How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

You can assess the LV systolic function by POCUS by just zeroing in on the following cardiac parameters: 1. Anterior mitral valve leaflet motion in early diastole; 2. Change in LV chamber diameter; and 3. LV wall thickness during systole.1

First assess the anterior mitral valve leaflet motion towards the interventricular septum in early diastole in the parasternal long axis view (Figure). Estimated or measured distance between anterior mitral valve leaflet and the interventricular septum is called E-point septal separation (EPSS). When LV systolic function is normal, anterior mitral valve leaflet opens fully in early diastole, resulting in a small or minimal separation between it and the interventricular septum. Due to the fixed length of the chordae and the enlarged LV chamber size, anterior mitral valve leaflets are unable to fully open as systolic function worsens. This results in increased separation between the anterior mitral valve leaflet and the interventricular septum. An estimated EPSS greater than 10 mm is considered abnormal and suggests LV dysfunction.1,2

You can also estimate the LV ejection fraction (LVEF) quantitatively  by utilizing the following formula:3

LVEF (%)=75.5 – 2.5xEPSS (mm)

Keep in mind that aortic insufficiency and mitral stenosis can affect the accuracy of this formula.1

As for assessing the LV chamber diameter and wall thickness, recall that these parameters are also dynamic throughout the cardiac cycle. In systole, LV diameter should decrease by 30-40% while LV wall thickness should increase by approximately 40%. Using this as a guide, you can perform qualitative assessment by “eyeballing” the LV systolic function in parasternal long axis, parasternal short axis, apical 4-chamber and subcostal 4-chamber views. Beware that in parasternal long axis, apical 4-chamber and subcostal 4-chamber views, off axis of images can foreshorten the chamber size, resulting in overestimation of systolic function. Also be sure to use the midventricular papillary muscle view when assessing systolic function in the parasternal short axis.1   

Once you have obtained all the necessary images, feel free to categorize the systolic function as either “hyperdynamic”, “normal”, “reduced” or “severely reduced” (watch video below).1

Bonus pearl:  Did you know that qualitative assessment of the LV systolic function  following brief training sessions have been shown to significantly correlate with that obtained by formal echocardiography (k = 0.77, p <0.001).1,4,5 

Contributed by Woo Moon, D.O, Director POCUS Training Program, Mercy-St. Louis Hospital, St. Louis, Missouri

Figure: EPSS in normal vs reduced EF 

Note: EPSS (yellow arrows) is narrow in normal but wide in reduced EF

Video: Four categories of systolic function

 

References

  1. Soni MD MS NJ, Arntfield MD FRCPC R, Kory MD MPA P. Point of Care Ultrasound. 2nd ed. St. Louis, MO: Elsevier; 2019. . https://www.elsevier.com/books/point-of-care-ultrasound/soni/978-0-323-54470-2
  2. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK, Wolfson T. Cardiopulmonary limited ultrasound examination for “quick-look” bedside application. Am J Cardiol 2011;108(4):586–90. https://linkinghub.elsevier.com/retrieve/pii/S0002-9149(11)01424-X
  3. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol 2006;97(1):137–40. https://www.ajconline.org/article/S0002-9149(05)01683-8/fulltext
  4. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest 2009;135(6):1416–20. https://journal.chestnet.org/article/S0012-3692(09)60341-X/fulltext 
  5. Johnson BK, Tierney DM, Rosborough TK, Harris KM, Newell MC. Internal medicine point-of-care ultrasound assessment of left ventricular function correlates with formal echocardiography. J Clin Ultrasound 2016;44(2):92–9. https://onlinelibrary.wiley.com/doi/10.1002/jcu.22272

 

 

 

 

 

 

 

How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

My patient with COPD on prednisone with recurrent pneumonia has a low serum IgG level.  Can corticosteroids lower serum immunoglobulin levels?

Yes! Both exogenous and endogenous hypercortisolism may be associated with a drop in serum immunoglobulin levels, particularly IgG, which may persist even after discontinuation of steroid treatment.1-4 This means that a low serum IgG level in a patient on corticosteroids should be interpreted with caution and may not necessarily suggest primary antibody deficiency.

Although some early studies did not find a significant impact of corticosteroids on immunoglobulin levels, several subsequent studies found otherwise.  A 1978 study involving atopic asthmatic patients (averaging 16.8 mg prednisone daily) found that mean serum IgG significantly decreased (-22%) with milder drop in IgA levels (-10%) and no drop in serum IgM levels.2 Of interest, IgE level increased significantly initially but later dropped as well. More importantly, mean serum IgG levels remained significantly decreased an average of 22 days after corticosteroids were discontinued.

More recently, in a study involving patients with giant cell arteritis and polymyalgia rheumatica on corticosteroids, 58% developed antibody deficiency with the great majority involving IgG, either alone or along with other immunoglobulins.3 The reduction of IgG persisted even after discontinuation of corticosteroids in nearly 50% of patients, and observed in nearly one-quarter of patients for at least 6 months! Whether low serum immunoglobulins due to corticosteroids alone significantly increase susceptibility to infections is unclear, however.

