My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?

Absolutely! As early as 1959, Guyton and Lindsey demonstrated the importance of serum colloid osmotic pressure in the pathogenesis of pulmonary edema1.

Specifically, they found that in dogs with normal plasma protein concentrations fluid began to transudate into the lungs when the left atrial pressure rose above an average of 24 mm Hg vs only 11 mm Hg when plasma protein concentration was reduced by about 50%.

Fast forward to 2003, Arques et al studied serum albumin and pulmonary artery wedge pressures in 4 groups of patients: acute HFpEF, heart failure with reduced ejection fraction (HFrEF), acute dyspnea from pulmonary origin and normal controls2.   Patients with HFpEF were significantly more likely to have hypoalbuminemia , compared to those with HFrEF, pulmonary disease or normal controls.  The main cause of hypoalbuminemia in the HFpEF was malnutrition in 77% and/or sepsis in 41% of patients.   Hypoalbuminemia was inversely related to age and plasma C-reactive protein.

Perhaps, we should pay more attention the nutritional status of our patients with HFpEF!

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References

  1. Guyton AC, Lindsey AW. Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pulmonary edema. Circ Res 1959;7: 649-657.
  2. Arquès S, Ambrosi P, Gélisse R et al. Hypoalbuminemia in elderly patients with acute diastolic heart failure. J Am Coll Card 2003;42:712-16. http://www.onlinejacc.org/content/42/4/71                                                                                                    
My elderly patient with acute heart failure with preserved ejection fraction (HFpEF) has a low serum albumin. Can hypoalbuminemia be associated with HFpEF?

What is the mechanism of pericardial effusion formation in heart failure?

Pericardial space contains 15-35 ml of fluid under physiologic conditions (1). Pericardial formation is dependent on the ultrafiltration of plasma across epidcardial and parietal pericardial capillaries a well as interstitial fluid traversing the epicardium, and is removed by the lymphatic system (1). The prevalence of pericardial fluid in congestive heart failure is 12-20%.

Experimental animal data and observations from human studies suggest that pericardial effusion in heart failure only occurs in the setting of high right-sided filling pressures. In a retrospective study of patients with primarily left ventricular dysfunction with or without pericardial effusion, enlarged right ventricular diastolic internal dimension on echocardiography was strongly correlated with the presence of pericardial effusion while systolic and diastolic internal dimensions were not (2).  Thus in patients with heart failure and pericardial effusion, high right-sided filling pressures should be suspected.

 

References

  1. Natanzon A, Kronzon I. Pericardial and pleural effusions in congestive heart failure—anatomical, pathophysiologic, and clinical considerations. Am J Med Sci 2009;338:211-216. https://www.ncbi.nlm.nih.gov/pubmed/19574887
  2. Kessler KM, Rodriguez D, Rahim A, et al. Echocardiographic observations regarding pericardial effusions associated with cardiac disease. Chest 1980;78:736-40. https://www.ncbi.nlm.nih.gov/pubmed/7428456
What is the mechanism of pericardial effusion formation in heart failure?

What is the mechanism of pleural fluid formation in congestive heart failure (CHF)?

The pleural fluid in CHF originates from increase filtration of plasma across the capillaries of the visceral pleura and, more importantly, excess fluid in the interstitial spaces of the lung, both related to the increased hydrostatic and capillary wedge pressures (1).

It is postulated that leak of edema fluid into the pleural space may serve as a “safety valve” to mitigate overflooding of alveoli (2). 

Interestingly, although the pleural effusion is commonly bilateral in CHF, when unilateral, it is more likely on the right (1). The reason for this finding is unclear but several hypotheses have been put forth including compression of the azygous vein (which drains a portion of the parietal pleura of right lung) due to the dilatation of the right heart, and compression of the right pulmonary veins by an enlarged right atrium (1).  

Bonus Pearl: A minimum of 50 ml and 200 ml of pleural fluid are required for visibility on lateral and posteroanterior views of a chest radiograph, respectively (3).

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References

  1. Natanzon A, Kronzon I. Pericardial and pleural effusions in congestive heart failure—anatomical, pathophysiologic, and clinical considerations. Am J Med Sci 2009;338:211-216. https://www.ncbi.nlm.nih.gov/pubmed/19574887
  2. Zocchi L. Physiology and pathophysiology of pleural fluid turnover. Eur Respir J 2002;20:1545-1558. http://erj.ersjournals.com/content/20/6/1545.short
  3. Mammarappallil JG, Anderson SA, Danelson KA, et al. Estimation of pleural fluid volumes on chest radiography using computed tomography volumetric analysis: an update of the visual prediction rule. J Thorac Imaging 2015;30:336-339.https://www.ncbi.nlm.nih.gov/pubmed/25811356

 

What is the mechanism of pleural fluid formation in congestive heart failure (CHF)?

My bed-bound, debilitated patient is being transferred to a long-term facility (LTF). Should I continue the venous thromboembolism (VTE) prophylaxis she has been receiving in the hospital?

