Cardiovascular

PAINE #PANCE Pearl – Emergency Medicine

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Question

You have a patient in the ED with an aortic dissection and are managing them while awaiting the cardiovascular surgeon to arrive.

  1. What are the two most important things to control?
  2. How do you go about doing that?

Answer

  1. The main aims of acute medical management of aortic dissections are to decrease the rate of left ventricular contraction and decrease the velocity of the contraction, which will overall decrease the shear stress at the site of the tear and slow progression.
  2. Start with intravenous beta-blockade and titrate to a heart rate of 60 betas/minute
  1. If systolic blood pressure is > 120 mmHg after successful beta-blockade, then add a vasodilator or afterload reducer.

For a deep dive into aortic dissections, check out the podcast

References

  1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010; 121(13):e266-369. [pubmed]
  2. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation. 2005; 112(24):3802-13. [pubmed]

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Jones Criteria

 

Other Known Aliases – diagnostic criteria for acute rheumatic fever

 

Definition – clinical criteria to help diagnose acute rheumatic fever.  There are divided into major and minor criteria as follows:

  • Major
    • Polyarthritis
    • Carditis
    • Subcutaneous nodules
    • Erythema marginatum
    • Sydenham’s chorea
  • Minor
    • Fever
    • Arthralgia
    • Elevated ESR or CRP
    • Leukocytosis
    • 1st degree heart block

Clinical Significance – a diagnosis of acute rheumatic fever is either two major or one major and two minor criteria

 

History – Named after T. Duckett Jones (1899-1954), an American cardiologist who received his medical doctorate from the University of Virginia in 1923.  With a keen interest in rheumatic fever and heart disease, he practiced at Massachusetts General Hospital and House of Good Samaritan in Boston for over 20 years.  He became the medical director of the Helen Way Whitney Foundation to pursue his passion for public health, which led to one of the first tweleve appointments to the National Advisory Heart Council in 1948.  He published his seminal paper entitled “The Diagnosis of Rheumatic Fever” in JAMA in 1944 which described these findings.  Dr. Jones unfortunately died as a result of malignant hypertension in 1954 at the age of 55.

First page PDF preview

 

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. White PD.  T. Duckett Jones, 1899-1954.  Circulation.  1955.
  7. Shulman ST. T. Duckett Jones and his criteria for the diagnosis of acute rheumatic fever. Pediatric annals. 1999; 28(1):9-12. [pubmed]
  8. Jones TD.  The Diagnosis of Rheumatic Fever.  JAMA. 1944;126(8):481-484 [article]

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May-Thurner Syndrome

 

Other Known Aliases – Illiac vein compression syndrome

Definition – Compression of the left common illiac vein by the right common illiac artery

Iliac veins.gif

Clinical Significance – This anatomic compression causes extensive deep venous thrombosis of the left lower extremity and is the cause of up to 5% of all spontaneous DVT occurrences.  It is more common in women (3x) and classically presents in the 2nd to 4th decade of life.  This should be considered in any patient with a spontaneous DVT and no other hypercoagulable causes. 

Image result for may-thurner syndrome

History – Named after May and Thurner in 1957 after they published their findings and built on the work of James McMurrich, who was an anatomist at the University of Michigan, and published his anatomic description of this phenomenon in 1908.  It was further defined clinically by Cockett and Thomas in 1965, but the eponym goes to May and Thurner.   There really is not a lot written about May and Turner and my internet detective skills did not turn up much on these physicians, so I apologize in advance for the paucity of personal information on these physicians that I usually try to provide on these posts.

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. McMurrich JP. The occurrence of congenital ahhesions in the common iliac veins and their relations to thrombosis of the femoral and iliac veins.
    The American Journal of the Medical Sciences. 1908;135:342
  6. May R, Thurner J. The cause of the predominantly sinistral occurrence of thrombosis of the pelvic veins. Angiology. 1957; 8(5):419-27. [pubmed]
  7. Cockett FB, Thomas ML. The iliac compression syndrome. The British journal of surgery. 1965; 52(10):816-21. [pubmed]

PAINE #PANCE Pearl – Cardiovascular

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Question

 

64yo male, with a history of HTN, DMII, and hyperlipidemia, is brought in by EMS to the ED with a 2 hour history of lightheadedness and palpitations.  He states both these symptoms seem to fluctuate and nothing seems to make them better or worse when they occur.  He has never had anything like this before.  He denies syncope, chest pain, dyspnea, nausea, vomiting, diaphoresis, or vision changes.

