Cardiovascular Third Degree PDF

MEHLMANMEDICAL.COM - Answer = “Pulmonary arteriovenous fistula” (leading to high-output failure); diagnosis is hereditary hemorrhagic telangiectasia. USMLE will basically always show you a pic of red dot...

MEHLMANMEDICAL.COM - Answer = “Pulmonary arteriovenous fistula” (leading to high-output failure); diagnosis is hereditary hemorrhagic telangiectasia. USMLE will basically always show you a pic of red dots on the tongue/mouth or finger in a patient with nosebleeds. - Likewise, be aware intraosseous AV fistulae can occur in Paget, as mentioned before. HY Murmur / ECG points for USMLE - Described as “irregularly irregular” rhythm with absent p-waves. - Notice how the QRS complexes are at random and irregular distances from one another. This is the “irregularly irregular” pattern. - AF is hugely important because it can cause turbulence/stasis within the left atrium that leads to a LA mural thrombus formation. This thrombus can launch off (i.e., become an embolus) and go to brain (stroke, TIA, retinal artery Atrial fibrillation (AF) occlusion), SMA/IMA (acute mesenteric ischemia), and legs (acute limb ischemia). - AF HY in older patients, especially over 75. Vignette will usually be an older patient with a stroke, TIA, or retinal artery occlusion, who has normal blood pressure (this implies carotid stenosis is not the etiology for the embolus). - AF usually is paroxysmal, which means it comes and goes. The vignette might say the patient is 75 + had a TIA + BP normal + ECG shows sinus rhythm with no abnormalities à next best step is Holter monitor (24-hour ambulatory ECG monitor) to pick up the paroxysmal AF (e.g., when the patient goes home and has dinner). - After AF is diagnosed with regular ECG or Holter, 2CK wants echocardiography as the next best step to visualize the LA mural thrombus. - Patient who has severe abdominal pain in setting of AF or hyperthyroidism (which can cause AF), diagnosis is acute mesenteric ischemia; next best step is mesenteric angiography; Tx is laparotomy if unstable (answer on NBME). MEHLMANMEDICAL.COM 17  MEHLMANMEDICAL.COM - Severe pain in a leg + absent pulses in patient with irregularly irregular rhythm = acute limb ischemia; USMLE wants “embolectomy” as answer. - Any structural abnormality of the heart, either due to LV hypertrophy, ischemia, growth hormone/anabolic steroid use, prior MI, etc., can lead to AF. - You need to know AF patient will get either aspirin or warfarin. This is determined by the CHADS2 score. There are variations of the score, but the simple CHADS2 suffices for USMLE à CHF, HTN, Age 75+, Diabetes, Stroke/TIA/emboli. Each component is 1 point, but stroke/TIA/emboli is 2 points. If a patient has 0 or 1 points, give aspirin; if 2+ points, give warfarin. - “Emboli” refers to Hx of AF leading to stroke, TIA, acute, mesenteric ischemia, or acute limb ischemia – i.e., any Hx of embolic event. 2CK IM form gives short vignette of 67F with chronic AF + Hx of acute limb ischemia + no other info relating to CHADS, and answer is warfarin to prevent recurrence; aspirin is wrong. - Some students will ask about NOACs, e.g., apixaban, etc., for non-valvular AF à I’ve never seen NBME care about this stuff. They seem to be pretty old- school and just have warfarin as the answer, probably because there isn’t debate around whether it can be used; use of NOACs is less textbook. - AF patient should also be on rate control before rhythm control. The USMLE actually doesn’t give a fuck about this component of management, although in theory metoprolol or verapamil is standard. You could be aware for Step 3 that flecainide is first-line for rhythm control if patients fail rate-control and have a structurally normal heart and no coronary artery disease. - NBME for 2CK has “electrical cardioversion” as the answer for patient with AF who has hemodynamic instability (i.e., low BP). What you need to know is: sometimes AF can trigger “rapid ventricular response,” where HR goes >150 and low BP can occur. - Has classic sawtooth appearance. Atrial flutter - Low yield for USMLE. I think it’s asked once on a 2CK NBME. But as student you should know it exists / the basic ECG above. - Causes wide-complex QRS complexes (>120 ms; normal is 80-120 ms). Ventricular tachycardia (VT) - Exceedingly HY for 2CK that you know VT is wide-complex, whereas SVT is narrow-complex. If you look at above ECG, even if you say, “No idea what I’m looking at.” You can tell the complexes look wide like mountains in comparison to a typical ECG. MEHLMANMEDICAL.COM 18  MEHLMANMEDICAL.COM - VT is treated with anti-arrhythmics – i.e., amiodarone. If patient has coma or hemodynamic instability (low BP), the NBME answer is direct current countershock or cardioversion (same thing). - Premature ventricular complex (PVC) is asked on 2CK. - Note on the above strip, we have a wide complex (meaning ventricular in origin) that occurs earlier (hence premature). What they do on the NBME is show you this strip and ask where this abnormality originates from, then the answer is just “ventricle.” - Don’t treat PVCs on USMLE. - Causes narrow / needle-shaped complexes. Make sure you’re able to contrast this with VT above, which is wide-complex. Supraventricular tachycardia (SVT) - Notice the complexes are narrow / look like needles. This means the tachy originates above the ventricles (hence SVT). - Treatment of SVT exceedingly HY on 2CK. - First step is carotid massage (aka vagal maneuvers). In pediatrics, they can do icepack to the face. - If the above doesn’t work, the next step is give adenosine (not amiodarone). - Same as with VT, if the patient has coma or low BP, shocking the patient is the first step. In other words, for both SVT and VT, you must shock first in the setting of coma or hemodynamic instability. It’s for stable SVT and VT that the treatments differ on USMLE. - Will present as ST-elevations in 3-4 contiguous leads. Acute MI (STEMI) MEHLMANMEDICAL.COM 19  MEHLMANMEDICAL.COM - The above is an inferior MI, as evidenced by ST-elevations in leads II, III, and aVF. The answer for the affected vessel is the posterior descending artery (PDA supplies the diaphragmatic surface of the heart); since >85% of people have right-dominant circulation (meaning the PDA comes of the right main coronary), sometimes the answer for inferior MI can just be “right coronary artery.” - If the Q says left-dominant circulation, the sequence USMLE wants is: left main coronary à left circumflex à PDA. - The apex of the heart is supplied by the left anterior descending artery (LAD). If there are ST-elevations in leads V1-V3, choose LAD as the answer. - The left-lateral heart is supplied by the left circumflex artery. If there are ST- elevations in leads V4-V6 for lateral MI, choose left circumflex. - Reciprocal ST-depressions in the anterior leads V1-V3 can reflex posterior wall MI (i.e., we have “elevations” out the back of the heart, so they look like depressions on the anterior wall leads). - As discussed earlier, if patient has MI followed by new-onset systolic murmur hours to days later, with or without dyspnea, that’s mitral regurg. - Stroke-like presentation in patient who had MI weeks ago à “embolus from ventricular septal aneurysm” (on 2CK form). - Most common cause of death due to MI is ventricular fibrillation (VF). - Fibrosis of myocardium in the months-years post-MI increases risk of arrhythmias such as AF, SVT, VT, etc. There’s no specific arrhythmia you need to memorize. Just know the risk is there in the future. - Q waves on an ECG mean old MI / history of MI. The vignette might give you patient who has light-headedness / fainting + they say patient has Q waves in II, III, aVF, and the answer will be something like “paroxysmal supraventricular tachycardia.” Student thinks this specific arrhythmia matters, but it doesn’t. The point is that Hx of MI means patient is at risk for nearly any arrhythmia now. - MI classically causes coagulative necrosis of the myocardium. - With cardiogenic shock as a result of MI, the arrows USMLE wants are: ¯ cardiac output, ­ peripheral vascular resistance, ­ PCWP. - MI can lead to acute tubular necrosis from cardiogenic shock à acute drop in renal perfusion. This is not pre-renal. I discuss this in detail in the renal section. - First treatment for MI is aspirin. After aspirin is given, the next drug to give is clopidogrel (an ADP P2Y12 blocker) as dual anti-platelet therapy. - USMLE wants you to know anyone with acute coronary syndrome (i.e., MI or unstable angina) gets coronary catheterization. This is answer on new 2CK NBME exam. - It’s to my observation that more extensive management of MI on USMLE, such as use of beta-blockers, nitrates, morphine, oxygen, statin, percutaneous coronary intervention, etc., isn’t assessed in detail. I can comment, however, that one 2CK Q wants you to know nitrates are contraindicated in right-heart MIs, which includes inferior MI in most people due to the right coronary supplying the PDA. This is because right-sided MIs are preload-dependent, which means they need sufficient preload to maintain BP. - Percutaneous coronary intervention (PCI) is done in patients with STEMIs within 90 minutes of reaching hospital. - Shows up on ECG as diffuse ST-elevations (i.e., in all leads rather than 3-4 contiguous leads as with MI). PR depressions can also be seen, but I’ve never seen the USMLE give a fuck about the latter. - Patient will have pain that’s worse when lying back, better when leaning forward. In turn, the patient can present walking through the door bent over at Pericarditis the waist. - Serous pericarditis will be post-viral, secondary to autoimmune disease, or due to cocaine use. - NBME Q gives pericarditis + a bunch of different organism types (i.e., bacterium, fungus, etc.), and answer is “virus.” MEHLMANMEDICAL.COM 20  MEHLMANMEDICAL.COM - Patient with rheumatoid arthritis or SLE notably at risk for pericarditis. In other words, don’t get confused if they mention pericardial friction rub in vignette of RA or SLE; this is common. - For cocaine use, they’ll say a 22-year-old male has chest pain after a night of