HY Cardio PDF - Heart Failure & Abnormalities

MEHLMANMEDICAL HY CARDIO  MEHLMANMEDICAL.COM YouTube @mehlmanmedical Instagram @mehlman_medical MEHLMANMEDICAL.COM 2  MEHLMANMEDICAL.COM HY Cardio – by Dr Mike Mehlman...

MEHLMANMEDICAL HY CARDIO  MEHLMANMEDICAL.COM YouTube @mehlmanmedical Instagram @mehlman_medical MEHLMANMEDICAL.COM 2  MEHLMANMEDICAL.COM HY Cardio – by Dr Mike Mehlman Important basic heart failure points - Presents as pulmonary findings (i.e., pulmonary edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea). - This is because left-heart problems cause a backup of pressure onto the pulmonary circulation, leading to increased pulmonary capillary hydrostatic pressure à transudation of fluid into the alveolar spaces (pulmonary edema). Sometimes this can also cause pleural effusion. - Left atrial pressure (LAP) = pulmonary capillary wedge pressure (PCWP). Left heart failure - Therefore, if there is left heart pathology, PCWP is high (exceedingly HY). - Conversely, if a Q gives you normal PCWP, you know there’s nothing wrong with the left heart. Qs will often give high PCWP and low BP, where you need to know immediately that means cardiogenic shock. - What USMLE will do is give you some sort of left-heart pathology + dyspnea, and then ask for the cause of the dyspnea à answer = “increased pulmonary capillary hydrostatic pressure.” Another answer in this case is “increased alveolar-arteriolar (A-a) oxygen gradient.” - Presents as systemic findings – i.e., jugular venous distension (JVD) and peripheral edema. - Since blood cannot enter the right heart as easily, it backs up to the neck veins (JVD) and venous circulation (increased hydrostatic pressure in veins à transudation of fluid into legs). The Q might mention that central venous Right heart failure pressure is high. - Hepatosplenomegaly can also be seen in RHF but is very rare on USMLE. - Normal jugular venous pressure (JVP) is 3cm above the sternal angle. JVD would be higher than this. Sometimes questions can write that jugular venous pulsations are seen 3cm above the sternal angle and the student erroneously thinks this means JVD, but this is not the case. - Congestive heart failure = left heart failure + right heart failure. - The most common cause of right heart failure is left heart failure. Simply adding the two together, we now call that congestive heart failure. Congestive heart failure - In congestive heart failure, we’ll see both left- and right-heart failure findings – i.e., patient will have dyspnea, JVD, and peripheral edema. - PCWP is elevated in these patients, since the left heart has pathology. - Cor pulmonale is defined as right-heart failure due to a pulmonary cause. In other words, the left heart is completely normal in cor pulmonale and PCWP is normal. - Cor pulmonale will be a patient who has JVD and peripheral edema in the setting of obvious and overt lung disease, such as 100-pack-year smoking history, cystic fibrosis, or pulmonary fibrosis. These can present with lung findings such as wheezes, where you as the student need to say, “It just doesn’t seem like they’re focusing on left-heart failure as the cause of the right-heart failure here. It seems the 100-pack-year smoking Hx causing Cor pulmonale COPD is why the right heart is failing.” - Can occur due to bronchopulmonary dysplasia in premature neonates or obstructive sleep apnea, since the lung disease backs up to the right heart. - The patient can have a “boot-shaped” heart colloquially, which refers to right ventricular hypertrophy without left ventricular hypertrophy. - If the patient has COPD, the massively hyperinflated lungs will push the heart to the midline, causing a long, narrow cardiac silhouette, with a point of maximal impulse in the sub-xiphoid space. - You must know that pulmonary hypertension is the reason the right heart decompensates. In both cor pulmonale and congestive heart failure, the MEHLMANMEDICAL.COM 3  MEHLMANMEDICAL.COM right heart experiences increased afterload because of pulmonary hypertension. - Endothelin 1 is vasoconstrictor and key mediator in pulmonary hypertension. USMLE wants you to know this is increased in both cor pulmonale and left heart failure. Bosentin is an endothelin 1 receptor antagonist. - Nitric oxide synthase, in contrast, USMLE wants you to know is decreased in pulmonary hypertension (makes sense, since NO dilates). - A loud P2 and tricuspid regurgitation are HY findings in cor pulmonale. I discuss these in more detail in the tables below. Hyper-quick causes of bilateral pitting peripheral edema - Right heart failure (either due to cor pulmonale or congestive) à ¯ ability to fill right heart à ­ central venous pressure à ­ systemic venous hydrostatic pressure à transudation of fluid from systemic veins/venules into interstitium of legs. - Tangential, but Step 1 NBME asks why HTN doesn’t automatically cause peripheral Cardiac edema à answer = “increased pre-capillary resistance.” The USMLE wants you to know that arterioles are responsible for the majority of peripheral resistance; in the setting of high BP, the reason capillary hydrostatic pressure isn’t automatically high enough where the transudation threshold is reached is because arterioles constrict, thereby ­­ resistance and reducing excessive blood flow through the capillaries. - Cirrhosis à ¯ hepatic production of albumin à ¯ intravascular oncotic pressure à Hepatic transudation of fluid from systemic veins/venules into interstitium of legs. - Proteinuria à hypoalbuminemia à ¯ intravascular oncotic pressure à transudation Nephrogenic of fluid from systemic veins/venules into interstitium of legs. - Dihydropyridine calcium channel blockers (i.e., amlodipine, nifedipine). Drugs - Imatinib (targets BCR/ABL tyrosine kinase in CML). - Miscellaneous mechanisms not important for USMLE. Just know above drugs do it. - Strict vegetarianism or veganism à ¯ dietary protein consumption à ¯ intravascular Dietary oncotic pressure à transudation of fluid from systemic veins/venules into interstitium of legs. Pregnancy - A little bit of peripheral edema is normal in pregnancy due to compression of IVC. Hyper-quick causes of unilateral non-pitting edema - Malignancy (e.g., peau d’orange of breast), Hx of surgery (e.g., mastectomy), Lymphatic insufficiency Wuchereria bancrofti (elephantiasis). - Pretibial myxedema (Graves) à mucopolysaccharide deposition in skin + surrounding edema. - Myxedma (severe hypothyroidism) à despite the name, it refers to general “severe hypothyroidism,” not just skin changes; can cause carpal tunnel Thyroid syndrome. - “Pretibial myxedema” is only seen in Graves. Paradoxical hyperthyroidism seen in Hashimoto causing pretibial myxedema is astronomically rare and will get you questions wrong on USMLE. MEHLMANMEDICAL.COM 4  MEHLMANMEDICAL.COM HY Valvular / flow abnormalities on USMLE - Fixed splitting of S2 - Can sometimes be associated with a systolic flow murmur, since more blood L à R from the LA à RA means more blood flow across the pulmonic valve. So Q might say “fixed splitting of S2 and a systolic murmur.” - Sometimes can be seen in Qs as “wide, fixed splitting.” I only mention this because some students get pedantic / ask about this. “Wide splitting” just means right ventricular hypertrophy. So if the Q says “wide, fixed splitting,” they’re saying the patient has RVH due to an ASD. - Patent foramen ovale = ASD on USMLE. Don’t confuse with patent ductus arteriosus (discussed below). - USMLE loves asking questions showing you change in oxygen in the chambers of the heart and making you choose ASD, VSD, etc. Atrial septal defect - For example, you can see above that somehow O2 increases from the SVC to the RA, which is ordinarily impossible. The only way this could occur is if an ASD is present, where oxygenated blood moved from LA à RA. - ASDs can sometimes be responsible for “paradoxical