 

Medications

Lisinopril 10mg

Metformin 1000mg

Simvastatin 20mg

 

Physical Exam

General – NAD, A&Ox3

HEENT – no diaphoresis, no gaze deviation, no facial palsies

CV – irregular, no M/G/R

Pulm – CTA bilaterally

MSK – 5/5 strength throughout

Neuro – CN II-XII grossly intact, MAE

 

While getting set up for a formal 12 lead EKG, the paramedic hands you the rhythm strips from transport:

 

What is the diagnosis????

 

Image result for sick heart yeti

 

Answer – Sick Sinus Syndrome

 

Definition

SSS is characterized by chronic sinoatrial node dysfunction with chronotropic incompetence and inappropriate heart rate responses to physiologic demands.  Classically, patients have bouts of bradycardia, tachyarrythmias, and sinus pauses or arrests.

 

Signs and Symptoms

  • fatigue
  • lightheadedness
  • palpitations
  • pre-syncopy and/or syncope

 

References

  1. Jensen PN, Gronroos NN, Chen LY. Incidence of and risk factors for sick sinus syndrome in the general population. Journal of the American College of Cardiology. 2014; 64(6):531-8. [pubmed]

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Mobitz, Wenckebach, and Hay AV Blocks

 

Other Known Aliases – Second degree AV blocks

 

Definition – Second degree AV block refers to the inability of the P-wave to initiate a QRS complex.  In Type I (Wenckebach), there is progressive elongation of the PR interval until a beat is dropped.

Image result for mobitz type I

In Type II (Hay), there is no progressive elongation, but there are dropped beats.

Image result for mobitz type II

 

Clinical Significance – Mobitz Type I is generally considered a benign entity due to absence of structural changes on histology.  Mobitz Type II is concerning because it can progress to a complete heart block with sudden cardiac arrest.

 

History – Named after Woldemar Mobitz (1889-1951), who was a Russian-German physician and earned his doctorate of medicine in 1914 from the Universities of Freiburg and Munich.  He researched heart block extensively in the early 1900’s which culminated in his landmark paper in 1924, where he classified the two distinct types of second degree heart block. 

Woldemar Mobitz The Apical View The Journey Continues To the end of the

Woldemar Mobitz

 

Interestingly, these two types were already described by:

1) Karel Frederik Wenckebach (1864-1940), who was a Dutch physician and anatomist in Hague and recieved his medical doctorate from the University of Groningen.  He published his findings of a irregular pulses due to partial blockage of the AV conduction system causing progressive lengthening of conduction time in cardiac tissue in 1899.

Wenckebach1.jpg

2) John Hay (1873-1959), who was an English physician and received his medical doctorate from Victoria University of Manchester in 1901.  He first described what would become Type II AV block in 1905 in a 65yo man with a 2.5 year history of dyspnea on exertion.  Interestingly, he did this without the benefit of elctrocardiography.

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Silverman ME, Upshaw CB, Lange HW. Woldemar Mobitz and His 1924 classification of second-degree atrioventricular block. Circulation. 2004; 110(9):1162-7. [pubmed]
  6. Mobitz W. Über die unvollständige Störung der Erregungsüberleitung zwischen Vorhof und Kammer des menschlichen Herzens. Zeitschrift für die Gesamte Experimentelle Medizin, Berlin 1924, 41: 180–23.
  7. Wenckebach KF. De Analyse van den onregelmatigen Pols. II. Over eenige Vormen van Allorhythmie en Bradycardie. Nederl Tijdschr Geneesk 1899;35:665.
  8. Hay J. Bradycardia and cardiac arrhythmia produced by depression of certain of the functions of the heart. The Lancet 1906, 1: 139–143
  9. Upshaw CB, Silverman ME.  John Hay: Discoverer of Type II Atrioventricular Block.  Clin Cardiol.  2000;23:869-871

#38 – Cardiac Murmurs

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***LISTEN TO THE PODCAST HERE***

 

Aortic Stenosis

 

Causes

  • Congenitally abnormal valve (bicuspid)
  • Calcific disease –> most common in US
  • Rheumatic valve disease –> most common world wide

Signs and Symptoms

  • Dyspnea on exertion
  • Exertional dizziness or syncope
  • Angina

Description

  • High-pitched, crescendo-decrescendo (diamond shaped), midsystolic murmur
  • Soft S2
  • S4 may be present