heavy partying + ECG shows diffuse ST-elevations à Dx = pericarditis. - Uremic pericarditis is HY for 2CK. Q will give ultra-high creatinine and BUN and say there’s a friction rub à treatment = hemodialysis. - Treatment for pericarditis is same as acute gout à NSAIDs, colchicine, steroids. - Fibrinous pericarditis is post-MI and occurs as two types: 1) literally “post-MI fibrinous pericarditis,” which will simply be friction rub within days of an MI; 2) Dressler syndrome (antibody-mediated fibrinous pericarditis occurring 2-6 weeks post-MI). - ECG is first step in Dx of pericarditis, but USMLE wants echocardiography as next best step in order to visualize a concomitant effusion that can occur sometimes. Vignette will give you stereotypical pericarditis + will ask for next best step in diagnosis; ECG might not be listed and you’re like huh? à Answer is echocardiography to look for potential effusion concomitant to the pericarditis. - I should make note that chronic constrictive pericarditis is a separate condition that doesn’t present with the standard pericarditis findings as described above. - This is low-yield for USMLE, but students ask about it because it can be confused with tamponade. - There’s two ways this can show up: 1) Tuberculosis is a classic cause; there may or may not be calcification around the heart on imaging. So if you get a Q where patient has TB + some sort of heart-filling impairment à answer = chronic constrictive pericarditis. 2) Kussmaul sign will be seen in the Q, where JVD occurs with inspiration rather than expiration. - Normally, inspiration facilitates RA filling (¯ intrathoracic pressure à ­ Chronic constrictive pulmonary vascular compliance/stretching à ­ high-low pressure gradient pericarditis from right heart to the lungs à ¯ in afterload on RV from the lungs à blood moves easier from right heart to the lungs à blood is pulled easier from SVC/IVC to the RA). - However, if there is ­ compressive force on the heart, the ­ in negative intrathoracic pressure during inspiration is not transmitted to the right side of the heart, so JVP does not ¯ (and can even paradoxically can ­). - In tamponade, however, as discussed below, the ­ in negative intrathoracic pressure during inspiration is able to be transmitted to the right side of the heart, so Kussmaul sign does not occur. This is likely because in constrictive pericarditis, the rigid pericardium prevents expansion of the right heart altogether, whereas in tamponade, the pericardium isn’t rigid per se, but is just filled with blood that can move/shift during the respiratory cycle, thereby allowing right heart expansion during inspiration. - Cardiac tamponade = pericardial effusion + low blood pressure. - What determines whether we have a tamponade or not is the rate of accumulation of the fluid, not the volume of the fluid – i.e., a stab wound or post-MI LV free-wall rupture resulting in fast blood accumulation, even if smaller volume, might cause tamponade, but cancer resulting in slow, but large, Pericardial effusion / accumulation might not cause tamponade. Cardiac tamponade - Tamponade presents as Beck triad: 1) hypotension, 2) JVD, 3) muffled/distant heart sounds. The question will basically always give hypotension and JVD. Occasionally they might not mention the heart sounds. But you need to memorize Beck triad as HY for tamponade. - Pulsus paradoxus (i.e., drop in systolic BP >10 mm Hg with inspiration) is classically associated with tamponade, although not frequently mentioned in MEHLMANMEDICAL.COM 21  MEHLMANMEDICAL.COM vignettes. I’ve seen a 2CK NBME Q where they say “the pulsus paradoxus is 200 ms). Should normally be 80-120 ms. First degree - Note that above on the ECG, the PR-segment in particular (just prior to the QRS complex) is extra-long. - Not really assessed on USMLE. Just know the definition. - Don’t treat on USMLE. MEHLMANMEDICAL.COM 23  MEHLMANMEDICAL.COM - Gradually prolonging PR interval until QRS drops. Then cycle repeats. Second degree Mobitz type I (aka Wenckebach) - Don’t treat on USMLE. - No gradual prolongation of PR interval, followed by a random dropping of the QRS. - Can also sometimes occur as patterns of 2:1, 3:1, etc., where there will be a P to QRS ratio of 2:1 or 3:1, etc. Second degree Mobitz type II - Regardless as to whether the dropped QRS is random or in a numerical pattern, there is no gradual prolongation of the QRS before the dropped complex. - More dangerous than Mobitz I. This is because Mobitz II has higher chance of progression into type III heart block. - Treatment on USMLE is insertion of pacemaker. This is asked on a new 2CK NBME exam. - Two things you want to look for on ECG: - 1) Ultra-slow HR (i.e., 30-40). You’ll see the QRS’s are super far apart. This is the ventricular escape rhythm. - 2) No relationship between the P-waves and QRS complexes. Third degree - Treatment on USMLE is insertion of pacemaker. - So what you want to remember is that Mobitz II and 3rd-degree are the ones where we insert pacemaker; 1st-degree and Mobitz I we don’t. MEHLMANMEDICAL.COM 24