emboli,” where a DVT leads to stroke. This is ordinarily impossible, since a clot embolizing to the lungs via the venous circulation has no way of reaching the arterial circulation. But if an ASD is present, the clot can go RA à LA à LV à up to the brain, causing stroke. - 2CK: ASDs do not need to be repaired unless patient has evidence of pulmonary hypertension, RVH, or develops an arrhythmia (i.e., usually AF). - If adult with ASD has paradoxical embolus (DVT going through the ASD to the brain/arterial circulation), this is also indication for repair. - Holosystolic (aka pan-systolic) murmur at lower left sternal border. - Can be associated with a diastolic rumble or enlarged left atrium (if more blood going L à R across VSD, then more blood is returning to the LA from the lungs à LA dilatation). - Seen as part of tetralogy of Fallot (VSD, RVH, overriding aorta, pulmonic stenosis). - If a VSD is repaired, USMLE wants ­ LV pressure, ¯ RV pressure, and ¯ LA Ventricular septal defect pressure as the changes now seen in the heart. - VSD does not cause cyanosis at birth. Only years later after the higher blood flow to the lungs results in pulmonary hypertension, followed by right ventricular hypertrophy and reversal R à L (Eisenmenger) can the patient become cyanotic. - Murmur can be silent or soft at birth, followed by loud at 7 days of life. The USMLE will ask why the murmur is louder now à answer = decreased pulmonary vascular resistance – i.e., the lungs open up during the first MEHLMANMEDICAL.COM 5  MEHLMANMEDICAL.COM week of life, resulting in decreased RV pressure and an increase in the L à R pressure gradient (louder murmur). - Conversely, if they ask why the murmur was softer at birth compared to now, the answer is “increased pulmonary vascular resistance,” where the lungs were still closed at the time, so there was a lesser gradient L à R (softer murmur) at birth. - Similar to ASD Qs, USMLE loves giving you diagrams with changes in O2 between the chambers and then making you infer we have a VSD. - NBME loves this style of Q. You can see O2 somehow increased from RA to RV. The only way this is possible is if we have a VSD where oxygenated blood moves from LV à RV. - This one might initially appear a little more difficult. This is Eisenmenger syndrome, where we have a reversal of flow from RV à LV across the VSD. The NBME is known to show this diagram as well. - If you’re wondering why oxygen % goes from 99 to 96 from the pulmonary circulation to the LA, this is because of thebesian veins draining the myocardium itself, which open into the different heart chambers, including the LA. If you think that’s weird, take it up with NBME, not me, since they have the 99 to 96 drop-down on their diagrams. - 2CK: VSDs are repaired if patient develops pulmonary hypertension, RVH, arrhythmia, Eisenmenger syndrome, recurrent endocarditis (turbulence of blood due to VSD can ­ risk of valve infections), or aortic regurgitation (if VSD located near the aortic valve). - Seen in Down syndrome. Atrioventricular septal defect - Between the atrium and ventricle, aka “endocardial cushion defect,” although this latter term can also apply to ASD and VSD in Downs. MEHLMANMEDICAL.COM 6  MEHLMANMEDICAL.COM - Holosystolic (pan-systolic) or just regular “systolic,” 29 times out of 30. - Q on NBME 20 offline for Step 1 has MR as “mid-systolic,” but I contend this is erratum. - Most USMLE questions will not mention it radiating to the axilla. - Highest yield cause of MR on USMLE is post-MI papillary muscle rupture. USMLE is obsessed with this. They’ll say hours to days after an MI, patient has new-onset systolic murmur à answer = MR. - Seen acutely in rheumatic heart disease (valve scars over years later and becomes mitral stenosis). - Can be caused by general ischemia / dilated cardiomyopathy. - Can cause JVD (i.e., back up all the way to the right heart); this is asked Mitral regurgitation multiple times on the new Step 1 NBMEs. - For 2CK: You do not do preoperative stress tests to determine perioperative MI risk if the patient has mere mitral regurg without other risk factors. For example, one of the Surg forms gives a Q where smoker with MR has no shortness of breath or chest pain with exertion, and the answer is “no further management indicated,” where exercise stress test is wrong. - If the patient has Sx of heart failure or ischemia, then we do pre-op stress test to determine MI risk. I discuss stress tests later in this chapter. - The mitral valve is replaced if the patient develops severe pulmonary symptoms (i.e., shortness of breath / reduced exercise tolerance), reduced ejection fraction, arrhythmia, or endocarditis if valve function is destroyed. - Described as “rumbling diastolic murmur with an opening snap”; can also be described as “decrescendo mid-late diastolic murmur” (i.e., following the opening snap). - Can cause a right-sided S4 if the pressure backs up all the way to the right heart (seen on NBMEs sometimes; this confuses students because they think S4 must be LV, but it’s not the case). An S4 is a diastolic sound heard in either the LV or RV when there is diastolic stiffening due to high afterload. - 99% of mitral stenoses are due to Hx of rheumatic heart disease (i.e., the patient had rheumatic fever as a child, where at the time it was mitral regurg, but years later it has now become mitral stenosis). - One 2CK NBME Q mentions patient with history of rheumatic heart disease who, years later, now has 4/6 rumbling diastolic murmur without an opening snap; this is still mitral stenosis. Although opening snap is buzzy for MS, just be aware it’s not mandatory and that this Q exists on NBME. - Other HY presentation on USMLE is pregnant women with new-onset Mitral stenosis dyspnea in 2nd trimester and a diastolic murmur. This is because 50% increase in plasma volume by 2nd trimester causes the underlying subclinical MS to become symptomatic. Don’t confuse this with severe dyspnea and peripheral edema in late third-trimester, which is instead peripartum cardiomyopathy (antibody-mediated). - The 1% of MS that’s not due to Hx of RF can be marantic (non-bacterial thrombotic endocarditis; NBTE) à endocarditis seen due to hypercoagulable state in the setting of malignancy, where the vegetations are small and verrucous, on both sides of the valve. This is in contrast to bacterial endocarditis, which causes large, floppy vegetations that lead to MR, not MS. - Libman-Sacks endocarditis seen in SLE is due to antiphospholipid antibodies and is a type of NBTE. - 2CK: Balloon valvuloplasty is the 1st-line Tx for mitral stenosis. This is done if patient has minimal calcification of the valve + has pulmonary HTN. - Mitral valve replacement is done if balloon valvuloplasty fails, if patient has severe MS with dyspnea, arrhythmia, or calcification of the valve. MEHLMANMEDICAL.COM 7  MEHLMANMEDICAL.COM - Most common murmur. - Described as mid-systolic click. - “Myxomatous degeneration” is buzzy term that refers to connective tissue degeneration causing MVP in Marfan and Ehlers-Danlos. - Almost always asymptomatic. On 2CK forms, they want you to know about “mitral valve prolapse syndrome,” which is symptomatic MVP that presents as repeated episodes of “fleeting chest pain” on the left side in an otherwise healthy patient 20s-30s. They might say there is Hx of MI in the family, but this is MVPS, not MI. Answer on surgery form is “no treatment Mitral valve prolapse necessary." - USMLE loves using MVP as a distractor in panic disorder questions, particularly on the 2CK Pysch CMS forms. They will give long paragraph about panic attack/disorder + also mention there’s a mid-systolic click; they’ll ask for cause of patient’s presentation à answer = panic disorder, not MVP à student is confused because they say mid-systolic click, but the MVP isn’t the cause of the patient’s presentation; the