Low-pressure cardiac tamponade: A case report

Abstract

A 57-year-old woman presented with a large idiopathic pericardial effusion with subsequent cardiac tamponade, in whom the intrapericardial pressure measured by pericardiocentesis was not elevated. The patient did not present with the classical clinical features of cardiac tamponade, requiring echocardiographic follow-up to make accurate diagnosis and treatment. This entity called low-pressure cardiac tamponade has been diagnosed anecdotally being an insidious condition that requires a high degree of suspicion.

<Learning objective: Low-pressure cardiac tamponade is a clinical condition whose clinical diagnosis is highly difficult due to the dramatic loss of sensitivity of the classical clinical findings (dyspnea, tachycardia, hypotension, central venous pressure, and paradoxical pulse), making the diagnosis challenging. It requires a high index of suspicion at the echocardiographic study moment, and as in the classic cardiac tamponade many cases eventually require pericardiocentesis for confirmation and treatment.>

Case report

We present a case of a 57-year-old woman with breast carcinoma in complete remission for the past 10 years and no other relevant medical history, who was referred to the cardiology clinic after an incidental finding of an enlarged cardiac silhouette in a routine chest X-ray. The patient was asymptomatic. The physical examination was normal without venous plethora signs. The intensity of cardiac tones was decreased, but no rub, murmurs, or other extra sounds were found.

The electrocardiogram showed sinus rhythm at 60 bpm, low-voltages with phasic changes in complex amplitudes, both respiratory and electrical alternans.

Transthoracic echocardiogram (TTE) showed large pericardial effusion (PE), without adhesions or fibrin strands; M-mode analysis revealed 32 mm separation between pericardial layers; left ventricle (LV) was normal in size and systolic function; left atrium, right atrium (RA), and right ventricle (RV) were of normal size; estimated pulmonary systolic pressure was 24 mmHg. Inferior vena cava (IVC) was normal. Pulsed wave Doppler did not show significant respiratory variations in either right or left inflow and outflow tracts.

As the patient was asymptomatic with no signs of cardiac tamponade, close outpatient monitoring was recommended. Further tests ruled out any tumor recurrence. Diagnoses of metabolic disorders or thyroid disease were also discarded.

Two months later, an overall progression of PE was documented with echocardiographic signs of incipient cardiac tamponade (Fig. 1); however, she remained hemodynamically stable. Low-pressure cardiac tamponade was suspected, and the patient was admitted for pericardiocentesis.

Fig. 1.

Echocardiographic findings of cardiac tamponade. (A) Two-dimensional echocardiography in apical 4-chamber view. There is a large pericardial effusion and systolic collapse of the RA free wall during expiration (arrow). (B) M-mode detail of RA free wall collapse less pronounced during inspiration. (C) PW-Doppler at LV inflow tract showing respiratory variations of E wave peak velocities greater than 25%. (D) Subcostal M-mode showing a non-dilated IVC with normal inspiratory collapse (arrow), suggesting absence of venous plethora and compatible with normal pressures of right chambers in euvolemic situation. Exp, expiration; Insp, inspiration; LV, left ventricle; RV, right ventricle; RA, right atrial; LA, left atrial; PE, pericardial effusion; IVC, inferior vena cava.

In the catheterization laboratory, the findings consistent with low-pressure cardiac tamponade were confirmed both during pericardiocentesis and with a new TTE: IVC <10 mm and inspiratory collapse >50%; variations in pulsed wave Doppler mitral >25% and in LV outflow tract >15%; and marked expiratory collapse of RA and RV free walls during its respective diastole. A right heart catheterization with simultaneous intrapericardial pressure (IPP) recording was performed showing RV pressure: 21/1 mmHg; RA mean pressure (RAP): 5 mmHg with prominent X descent; IPP: 7 mmHg and its curve showed equalization with RAP during expiration. Respiratory phasic variations and echocardiographic signs of CT disappeared progressively with pericardial fluid removal. After pericardiocentesis of 450 mL of serous fluid the IPP decreased to 1 mmHg and RAP to 3 mmHg, with subsequent separation of IPP and RAP curves (Fig. 2). The total volume of pericardial fluid removed was 1100 mL with negative cytology and microbiological study. The patient was discharged from hospital and presented a favorable clinical course without recurrence of PE after 1 year of follow-up.

Fig. 2.

Simultaneous recording of IPP and RA pressure during pericardiocentesis: (A) Immediately after pericardial puncture, despite IPP being <7 mmHg it is higher than RA pressure. Panels (B) and (C) As pericardial fluid is removed, IPP decreases. (D) Final situation. IPP is <1 mmHg and RA curve has returned to normality. IPP, intrapericardial pressure; RA, right atrial; Exp, expiration; Insp, inspiration.

Discussion

The initial description by Antman et al. [1] of a case with low-pressure cardiac tamponade was correlated by a state of dehydration, characterized as a PE associated with severe intravascular volume depletion.

Subsequent descriptions, such as that by Boltwood et al. [2], have emphasized the important therapeutic repercussion of pericardiocentesis on cardiac output in contrast to the limited benefit of vasoactive amines and volume repletion, despite the state of hypovolemia with sufficient hemodynamic impact to generate both right cavities and LV collapse [3]. In addition, the diagnosis should be made under a high degree of clinical suspicion, owing to a dramatic lack of sensitivity in the classical clinical findings (tachycardia, hypotension, venous plethora, and arterial pulsus paradoxus), being explained by the depletion of intravascular volume [4].

As opposed to the hemodynamic status of patients initially published, our patient was euvolemic, without any comorbidity able to compromise her cardiac output. However, she did not show clinical signs of cardiac tamponade during physical examination; it was only through echocardiographic follow-up that the correct diagnosis was made.

The clinical features published by Sagristà-Sauleda et al. [5] in a retrospective registry of 29 patients with low-pressure cardiac tamponade for 19 years show many similarities with the patient presented in this case report. Low-pressure cardiac tamponade was diagnosed when IPP was <7 mmHg before pericardiocentesis and RAP become <4 mmHg after IPP had been lowered to near 0 mmHg by pericardiocentesis. Importantly, only 24% of the patients with low-pressure cardiac tamponade had the classic signs of cardiac tamponade, most of them being euvolemic, compared with 71% of the patients with conventional cardiac tamponade; there were no differences according to the prevalence of volume depletion.

A potential limitation in the present case report is that unfortunately cardiac output was not measured during the pericardiocentesis.

Low-pressure cardiac tamponade is an insidious condition that usually presents few clinical features, making its diagnosis challenging, and requiring a high index of suspicion at the moment of echocardiographic study. As it has been shown in classical cardiac tamponade, many cases eventually require pericardiocentesis for confirmation and treatment.

Conflict of interest

Authors declare no conflict of interest.