Interstital Lung Disease and Pericardial Effusion/Tamponade

Today's case centred around an elderly woman who had presented to hospital with imaging findings of diffuse interstitial lung disease and a large pericardial effusion.  There were a lot of really good learning points:

-We spend a lot of time looking after people with multiple medical problems who are on quite a number of medications.  It is always good practice to review their conditions and medications to ensure they are on all appropriate medications (we had a good discussion about primary prevention with ASA) and that they are off inappropriate medications (PPI’s are the usual culprits).

-We talked about constitutional symptoms which are frequently overlooked in the history. These are: the presence of fever, loss of greater than 10% of total body weight in 6 months, drenching night sweats (we usually ask if they need to change their clothes at night), and anorexia.  These are important because they are suggestive of a systemic process such as an infection, a malignancy, or a connective tissue disease.

-This patient was found on imaging to have a pericardial effusion.  The first question concern around anyone with a large (or small) pericardial effusion is related to pericardial tamponade.  This is a process through which fluid accumulating in the rigid pericardium impairs the ability of (mainly) the right heart to fill.  Physical examination and other findings and their rationale are as follows:

• ·      Elevated JVP due to high transmitted intracardiac pressures to the neck veins
• ·      A sharp X-descent due to rapid right atrial filling with an abrupt stop during ventricular systole (you can picture the ventricle contracting leaving a momentary reduction in atrial pressure as it occupies less space)
• ·      Muffled heart sounds due to impaired transmission through pericardial fluid
• ·      Hypotension due to impending obstructive shock from the inability to fill the RV
• ·      Pulsus Paradoxus – a reduced systolic blood pressure during inspiration

o   The pulsus paradoxus is actually a misnomer because it occurs in healthy individuals, just to a lesser extent.

o   There are two postulated mechanisms for the pulsus paradoxus – many sources quote that inspiration leads to a fall in intrathoracic pressure, leading to an increase in RA/RV inflow, leading to bowing of the septum and encroachment of the LV’s ability to fill.  The problem with this explanation is that (1) you do not see bowing of the septum when you look at the heart of someone in tamponade with an echocardiogram and (2) a pulsus paradoxus is actually commonly caused by other things such as asthma and COPD exacerbations

o   The other explanation is that, in order for blood to flow from your pulmonary veins into your left atrium, the pressure in the pulmonary veins must exceed the pressure in your left atrium.  If you either have high pressure in your left atrium (as in cardiac tamponade) or very low pressure in your pulmonary veins (as in an asthma exacerbation in which someone is generating negative intrathoracic pressures) then you impair venous return to the heart during inspiration.  This also explains why people do not get a pulsus paradoxus with cardiac tamponade if they have an atrial septal defect.

·      The JAMA Rational Clinical Examination Series looked at Cardiac Tamponade – helpful things to rule in or out tamponade were:

o   Pulsus paradoxus > 10mmHg (LR+ 5.9, LR- 0.03)

o   Tachycardia (77% sensitive)

·     Echocardiographic findings are supportive if they show the right atrium and later the right ventricle collapsing during inspiration.  Cardiac tamponade is a clinical diagnosis meaning that the clinical picture does not always correspond with the echocardiographic one.

We also talked about interstitial lung disease given that this patient’s chest radiograph showed diffuse reticular-nodular patterns.  Some people divide the differential diagnosis into upper lobe predominant disease (cystic fibrosis, sarcoidosis, tuberculosis, silicosis, ankylosing spondylitis, radiation-induced pneumonitis) and lower lobe predominant disease (IPF, connective tissue diseases, asbestosis, aspiration pneumonia, and bronchiectasis).  A helpful tool for your differential diagnosis is to think of what can cause these problems:

• ·      Idiopathic Disease (IPF, sarcoidosis etc.)
• ·      Connective Tissue disease (Systemic sclerosis, SLE, RA)
• ·      Exposures

o   Medications – Amiodarone, methotrexate

o   Silicosis, asbestosis

o   Hypersensitivity pneumonitis

• ·      Infections

o   Viruses

o   Bacteria

o   Fungi

• ·      Malignancy

o   Primary

o   Secondary

Hopefully we will hear about a resolution to this case soon!

Further reading:

Spodick, D. H. (2003). Acute cardiac tamponade. New England Journal of Medicine, 349(7), 684-690.

Raghu, G. (1995). Interstitial lung disease: a diagnostic approach. Am J Respir Crit Care Med, 151, 909-914.

Roy, C. L., Minor, M. A., Brookhart, M. A., & Choudhry, N. K. (2007). Does this patient with a pericardial effusion have cardiac tamponade?. JAMA, 297(16), 1810-1818.