In our patient with COPD on prednisone, if serum IgG level is found to be low and a primary antibody deficiency is still suspected, a functional assessment of the antibody production after active immunization (eg, polysaccharide pneumococcal vaccine, tetanus toxoid) may be necessary. 1 An adequate antibody response to active immunization makes primary immunodeficiency unlikely. 

 

Bonus Pearl: Did you know that corticosteroid-induced hypogammaglobulinemia may be in part related to reduced IgG production as well as an increase in IgG catabolism?1,4

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References

  1. Sarcevic J, Cavelti-Weder C, Berger CT, et al. Case report-secondary antibody deficiency due to endogenous hypercortisolism. Frontiers in Immunology 2020;11:1435. https://www.frontiersin.org/articles/10.3389/fimmu.2020.01435/full
  2. Settipane GA, Pudupakkam RK, McGowan JH. Corticosteroid effect on immunoglobulins. J Allergy Clin Immunol 1978;62: 162-6. https://www.jacionline.org/article/0091-6749(78)90101-X/pdf
  3. Wirsum C, Glaser C, Gutenberger S, et al. Secondary antibody deficiency in glucocorticoid therapy clearly differs from primary antibody deficiency. J Clin Immunol 2016;36:406-12. https://link.springer.com/article/10.1007/s10875-016-0264-7
  4. McMillan R, Longmire R, Yelenosky R. The effect of corticosteroids on human IgG synthesis. J Immunol 1976;116:1592-1595. https://www.jimmunol.org/content/116/6/1592

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient with COPD on prednisone with recurrent pneumonia has a low serum IgG level.  Can corticosteroids lower serum immunoglobulin levels?

Why do we often prescribe ceftriaxone in preference to fluoroquinolones for prophylaxis of infections in patients with cirrhosis and upper GI bleed?

Preference of ceftriaxone over fluoroquinolones (FQs) for prophylaxis of infection in patients with cirrhosis and upper GI bleed (UGIB) can often be traced back to a small 2006 Spanish randomized controlled trial (RCT)1 which found a significantly lower rate of proved or possible bacterial infection and lower rate of fermentative Gram-negative bacilli infection in the ceftriaxone group (vs norfloxacin) over a 10-day period (11% vs 33% and 0% vs 11%, respectively). There was no significant difference in the incidence of proved bacterial infection (spontaneous bacterial peritonitis or bacteremia, P=0.07) or 10-day mortality between the 2 groups.   

It’s worth emphasizing that the primary impetus for this study was evaluation of the efficacy of ceftriaxone in patients with cirrhosis and UGIB in a setting where FQ Gram-negative bacilli was thought to be highly prevalent. Parenthetically, a similar RCT performed where the prevalence of FQ resistance was considered low failed to find a significant difference in breakthrough bacterial infection, rebleeding or mortality when ceftriaxone was compared to IV ciprofloxacin.2

Another caveat of the 2006 study was that an IV antibiotic (ceftriaxone) was compared to a oral antibiotic (norfloxacin) which, in the setting of active UGIB, may be problematic.

Despite these limitations, its favorable safety profile compared to FQs coupled with its ease of administration has often made ceftriaxone the drug of choice for prophylaxis of infections in patients with cirrhosis and UGIB. The 2016 Practice Guidance by the American Association for the Study of Liver Diseases considers ceftriaxone as the first choice in patients with advanced cirrhosis, on FQ prophylaxis, and in hospital settings with high prevalence of FQ resistant bacterial infection.3

Bonus Pearl: Did you know that the prevalence of FQ resistant in Enterobacteriaceae may be as high as 30% in certain regions of U.S. and >50% in certain regions of the world? 4

Also see related 2 P4P pearls (1, 2) on the association of UGIB bleed with infections in patients with cirrhosis.

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Subscribe to Blog via Email

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References

  1. Fernandez J, Del Arbol LR, Gomez C, et al. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage. Gastroenterol 2006;131:1049-1056. https://pubmed.ncbi.nlm.nih.gov/17030175/
  2. Pittayanon R, Reknimir R, Kullavanijaya P, et al. Intravenous ciprofloxacin vs ceftriaxone for the prevention of bacterial infections in cirrhotic patients with gastrointestinal bleeding:A randomized controlled trial. Thai J Gastroenterol 2016;17:24-30. http://www.thaigastro.com/books.php?act=content&content_id=476&book_id=61
  3. Garcia-Tsao G, Abraldes JG, Berzigotti A, et al. Portal hypertensive bleeding in cirrhosis:risk stratification, diagnosis and management: 2016 Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology 2017;65:310-335. https://pubmed.ncbi.nlm.nih.gov/27786365/
  4. Spellberg B, Doi Y. The rise of fluoroquinolone-resistant Escherichia coli in the community:scarier than we thought. J Infect Dis 2015;212:1853-1855. https://pubmed.ncbi.nlm.nih.gov/25969562/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Why do we often prescribe ceftriaxone in preference to fluoroquinolones for prophylaxis of infections in patients with cirrhosis and upper GI bleed?