Ep-PAINE-nym



Korotkoff Sounds

Other known aliasesnone

Definitionsounds heard during auscultation of the brachial artery during blood pressure measurements

Clinical Significancethese sounds are generated as the sphygmomanometer cuff is slowly being deflated to the point that the maximal impulse of the pressure wave is more than cuff, but the cuff still occluded the artery at the nadir of the impulse. This pressure difference produces turbulence in the blood flow and the characteristic sound on auscultation. There are five phases to the Korotkov sounds with the initiation of Phase 1 as the systolic pressure and the end of Phase 4 as the diastolic pressure.

Historynamed after Nicholai Korotkov (1874-1920), who was a Russian surgeon and earned his medical degree from Moscow University in 1895. He had a prestigious career as a military physician and surgeon earning him an appointment as professor of surgery at the Military Medical Academy at St. Petersberg in 1903. He was preparing his doctoral thesis on vascular surgery when he described his now famous technique for measuring blood pressure in only a 281 word excerpt from a presentation to the Imperial Military Medical Academy entitled “Izvestie Imp. Voiennomedicinskoi Akademii” in 1905.

Nicolai Korotkov
Korotkov’s personal sphygmomanomter

References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • Shevchenko YL, Tsitlik JE. 90th Anniversary of the development by Nikolai S. Korotkoff of the auscultatory method of measuring blood pressure. Circulation. 1996; 94(2):116-8. [pubmed]

#46 – Heart Failure



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Definition of Heart Failure

  • Complex clinical syndrome resulting from conditions that affect the structure and/or function of the heart culminating in reduced systemic perfusion that is inadequate to meet the metabolic demands of the body
    • Main effect is decreased cardiac output
  • No more “congestive”

Epidemiology

  • 5.7 million adults in US
    • 550,000 new cases each year
    • 1.4 million are under 60 years of age
  • Annual incidence is 10 per 1,000 population AFTER 65 years of age
  • 287,000 deaths per year
    • 1 in 9 deaths included heart failure as contributing causes
    • Most common diagnosis in hospital patients over 65 years of age
  • Responsible for 11 million office visits each year in the US and more hospitalizations than all cancers COMBINED
  • 50% of adults who develop heart failure die within 5 years
  • Cost to US is ~$30 billion/year

Causes and Pathophysiology

Any condition that leads to alteration in left ventricular structure or function can cause heart failure and the specific causes depends on the preservation of ejection fraction.  There is considerable overlap between these with coronary artery disease and hypertension causes the majority of cases.

The problem is that the rest of the body feel the effects of the decreased cardiac output and activate the neurohormonal systems to compensate.  The issue is that this makes the heart failure worse and it is a vicious cycle until it can be broken.


Signs and Symptoms

  • History
    • Reduced cardiac output
      • Fatigue, weakness
    • Excessive fluid accumulation
      • Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, leg swelling, abdominal discomfort, palpitations
  • Physical Examination
    • Appearance and Vital Signs
      • Resting sinus tachycardia
      • Narrow pulse pressure
      • Cool, pale skin (peripheral vasoconstriction)
    • Volume Assessment
      • Pulmonary congestion
        • Rales on auscultation
        • AUDIO
      • Peripheral edema
        • Leg swelling, hepatic congestion, ascites, scrotal edema
      • Elevated jugular venous pressure
        • Hepatojugular reflux
  • Cardiac
    • S3 with gallop (if systolic failure)
    • S4 (if diastolic failure)
    • Displaced PMI past midclavicular line and below the 5th intercostal space
    • Pulsus alternans
      • Evenly spaced alternating strong and weak peripheral pulses
Pulsus Alternans

Framingham Clinical Criteria for Heart Failure


Clinical Decision Rule for Heart Failure

  • Age
    • < 60 = 0 points
    • 60-70 = 4 point
    • 71-80 = 7 points
    • > 80 = 10 points
  • History of coronary disease = 15 points
    • AMI, CABG, PCI
  • Loop diuretic = 10 points
  • Displaced PMI = 20 points
  • Rales = 14 points
  • Irregularly irregular pulse = 11 points
  • Heart murmur = 10 points
  • Pulse Rate = (HR-60)/3 points
  • Elevated jugular venous pressure = 12 points
  • NT-proBNP (pg/mL)
    • < 100 = 0 points
    • 100-200 = 8 points
    • 200-400 = 16 points
    • 400-800 = 24 points
    • 800-1600 = 32 points
    • 1600-3200 = 40 points
    • > 3200 = 48 points
  • Interpretation
    • < 13 points = < 10% probability of heart failure
    • > 54 points = > 70% probability of heart failure

