We have watched thousands of international medical graduates open a Step 1 vignette, see the phrase “a high pitched blowing decrescendo murmur best heard at the left sternal border,” and freeze. They knew the buzzwords. They had flashcards. They could recite tables. And yet the answer slipped through their fingers.
Here is the truth almost no review book tells you. Memorization alone breaks the moment NBME twists a single clue. The exam writes vignettes that flip one variable. The pulse pressure shifts. The maneuver changes. The location is unusual. Suddenly the buzzword fails and the student picks the wrong valve.
Murmurs are not a memory test. Murmurs are a physics test wearing a clinical disguise. Once you understand what blood is actually doing inside the heart at each moment of the cardiac cycle, every murmur on the exam becomes obvious. We will teach you physics, then layer the clinical features on top, then show you exactly how NBME tries to trick you.
| What This Guide Gives You A single framework that solves every murmur instead of memorizing isolated facts. A master comparison table covering timing, location, radiation, maneuvers, and buzzwords. Pathophysiology explained from pressure gradients, not flashcards. Maneuver logic broken down with flowcharts and clinical reasoning. Memorable mnemonics built around mechanisms, not rote letters. Fifteen NBME style vignettes with detailed explanations. A one page revision sheet you can print before exam day. |
Every murmur question on Step 1 is built on the same three questions. Get all three right, and the answer falls out. Skip one, and you guess.
The cardiac cycle has two phases. Systole is when the ventricles contract. Diastole is when the ventricles relax and fill. S1 marks the beginning of systole. S2 marks the beginning of diastole.
During systole the mitral and tricuspid valves must stay closed (otherwise blood leaks backward into the atria) and the aortic and pulmonic valves must open (so blood can leave the heart). During diastole the situation reverses.
That single fact sorts every murmur. If a valve that should be closed is leaky during systole, you get a systolic regurgitant murmur. If a valve that should be open during systole is narrowed, you get a systolic ejection murmur. Same logic applies in reverse for diastole.
| The Mechanical Rule That Runs Everything Blood always flows from high pressure to low pressure. A murmur is just turbulent blood. So the question is always: where is blood trying to go, what is in its way, and does the pressure gradient favor the abnormal flow? |
A valve can fail in exactly two ways. It can fail to open all the way (stenosis), or it can fail to close all the way (regurgitation, also called insufficiency). That is the whole story. Stenosis blocks forward flow. Regurgitation lets backward flow happen.
Now combine that with timing. A valve that is supposed to be open during systole (aortic, pulmonic) causes a systolic murmur when it is stenotic. A valve that is supposed to be closed during systole (mitral, tricuspid) causes a systolic murmur when it is regurgitant. Flip everything for diastole.
This is the maneuver question and it is the reason students lose easy points. Two physiological levers move every murmur on the exam: preload (how much blood returns to the heart) and afterload (how hard the heart has to push against the systemic pressure). We will give you the full flowchart in section 5, but for now hold this idea in your head: maneuvers shift one of those two variables, and that shift either helps or hurts each specific pathology in a predictable way.
Print this. Memorize the columns, then build the cells through reasoning rather than rote. Once you understand why each row reads the way it does, you can rebuild this table from scratch on exam day even if you forget a single fact.