panic disorder is; MVPs are usually incidental, benign, and asymptomatic. - MVP does not progress to mitral regurg almost always. So don’t think that MVP and MR are the same. - Decrescendo holo-diastolic (pan-diastolic) murmur; can also be described as “early diastolic murmur,” or “diastolic murmur loudest after S2.” - Causes wide pulse pressure (i.e., big difference between systolic and diastolic pressures, e.g., 160/50, or 120/40) à results in head-bobbing and bounding pulses (don’t confuse with slow-rising pulses of aortic stenosis). - The bounding pulses can be described on NBME as “brisk upstroke with precipitous downstroke.” In turn, they can just simply say, “the pulses are brisk,” meaning the systolic component is strong. - I would say 4/5 times bounding pulses means AR. The other 1/5 will be PDA and AV fistulae (discussed below). Bounding pulses occur when blood Aortic regurgitation quickly leaves the arterial circulation. In AR, the blood quickly collapses out of the aorta back into the LV. In PDA, it leaves the aorta and enters the ductus arteriosus; in AV fistulae, it leaves for a vein. - Highest yield cause on USMLE is aortic dissection à can retrograde propagate toward the aortic root causing aortic root dilatation and AR. - Even though MVP is most common in Marfan and Ehlers-Danlos, AR is second most common in these patients, since if they get aortic dissection, this can lead to AR. - Can lead to volume overload on the LV and eccentric hypertrophy. - 2CK: Valve is replaced if patient has EF 80% asymptomatic, then do endarterectomy. “Symptomatic” = stroke, TIA, or retinal artery occlusion. A mere bruit is not a symptom; that is a sign. - If under these thresholds, do medical management only, which requires a triad of: 1) statin; 2) ACEi or ARB; and 3) anti-platelet therapy. - The USMLE will not force you to choose between low- and high-potency statins. - USMLE tends to list lisinopril as their favorite ACEi for HTN control. - It’s to my observation aspirin alone is sufficient on NBME exams for anti- platelet therapy, even though in real life patient can receive either aspirin alone; the combo of aspirin + dipyridamole; or clopidogrel alone. - USMLE will not give borderline carotid occlusion thresholds – i.e., they’ll say either 30% or 90%. If they list the % as low, look at the vignette for the drugs they list the patient on. Sometimes they’ll show the patient is already on statin, lisinopril, and aspirin, and then the answer is just “continue current regimen.” I have once seen “add clopidogrel” as a wrong answer in this setting, which makes sense, since the combo of aspirin + clopidogrel is never given anyway. - Sometimes they will give you a low carotid occlusion % + say the patient is on 2 of 3 drugs in the triad, and then the answer is just “add aspirin,” or “add statin,” or “add lisinopril.” - If the vignette doesn’t mention elevated BP but says you have some random dude over 50 with a stroke, TIA, or retinal artery occlusion, the next best step is carotid ultrasonography to look for carotid stenosis. In other words, it is assumed the patient has a carotid plaque in this setting. - If the vignette gives patient with episodes of unexplained syncope or light-headedness, but not stroke, TIA, or retinal artery occlusion, then the next best step is ECG, followed by Holter monitor, looking for atrial fibrillation (AF causes LA mural thrombus that launched off to brain/eye). - The triad of 1) statin; 2) ACEi or ARB; and 3) anti-platelet therapy is also done for general peripheral vascular disease unrelated to carotid stenosis (i.e., if a patient has intermittent claudication). - Stroke, TIA, or retinal artery occlusion, if they don’t mention HTN, but they mention an abdominal bruit, you will still do a carotid duplex ultrasound. The implication is that the bruit in the abdomen could be a AAA or RAS, where atherosclerosis in one location means atherosclerosis everywhere, so the patient likely has carotid stenosis by extension. They once again need not mention carotid bruit; apparently it is not a sensitive finding (i.e., we cannot rule-out ­ occlusion just because we don’t hear it). - Classically presents as severe upper chest pain radiating to the back between the scapulae. Aortic dissection - As discussed above in the aortic regurg section, USMLE loves this as most common cause of AR due to retrograde propagation toward the aortic root. For example, patient with Hx of HTN, cocaine use, or a connective MEHLMANMEDICAL.COM 13  MEHLMANMEDICAL.COM tissue disorder (i.e., Marfan, Ehlers-Danlos) who has a diastolic murmur, you should be thinking immediately that this is dissection. - “Medial necrosis” is a term that is used on NBME exams to describe changes to the aorta in dissection. In the past, “cystic medial necrosis” used to be buzzy for dissection due to Marfan syndrome, but I haven’t seen USMLE care about this. I have, however, seen a dissection Q on NBME where it is due to hypertension, and simply “medial necrosis” is the answer. - As mentioned above, 3/4 Qs where BP is different between the arms refers to aortic dissection. A Q on 2CK IM form 7 has “thoracic aortic dissection” where not only is the BP different between the arms, but it’s also different between the L and R legs (i.e., L-leg BP is different from R-leg BP) à sometimes thoracic aortic dissections can anterograde propagate all the way down to the abdominal aorta. - You do not need to memorize these aortic aneurysm types. I’m just showing you that if the common iliacs are involved (as with left image), BP can differ as well between the legs. For 2CK: - CXR is done first to view ”widening of the mediastinum.” The next step is ”CT of the chest,” or “CT angiography.” They refer to same thing in this setting. If not listed, choose “aortic angiography” and “aortography.” - Tx for ascending aortic aneurysm (type A) = labetalol + surgery. - Tx for descending aortic aneurysm (type B) = labetalol alone initially. - Caused by deceleration injury. Most common cause of death due to car accident or fall. Exceedingly HY on 2CK. - Will be described as patient following an MVA who has “widening of the mediastinum” on CXR. Next best step is CT of chest or CT angiography. If not listed, choose aortography or aortic angiography. - Labetalol used first-line in aortic dissection and traumatic rupture of the aorta. If they force you to choose another drug after, nitroprusside is the Traumatic rupture answer on NBME. of the aorta - Labetalol is answer on NBME even in patient who has low BP due to rupture or dissection due to the drug ¯ shearing forces. I’ve seen students get this wrong saying, “But patient has low BP though.” My response is, file a complaint with the exam not with me. - 2CK Q gives “esmolol + nitroprusside” as answer to a traumatic rupture Q, but almost always, they will just want “labetalol.” - Emergency surgical repair is indicated following IV drug administration. - Can present as “visible pulsation” on USMLE. Aortic aneurysm - For aortic aneurysm, they can say “visible pulsation above the manubrium,” or “pulsatile mass above the manubrium.” There can also be MEHLMANMEDICAL.COM 14  MEHLMANMEDICAL.COM a tracheal shift. I’ve seen students select pneumothorax here. But for whatever reason you can get tracheal shift in thoracic aortic aneurysm. For AAA, there can be “visible pulsation in the epigastrium.” - Biggest risk factor for AAA is smoking. - For Family Med, do a one-off abdominal ultrasound in both men and women 65+ who are ever-smokers. This screening used to be just performed on men, but now it includes women. - For Surgery, AAA repair is indicated if the aneurysm is >5.5 cm or the rate of change of size increase is >0.5cm/month for 6 months. This is on Surgery form, where they give a patient with a 4-cm AAA and ask why serial ultrasounds are indicated à answer = “size of aneurysm.” - Don’t