Diagnostic Studies

  • Electrocardiogram
    • Not really diagnostic, but can evaluate for current ischemia, past infarction, low voltage, dysrhythmias
    • A normal EKG makes systolic dysfunction unlikely (98% NPV)
  • Laboratory studies
    • Brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP)
      • Released from ventricles  when stretched
      • < 100 pg/mL = very high NPV and rule out heart failure
    • Cardiac enzymes
    • CBC
    • CMP
  • Chest Radiography
    • Increased cardiothoracic ratio
    • Cephalization of pulmonary vessels
    • Kerley B-lines
    • Pleural effusions
  • Echocardiography
    • Recommended for all patient with dyspnea and suspicion of heart failure
    • Provides vital information on:
      • Ejection fraction
        • < 40% = reduced = systolic
        • > 50% = preserved = diastolic
      • Valvular disease
        • Aortic and mitral regurgitation/insufficiency
      • Atrial and Ventricular size and function
        • Enlarged left ventricle = systolic
        • Left atrial enlargement with normal/small left ventricle = diastolic
      • Left ventricular wall size
        • Thin = systolic
        • Thick = diastolic
  • Exercise/Stress Testing
    • Evaluate for underlying coronary disease, as well as potential candidates for transplantation
      • Patients with a peak oxygen uptake (VO2) < 14 mL/kg/min have better outcomes with transplanted
  • Coronary angiography
    • Not strongly recommended as part of the work-up, but can be useful to evaluate for underlying coronary disease and get an accurate ejection fraction

Classification and Grading


Current Nomenclature

Heart failure with reduced ejection fraction (HFrEF)

  • Systolic
  • < 40% EF

Heart failure with preserved ejection fraction (HFpEF)

  • Diastolic
  • > 50% EF

Management

  • Heart failure with reduced ejection fraction (HFrEF)
    • Lifestyle Modifications
      • Smoking cessation
      • Restrict sodium to < 3g/day
      • Restrict fluid to < 2L/day
    • Pharmacotherapy
      • Loop diuretic (if overload is present)
        • Furosemide, bumetanide, torsemide
      • ACE inhibitors
        • Lisinopril, enalapril
      • Angiotension receptor-neprilysin inhibitor (ARNI)
        • NYHA II or III and:
          • BNP > 150 ng/mL or hospitalized with last 12 months
          • SBP > 100 mmHg
          • GFR > 30 mL/min
          • No history of angioedema
      • ARB
        • Candesartan, valsartan
      • Beta blockers
        • Carvedilol, metoprolol, bisoprolol
      • Mineralcorticoid receptor antagonist (MRA)
        • Spironolactone, eplerenone
      • Selective sinus node inhibitor
        • Ivabradine
        • Need a resting HR > 70 bpm on maximum BB therapy
    • Ischemic heart disease
      • Increase coronary perfusion
      • Decrease myocardial demand
    • Hyperlipidemia
      • High-intensity statin
    • Cardiac rehabilitation
  • Heart failure with preserved ejection fraction (HFpEF)
    • Differences with HFrEF
      • ACEI/ARB not as useful
      • MRA used more often
      • Diuretics OK but be careful for volume depletion
      • Don’t use BB unless compelling indication


References

  1. Tan LB, Williams SG, Tan DK, Cohen-Solal A. So many definitions of heart failure: are they all universally valid? A critical appraisal. Expert review of cardiovascular therapy. 2010; 8(2):217-28. [pubmed]
  2. CDC Heart Failure Data Sheet. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_failure.htm
  3. Emory Healthcare Heart Failure Statistics. https://www.emoryhealthcare.org/heart-vascular/wellness/heart-failure-statistics.html
  4. Mann DL, Chakinala M. Heart Failure: Pathophysiology and Diagnosis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com.ezproxy.uthsc.edu/content.aspx?bookid=2129&sectionid=192028958
  5. Davie AP, Francis CM, Caruana L, Sutherland GR, McMurray JJ. Assessing diagnosis in heart failure: which features are any use? QJM : monthly journal of the Association of Physicians. 1997; 90(5):335-9. [pubmed]
  6. Kelder JC, Cramer MJ, van Wijngaarden J, et al. The diagnostic value of physical examination and additional testing in primary care patients with suspected heart failure. Circulation. 2011; 124(25):2865-73. [pubmed]
  7. Davie AP, Francis CM, Love MP, et al. Value of the electrocardiogram in identifying heart failure due to left ventricular systolic dysfunction. BMJ (Clinical research ed.). 1996; 312(7025):222. [pubmed]
  8. Maisel A. B-type natriuretic peptide levels: diagnostic and prognostic in congestive heart failure: what’s next? Circulation. 2002; 105(20):2328-31. [pubmed]
  9. Knudsen CW, Omland T, Clopton P, et al. Diagnostic value of B-Type natriuretic peptide and chest radiographic findings in patients with acute dyspnea. The American journal of medicine. 2004; 116(6):363-8. [pubmed]
  10. Badgett RG, Mulrow CD, Otto PM, Ramírez G. How well can the chest radiograph diagnose left ventricular dysfunction? Journal of general internal medicine. 1996; 11(10):625-34. [pubmed]
  11. Bart BA, Shaw LK, McCants CB, et al. Clinical determinants of mortality in patients with angiographically diagnosed ischemic or nonischemic cardiomyopathy. Journal of the American College of Cardiology. 1997; 30(4):1002-8. [pubmed]
  12. Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. Journal of the American College of Cardiology. 1993; 22(4 Suppl A):6A-13A. [pubmed]
  13. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013; 128(16):1810-52. [pubmed]
  14. Yancy CW, Jessup M, et al. 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2016; 134(13):e282-93. [pubmed]
  15. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European heart journal. 2016; 37(27):2129-2200. [pubmed]
  16. Parch J, Powell C. No longer failing to treat heart failure: A guideline update review. JAAPA : official journal of the American Academy of Physician Assistants. 2019; 32(1):11-15. [pubmed]