| Murmur | Timing | Location | Radiation | Maneuvers | Sound | NBME buzzwords |
|---|---|---|---|---|---|---|
| Aortic stenosis | Mid systolic | Right 2nd ICS | Carotids | Louder squat, softer handgrip | Harsh crescendo decrescendo | Syncope on exertion, slow rising pulse |
| Mitral regurg | Holosystolic | Apex | Left axilla | Louder handgrip and squat | Blowing plateau | Post MI papillary muscle, rheumatic |
| Tricuspid regurg | Holosystolic | Left 4th ICS | None | Louder inspiration (Carvallo) | Blowing plateau | IV drug use, endocarditis |
| VSD | Holosystolic | Left lower sternal | None | Louder handgrip | Harsh plateau | Down syndrome, FAS, smaller is louder |
| MVP | Mid to late systolic | Apex | None | Earlier click standing or Valsalva | Midsystolic click then murmur | Young woman, Marfan, anxiety |
| HOCM | Mid systolic | Left lower sternal | None | Louder Valsalva and standing | Crescendo decrescendo | Young athlete sudden death, S4 |
| Aortic regurg | Early diastolic | Erb point | None typical | Louder handgrip and squat | Decrescendo blowing | Wide pulse pressure, water hammer pulse |
| Mitral stenosis | Mid to late diastolic | Apex (bell) | None | Louder left lateral decubitus | Opening snap then rumble | Rheumatic, dysphagia, hoarseness |
| Pulmonic regurg | Early diastolic | Left 2nd ICS | None | Louder inspiration | Decrescendo | Pulmonary HTN, Graham Steell murmur |
| Tricuspid stenosis | Mid diastolic | Left 4th ICS | None | Louder inspiration | Rumble with opening snap | Rheumatic, almost always with mitral stenosis |
| PDA | Continuous | Left 2nd ICS infraclavicular | None | Louder handgrip | Machinery murmur | Congenital rubella, premature infant |
| How To Read This Table The Right Way Do not memorize cells in isolation. Notice the patterns. Every regurgitation gets louder with handgrip because handgrip raises afterload and more blood leaks backward. HOCM and MVP both improve with bigger ventricles and worsen with smaller ones. Right sided murmurs (tricuspid, pulmonic) get louder on inspiration because inspiration sucks blood into the right heart. Patterns beat rote memorization every time. |
We will go through each one with the same structure: what is broken, what blood is doing, where to hear it, how maneuvers change it, and the exact phrasing NBME uses. Read each section like a teaching round, not a flashcard.
The aortic valve is narrowed, so during systole the left ventricle has to push blood through a tiny opening, creating turbulence and a pressure gradient between the ventricle and the aorta.
Causes By Age
Auscultation
A harsh crescendo decrescendo systolic ejection murmur, best heard at the right second intercostal space, radiating to the carotids. The sound starts soft after S1, peaks in mid systole, then fades before S2. The later the peak, the more severe the stenosis.
Maneuver Behavior
Classic NBME Clues
Pressure And Volume Logic
The left ventricle hypertrophies concentrically because it must generate enormous pressure to overcome the stenotic valve. This produces a small, stiff cavity with reduced compliance. That is why an S4 appears, and that is why these patients are exquisitely preload dependent.
| Why Exertional Syncope Matters During exercise, systemic vascular resistance drops to deliver blood to muscles. A normal heart compensates by increasing cardiac output. The aortic stenosis patient cannot increase output through the narrowed valve, so blood pressure crashes and the patient faints. This single mechanism explains the dreaded vignette. |
Pathophysiology In One Sentence
The mitral valve does not close completely during systole, so blood leaks from the left ventricle back into the left atrium throughout systole.
Causes To Know
Auscultation
A holosystolic (pansystolic) blowing murmur at the apex, radiating to the left axilla. The murmur begins with S1 and continues through S2 because the pressure gradient between LV and LA exists throughout the systole.
Maneuver Behavior
Classic NBME Clues
Pathophysiology In One Sentence
Myxomatous degeneration of the mitral leaflets causes them to balloon backward into the left atrium during systole, often with a small jet of regurgitation.
Auscultation
The classic finding is a mid systolic click followed by a late systolic murmur, best heard at the apex. The click is the sudden tensing of the redundant leaflet as it reaches its maximum prolapse.