do AAA repair on USMLE in patient who has advanced comorbidities or terminal disease, e.g., stage 4 lung cancer. - In general, perioperative MI risk is assessed using a pre-op stress test. 2CK NBME Q has dipyridamole and thallium pharmacologic stress test as answer in patient with 6-cm AAA prior to surgery. - Diabetes is protective against aneurysm. Non-enzymatic glycosylation of endothelium causes stiffening of the vascular wall. - Tangential: 2CK Surg loves “pulsatile hematoma” in the neck in trauma patients, where the answer is “endotracheal intubation.” Sounds nitpicky, but shows up repeatedly. - Can be idiopathic, iatrogenic (i.e., dialysis), from injury (i.e., stab wound), or caused by other disease (i.e., hereditary hemorrhagic telangiectasia or Paget disease of bone). - Similar to aortic aneurysms, AV fistulae can sometimes present with pulsatile mass, but in a weird location, e.g., around the left ear in patient with tinnitus (on NBME exam). Student says, “Why is it at the left ear though?” à No fucking idea. Take it up with NBME. - Highest yield point is they can cause high-output cardiac failure. This is because blood quickly enters the venous circulation from the arterial circulation à combo of ­ preload back to right heart + poorer arterial perfusion distal to the fistula à compensatory ­ CO. - AV fistulae can sometimes present with a continuous machinery murmur Arteriovenous fistula similar to a PDA, since blood is continuously flowing through it. They might say a continuous machinery-like murmur is auscultated in the leg at site of prior stab wound. - As discussed earlier, they can present with bounding pulses similar to AR. - Student says, “Well how am I supposed to know if it’s AV fistula then if it sounds like other conditions too?” à by paying attention to HY points like, “Is there lone S3 or S3/4 combo or EF >70%? Is there Hx of penetrating trauma? Or does the patient have Paget? Etc.” - 2CK NBME Q shows you obscure angiogram of a fistula in the leg + tells you there’s a continuous machinery murmur; they ask what most likely determines prognosis in this patient à answer = “size of lesion.” MEHLMANMEDICAL.COM 15  MEHLMANMEDICAL.COM - NBME exam shows obscure image similar to above (without the arrow) + they tell you there’s continuous murmur à answer = “size of lesion.” - Another NBME Q gives 45-year-old male will nosebleeds since adolescence + S3 heart sound + dyspnea + they show you pic of tongue; they ask for the cause of dyspnea. - 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. MEHLMANMEDICAL.COM 16  MEHLMANMEDICAL.COM 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 occlusion), SMA/IMA (acute mesenteric ischemia), and legs (acute limb ischemia). These vignettes are higher yield for 2CK, but the concept is important for Step 1. - 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). Atrial fibrillation (AF) - 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. - For 2CK, 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. This is important for 2CK. - “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 7 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 9 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. MEHLMANMEDICAL.COM 17  MEHLMANMEDICAL.COM - 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). - 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. - VT is treated with anti-arrhythmics – i.e., amiodarone. If patient has coma or Ventricular tachycardia hemodynamic instability (low BP), the NBME answer is direct current (VT) 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. Supraventricular - Causes narrow / needle-shaped complexes. Make sure you’re able to contrast tachycardia this with VT above, which is wide-complex. (SVT) MEHLMANMEDICAL.COM 18  MEHLMANMEDICAL.COM - 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) - 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). MEHLMANMEDICAL.COM 19  MEHLMANMEDICAL.COM - USMLE wants you to know gross appearance of fresh vs several-day-old myocardial infarcts: At 12-24 hours, fresh infarcts show dark mottling (green arrow); by 10-14 days, an infarct becomes a yellow, softened area (pink arrow). - Old infarcts will appear white. There is an NBME Q that shows image similar to the following, where the answer is “congestive heart failure resulting from repeated infarcts”: Note the old infarcts are white in appearance (black arrows). - Left ventricular free-wall rupture can cause tamponade (Beck triad): MEHLMANMEDICAL.COM 20  MEHLMANMEDICAL.COM Note the myocardial free-wall rupture at the lower left aspect. - Ventricular septal rupture has similar image: Note the thinned/ruptured area of the interventricular septum (white arrow). - Post-MI papillary muscle rupture resulting in mitral regurg is exceedingly HY. 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 Neuro 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. MEHLMANMEDICAL.COM 21  MEHLMANMEDICAL.COM - USMLE wants you to know anyone with acute coronary syndrome (i.e., MI or unstable angina) gets cardiac 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. - 2CK: 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 the waist. - Serous pericarditis will be post-viral, secondary to autoimmune disease, or due to cocaine use. - Step 1 NBME Q gives pericarditis + a bunch of different organism types (i.e., bacterium, fungus, etc.), and answer is “virus.” - 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 Pericarditis heavy partying + ECG shows diffuse ST-elevations à Dx = pericarditis. - 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). - Uremic pericarditis is HY for 2CK. Q will give ultra-high creatinine and BUN and say there’s a friction rub à treatment = hemodialysis. - 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. - Treatment for pericarditis is same as acute gout à NSAIDs, colchicine, steroids. - 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 + Chronic constrictive some sort of heart-filling impairment à answer = chronic constrictive pericarditis 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 ­ pulmonary vascular compliance/stretching à ­ high-low pressure gradient 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). MEHLMANMEDICAL.COM 22  MEHLMANMEDICAL.COM - 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 ­). - 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, accumulation might not cause 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 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. - 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 Second degree Mobitz type II be a P to QRS ratio of 2:1 or 3:1, etc. - 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. MEHLMANMEDICAL.COM 25  MEHLMANMEDICAL.COM - 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. HY Cardiomyopathy points for USMLE - Can be isolated ventricular or diffuse 4-chamber dilation. Causes are multifarious, but a key feature is systolic dysfunction, where ejection fraction is reduced (i.e., 30mm. - Septal myectomy is done if the left ventricular outflow tract pressure gradient is >50mm Hg. But it should be noted ICD is usually first-line. - Heart failure due to diastolic dysfunction, where HTN is not the cause. - JVD is HY for RCM. An S4 can also be seen. The heart will not be dilated. Restrictive (RCM) - HY causes are Hx of radiation (leads to fibrosis), amyloidosis, and hemochromatosis. MEHLMANMEDICAL.COM 27  MEHLMANMEDICAL.COM - Student might say, “I thought you said hemochromatosis was DCM. So if we have to choose on the exam, which one is it?” The answer is, whichever the vignette gives you. If they say a large cardiac silhouette with an S3 and lateralized apex beat, that’s DCM. If they say JVD + S4 + nothing about a lateralized apex beat, you know it’s RCM. - Amyloidosis is protein depositing where it shouldn’t be depositing. Highest