HY lecture material:
Fat embolism –> long bone fracture(s) + petechiae on the chest (thrombocytopenia from fat binding platelets).
Pulmonary contusion vs myocardial contusion:
MVA + rib fractures + underlying infiltrates in lung + low O2 sats –> pulmonary contusion.
MVA + no rib fractures + non-central chest pain + pulmonary infiltrates underlying the painful area –> pulmonary contusion (resources will say “white out of the lung” for pulmonary contusion, but this is buzzywordy and never shows up on actual NBME material).
MVA + pulmonary infiltrates + low O2 sats + bolus of normal saline given, resulting in worsening of O2 sats –> pulmonary contusion (contused lung is very sensitive to fluid overload).
MVA + bruising/pain over the sternum +/- rib fractures –> myocardial contusion.
MVA + bruising/pain over sternum + pulmonary infiltrates + O2 sats get worse when saline is given –> answer = myocardial contusion (“Wait, but I thought you said that latter finding means pulmonary contusion” –> it does, and it’s HY for pulmonary contusion, but “bruising/pain over the sternum” wins if it’s listed; this is on a 2CK NBME).
Important point about Mx of myocardial contusion –> do troponins + must monitor for arrhythmia.
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MVA + widened mediastinum seen on CXR –> answer = thoracic aortic rupture. Super HY. You need to know this is the most common cause of death after deceleration injury (i.e., falls, MVAs).
MVA + widened mediastinum seen on CXR; next best step in Mx? –> labetalol (must give beta-blocker to decrease shearing forces). Sodium nitroprusside is the wrong answer. Labetalol is the specific beta-blocker that shows up repeatedly for the med you give in dissection + thoracic aortic rupture.
MVA + widened mediastinum seen on CXR; next best step in Mx? –> (you don’t see labetalol listed; all the answers are interventions) –> aortic arteriography (aortography), then surgery.
“Dissection” implies a false lumen within the vascular wall secondary to hypertension or a connective tissue disorder as the etiology; traumatic aortic rupture is literally a traumatic rupture; it’s not a dissection. Regardless, choose labetalol.
Hypertensive emergency = BP >180/120 (if either number is exceeded PLUS end-organ damage secondary to the hypertension) –> i.e., hypertensive retinopathy w/ AV nicking; high Cr from renal damage, etc. –> answer = sodium nitroprusside (don’t decrease BP more than 25% in first six hours; bottom line is, don’t reduce too much too soon) + IV nicardipine (hard-hitting dihydropyridine CCB) + fenoldopam (D1 agonist that keeps renal afferent arterioles dilated + kidneys perfused in the setting of dilating arterioles with former two drugs that could otherwise reduce renal perfusion).
Hypertensive urgency = severe hypertension without end-organ damage (i.e., you just record the BP) –> Tx with oral captopril. This was asked in UWorld for Step 3 twice.
Aortic regurg –-> decrescendo holodiastolic murmur (aka decresendo pan-systolic) that can radiate down left sternal border –> bounding pulses + head-bobbing –> wide pulse-pressure (big difference between systolic and diastolic BP) –> question will usually say BP is 160/60 or 120/40. I point this out because often times if students miss an AR question, I’ll say, “What do you make of the BP?” So pay attention to BP in AR.
Pulses in AR will often be described as “brisk upstroke with precipitous downstroke,” which reflects the bounding pulses. The basis for it is that blood quickly leaves the arterial circulation after entering. Bounding pulses can also be seen in arteriovenous fistulae (i.e., Paget disease of bone, hereditary hemorrhagic telangiectasia, or dialysis patients).
So bounding pulses on the USMLE, you should think: AR or AVF.
AR is associated with fluid overload on the left ventricle –> increased preload + eccentric hypertrophy.
AR is caused by connective tissue disorders (e.g., Marfan, Ehlers-Danlos) or aortic root dilation (e.g., ascending aortic arch dissection, tertiary syphilis, Takayasu arteritis).
Aortic stenosis –> crecendo-decrescendo systolic murmur (aka mid-systolic) that can radiate to the carotids –> slow-rising pulses (“pulsus parves et tardus”) –> can sometimes be described as “late-peaking systolic murmur with an ejection click” –> this can fuck with some students who are like, “wait, I thought ‘systolic click’ meant mitral valve prolapse”; what you need to know is: mid-systolic click = MVP; ejection click = AS.
AS is associated with pressure overload on the left ventricle –> increased afterload + concentric hypertrophy –> can result in S4 heart sound (stiff LV).
Classic triad for AS is SAD –> Syncope + Angina + Dyspnea; but by all means Qs don’t have to mention them.
AS is usually caused by bicuspid aortic valve (autosomal dominant familial, or Turner).
Murmurs get worse with more volume in the heart –> lying down, squatting, leg raise while supine, hand-grip.
HOCM and MVP are the two murmurs that get worse with less volume in the heart –> nitrates, standing/sitting up, Valsalva.
USMLE likes Qs about oxygen at different locations in the heart / vena cava, where they want you to infer the heart defect. For instance:
If blood oxygen goes up from SVC –> RA, then answer is ASD.
If blood oxygen goes up from RA –> RV, then answer is VSD.