Maneuver Behavior (High Yield)
Classic NBME Clues
| MVP Click Logic Decoded Smaller ventricle (Valsalva, standing) = the redundant leaflets reach their prolapse point sooner, so the click comes earlier and the murmur lasts longer. Bigger ventricle (squat) = leaflets take longer to prolapse, so click is later and murmur is shorter. This is the single most tested maneuver concept on Step 1. |
Pathophysiology In One Sentence
Asymmetric septal hypertrophy plus systolic anterior motion of the mitral valve creates a dynamic obstruction of the left ventricular outflow tract during systole.
Auscultation
A harsh crescendo decrescendo systolic murmur at the left lower sternal border. Crucially, it does not radiate to the carotids (this is how you distinguish it from aortic stenosis).
Maneuver Behavior (The Famous Outlier)
Classic NBME Clues
Pathophysiology In One Sentence
The aortic valve fails to close completely during diastole, so blood leaks from the aorta back into the left ventricle, raising LV end diastolic volume and widening pulse pressure.
Causes To Know
Auscultation
A high pitched blowing early diastolic decrescendo murmur, best heard at Erb point (left third intercostal space) with the patient sitting up, leaning forward, and in held exhalation. The murmur starts loud right after S2 and fades.
Peripheral Findings (These Win Exam Questions)
Maneuver Behavior
Pathophysiology In One Sentence
The mitral valve is narrowed, so during diastole blood struggles to move from left atrium to left ventricle, raising left atrial pressure and eventually causing pulmonary hypertension.
Causes
Auscultation
Listen with the bell at the apex with the patient in the left lateral decubitus position. You will hear an opening snap shortly after S2, followed by a low pitched mid diastolic rumble. Often there is also a loud S1 in early disease.
Severity Clue
The shorter the A2 to the opening snap interval, the more severe the stenosis (because the higher left atrial pressure forces the valve to open sooner after S2). This is a high yield exam point.
Classic NBME Clues
Pathophysiology In One Sentence
A hole in the interventricular septum allows blood to shunt from the high pressure left ventricle to the lower pressure right ventricle during systole.
Auscultation
A harsh holosystolic murmur at the left lower sternal border (tricuspid area). The murmur does not radiate to the axilla, which distinguishes it from mitral regurgitation.
Counterintuitive Rule
Smaller VSDs are louder. A tiny defect creates more turbulence and a steeper pressure gradient. A large VSD may produce only a soft murmur because pressures equalize quickly. This is my favorite NBME trick.
Classic NBME Clues
Pathophysiology In One Sentence
The ductus arteriosus fails to close after birth, leaving a connection between the aorta and the pulmonary artery so blood shunts continuously from aorta to pulmonary artery.
Auscultation
A continuous machinery murmur (sometimes called a Gibson murmur) best heard at the left second intercostal space, often radiating to the infraclavicular region. The murmur builds through systole, peaks at S2, and continues into diastole.
Classic NBME Clues
Almost every Step 1 vignette that tests murmur identification will throw in a maneuver. Once you understand that each maneuver moves either preload or afterload, you can solve every variation without memorization. Here is the full logic in one image.
Squatting compresses the leg veins and the abdominal aorta. This does two things at once: it increases venous return (preload up) and increases systemic vascular resistance (afterload up). Almost every murmur gets louder because more blood is flowing through everything. The two exceptions are HOCM and MVP, which both improve with a fuller ventricle.
Standing pools blood in the legs. Valsalva increases intrathoracic pressure and compresses the venae cavae. Both reduce venous return (preload down). Smaller ventricle, less flow. Most murmurs get softer. HOCM gets louder. MVP click moves earlier.
Sustained handgrip raises systemic vascular resistance dramatically without changing preload much. Higher afterload makes it harder to push blood forward through the aortic valve, so aortic stenosis gets softer. Higher afterload also pushes more blood backward through leaky valves, so mitral regurgitation, aortic regurgitation, and VSD all get louder.
