Errors in First Aid for the USMLE (2007): Cardiovascular System

As always, this is from an email sent to the First Aid team.

Cardiovascular (BRS Physiology, Merck Manual and Robbins Basic Pathology)

  1. P.235, Myocardial action potential
    1. The line indicating the flow of currents omits the K+ current responsible for Phase 1, and instead shows the K+ current active midway through Phase 2. This missing current is voltage-gated, above and beyond the “leak” current shown.
  2. P.241, Normal Pressure
    1. Normal pressures for the Aorta are listed as “<130/90.” Other texts put this diastolic value at 70mmHg (leading to an aortic MAP of 90).
  3. P.241, Congenital Heart Disease
    1. “Children may squat to increase venous return” is not correct. Squatting posture is used to increase systemic vascular resistance and thereby reduce the R-L shunting seen in the Tetralogy of Fallot. Increasing venous return would increase Preload, SV, and CO from the R ventricle, exacerbating the R-L shunt that is causing the cyanosis. This should be changed to “Children may squat to increase Systemic Vascular Resistance and thereby decrease R-L shunting.”
  4. P.241, Congenital Heart Disease
    1. When discussing the L-R shunts, a brief explanation for Eisenmenger’s syndrome is given. On the very next page, this is explained much better. I think this could be shortened to “Uncorrected L-R shunts may lead to Eisenmenger’s Syndrome.”
  5. P.242, Tetralogy of Fallot
    1. The physiological explanation given should have the bold words added: “Patient leans to squat to improve symptoms: compression of femoral arteries increases Systemic Vascular Resistance, thereby decreasing the R-L shunt.”
  6. P.242, Transposition of great vessels
    1. “Not compatible with life unless a shunt is present to allow adequate mixing of blood ( e.g. VSD, PDA, or patent foramen ovale [?]” I do not understand why “patent foramen ovale” is used here since any ASD would do (e.g. foramen primum, sinus venosum). I think this should be changed to “( e.g. VSD, ASD, PDA)”
  7. P.243, Congenital cardiac defect associations
    1. After listing “22q11,” I think including “(DiGeorge)” might save people some time looking it up.
    2. “Aortic insufficiency” is not a congenital defect in Marfan’s. Ruptured Aortic Aneurysm is a late complication of Marfan’s, as is Mitral Insufficiency, but not one of these is present at birth and so cannot be considered “congenital.” I think this should be removed.
  8. P.244, Atherosclerosis
    1. I have attached a picture below to help people remember the incidence for plaques at each location.
  9. P.244, Infarcts: red vs. pale
    1. The liver is not listed under red infarcts but is included in the illustration. I think this should be included in the write up as well.
    2. The brain is listed under pale infarcts. The brain is subject to both red and pale infarcts, depending on location. Red infarcts occur in “watershed areas” where cerebral arteries overlap their supply and white infarcts where there is a single arterial supply ( e.g. the thalamus).
  10. P.245, Evolution of MI
    1. “Risk for arrhythmia” is listed under “2-4 days.” While true that most arrhythmias occur within the first 4 days, the striking example of this in sudden cardiac death is within the first few hours. This is mentioned on P.246, under “MI Complications,” but needs to be listed consistently between the two pages. I suggest adding “Sudden cardiac death from arrhythmia” after “No visible change by light microscopy in first 2-4 hours.”
  11. P.246, MI complications
    1. Bullet 4: “can lead to cardiac tamponade” is listed as an outcome of the preceding three complications of ventricular free wall rupture, iv septum rupture, and rupture of the papillary muscles. This is confusing and omits the specific outcomes associated with each. I think this should be rewritten:
    2. Rupture (in order of incidence):
      1. IV septum – L-R shunt
      2. Papillary muscle – severe mitral regurgitation
      3. Ventricular free wall – cardiac tamponade, almost always fatal.
  12. P.247, Heart Murmurs
    1. I would change both the picture and description of Mitral prolapse. The description should follow the order of events, so I feel that “ Midsystolic click followed by late systolic murmur” is less confusing than “Late systolic murmur with midsystolic click”. The picture does not show the midsystolic click . The picture shows the late systolic murmur as a mid-to-late crescendo rumbling. The murmur is more commonly listed as being “barely audible to holosystolic (after the click)”. I have attached a drawing based on the mitral valve prolapse phonocardiography available at the American Family Physician website.
