Current Thinking in Acute Congestive Heart Failure and Pulmonary Edema

Login or register to view PDF.
Citation
US Cardiology 2004;2004:1(1):1-6

Pages

Introduction

Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to maintain the circulation of blood adequately. The most severe manifestation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.

CHF can be categorized as forward or backward ventricular failure. Backward failure is secondary to elevated systemic venous pressure, while left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. Furthermore, heart failure can be subdivided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a dilated left ventricle with impaired contractility, while diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

The New York Heart AssociationÔÇÖs (NYHAÔÇÖs) functional classification of CHF is one of the most useful. Class I describes a patient who is not limited with normal physical activity by symptoms. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activity.

CHF is best summarized as an imbalance in starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction.This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium.

Maintenance of plasma oncotic pressure (generally about 25mmHg) higher than pulmonary capillary pressure (about 7-12mmHg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry.

Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. When the capacity of lymphatic drainage is exceeded, however, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF.

Pages

References
  1. Edwards J D, Grant P T and Plunkett P, "The hemodynamic effects of sublingual nitroglycerin spray in severe left ventricular failure", Intensive Care Med. (1989), 15: pp. 247-249.
    Crossref | PubMed
  2. Gordon H S, Harper D L and Rosenthal G E "Racial variation in predicted and observed in-hospital death:A regional analysis", JAMA (1996), 276: pp. 1,639-1,644.
    Crossref | PubMed
  3. Hamilton R J, Carter W and Galahger E J, "Rapid improvement of acute pulmonary edema with sublingual captopril", Academic Emergency Medicine (1996), 3: pp. 205-212.
    Crossref | PubMed
  4. Harlan W, Oberman A and Grimm R,"Chronic congestive heart failure in coronary artery disease: Clinical criteria", Ann. Intern. Med. (1977), 86: pp. 133-138.
    Crossref | PubMed
  5. Lin M,"Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema", Chest (1995), 107: pp. 1,379-1,386.
    Crossref | PubMed
  6. Melandri G, Semprini and Branzi A, "Comparative hemodynamic effects of transdermal vs intravenous nitroglycerin in acute myocardial infarction with elevated pulmonary artery pressure", Eur. Heart J. (1990), pp. 649-655.
    PubMed
  7. Polese A, Fiorenti C and Olivari M T,"Clinical use of nifedipine in acute pulmonary edema",Am.J.Med. (1979), 66: pp.825-830.
    Crossref | PubMed
  8. Andersson B and Waagstein F, "Spectrum and outcome of congestive heart failure in a hospitalized population", Am. Heart J. (1993), Sep; 126 (3 Pt 1): pp. 632-640.
    Crossref | PubMed
  9. Annane D, Bellissant E and Pussard E, "Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema", Circulation (1996), Sep 15; 94 (6): pp. 1,316-1,324.
    Crossref | PubMed
  10. Chen J T, "Radiographic diagnosis of heart failure", Heart Dis. Stroke (1992), Mar-Apr; 1 (2): pp. 58-63.
    PubMed
  11. Clinical Quality Improvement Network Investigators, "Mortality risk and patterns of practice in 4606 acute care patients with congestive heart failure,The relative importance of age, sex, and medical therapy", Arch. Intern. Med. (1996) Aug 12-26; 156 (15): pp. 1,669-1,673.
    Crossref | PubMed
  12. Connors A F, Jr, Speroff T, Dawson N V,"The effectiveness of right heart catheterization in the initial care of critically ill patients", JAMA (1996), 276: pp. 889-897.
    Crossref | PubMed
  13. Goldstein R E, Boccuzzi S J and Cruess D, "Diltiazem increases late onset congestive heart failure in post myocardial infarction patients with early reduction in ejection fraction", Circulation (1991), 83: pp. 52-60.
    Crossref | PubMed
  14. Kannel W B and Pinsky J L,"Trends in cardiac failure incidence and causes of three decades in the Framingham study", J.Am. Coll. Cardiol. (1991), 17: p. 87A.
    Crossref
  15. Kiyingi A, Field M J and Pawsey C C,"Metalozone in treatment of severe refractory congestive cardiac failure", Lancet (1990), 335: pp. 29-31
    Crossref | PubMed
  16. Kostuk W, Barr J W and Simon A L, "Correlations between the chest film and hemodynamics in acute myocardial infarction", Circulation (1973), 48: pp. 624-632.
    Crossref | PubMed
  17. Massie B M,"Congestive heart failure: Current controversies and future prospects", Am. J. Cardiol. (1990).
  18. Mehta S, Jay G D and Woolard R H,"Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema", Crit. Care Med. (1997), Apr; 25 (4): pp. 620-628.
    Crossref | PubMed
  19. Parmley W W, "Pathophysiology and current therapy of congestive heart failure", J. Am. Coll. Cardiol. (1989), 13(4): pp. 771-785.
    Crossref | PubMed
  20. Maisel A S, Krishnaswamy P, Nowak R M et al.,"Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure", N. Engl. J. Med. (2002), 347: pp. 161-167.
    Crossref | PubMed
  21. Mueller C, Scholer A, Laule-Kilian K, et al., "Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea", N. Engl. J. Med. (2004), 350; pp. 647-654.
    Crossref | PubMed
  22. McCullough P A, Nowak R M, McCord J, et al., "B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study", Circulation (2002), 106: pp. 416-422.
    Crossref | PubMed
  23. Wright S P, Doughty R N, Pearl A et al., "Plasma amino-terminal pro-brain natriuretic peptide and accuracy of heart-failure diagnosis in primary care: a randomized, controlled trial", J.Am. Coll. Cardiol. (2003), 42: pp. 1,793-1,800.
    Crossref | PubMed
  24. Peacock, et al., "Prospective randomized outcomes study of acutely decompensated CHF treated initially in outpatients with Natrecor (PROACTION)", J.Am. Coll. Cardiol. (2003), 4 (Suppl A): 336A, CHF and Pulmonary Edema.