yield cause of amyloidosis on USMLE is multiple myeloma, which will lead to RCM. Cardiac amyloidosis. Myocardium is pink; amyloid is white. - Since RCM is diastolic dysfunction, the arrows are the same as HCM, which are: « EF; « LVEDV; ­ LVEDP. Important points about atherosclerosis for USMLE - Endothelial cell damage / dysfunction (e.g., from HTN or smoking) à monocytes leave blood and accumulate beneath internal elastic lamina of artery à monocytes within tunica media of artery are now called macrophages à phagocytosis of oxidized LDL particles à macrophages are now called foam cells à accumulation of foam cells leads to fatty streak/plaque à stimulates vascular smooth muscle cell migration/proliferation within plaque à cap thinning + rupture à myocardial infarction, etc. Mechanism - Most acceleratory risk factors are diabetes mellitus (I and II), followed by smoking, HY points followed by HTN, in that order. MEHLMANMEDICAL.COM 28  MEHLMANMEDICAL.COM - HTN is most common risk factor, but DM and smoking are worse. I talk a lot about this stuff in my HY Risk Factors PDF if you want extensive detail. - HTN is most acceleratory specifically for carotid stenosis (systolic impulse pounds carotids à endothelial damage). - Stroke, TIA, or retinal artery occlusion in patient with high BP is due to carotid plaque launching off to the brain/eye. If patient has normal BP, think AF instead, with left atrial mural thrombus launching off. - Patient over 50 with Hx of cardiovascular risk factors who now has accelerated HTN, think renal artery stenosis (narrowing due to atherosclerosis). - Plaques can calcify. The more calcium there is in a plaque, the more mature it is often considered to be. Calcium scoring is routinely done in patients who have coronary artery disease in the assessment of plaque progression. - Statins have 2 HY MOAs on USMLE: 1) inhibit HMG-CoA reductase; 2) upregulate LDL receptors on hepatocytes. - Ezetimibe blocks cholesterol absorption in the small bowel. - Bile acid sequestrants (e.g., cholestyramine) result in the liver pulling more cholesterol out of the blood. - Fibrates upregulate PPAR-a and lipoprotein lipase; best drugs to decrease triglycerides. HY Angina points for USMLE - Chest pain that occurs predictably with exercise. - Due to atherosclerotic plaques causing >70% occlusion; can be calcific. - Classically causes ST depressions on ECG. - Nitrates (e.g., sublingual isosorbide dinitrate) used as Tx à nitrates “donate” nitric oxide (NO) that upregulates guanylyl cyclase within venous smooth muscle à increased cGMP à relaxation of venous smooth muscle Stable angina à increased venous pooling of blood à decreased venous return à decreased myocardial oxygen demand à mitigation of chest pain. - Nitrates are contraindicated with PDE-5 inhibitors (e.g., Viagra) due to risk of low blood pressure. - Sodium nitroprusside used for hypertensive emergencies dilates arterioles in addition to the veins. If USMLE asks you where this drug acts, choose arterioles. - Chest pain that is unpredictable and can occur at rest. - Due to partial rupture of atherosclerotic plaque leading to partial occlusion. Unstable angina - ST depressions on ECG. - Diltiazem is answer on new 2CK NBME for patient with unstable angina. - Patients need cardiac catheterization. - Vasospastic angina that occurs at rest (i.e., watching TV or while sleeping) in younger adults; it is not caused by atherosclerosis. - ST elevations are seen on ECG. - You must know that Prinzmetal is also known as variant angina pectoris. There is an NBME Q that gives vignette of Prinzmetal, but answer is Prinzmetal angina “variant angina pectoris.” (variant angina pectoris) - Treatment is nitrates (can cause coronary artery dilation unrelated to the venous pooling effects) or dihydropyridine calcium channel blockers (e.g., nifedipine). Avoid a1-agonists in these patients (cause vasoconstriction), as well as non-selective b-blockers like propranolol (can cause unopposed a effects). MEHLMANMEDICAL.COM 29  MEHLMANMEDICAL.COM HY histopath / cardiac marker points for MI - Coagulative necrosis occurs within the first day of the MI. USMLE wants you to know cellular architecture is maintained in coagulative necrosis. Histopath - Neutrophils will infiltrate at 1-3 days. - Macrophages will infiltrate at 3-14 days. - Scar formation occurs from ~2 weeks onward. - Percutaneous coronary intervention used to open blocked coronary artery can cause reperfusion injury, where fast influx of oxygen to tissue results in high density of oxygen free radicals and peroxidation of lipid membranes à further myocardial HY random points necrosis. But this outcome is superior to non-intervention. - Adenosine is molecule that causes cardiac pain in MI and angina. It is main autoregulator of coronary blood flow. It is increased in MI due to exhaustion of ATP. - USMLE wants you to know during acute MI, cardiac markers are not initially elevated. We rely on the ECG to show us ST elevations. - Troponin rises the most and stays elevated the longest. - CK-MB is the answer if they ask about recurrent MI. This is because its shorter duration of elevation makes it useful to discern a new cardiac event has occurred. Cardiac markers Hypertensive Emergency + urgency (Steps 2CK/3 only) - HTN >180/120 + signs of end-organ damage. - The latter can be hypertensive encephalopathy (confusion), nephropathy (poor renal function tests), retinopathy, acute heart failure, etc. Emergency - BP should be ¯ by no more than 20-25% in the first hour, as drastic ¯ can compromise perfusion to the brain and vital organs. - Blood pressure should be brought under 160/100 by 24-48 hours. - Drugs used are IV sodium nitroprusside, IV nicardipine, IV labetalol, and oral captopril. - HTN >180/120 + no signs of end-organ damage. Urgency - Blood pressure should be brought under 160/100 by 24-48 hours. - Drugs used are IV sodium nitroprusside, IV nicardipine, IV labetalol, and oral captopril. HY Endocarditis points - Bacterial infection of valve in patient with no previous heart valve problem. - Caused by Staph aureus on USMLE. - Left-sided valves (i.e., aortic and mitral) most commonly affected because of Acute endocarditis greater pressure changes (i.e., from high to low) within left heart, resulting in turbulence that enables seeding. - IV drug users à venous blood inoculated with S. aureus à travels to heart and causes vegetation of tricuspid valve. MEHLMANMEDICAL.COM 30  MEHLMANMEDICAL.COM - Bacterial infection of valve in patient with history of valve abnormality (i.e., congenital bicuspid aortic valve, Hx of rheumatic heart disease). - Caused by Strep viridans on USMLE. You need to know S. viridans can be Subacute endocarditis further broken down into: S. sanguinis, S. mutans, and S. mitis. - Hx of dental procedure is HY precipitating event, where inoculation of blood occurs via oral cavity à previously abnormal valve gets seeded. - New-onset murmur + fever = endocarditis till proven otherwise on USMLE. - Reactive thrombocytosis (i.e., high platelets) can occur due to infection. This is not unique to endocarditis, but it is to my observation USMLE likes endocarditis as a notable etiology for it. In other words, if you get an endocarditis question and you’re like, “Why the fuck are platelets 900,000?” (NR 150-450,000), don’t be confused. Random points - Hematuria can occur from vegetations that launch off to the kidney. - Endocarditis + stroke-like episode (i.e., focal neurologic signs) = septic embolus, where a vegetation has launched off to the brain. - Janeway lesions, Osler nodes, splinter hemorrhages, etc., are low-yield for USMLE and mainly just school of medicine talking points. - HACEK organisms nonexistent on USMLE. - Blood cultures before antibiotics is important for 2CK. - Transesophageal echocardiography (TEE) confirms diagnosis after blood cultures. Transthoracic