Deep inspiration creates negative intrathoracic pressure, which sucks more blood into the right side of the heart. All right sided murmurs (tricuspid regurg, tricuspid stenosis, pulmonic stenosis, pulmonic regurgitation) get louder. Left sided murmurs are not significantly affected.
| The Carvallo Trick If a vignette says “the murmur becomes louder on inspiration,” think right side immediately. The two most tested right sided murmurs are tricuspid regurgitation (IV drug user with fever) and pulmonic stenosis (Noonan syndrome). |
A vasodilator that drops afterload sharply. Therefore it does the opposite of handgrip. Aortic stenosis gets louder, mitral regurgitation gets softer, HOCM gets louder.
We do not believe in memorizing meaningless letter strings. Every mnemonic here is built around a real mechanism, so even if you forget the words you can rebuild the meaning.
| MR. ASS = Mitral Regurg, Aortic Stenosis (and friends) Systolic murmurs include: Mitral regurgitation, Tricuspid regurgitation, MVP, HOCM, Aortic stenosis, Pulmonic stenosis, VSD. Memory trick: anything that should be closed in the systole but is leaky (MR, TR, VSD) or anything that should be open in the systole but is blocked (AS, PS, HOCM). |
| MS. ARP = Mitral Stenosis, Aortic Regurg, Pulmonic Regurg Diastolic murmurs include: Aortic regurgitation, Pulmonic regurgitation, Mitral stenosis, Tricuspid stenosis. Memory trick: anything that should be closed in diastole but is leaky (AR, PR) or anything that should be open in diastole but is blocked (MS, TS). Diastolic murmurs are almost always pathological. Systolic murmurs can be innocent in children and pregnancy. This single rule saves you on screening questions. |
| The HOCM and MVP rule (the one rule that breaks every other rule) Almost every murmur LOUDER with squatting, SOFTER with Valsalva and standing. HOCM and MVP do the opposite: SOFTER with squatting, LOUDER with Valsalva and standing. Why: HOCM and MVP both benefit from a larger ventricle (squatting). They worsen with a smaller ventricle (Valsalva and standing). If you remember nothing else about maneuvers, remember this paradox. NBME asks it constantly. |
Right Sided Murmurs get louder on inspiration (RILE: Right side Inspiration, Left side Expiration). Inspiration pulls blood into the right heart via negative intrathoracic pressure.
Left Sided Murmurs get louder on expiration (such as aortic regurgitation, classically auscultated with the patient leaning forward in held exhalation).
APE TM, read from top to bottom along the chest:
After reviewing thousands of NBME items, we can tell you exactly how the exam wraps a simple murmur in a confusing vignette. Here are the seven traps that catch IMGs most often.
A vignette mentions “a crescendo decrescendo murmur” and you immediately think of aortic stenosis. But the vignette places it at the left lower sternal border with no radiation to the carotids. That is HOCM, not AS. Always read the location before committing.
Both AS and HOCM produce a systolic ejection murmur. The maneuver question separates them. Handgrip softens AS and softens HOCM (both ejection murmurs). Valsalva softens AS but LOUDENS HOCM. Squatting LOUDENS AS but softens HOCM. The single most discriminating maneuver is squat or Valsalva, not handgrip.
| AS vs HOCM Cheat Code Same shape (crescendo decrescendo), different location, different maneuvers. Carotid radiation? Aortic stenosis. Pulse character? AS has pulsus parvus et tardus. HOCM has a brisk bifid pulse. Valsalva louder? HOCM. Valsalva softer? AS. Young athlete with a family history of sudden death? HOCM until proven otherwise. |
A child with a soft systolic ejection murmur at the left sternal border that decreases with standing is usually a Still murmur (benign). Anything diastolic, anything that radiates, anything with a thrill, anything over grade 3 in adults: that is pathological until proven otherwise.
Day 2 to 7 after an inferior MI, a patient develops sudden dyspnea and a new holosystolic murmur at the apex. That is papillary muscle rupture causing acute mitral regurgitation. Day 2 to 7 with a new holosystolic murmur at the left sternal border is more likely a ventricular septal rupture. Day 3 to 14 with sudden hypotension, jugular venous distension, and muffled heart sounds is free wall rupture and tamponade. Same time window, three different murmurs, very different prognoses.
