P.H. .Slonim A.D. . Echocardiographic diagnosis of cardiac tamponade.Loeb M.S..Davis K.J.. Critical Care Ultrasonography.  :135-141 [PubMed]journal
 
Otto C.M. . Pericardial disease. Textbook of Clinical Echocardiography.  :254-270 [PubMed]journal
 
Spodick D.H. . Acute cardiac tamponade. N Engl J Med. 2003;349:684-690 [PubMed]journal. [CrossRef] [PubMed]
 
Salem K. .Mulji A. .Lonn E. . Echocardiographically guided pericardiocentesis—the gold standard for the management of pericardial effusion and cardiac tamponade. Can J Cardiol. 1999;15:1251-1255 [PubMed]journal. [PubMed]
 
Arsura E.L. . Purulent pericarditis misdiagnosed as septic shock. South Med J. 1999;92:285-288 [PubMed]journal. [CrossRef] [PubMed]
 
Shiber J. . Purulent pericarditis: acute infections and chronic complications. Hosp Phys. 2008;44:9-17 [PubMed]journal
 
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