echocardiography (TTE) is not done for endocarditis. - For 2CK, empiric treatment for endocarditis is vancomycin, PLUS either gentamicin or ampicillin/sulbactam. - Vancomycin targets gram-positives (including MRSA). Gentamicin targets gram-negatives. - Endocarditis prophylaxis given prior to a dental procedure is usually ampicillin or a second-generation cephalosporin, such as cefoxitin. Management - Indications for endocarditis prophylaxis are: 1) Hx of endocarditis (obvious); 2) If there is any prosthetic material in the heart whatsoever; 3) If there is any congenital cyanotic heart disease that has not been completely repaired (if it’s been completely repaired with prosthetics, give prophylaxis); 4) Hx of heart transplant with valvular regurgitation of any kind. - Highest yield point for USMLE about endocarditis prophylaxis is that mitral valve prolapse (MVP) and valve regurgitations or stenoses are not an indication. In other words, do not give prophylaxis if the patient has MVP, MR, AS, etc. In addition, bicuspid aortic valve is not an indication. Rheumatic heart disease (rheumatic fever) HY points - Strep pyogenes (Group A Strep) oropharyngeal infection results in production of antibodies against S. pyogenes’ M-protein that cross-react with the mitral valve (i.e., molecular mimicry; type II hypersensitivity). - Can occur with the aortic valve in theory, but on USMLE, it is always mitral valve. - Results in mitral regurgitation acutely and mitral stenosis late, as discussed earlier. - Presents as JONES (J©NES) à Joints (polyarthritis), © Carditis, subcutaneous Nodules, Erythema marginatum (annular, serpent-like rash), Sydenham chorea (autoimmune basal ganglia dysfunction that results in dance-like movements of the limbs). - Cutaneous Group A Strep infections don’t cause rheumatic fever, but can still cause PSGN. - Treatment is penicillin. MEHLMANMEDICAL.COM 31  MEHLMANMEDICAL.COM Conditions confused for cardiac path - Psych forms love trying to make you think this is an MI. - They’ll give you young, healthy patient who feels doom / like he or she is going to die. - Sometimes they mention in stem Hx of MI in family as distraction. Panic attack - They can say patient has mid-systolic click, as discussed earlier, and then they ask for cause of patient’s symptoms à answer = panic disorder, not MVP. Student gets confused, but MVP is almost always asymptomatic, where panic attack is clearly cause of the patient effusively hyperventilating. - Treat with benzo. - Orthostatic hypotension is defined as intravascular fluid depletion causing a drop of systolic BP >20 mmHg and diastolic BP >10 mmHg when going from supine to standing. Orthostasis - Shows up on 2CK IM form as exactly a drop of 20 and 10, respectively, for systolic and diastolic BPs in a patient with fainting à answer = “intravascular fluid depletion.” - Diuretic use is big risk factor. - Fainting in response to stressor (e.g., emotional trigger). - Stress triggers an initial sympathetic response, which in turn triggers a compensatory parasympathetic response. This latter response is excessive in Vasovagal syncope some people, where the peripheral arterioles dilate and the heart slows too much à decreased cerebral perfusion à lightheadedness/fainting. - 2CK wants you to know a tilt-table test can be used to diagnose, where a reproduction of symptoms can occur. - USMLE likes this for both Steps 1 and 2. - They’ll say dude was shaving then got lightheadedness or fainted. Carotid sinus Mechanism is ­ stretch of carotid sinus baroreceptors à ­ afferent CN IX hypersensitivity firing to solitary nucleus of the medulla à ­ efferent CN X parasympathetic firing down to cardiac nodal tissue à ¯ HR à ¯ CO à ¯ cerebral perfusion. - Inflammation of cartilage at rib joints. - Will present as chest pain that worsens with palpation or when patient Costochondritis reaches over the head or behind the back. These two findings are clear indicators we have an MSK condition, not cardiac. - Can be idiopathic, caused by strain (e.g., at the gym), or even post-viral. - MSK condition asked twice on NBMEs that has nothing to do with the lungs, despite the name. - This is viral infection (Coxsackie B) causing sharp lateral chest pain due to Pleurodynia intercostal muscle spasm. Sometimes students choose pericarditis, etc., even though the presentations are completely disparate. - Creatine kinase can be elevated in stem due to ­ tone of muscle. - Viral infection causing inflammation of the pleura (layers covering the lungs), leading to sharp chest pain. Viral pleurisy - If this is the answer, CK will be normal (unlike pleurodynia, because it’s not MSK). - Can cause angina-like pain in patient without cardiovascular disease. Diffuse esophageal spasm - I discuss this in detail in HY Gastro PDF. - Can present as chest pain confused for MI. ECG will be normal, clearly. Gastroesophageal reflux - I discuss GERD in detail in HY Gastro PDF. MEHLMANMEDICAL.COM 32  MEHLMANMEDICAL.COM Arterial vs venous disease - Caused by atherosclerotic disease; presents as diminished peripheral pulses in patient over 50 who has risk factors – i.e., diabetes, smoking, HTN. - Lower legs can be shiny and glabrous (trophic changes). - Arterial ulcers are small and punched-out; located on tops/bottoms of feet and toes. Arterial disease - Ankle-brachial indices (ABIs) are first step in diagnosis (exceedingly HY on 2CK), which compare BP in ankle to the arm; if R from LA –> RA (pressure is always greater on the left side). So the effects of inhalation/exhalation are minimized in terms of the A2-P2 split bc you’ll always have relatively constant LA à RA flow (and resultant steady RA preload) irrespective of inspiration. The sound can also be described as “wide, fixed splitting” bc of increased RV preload à delayed closure of P2 relative to A2 à slight widening, but it’s still fixed for the reasons explained above. - What is the fossa ovalis? à impression in the interatrial septum following closure of the wall during embryological development. Failure of closure leads to patent foramen ovale, which is a type of ASD. - ASD/VSD in relation to blood pO2? à USMLE loves making you guess whether you have an ASD or VSD based on info they give you about blood pO2. If they say pO2 increases from SVC to RA, you MEHLMANMEDICAL.COM 51  MEHLMANMEDICAL.COM know the answer is ASD. If they say pO2 increases from RA to RV, you know VSD is the answer. Path of blood through the heart/lungs (IVC/SVC à RA à RV à pulmonary arteries (deoxygenated) à pulmonary veins (oxygenated) à LA à LV à aorta). - What does MVP sound like? à as mentioned earlier, mid-systolic click, over 4th intercostal space, left mid-clavicular line. - Who gets MVP? à most common heart murmur; polygenic; usually benign + incidental; can also get in connective tissue disorders (i.e., Marfan syndrome, Ehlers-Danlos). - Murmurs seen in connective tissue disorders à MVP or AR. - What does myxomatous degeneration mean? à answer = MVP à connective tissue degeneration. - What does MR sound like? à holosystolic (pansystolic) murmur over 4th intercostal space, left mid- clavicular line; classically radiates to the axilla but by all means doesn’t have to. - Most common cause of MR? à ischemia; student says “what do you mean?” à atherosclerosis (i.e., due to diabetes, smoking, HTN, familial) à ischemia à structural heart change (LVH + LV dilatation) + papillary muscle weakening à MVP. This is not the same thing as full-blown papillary muscle rupture following an MI; mere ischemia in the absence of MI can cause MR. - 68M + T2DM + dilated heart on CXR + S3 heart sound + 2/6 holosystolic murmur over left chest; Dx? à MR due to ischemia from atherosclerosis. - 68M + T2DM + crushing central chest pain + 3 days later has sudden-onset 4/6 holosystolic murmur over left chest; Dx? à MR from papillary muscle rupture. - 22M + obvious