PAINE #PANCE Pearl – Cardiovascular



Question

Hypercholesterolemia is most commonly a laboratory diagnosis, but there are some class physical examination findings that can be seen. What are they?



Answer

There are five (5) classic physical exam findings associated with hypercholesterolemia and are more common in familial, genetic hyperlipoprotenemias.

  • Tendon xanthomas (most commonly at the achilles tendon and hands)
  • Planar xanthomas on hands and feet
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)
  • Planar xanthomas on hands and feet
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)
  • Xanthelasmas (soft, cholesterol filled, yellow plaques on the upper eyelids)
  • Corneal arcus (white/grey/yellow ring around cornea)
  • Lipemia retinalis (white colored retinal vessels associated with hypertriglyceridemia)

Ep-PAINE-nym



Bundle of Kent

Other known aliases atrioventricular bypass tract

DefinitionAs discussed in the WPW eponym, the Bundle of Kent is an accessory conduction pathway between the atrium and ventricle on either the right or left side of the heart.

Clinical Significancethis pathway occurs in up to 0.3% of patients and the cause of Wolff-Parkinson-White syndrome. It bypasses the traditional conduction system and allows for pre-excitation tachydysrthymias.

HistoryNamed after Albert Frank Stanley Kent (1863-1958), an English physiologist who received his degree in 1886 from the Magdalen College of Oxford. He first described lateral atrioventricular connections in a monkey heart in 1893 and erroneously believed these were part of the normal specialized conduction system. These findings generated a lot of controversy at the time and were actually rejected by several notable anatomists and physiologists. In fact, in 1955, Lev and Learner dissected 33 neonatal hearts and found no evidence of “normal” lateral conduction systems.


References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • Kent AF. Researches on the Structure and Function of the Mammalian Heart. The Journal of physiology. 1893; 14(4-5):i2-254. [pubmed]
  • LEV M, LERNER R. The theory of Kent; a histologic study of the normal atrioventricular communications of the human heart. Circulation. 1955; 12(2):176-84. [pubmed]

Ep-PAINE-nym



Wolff-Parkinson-White Syndrome

Other known aliasesventricular pre-excitation with arrhythmia, auriculoventricular accessory pathway syndrome

Definitionparoxysmal supraventricular tachycardia caused by conduction through an abnormal accessory bypass tract between the atria and ventricles known as the Bundle of Kent. There are two types depending on the side of the heart it effects; Type A is between the right atrium and ventricle and Type B is between the left atrium and ventricle.

Clinical SignificancePatients with WPW can numerous cardiac dysfunction symptoms including tachydysrhythmias, palpitations, dyspnea, presyncope, syncope, and sudden cardiac arrest. It is characterized by the triad of abnormalities on EKG of widened QRS, shortened PR interval, and slurring of the initial part of the QRS (called a delta wave).

HistoryNamed after Louis Wolff (1898-1972), Sir John Parkinson (1885-1976), and Paul Dudley White (1886-1973). Dr. Wolff was an American cardiologist who received his medical doctorate from Harvard Medical School in 1922. Dr. Parkinson was an English cardiologist who received his medical doctorate from University of Freiburg in 1910 and was also knighted by King George in 1948. Dr. White was an American cardiologist who received his medical doctorate from Harvard Medical School in 1911 and one of the founding presidents for the American Heart Association. He was a prominent advocate for preventive medicine receiving many national and international awards for his efforts to advance the importance of diet, exercise, and weight control in the prevention of cardiovascular disease. They collaborated to publish a series of 11 cases entitled “Bundle‐Branch Block with Short P‐R Interval in Healthy Young People Prone to Paroxysmal Tachycardia” in the American Heart Journal in 1930. It should be noted that Dr. Frank Norman Wilson and Dr. Alfred Wedd both described and published these findings in 1915 and 1921.


References

  • Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  • Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  • Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  • Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  • Up To Date. www.uptodate.com
  • Wolff L, Parkinson J, White PD. Bundle‐Branch Block with Short P‐R Interval in Healthy Young People Prone to Paroxysmal Tachycardia. American Heart Journal. 1930;5(6):985-704 [article]