    2. I would change both the picture and description of Aortic regurgitation. The picture shows the diastolic murmur as being a crescendo-decrescendo murmur. As the pressure in the aorta is falling down a gradient, this does not make sense. The murmur of aortic regurgitation is regularly described as an early diastolic decrescendo rumbling.
      1. I think this is also the appropriate time to mention the Austin Flint murmur with the following description: Pure aortic regurgitation without interference from aortic valves. Returning blood pushes against mitral valves, causing diastolic vibration mimicking Mitral stenosis. Unlike Mitral stenosis, no opening snap is present.
      2. I have attached pictures for both Austin Flint and Aortic Regurgitation
  13. P.248, Cardiac tamponade
    1. “Compression of heart by fluid (i.e. blood)” is incorrect as a definition. Cardiac tamponade often results from pericarditis with serous, serosanguinous, hemorrhagic, chylos, or suppurative pericardial effusions. I think it should be changed:
      1. “Compression of heart by fluid (e.g. blood, pericardial effusions)”
    2. “Equilibration of pressures in all 4 chambers” is not complete. This should say “Equilibration of diastolic pressures in all 4 chambers of the heart with intrapericardial pressure.”
  14. P.249, Pericarditis
    1. Findings of pericarditis do not include “diffuse ST elevations in all leads.” One of the EKG hallmarks of pericarditis is “diffuse ST elevations in all leads except aVR and V1.” There is also an absence of pathologic Q waves, further helping one distinguish it from a transmural MI.
  15. P.250, Cardiac tumors
    1. Kussmaul’s sign is mentioned here but there is no mention that this occurs in any cardiac restriction ( e.g. cardiac tamponade, pericarditis). I think it is worth mentioning this with each of the previous entries, or giving it its own section:
      1. Kussmaul’s sign: paradoxical [up arrow] in systemic venous pressure on inspiration. Caused by pathologic [down arrow] in RV filling ( e.g. restrictive cardiomyopathy, constrictive pericarditis, right heart failure, cardiac tamponade).
  16. P.251, Antihypertensive drugs
    1. Captopril is listed as having “Proteinuria” as an adverse side effect. This is incorrect. By decreasing levels of angiotensin II, the efferent arteriole dilates, thereby decreasing GFR. This leads to a decrease in proteinuria. “Proteinuria” should either be omitted from the mnemonic or changed to “ Prevents proteinuria “
      1. The plot thickens and I eat crow. Captopril is used to treat (and even delay the onset of) proteinuria. It does this by the mechanism I have described. Its toxicity, however, can also cause proteinuria. So the First Aid is incomplete but not incorrect. The mnemonic is fine.
  17. P.252, Antianginal therapy
    1. The table says that Beta Blockers “affect afterload.” This is not true. They affect contractility . This is specifically true for the cardioselective beta blockers that would be used in cases of angina. B1 = contractility.
    2. Nitrates + Beta-blockers is listed as having “Little/no effect” on contractility. As B-blockers have their principle effect on contractility, I do not see how this is possible. In combination, the reflex increase in contractility seen in nitrate use would be blunted by the B-blocker and any basal sympathetic activity would also be blunted, leading to a decrease in contractility.
  18. P.254, Cardiac Glycosides
    1. To help make the hypokalemia/hyperkalemia relationship with digoxin more obvious and intuitive, I think that “Direct inhibition of Na/K ATPase” should be changed to ” Competitively inhibits Na/K ATPase at K-binding site.”
    2. “+ IONOtropy” should be “+ INOtropy”
    3. “Hypokalemia (potentiates drug’s effects),” while true, is not at play clinically. In acute digoxin toxicity, hyperkalemia results. In chronic digoxin use (or when combined with a K-wasting diuretic), hypokalemia can result and this then leads to digoxin toxicity. I think this should be rewritten:
      1. “hypokalemia (when combined with a diuretic), hyperkalemia (in digoxin overdose);”
      2. I’ve omitted the “potentiates drug’s effects” part because this is covered when we state that digoxin “competitively inhibits Na/K ATPase at K-binding site.”
    4. “anti-dig Fab fragments (Digibind).”
  19. P.257, Antiarrhythmials – Ca2+ channel blockers
    1. “Phase 2 (Ica and Ik)” should be “Phase 2 (Ica) and Phase 3 (Ik)”.
  20. P.257, Other antiarrhythmials
    1. “K+ — depresses ectopic pacemakers, especially in digoxin toxicity.” should be changed to “K+ — depresses ectopic pacemakers in hypokalemic digoxin toxicity.”