Aortic stenosis radiates to the carotids. Mitral regurgitation radiates to the axilla. If the vignette says “radiating to the back” that is aortic dissection or coarctation, not a typical valvular murmur.
The exam loves to add the word “continuous” to a murmur description. That almost always means PDA. Other rare continuous murmurs include arteriovenous fistula and ruptured sinus of Valsalva aneurysm. If the patient is an infant, especially premature, PDA is the answer.
At IMG Helping Hands, our UIT mentorship system was built on three principles that separate students who pass Step 1 from students who score over 250.
We do not start with flashcards. We start with the underlying physiology. When you understand why aortic stenosis causes syncope on exertion, you do not need to memorize the symptom. It becomes obvious. This blog is a small example of that philosophy applied to murmurs.
Cardiology does not live in a vacuum. A patient with mitral stenosis has a dilated left atrium, which causes atrial fibrillation, which causes embolic stroke. That is cardiology, neurology, and pharmacology in one vignette. Our teaching connects systems instead of siloing them.
Every concept in our curriculum is taught the way an attending teaches on rounds. You will hear us say things like “this is what you do when the pulse is bounding,” not “memorize this list.” That is how Step 1 high scorers and matched residents think.
| Why IMGs Choose UIT Concept driven physiology and pathology, built for international medical graduates. Reasoning frameworks that survive twisted NBME vignettes. Mentorship from physicians who have been through the same match journey. Integration with the broader IMG Helping Hands ecosystem including match strategy, externships, and licensure guidance. |
Print this section. Read it the morning of your exam. It is everything you need in a single page of decision logic.
Step 1: Where in the cycle? Systolic (between S1 and S2) or diastolic (between S2 and the next S1) or continuous.
Step 2: Where on the chest? Right 2nd ICS, left 2nd ICS, Erb point, left 4th ICS, or apex.
Step 3: What shape? Crescendo decrescendo, holosystolic plateau, decrescendo, rumble, click plus murmur, or machinery.
Step 4: What does it do with maneuvers? Apply the preload and afterload logic.
Step 5: Confirm with NBME buzzwords and demographics.
Cover the explanations with your hand. Reason through each one using the framework. Then check your logic.
A. Mitral valve prolapse with regurgitation
B. Calcified aortic valve with reduced opening
C. Dilated aortic root with regurgitant jet
D. Asymmetric septal hypertrophy
E. Thickened mitral leaflets with diastolic doming
| Answer: B. Calcified aortic valve with reduced opening. The classic triad of syncope, angina, and dyspnea on exertion in an elderly patient with a harsh crescendo decrescendo murmur radiating to the carotids and pulsus parvus et tardus is aortic stenosis. In a patient over 70, the cause is age related calcific degeneration. |
A. Systolic ejection murmur softer with Valsalva
B. Systolic ejection murmur louder with Valsalva
C. Holosystolic murmur at the apex
D. Decrescendo diastolic murmur at Erb point
E. Continuous murmur at the left infraclavicular region
| Answer: B. Systolic ejection murmur louder with Valsalva. Sudden cardiac death in a young athlete with a family history points to hypertrophic obstructive cardiomyopathy. HOCM produces a systolic ejection murmur that becomes LOUDER with Valsalva because reduced preload shrinks the ventricle and worsens the LVOT obstruction. |
A. Aortic stenosis
B. Mitral regurgitation from rheumatic disease
C. Mitral valve prolapse
D. Tricuspid regurgitation
E. Ventricular septal defect
| Answer: C. Mitral valve prolapse.Marfan features plus a mid systolic click and late systolic murmur at the apex equals MVP. Squatting increases preload, fills the ventricle, and delays the prolapse, so the click moves later. The opposite happens with standing or Valsalva. |