Marfan syndrome in vignette + stethoscope Q where it starts hovering over aortic valve region; what do you do? à you’re listening for either AR or MVP, so if you don’t hear anything, just move the stethoscope to the mitral area and you’ll hear the mid-systolic click. - 32M + fleeting/stabbing chest pain along the left-lateral chest wall + has had 20-30 episodes like this in the past + mid-systolic click; Dx? à mitral valve prolapse syndrome à do not need to treat overwhelming majority of the time, even when the patient is symptomatic; on the 2CK NBMEs, they give a symptomatic presentation just like this, and the answer is reassurance/observation, not propranolol. - What does mitral stenosis sound like? à diastolic opening snap with a decrescendo mid-late diastolic murmur. MEHLMANMEDICAL.COM 52  MEHLMANMEDICAL.COM - Who gets MS? à 99% due to previous rheumatic fever as a kid. - What is mechanism for rheumatic fever? à type II hypersensitivity against M-protein of Group A Strep (S. pyogenes) à immune system makes antibodies against Group A Strep M-protein that cross- react with the mitral valve (molecular mimicry). - How does rheumatic fever present? à JONES (J©NES) à Joints (polyarthritis) + © (myocarditis / mitral valve disease) + Nodules (subcutaneous nodules over bony prominences) + Erythema marginatum (appears annular [ring-like] and serpiginous [snake-like]; important vocab words actually for medicine) + Sydenham chorea (antibody-mediated destruction of corpus striatum of basal ganglia) à my biggest advice here is to remember “marginatum” because it’s specifically seen in RF; don’t be that person going around saying “RF has……..erythema multiforme…..?” The latter is usually seen as one of the types of drug rashes. - 12F + red tongue + salmon body rash; Dx and Tx? à scarlet fever caused by Group A Strep. Must give penicillin to prevent RF. - RF caused by cutaneous Group A Strep? à No. Cutaneous infections (i.e., impetigo, erysipelas, cellulitis) can cause post-streptococcal glomerulonephritis (PSGN), but not RF. RF is caused by pharyngitis / scarlet fever (pharyngitis + body rash). - 40M + Hx of rheumatic fever as a child; what murmur does he most likely have now? à MS. - 40M + Hx of rheumatic fever as a child + rumbling diastolic murmur + S4 heart sound; Dx? à MS with a right-ventricular S4 (unusual to be right-sided, but this is on the 2CK NBME). - 40M + Hx of rheumatic fever as a child + rumbling diastolic murmur; which of the following is most likely part of his Hx as a child? à mitral regurgitation. à this is exceedingly HY à RF causes MR acutely in the child but will cause MS later in life as the valve scars over. - 12M + fever + sore throat + painful joints + annular skin rash + heart murmur; most likely murmur that he has? à MR, not MS. - 12M + fever + sore throat + painful joints + annular skin rash + 2/6 holosystolic murmur over left chest; as an adult, what might we expect in this patient? à answer = diastolic rumbling murmur with opening snap (MS); even though right now he has MR, later in life it will become MS. MEHLMANMEDICAL.COM 53  MEHLMANMEDICAL.COM - 33F + pregnant at 20 weeks + new-onset dyspnea + crackles in both lung fields + diastolic rumbling murmur; Dx? à mitral stenosis presenting symptomatically now that plasma volume has increased ~50% in pregnancy. - 33F + pregnant at 38 weeks + prominent bilateral ankle pitting edema + dyspnea; Dx? à peripartum dilated cardiomyopathy (antibody-mediated; idiopathic). - 33F + pregnant at 32 weeks + mild ankle edema; Dx? à normal edema seen in pregnancy. - 33F + peripartum dilated cardiomyopathy; next best step in Mx? à transthoracic echo (TTE) to check for ejection fraction (guides management based on severity). - Does peripartum dilated cardiomyopathy come back in subsequent pregnancies? à Yes, and it gets worse. - 33F + peripartum dilated cardiomyopathy; best way to predict prognosis if she goes on to have a future pregnancy? à TTE (ejection fraction predicts prognosis for future pregnancy). - If 99% of MS is due to Hx of rheumatic fever, what else can cause it? à Libman-Sacks endocarditis in SLE is associated with MS. 60% of those with LS endocarditis have anti-phospholipid antibodies (lupus anticoagulant). - 32F + SLE + diastolic rumbling murmur; most likely characteristic of valvular lesion? à answer = “verrucous vegetations on both sides of the mitral valve” for LS endocarditis. - 28M IV drug user + 2/6 holosystolic murmur at left sternal border that increases with inspiration + fever; most likely characteristic of valvular lesion? à “large, friable, floppy vegetation” à bacterial endocarditis (tricuspid regurg in this case bc IV drug user). - New-onset murmur + fever; Dx? à infective endocarditis (IE) until proven otherwise. Unlike rheumatic fever, this is actual bacterial colonization of a heart valve + production of vegetation; RF is a mere antibody response. - What is acute endocarditis? à no Hx of valve abnormality; caused almost always by S. aureus; classically seen in IV drug users); classic new-onset murmur + fever presentation. - What is subacute endocarditis? à Hx of valve abnormality, i.e., congenital defect, Hx of RF; classically occurs following dental procedures; S. viridans (same thing as S. sanguinis or S. mutans) is classic cause; USMLE wants you to know S. viridan’s production of limit dextrins (carbohydrates) enables binding to mitral + aortic valve. MEHLMANMEDICAL.COM 54  MEHLMANMEDICAL.COM - What is HACEK? à Gram (-) organisms that can cause endocarditis – Hemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae – the yield on the USMLE is extremely low so you do not need to memorize these, but I mention them because students occasionally ask about HACEK + the USMLE likes you to know for some magical reason that Eikenella corrodens is associated with human bites, grows white, and has a bleach-like odor. - For IE, blood cultures before Abx, or Abx before blood cultures? à Always blood cultures (draw three tubes of blood) before giving Abx. - Empiric Tx for endocarditis? à Gentamicin (aminoglycoside) PLUS either vancomycin or ampicillin/sulbactam. Add rifampin if patient has prosthetic valve. - If culture comes back positive for MSSA (not MRSA)? à switch to six weeks nafcillin (highly simplified, but the bottom line is if MSSA is confirmed, USMLE answer is you switch to the beta-lactam). - Why switch to beta-lactam if MSSA? Why not just stay on vanc? à Beta-lactams are way more efficacious than vanc à vanc is actually not a very good drug, but if the organism causing IE is MRSA, it’s first-line. - Who gets pulmonic stenosis and what does it sound like? à sounds like aortic stenosis (midsystolic murmur) but increases in intensity with inspiration because it’s right-sided; classically seen as part of tetralogy of Fallot in DiGeorge syndrome; also seen classically in Noonan syndrome (USMLE will not ask you about Noonan syndrome). - Who gets pulmonic regurg and what does it sound like? à sounds like aortic regurg (holodiastolic) but increases with inspiration; rare, but can be seen in endocarditis in IV drug users. - Who gets tricuspid regurg and what does it sound like? à same as mitral regurg (holosystolic murmur) but gets louder with inspiration; highest yield cause on USMLE is pulmonary hypertension / cor pulmonale (these don't cause pulmonic regurg, so sounds a bit weird). Can also be seen in IV drug user endocarditis and carcinoid syndrome. - Who gets tricuspid stenosis and what does it sound like? à sounds like mitral stenosis presumably (diastolic rumbling murmur, with or without opening snap; but would increase in intensity with inspiration in theory); very rare; I’ve never seen this in any USMLE question. MEHLMANMEDICAL.COM 55  MEHLMANMEDICAL.COM - How does isolated left heart failure present? à fluid in the lungs (pulmonary edema) +/- pleural effusion; orthopnea, paroxysmal