Return to First Aid Errors page.

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28 Responses to Errors in First Aid for the USMLE (2007): Cardiovascular System

  1. Wow, you’ve already read so much! I need to catch up!

  2. Jane Chuongsakul says:

    thank you very much for your help.
    i’m on the way to discuss with my friends about Tetralogy of Fallot (USMLE 2006)

    Thanks again

    PS. i’m a medical student in Thailand ^-^

  3. rakesh says:

    p231 diagram of pulmonic area:

    pulm. stenosis is a systolic murmur, not diastolic as written

  4. karen says:

    p250 pharmacology diagram: positive inotropes raise cardiac ouput (the + sign and the down arrow are confusing)

  5. Tina says:

    Also, on page 234. It says v waves are due to increased atrial pressure due to filling against a closed tricuspid valve. I believe that that describes a cannon a wave. A prominent v wave is due to tricuspid regurg.

  6. Brian says:

    “The mechanism of the v wave is the rise in right atrial and jugular venous pressure due to continued inflow of blood to the venous system during late ventricular systole when the tricuspid valve is still closed.” Kanu Chattarjee “Examination of the jugular venous pulse.” UpToDate

  7. Brian says:

    With regard to #17. According to Ch. 10 of G&G, 11th Ed., “Some β-receptor antagonists produce peripheral vasodilation…These mechanisms appear to contribute to the antihypertensive effects by enhancing hypotension, increasing peripheral blood flow, and decreasing afterload.”

  8. Julie says:

    Also, in addition to what Brian says above about #17. Beta Blockers reduce renin release, which leads to a reduction of aldosterone. Therefore, that reduces afterload. I think that’s what First Aid is getting at in the chart… (esp if you look at the diagram on the pg. 250).

  9. Julie says:

    woops i mean reduction of angiotensin II and aldosterone.

  10. Nelson says:

    The first error listed here (p235, myocardial action potential) doesn’t make sense to me. Can someone elaborate on what is wrong with the diagram in FA?

  11. Nelson says:

    Regarding #7, rupture, UpToDate lists the incidence as septal > free wall > papillary (see the link)

  12. Nelson says:

    #9 – I was under the impression that red vs pale infarcts referred only to coagulative necrosis (and the brain undergoes liquefactive necrosis).

    #15 Kussmaul’s sign is seen in constrictive pericarditis, but it is not seen in cardiac tamponade (see Lilly pathophysiology of heart disease 4th ed. p345)

    Regarding my previous comment, the “link” is when you click on my name :)

  13. Holly says:

    In response to #9 P.244, Infarcts: red vs. pale:
    Red infarcts occur in areas with dual circulation, like lung and liver, NOT in watershed areas. Watershed areas are defined as areas just distal to the supply of two arteries, so that if either of those arteries become ischemic, the watershed area is most susceptible to infarct, and I think it would be a pale infarct since it’s ischemic. Watershed areas are not areas of overlapping supply, but rather, of lack of overlapping supply.

  14. Holly says:

    In response to Nelson, the UptoDate link says that patients with septal rupture have the highest incidence of post-MI angina, NOT that septal rupture is the most common rupture.

  15. Brian says:

    pg 251
    Hydralazine:
    Mechanism is listed as “[up arrow] cGMP–> smooth muscle relaxation.” This is not the mechanism of hydralazine or minoxidil. This is the mechanism for NO and other nitro derived vasodilators. BRS Pharm: pg 91 Hydralzine and Minoxidil “effect is probably mediated by increasing K+ efflux and decreasing Ca2+ influx.” These serves to hyperpolarize the membrane and reduce the amount of Ca2+ available for contraction. Also one of minoxidil’s main side effects is hirsutism and this is taken advantage of to treat male pattern baldness and thinning hair which is not mentioned.

  16. Janet says:

    On page 255: I’m pretty sure Antiarrhythmics decrease the slope of phase 0 depolarization NOT phase 4.

  17. Janet says:

    I’m sorry, Just ignore my last comment. It’s correct. I just think it would be more clear if they put the word ALSO before that sentence.

  18. nyu says:

    on page 255, The Class Ia antiarrhythmics list amiodarone as a member. Amiodarone is Class III. The memory tool should read “the Queen Proclaims Diso’s Pyramid”

  19. Nick says:

    http://en.wikipedia.org/wiki/Amiodarone#Mechanism_of_action

    Amiodarone works in many ways, Class Ia, II, III, and IV, though it seems to be classified in III on the Wiki.

  20. Abe says:

    p. 243 Patent ductus arteriosus

    where it says “shunt becomes left to right with subsequent RVH”, that’s not correct…it should say “shunt becomes left to right with subsequent volume overload of pulmonary circulation, LA, LV, resulting in LVH and left-sided heart failure.”

    See Lilly, 3rd edition p. 360

  21. Sureshot says:

    On page 230 in vignette #3 it says ASD has a systolic murmur. On page 231 in the “Tricuspid area” it says it has a diastolic murmur.

    Which is right? You could say diastolic, because that is when the atria contract and the blood moves from LA –> RA, or you could go with systolic because the excess volume of blood that ends up in the RV can cause a flow murmur across the pulmonic valve. Maybe both are correct?

  22. chiviss says:

    In response to Sureshot, eMedicine say that the findings depend on the hemodynamic consequences of the left-to-right shunt, which in turn depends on the size of the defect, the diastolic properties of both ventricles, and the relative impedance in pulmonary and systemic circulation. ASDs with moderate-to-large left-to-right shunts produce a pulmonary outflow murmur that begins shortly after the S1, peaks in early-to-mid systole and that ends before the S2. # Increased right ventricular stroke volume across the pulmonary outflow tract and valve creates a crescendo-decrescendo midsystolic (ejection) murmur.

  23. Marc says:

    p.255 Na+ channel blockers decrease slope of phase 0, not phase 4, correct?

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