Best Auscultation Position

  • Right 2nd intercostal space

Special Notes

  • Radiate to carotid arteries

Aortic Regurgitation

 

Causes

  • Aortic root dilation
  • Congenital bicuspid valve
  • Calcific disease
  • Rheumatic heart disease –> most common world wide

Signs and Symptoms

  • Exertional angina and yspnea
  • Symptoms of heart failure
    • PND, orthopnea, pulmonary edema, lower extremity edema
  • Laterally and inferiorly displaced PMI with a thrill

Description

  • Soft, high-pitched, early diastolic, decrescendo murmur
  • Soft S1 with soft/absent A2
  • S3 may be present

Best auscultation position

  • Left 3rd intercostal space near sternal border (Erb’s point)

Special Notes

  • Accentuated by patient sitting up and leaning forward at end expiration

Mitral Stenosis

 

Causes

  • Rheumatic heart disease is most common causes
  • Mitral annular calcification
  • Radiation associated-valve disease (Hodgkin’s lymphoma)

Signs and Symptoms

  • Exertional dyspnea
  • Decreased exercise tolerance
  • Hemoptysis (increased pulmonary pressure)
  • Angina
  • Fatigue
  • Atrial fibrillation (elevated left atrial pressure)
  • Hoarseness

Description

  • Opening snap with low-pitched, diastolic murmur
  • Decrescendo after S2
  • Late, diastolic, crescendo before S1
  • Loud S1

Best auscultation position

  • Cardiac apex at left 5th intercostal space, midclavicular line

Special Notes

  • Patient in left lateral decubitus in held expiration
  • Using the bell

Mitral Regurgitation

 

Causes

  • Primary
    • Degenerative mitral valve disease à most common in US
      • Mitral valve prolapse
    • Rheumatic heart disease
    • Infective endocarditis
    • Trauma
    • Congenital valve cleft
    • Mitral annular calcification
  • Secondary
    • Coronary artery disease (regional wall motion abnormality)
    • Dilated cardiomyopathy
    • Hypertrophic cardiomyopathy

Signs and Symptoms

  • Exertional dyspnea
  • Fatigue
  • Atrial fibrillation
  • Heart failure

Description

  • High-pitched “blowing”, holosystolic murmur
  • Diminished S1

Best auscultation position

  • Cardiac apex at left 5th intercostal space, midclavicular line

Special Notes

  • Radiates to axilla
  • No variability in respiration
  • Decreases in intensity with valsalva

Mitral Valve Prolapse

 

Causes

  • Primary
    • Sporadic (myxomatous degeneration)]\
    • Familial (autosomal dominant with incomplete penetration)
      • 30-50% in 1st degree relatives
  • Secondary
    • Connective tissue disorders
    • 23CVInfective endocarditis
    • Coronary artery disease

Signs and Symptoms

  • Palpitations
  • Dyspnea
  • Exercise intolerance
  • Dizziness or syncope
  • Panic and anxiety disorders
  • Numbness or tinging

Description

  • Midsystolic click followed by a uniform, high-pitched, late systolic murmur

Best auscultation position

  • Cardiac apex at left 5th intercostal space, midclavicular line

Special Notes

  • Responds to dynamic auscultation
    • Increased in sudden standing
    • Decreased in sudden squatting

Tricupsid Stenosis

 

Causes

  • Rheumatic heart disease
  • Atrial myxoma
  • Carcinoid syndrome

Signs and Symptoms

  • Abdominal discomfort
    • Hepatic congestion and heptomegaly
  • Fluttering sensation in neck caused by jugular venous pulse
  • JVD, ascites, peripheral edema

Description

  • Soft, high-pitched, mid-diastolic

Best auscultation position

  • 4th intercostal space on the sternal border

Special Notes

  • Increased during inspiration, squatting, or leg raise

Tricuspid Regurgitation

 

Causes

  • Functional
    • Dilation of right atrium and ventricle with dilation of tricuspid annular leaflet
      • Pulmonary hypertension, left-sided heart failure, left-to-right shunt
  • Valvular
    • Valve damage from pacemaker or ICD
    • Infective endocarditis
    • Rheumatic heart disease
    • Ischemic heart disease

Signs and Symptoms

  • Majority are symptomatic
  • Right-sided heart failure
    • Hepatomegaly, hepatic congestion, ascites, hepatic venous hum, JVD, edema

