Congestive heart failure

My patient with acute exacerbation of heart failure and pulmonary edema also has pneumonia. How often do heart failure and pneumonia coexist?

FA Manian MD, MPH, , , Leave a comment

More often than you might think! The relationship between pneumonia and heart failure (HF) appears bidirectional with pneumonia precipitating heart failure (HF) and HF predisposing to it.

Although It’s often quoted that acute respiratory tract infection accounts for 3-16% of patients hospitalized with decompensated heart failure (HF) (based primarily on small observational studies),1 a 2016 large prospective study involving nearly 100,000 HF admission from 305 US hospitals has reported “pneumonia/respiratory process” as the most common precipitating clinical factor, present in 28.2% of cases (arrhythmia and medication noncompliance came in as 2nd and 3rd).2

Interestingly, the same study reported that pneumonia/respiratory process was most prevalent among patients with preserved (≥50%) ejection fraction (EF) compared to those with borderline ( 40%-49%) or reduced (<40%) EF (33% vs 30% vs 24%, respectively). 2

Pulmonary edema may in turn predispose to bacterial pneumonia through adverse effects of edema fluid on lung bacterial defense mechanisms and establishment of a culture medium for bacterial growth by the presence of fluid in the alveolar space.3

So don’t be surprised if you have to treat for both!

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References

  1. Thomsen RW, Kasatpibal N, Riis A, et al. The impact of pre-existing heart failure on pneumonia prognosis: Population-based cohort study. J Gen Intern Med 2008;23:1407-13. https://www.ncbi.nlm.nih.gov/pubmed/18574639
  2. Kapoor JR, Kapoor R, Ju C, et al. Precipitating clinical factors, heart failure characterization, and outcomes in patients hospitalized with heart failure with reduced, borderline, and preserved ejection fraction. JACC 2016;4:464-72. https://www.scholars.northwestern.edu/en/publications/precipitating-clinical-factors-heart-failure-characterization-and 
  3. Harris GD, Woods DE, Fine R, et al. The effect of intraalveolar fluid on lung bacterial clearance. Lung 1980; 158;91-100 Harris GD, Woods DE, Fine R, et al. The effect of intraalveolar fluid on lung bacterial clearance. Lung 1980; 158;91-100. https://link.springer.com/article/10.1007/BF02713708

 

 

My patient with acute exacerbation of heart failure and pulmonary edema also has pneumonia. How often do heart failure and pneumonia coexist?

Does methotrexate reduce the risk of cardiovascular events in patients with rheumatoid arthritis?

FA Manian MD, MPH, , , , , , , , 1 Comment

The weight of the evidence suggests that methotrexate reduces the overall risk of cardiovascular events (CVEs)—including myocardial infarction, congestive heart failure, stroke, and or major adverse cardiac events—in RA patients (RR 0.72, 95% CI 0.57-0.91)1.

Aside from its effect on controlling systemic inflammation, methotrexate has also been shown to increase HDL and reduce total cholesterol/HDL ratio in patients with RA compared with treated non-RA controls2. In vitro, methotrexate appears to activate mechanisms involved in reverse transport of cholesterol out of the cell to the circulation for eventual excretion3. Not surprisingly then, methotrexate has also been reported to decrease atherosclerotic plaque burden measured by carotid artery intima-media thickness2.

We tend to think of RA as a disease that primarily causes arthritis but its effects may extend far beyond the joints. Patients with RA have an increased risk of cardiovascular deaths compared to the general population4, likely due to a variety of factors, including accelerated atherosclerosis secondary to chronic inflammation. At baseline, RA patients also have an unfavorable lipid profile with decreased HDL and higher total cholesterol/HDL ratio.

Fun Final Fact: Did you know that methotrexate is on the WHO Model List of Essential Medicines (April 2015) not only as a cancer drug but for treatment of RA as well5?

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References:

  1. Roubille C, Richer V, Starnino T, McCourt C, McFarlane A, Fleming P, Siu S, Kraft J, Lynde C, Pope J, Gulliver W, Keeling S, Dutz J, Bessette L, Bissonnette R, Haraoui B. The effects of tumour necrosis factor inhibitors, methotrexate, non-steroidal anti-inflammatory drugs and corticosteroids on cardiovascular events in rheumatoid arthritis, psoriasis and psoriatic arthritis: a systematic review and meta-analysis. Ann Rheum Dis. 2015;74:480-9. https://www.ncbi.nlm.nih.gov/pubmed/25561362
  2. Georgiadis AN, Voulgari PV, Argyropoulou MI, Alamanos Y, Elisaf M, Tselepis AD, Drosos AA. Early treatment reduces the cardiovascular risk factors in newly diagnosed rheumatoid arthritis patients. Semin Arthritis Rheum 2008;38:13-9. https://www.ncbi.nlm.nih.gov/pubmed/18191989
  3. Reiss AB, Carsons SE, Anwar K, Rao S, Edelman SD, Zhang H, Fernandez P, Cronstein BN, Chan ES. Atheroprotective effects of methotrexate on reverse cholesterol transport proteins and foam cell transformation in human THP-1 monocyte/macrophages. Arthritis Rheum 2008;58:3675-83. https://www.ncbi.nlm.nih.gov/pubmed/19035488
  4. Aviña-Zubieta JA, Choi HK, Sadatsafavi M, Etminan M, Esdaile JM, Lacaille D. Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of observational studies. Arthritis Rheum 2008; 59:1690-7. https://www.ncbi.nlm.nih.gov/pubmed/19035419
  5. WHO Model List of Essential Medicines (April 2015). http://www.who.int/medicines/publications/essentialmedicines/en/