nocturnal dyspnea (PND); depending on the etiology of the heart failure, the structure of the heart will take on different characteristics, but the important point about LH failure is fluid in the lungs à also really important you know that pulmonary capillary wedge pressure (PCWP) is increased in any LH pathology (even if the pressure is within the acceptable range prior to full-blown LH decompensation, the PCWP is still increased relative to the patient’s original baseline in LH pathology). - What is PCWP? à equal to left atrial pressure; if you stick a catheter through the venous circulation all the way back to the right heart, and then into the pulmonary circulation, and then into a distal pulmonary capillary such that it can’t go any farther, the pressure reverberations are said to best reflect those of the left atrium. The USMLE is obsessed with PCWP; you need to know it is increased not just in cardiogenic shock, but also in LH pathology as I’ve stated above. - What is orthopnea? à reflective of LH decompensation à requirement to sleep on multiple pillows when supine to prevent fluid buildup in lungs; when supine, there’s greater venous return à greater preload à worsening of dyspnea because the heart cannot handle the volume (i.e., decompensates) because greater O2 demand by the LV with greater preload. - What is paroxysmal nocturnal dyspnea (PND)? à like orthopnea, reflective of LH decompensation à severe dyspnea that occurs while sleeping due to redistribution of fluid into the lungs; unlike orthopnea, does not immediately subside when sitting up. - How does isolated right heart failure present? à right ventricular hypertrophy (unless tricuspid pathology), jugular venous distension (JVD), peripheral edema, hepatosplenomegaly (late). - What’s the most common cause of right heart failure? à left heart failure. - What is congestive heart failure (CHF)? à right heart failure + left heart failure. - What causes left heart failure? à systemic HTN, ischemia (atherosclerosis), valvular abnormalities. - Since left heart failure is the most common cause of right heart failure, what usually causes isolated right heart failure? à lung pathology à when you have lung pathology causing RH failure, that’s called cor pulmonale. - “Wait, can you explain cor pulmonale a little more. I’ve heard that a lot but don’t really understand it.” à when you have a lung condition like COPD, cystic fibrosis, chronic asthma, etc., that leads to RH MEHLMANMEDICAL.COM 56  MEHLMANMEDICAL.COM failure, we call that cor pulmonale. Probably the most important piece of info regarding this condition is that PCWP is normal, which tells you the cause of the RH failure cannot be from LH origin. For instance, if you have a guy with COPD who also has heart disease, if his PCWP is elevated, then we cannot conclude that his right heart failure is a result of the lung disease in isolation because increased PCWP can lead to RH failure. - 45M + 70-pack-year Hx of smoking + JVD + peripheral edema; Dx? à cor pulmonale à signs of RH failure in someone who has lung disease. - 45M + 70-pack-year Hx of smoking + systemic HTN + JVD + peripheral edema + has crackles in lungs + dilated heart on CXR; Dx? à congestive heart failure; patient has combo of left and right heart failure signs. - 25M + cystic fibrosis + JVD + peripheral edema + crackles in lungs; Dx? à cor pulmonale à crackles due to CF, not LH failure. - If USMLE asks you for the mechanism of cor pulmonale, what’s the answer? à pulmonary hypertension à hypoxic vasoconstriction (e.g., in chronic bronchitis, CF) or obliteration of pulmonary parenchyma (emphysema) will cause a backup of blood and pulmonary HTN à increased afterload on RV à starts the process of cor pulmonale (mere pulmonary HTN is not cor pulmonale; there must be RH failure). Can also be due to fibrosis (e.g., CREST or radiation) + loss of lung parenchyma (emphysema). - How will USMLE describe pulmonary HTN? à Increased pulmonary vascular markings; loud P2; tricuspid regurg. Loud P2 means valve slams shut due to high pressure distal to it. Highest yield cause of tricuspid regurg on USMLE is pulmonary hypertension / cor pulmonale.. - 28F + non-smoker + dyspnea + JVD + increased pulmonary vascular markings; Dx? à primary pulmonary hypertension. - What is primary pulmonary HTN? à mutation in BMPR2 gene leading to narrowing of pulmonary vessels + RH failure. - Tx for pulmonary HTN à most patients will respond to dihydropyridine CCBs; if fail, can use agents like bosentan (endothelin-1 receptor antagonist), prostaglandins (i.e., epoprostenol), or sildenafil (yes, Viagra). MEHLMANMEDICAL.COM 57  MEHLMANMEDICAL.COM - 28F + non-smoker + dyspnea + JVD + increased pulmonary vascular markings; which of the following might describe her condition? à USMLE answer = increased endothelin-1 expression (which makes sense as we know bosentan is a Tx). - What is dilated cardiomyopathy (DCM) + what are the causes? à heart failure with dilatation of the LV cavity + systolic dysfunction with decreased ejection fraction; classic causes are systemic HTN and ischemia (coronary atherosclerosis), but may also be due to ABCD à Alcohol (EtOH directly damages myocardium); Beriberi (wet beriberi seen in thiamine [B1] deficiency; this is not the same as alcoholic cardiomyopathy; it’s coincidental that this also occurs in alcoholics; alcoholics can get DCM and need not be B1 deficient); Cocaine, Chagas disease (Trypanosoma cruzi), Coxsackie B virus; Doxorubicin (Adriamycin); DCM can also be caused by pregnancy (as discussed earlier) and hemochromatosis. - How does DCM present? à enlarged cardiac silhouette on CXR (dilated heart), lateralized apex beat (dilated heart); sometimes S3 heart sound; fluid in the lungs (pulmonary edema) +/- pleural effusion; can present with orthopnea, paroxysmal nocturnal dyspnea (PND). - Is HOCM the same thing as hypertrophic cardiomyopathy (HCM)? à Once again, no. HOCM is an AD condition (as discussed earlier). HCM is the diastolic dysfunction of the LV that ensues secondary to increased LV afterload (i.e., from systemic HTN, AS, or HOCM) à the USMLE will often give you an S4 heart sound for HCM. - What about restrictive cardiomyopathy (RCM)? à diastolic dysfunction with failure of the heart to expand; causes are fibrosis, amyloidosis, sarcoidosis, scleroderma, prior radiation, etc. - What are the important arrows for systolic dysfunction? à Ejection fraction – decreased; LV pressure – increased; LV volume – increased. - What are the important arrows for diastolic dysfunction? à Ejection fraction – normal; LV pressure – increased; LV volume – normal. - “Can you explain restrictive cardiomyopathy vs constrictive pericarditis?” à both are characterized by diastolic dysfunction (decreased ability of heart to expand), but in RCM this is due to myocardial stiffness / inelasticity, whereas in CP, the etiology is strictly pericardial, with TB being the most common cause of chronic constrictive pericarditis; CP is associated with calcification on CXR in about a third of patients; calcification is not seen in RCM. MEHLMANMEDICAL.COM 58  MEHLMANMEDICAL.COM - 22M + stab wound to left chest + JVD + muffled heart sounds + hypotension; Dx? à cardiac tamponade à Beck triad always seen in USMLE Qs = JVD + muffled heart sounds + hypotension; also associated with pulsus paradoxus. - What is pulsus paradoxus? à drop in BP of >10 mm Hg on inspiration à reflects inability of the heart to fill à seen in cardiac tamponade, severe lung disease (i.e., severe asthma, COPD), and sometimes severe sleep apnea à my observation is students love to focus on miscellaneous causes of PP, but in reality the USMLE only gives a fuck about cardiac tamponade; Qbank might venture down the asthma route once in a blue moon. - What’s the difference between pericardial effusion and cardiac tamponade? à all tamponades are