Description

  • High-pitched, holosystolic murmur

Best auscultation position

  • 4th intercostal space on the sternal border

Special Notes

  • Radiates to right sternal border
  • Increases with inspiration, leg raises, or squatting

Pulmonic Stenosis

 

Causes

  • Congenital (10% of children with congenital heart disease)
    • Tetralogy of Fallot
    • Noonan Syndrome
  • Bicuspid valves
  • Calcification

Signs and Symptoms

  • Exertional dyspnea
  • Right heart failure

Description

  • Midsystolic, high-pitched, crescendo-decrescendo
  • Pulmonary ejection click
  • Extends through the A2
  • Splitting of S2

Best auscultation position

  • Left 2nd intercostal space

Special Notes

  • Increased during inspiration

Pulmonic Regurgitation

 

Causes

  • Primary
    • Iatrogenic, infectious, rheumatic, congenital
  • Secondary
    • Pulmonary artery hypertension and/or dilation
  • Physiologic (incidental)

Signs and Symptoms

  • Asymptomatic until right ventricular dysfunction occurs
    • Exertional dyspnea, fatigue
    • Tachyarrythmias

Description

  • Soft, high-pitched, early diastolic decrescendo
  • Graham-Steele murmur (pulmonary HTN)
    • High-pitched, blowing with accentuated P2

Best auscultation position

  • Left 2nd intercostal space

Special Notes

  • Increased with inspiration

S3 (ventricular gallop)

 

Causes

  • Large amount of blood hitting a very compliant left ventricle
    • Systolic heart failure

Description

  • Low-pitched, early diastolic sound
  • Occurs after S2

Best auscultation position

  • Cardiac apex at left 5th intercostal space, midclavicular line

Special Notes

  • Present with bell and absent with diaphragm

S4 (atrial gallop)

 

Causes

  • Blood striking a non-compliant left ventricle
    • Diastolic heart failure, LVH

Description

  • Low-pitched, late-diastolic murmur

Best auscultation position

  • Cardiac apex at left 5th intercostal space, midclavicular line

Special Notes

  • Present with bell and absent with diaphragm

Cottage Physician

 

References

  1. Eveborn GW, Schirmer H, Heggelund G, Lunde P, Rasmussen K. The evolving epidemiology of valvular aortic stenosis. the Tromsø study. Heart (British Cardiac Society). 2013; 99(6):396-400. [pubmed]
  2. Enriquez-Sarano M, Tajik AJ. Clinical practice. Aortic regurgitation. NEJM. 2004; 351(15):1539-46. [pubmed]
  3. Horstkotte D, Niehues R, Strauer BE. Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. European heart journal. 1991; 12 Suppl B:55-60. [pubmed]
  4. Hull MC, Morris CG, Pepine CJ, Mendenhall NP. Valvular dysfunction and carotid, subclavian, and coronary artery disease in survivors of hodgkin lymphoma treated with radiation therapy. JAMA. 2003; 290(21):2831-7. [pubmed]
  5. Chandrashekhar Y, Westaby S, Narula J. Mitral stenosis. Lancet (London, England). 2009; 374(9697):1271-83. [pubmed]
  6. Freed LA, Benjamin EJ, Levy D. Mitral valve prolapse in the general population: the benign nature of echocardiographic features in the Framingham Heart Study. Journal of the American College of Cardiology. 2002; 40(7):1298-304. [pubmed]
  7. Strahan NV, Murphy EA, Fortuin NJ, Come PC, Humphries JO. Inheritance of the mitral valve prolapse syndrome. Discussion of a three-dimensional penetrance model. The American journal of medicine. 1983; 74(6):967-72. [pubmed]
  8. Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. Journal of the American College of Cardiology. 1994; 24(2):446-53. [pubmed]
  9. Snellen HA, Hartman H, Buis-Liem TN, Kole EH, Rohmer J. Pulmonic stenosis. Circulation. 1968; 38(1 Suppl):93-101. [pubmed]
  10. Nishimura RA, Otto CM, Bonow RO. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. 2014; 63(22):e57-185. [pubmed]
  11. Ozawa Y, Smith D, Craige E. Origin of the third heart sound. II. Studies in human subjects. Circulation. 1983; 67(2):399-404. [pubmed]
  12. Abrams J. Current concepts of the genesis of heart sounds. II. Third and fourth sounds. JAMA. 1978; 239(19):2029-30. [pubmed]
  13. Learn The Heart. https://www.healio.com/cardiology/learn-the-heart