A. Aortic valve
B. Mitral valve
C. Pulmonic valve
D. Tricuspid valve
E. Mitral and aortic valves together
| Answer: D. Tricuspid valve. IV drug use plus right sided endocarditis plus a holosystolic murmur louder on inspiration (Carvallo sign) is tricuspid regurgitation. Inspiration increases venous return to the right heart, amplifying right sided murmurs. |
A. Free wall rupture
B. Ventricular septal rupture
C. Posteromedial papillary muscle rupture
D. Acute pericarditis
E. Pulmonary embolism
| Answer: C. Posteromedial papillary muscle rupture. Acute mitral regurgitation after an inferior MI is classically due to posteromedial papillary muscle rupture because this papillary muscle has a single blood supply from the posterior descending branch of the right coronary artery. The murmur is holosystolic at the apex radiating to the axilla. |
A. Bicuspid aortic valve
B. Marfan syndrome
C. Rheumatic fever
D. Infective endocarditis
E. Carcinoid syndrome
| Answer: C. Rheumatic fever. Mitral stenosis in a young adult from a developing country is essentially always rheumatic in origin. Dysphagia and hoarseness (Ortner syndrome) come from the dilated left atrium compressing the esophagus and recurrent laryngeal nerve. |
A. Increased stroke volume from chronic volume overload
B. Aortic stenosis with reduced cardiac output
C. Right to left intracardiac shunting
D. Decreased systemic vascular resistance from sepsis
E. Severe anemia
| Answer: A. Increased stroke volume from chronic volume overload. Chronic aortic regurgitation increases left ventricular end diastolic volume. The ventricle compensates with a larger stroke volume, raising systolic pressure. Diastolic pressure falls because blood leaks back into the ventricle. Wide pulse pressure results. |
A. Stimulating prostaglandin synthesis
B. Inhibiting prostaglandin synthesis
C. Activating beta adrenergic receptors
D. Blocking calcium channels
E. Stimulating cyclic GMP
| Answer: B. Inhibiting prostaglandin synthesis. Patent ductus arteriosus in a premature infant is closed with indomethacin, which inhibits prostaglandin synthesis. Prostaglandins keep the ductus open. Prostaglandin E1 is used to keep the ductus open in ductal dependent lesions like transposition of the great arteries. |
A. Tricuspid regurgitation
B. Mitral regurgitation
C. Ventricular septal defect
D. Aortic stenosis
E. Mitral stenosis
| Answer: C. Ventricular septal defect. Holosystolic at the left lower sternal border without inspiratory change rules out tricuspid regurg. No axillary radiation rules out mitral regurg. VSD is the answer. Childhood respiratory infections are typical of a left to right shunt. |
A. Inspiration
B. Handgrip
C. Valsalva strain
D. Lying supine
E. Cold pressor test
| Answer: C. Valsalva strain. Valsalva strain decreases preload. Aortic stenosis murmur SOFTENS (less flow across a fixed obstruction). HOCM murmur LOUDENS (smaller ventricle worsens dynamic obstruction). This is the single most discriminating maneuver. |
A. Tetralogy of Fallot
B. Transposition of the great arteries
C. Endocardial cushion defect (AV septal defect)
D. Coarctation of the aorta
E. Ebstein anomaly
| Answer: C. Endocardial cushion defect (AV septal defect). Down syndrome is associated most strongly with endocardial cushion defects, which involve both atrial and ventricular septal defects plus AV valve abnormalities. |
A. Concomitant mitral stenosis
B. Austin Flint murmur from regurgitant jet hitting the mitral leaflet
C. Tricuspid stenosis
D. Left atrial myxoma
E. Constrictive pericarditis
| Answer: B. Austin Flint murmurs from a regurgitant jet hitting the mitral leaflet. The Austin Flint murmur is a classic mimic of mitral stenosis. The regurgitant jet from the aortic valve strikes the anterior mitral leaflet during diastole, producing a low pitched rumble at the apex. |