 

Contributed by Brian Li, Medical Student, Harvard Medical School

Does methotrexate reduce the risk of cardiovascular events in patients with rheumatoid arthritis?

My patient just had a run of ventricular tachycardia (VT) at a rate of 120 beats/min lasting 18 seconds without any symptoms. Does this arrhythmia meet the criteria for nonsustained VT (NSVT) and what is its significance?

FA Manian MD, MPH, , , Leave a comment

Although NSVT is often defined as 3 (sometimes 5) or more consecutive beats arising below the atrioventricular node with a heart rate >100 beats/min lasting <30 s, this definition is not universal. Other definitions of NSVT include >120 beats/min using a duration cutoff of 15 s,  or at times no strictly defined diagnostic criteria1.  

NSVT can be observed in a variety of individuals, ranging from apparently healthy people to those with significant heart disease.  Whether NSVT provokes sustained life-threatening arrhythmias or is merely a surrogate marker of a more severe underlying cardiac pathology is unclear in most clinical settings 1. 

Because our patient  meets the generally observed criteria for NSVT, we should exclude an underlying occult pathology responsible for the arrhythmia and, in the case of known cardiac disease,  risk-stratify the patient for appropriate management2.  

The prognostic significance of NSVT is heavily influenced by the type and severity of underlying heart disease.  Patients with NSVT in the setting of >24 h post-acute myocardial infarction and those with chronic ischemic heart disease with left ventricular ejection fraction <40%  have a less desirable prognosis2. The management of patients with NSVT is generally aimed at treating the underlying heart disease.

References

  1. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol 2012;60:1993-2004. http://www.onlinejacc.org/content/60/20/1993
  2. Katritisis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J 2004;25:1093-1099. https://academic.oup.com/eurheartj/article/25/13/1093/465312
My patient just had a run of ventricular tachycardia (VT) at a rate of 120 beats/min lasting 18 seconds without any symptoms. Does this arrhythmia meet the criteria for nonsustained VT (NSVT) and what is its significance?

What is the significance of hyponatremia in my patient with acute decompensated congestive heart failure (ADCHF)?

FA Manian MD, MPH, , , , , , Leave a comment

Hyponatremia, defined as a serum sodium <135 meq/L, is observed in ~20% of patients hospitalized with ADCHF, and is often dilutional, not “depletional” (ie, not associated with hypovolemia) in this condition1.

In ADCHF, hyponatremia is primarily caused by the production of arginine vasopressin (AVP) (also known as anti-diuretic hormone, or ADH) as a result of decreased perfusion pressures in the aortic arch and renal afferent arterioles, and increased thirst due to the activation of the renin-angiotensin system.  Hyponatremia correlates with the severity of ADCHF and adverse clinical outcomes2.   

 A common approach to dilutional hyponatremia in ADCHF is fluid restriction. Other potential therapies include angiotension converting enzyme inhibitors (by increasing cardiac output and decreasing thirst), loop diuretics (by reducing water reabsorption in the renal distal tubule), and AVP antagonists (eg, tolvapatan, satavaptan)1,3.  Otherwise, in the absence of symptoms, no specific therapy is generally indicated for serum sodium levels ≥ 120mEq/L.

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References 

  1. Verbrugge FH, Steels P, Grieten L, Nijst P, Tang WHW, Mullens W. Hyponatremia in acute decompensated heart failure: Depletion versus dilution. J Am Coll Cardiol 2015;65:480-92. https://www.sciencedirect.com/science/article/pii/S073510971407394X?via%3Dihub
  2. Leier CV, Dei Cas L, Metra M. Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia. Am Heart J. 1994;128:564.  https://www.sciencedirect.com/science/article/pii/0002870394906335
  3. Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec FS, Orlandi C, SALT Investigators. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. N Engl J Med. 2006;355:2099. https://www.ncbi.nlm.nih.gov/pubmed/17105757

 

Contributed by Ricardo Ortiz, Medical Student, Harvard Medical School

What is the significance of hyponatremia in my patient with acute decompensated congestive heart failure (ADCHF)?

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

FA Manian MD, MPH, , , , Leave a comment

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?

FA Manian MD, MPH, Leave a comment

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)?

FA Manian MD, MPH, , Leave a comment

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?

FA Manian MD, MPH, , , , , , , , , Leave a comment

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?

FA Manian MD, MPH, , , , , , 1 Comment

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?

FA Manian MD, MPH, , , , , , Leave a comment

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?