There are no randomized-controlled studies that examine the effectiveness of VTE prophylaxis in debilitated patients following discharge from the hospital, and currently  the literature does not recommend prophylaxis for chronic immobility as a single risk factor for VTE (1). However, given the expected morbidity, potential mortality and hospital readmission associated with VTE,  prophylaxis should be considered in residents of LTFs with the following comorbidities (2):

  • Acute exacerbation of congestive heart failure
  • Acute exacerbation of chronic obstructive pulmonary disease
  • Acute infection (e. g. pneumonia, urosepsis, skin and soft tissue infections, infectious diarrhea)
  • Acute exacerbation of inflammatory/autoimmune diseases
  • Active malignancy
  • Immobility and prior VTE

 

Unless contraindicated, patients should receive prophylactic doses of unfractionated heparin, enoxaparin, or other approved drugs. Mechanical VTE prophylaxis should be used only when the risk of bleeding is considered unacceptably high or when there are drug intolerances or adverse effects.

The need for VTE prophylaxis should be reassessed regularly taking into account patient’s overall health status, mobility, drug tolerance and goals of care.

 

References

  1. Pai M, Douketis JD. Preventing venous thromboembolism in long-term care residents: Cautious advice based on limited data. Cleveland Clin J Med 2010;77: 123-130.  https://www.ncbi.nlm.nih.gov/pubmed/20124270    
  2. Robinson Am. Venous thromboembolism prophylaxis for chronically immobilized long-term care residents. Ann Long-Term Care 2013;10:30. https://www.managedhealthcareconnect.com/article/venous-thromboembolism-prophylaxis-chronically-immobilized-long-term-care-residents
My bed-bound, debilitated patient is being transferred to a long-term facility (LTF). Should I continue the venous thromboembolism (VTE) prophylaxis she has been receiving in the hospital?

What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?

The evidence for the accuracy of crackles in CHF is not as robust as often assumed, with wide variations in its sensitivity (13%-70%), specificity (35%-100%), positive predictive value (19%-100%), and negative predictive value (17%-85%) (1).

In a study  of patients at high risk for CHF but without valvular heart disease, symptoms of CHF, or comorbid pulmonary disease,  the prevalence of baseline crackles in one or both lungs increased with age: 45-64 y , 11%; 65-79 y, 34%; and 80-95 y, 70%.  At best, fair or poor positive and negative likelihood ratios (LRs) have been reported for crackles in CHF (3.4, and 0.8, respectively) (2). 

The accuracy of crackles in diagnosing pneumonia in patients with cough and fever is not much better: sensitivity 19-67%, specificity 36-94%, and poor positive and negative LRs (1.8 and 0.8, respectively) (2).

So don’t overestimate the accuracy of crackles in CHF or pneumonia, especially if your suspicion for these conditions is high!

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References

  1. Kataoka H, Matsuno O. Age-related pulmonary crackles (rales) in asymptomatic cardiovascular patients. Ann Fam Med 2008;6:239-245.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2384982/ 
  2. McGee S. Auscultation of the lungs. In Evidence-based physical diagnosis (3rd ed.). Elsevier Saunders, Philadelphia, 2012.
What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?

How does obesity lower serum brain natriuretic peptide (BNP) levels in patients with heart failure?

The association between high body mass index (BMI) and low serum BNP levels  has been reported in heart failure patients with diminished or preserved left ventricular systolic function (1).  

However, The exact mechanism underlying the inverse relationship of BNP levels with BMI is unclear.  Decreased production of BNP by myocytes, increased clearance of BNP and decreased sensitivity of the myocytes to stretch have been proposed (1). 

Of interest, in obese patients who undergo gastric bypass surgery, serum BNP levels increases significantly postoperatively and correlates with weight loss  (2).  

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References 

  1. Stavrakis S, Pakala A, Thomas J et al. Obesity, brain natriuretic peptide levels and mortality in patients hospitalized with heart failure and preserved left ventricular systolic function. Am J Med Sci 2013;345:211-217. https://www.ncbi.nlm.nih.gov/pubmed/23422653
  2. Changchien EM, Shushmita A, Betti F, et al. B-type natriuretic peptide increases after gastric bypass surgery and correlates with weight loss. Surg Endosc 2011;25:2338-2343. https://www.ncbi.nlm.nih.gov/pubmed/21424205
How does obesity lower serum brain natriuretic peptide (BNP) levels in patients with heart failure?

Which patients outside of ICU setting should be placed on telemetry monitoring in the hospital?

Telemetry monitoring should be used in patients at increased risk of arrhythmias during hospitalization (1). While the American Heart Association provides expert opinion on telemetry for a variety of cardiac conditions (1), a more recent review (2) makes suggestions for common cardiac and non-cardiac diagnoses based on arrhythmia risk.

Telemetry is recommended for patients admitted for implantable cardioverter- defibrillator firing, second or third degree AV block, prolonged QT interval with ventricular arrhythmia, acute heart failure, acute cerebrovascular event,  acute coronary syndrome and massive blood transfusion.

Telemetry may be beneficial in syncope with arrhythmia as a suspected cause, gastrointestinal hemorrhage after endoscopy, atrial arrhythmias on rate or rhythm control therapy, electrolyte imbalance and subacute congestive heart failure.

Telemetry is not generally indicated in chest pain with normal EKG and cardiac markers, COPD exacerbation, PE if the patient is stable and on anticoagulation, and cases requiring minor blood transfusion. 

Contributed by Joome Suh, MD, Boston, MA

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References 

(1) Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care Nurses. Circulation 2004;110:2721–46. 

(2) Chen EH and Hollander JE. When do patients need admission to a telemetry bed? The Journal of Emergency Medicine 2007:33(1):53-60.

 

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 or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. 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!

Which patients outside of ICU setting should be placed on telemetry monitoring in the hospital?