A. Hypertrophic obstructive cardiomyopathy
B. Innocent flow murmur
C. Atrial septal defect
D. Mild aortic stenosis
E. Mitral valve prolapse
| Answer: B. Innocent flow murmur. Soft systolic ejection murmur, no radiation, no thrill, decreases with standing (which decreases preload, decreases flow, decreases murmur intensity), no symptoms or ECG abnormalities. This is an innocent murmur. |
A. Right atrial enlargement
B. Left atrial enlargement from chronic volume overload
C. Sinoatrial node ischemia
D. Wolff Parkinson White accessory pathway
E. Hyperthyroidism
| Answer: B. Left atrial enlargement from chronic volume overload. Chronic mitral regurgitation pushes a regurgitant jet into the left atrium with every beat. The left atrium dilates, the conduction tissue stretches, and atrial fibrillation develops. Same mechanism in mitral stenosis. |
A. Aortic stenosis
B. Hypertrophic obstructive cardiomyopathy
C. Mitral regurgitation
D. Pulmonic stenosis
E. Atrial septal defect
| Answer: C. Mitral regurgitation. Handgrip increases afterload, which increases the backward pressure gradient across the leaky mitral valve, making MR louder. Amyl nitrite drops afterload, doing the opposite. Aortic stenosis behaves in the reverse pattern (softer with handgrip, louder with amyl nitrite). HOCM also behaves opposite to MR for maneuvers that change afterload. |
These are the questions IMGs ask us most often before Step 1. We answer each one in the same humanized voice we would use sitting across from you during a tutoring session.
The easiest way is to stop memorizing and start reasoning. Master three layers in order: cycle timing (systole vs diastole), valve mechanics (stenosis vs regurgitation), and maneuver effects (preload, afterload, inspiration). Once those three layers are second nature, every murmur becomes a logic puzzle rather than a memory exercise. We teach this exact sequence inside our UIT Step 1 program.
Three features separate them reliably. First, location: AS at the right 2nd ICS with carotid radiation, HOCM at the left lower sternal border with no carotid radiation. Second, pulse: AS gives pulsus parvus et tardus (slow rising, weak), HOCM gives a brisk bifid pulse. Third, maneuvers: Valsalva strain SOFTENS AS but LOUDENS HOCM. If a vignette mentions a young athlete or sudden cardiac death in the family, HOCM. If it mentions an elderly patient with calcific disease, AS.
Handgrip raises systemic vascular resistance, which raises afterload. Higher afterload makes it harder for the left ventricle to push blood forward through the aorta. So forward flow murmurs like aortic stenosis get softer. At the same time, higher afterload increases the pressure gradient driving blood backward through any leaky valve. So regurgitant murmurs (mitral regurg, aortic regurg) and left to right shunts (VSD) get louder.
From our review of thousands of practice and retired NBME items, the most tested murmurs on Step 1 are aortic stenosis, mitral regurgitation, mitral valve prolapse, hypertrophic obstructive cardiomyopathy, aortic regurgitation, mitral stenosis, ventricular septal defect, and patent ductus arteriosus. Tricuspid regurgitation appears most often in IV drug use questions. Master these eight and you cover almost every murmur question on the exam.
Yes, in adults. Diastolic murmurs are essentially never innocent. If a vignette describes a diastolic murmur, it is testing aortic regurgitation, mitral stenosis, pulmonic regurgitation, or tricuspid stenosis. Systolic murmurs can be innocent (especially in children and pregnancy), but a diastolic murmur always demands a pathological explanation.
Mitral stenosis raises left atrial pressure, which dilates the left atrium over time. The enlarged left atrium compresses the left recurrent laryngeal nerve as it loops around the aortic arch, causing hoarseness. This is called Ortner syndrome. The same mechanism can cause dysphagia from compression of the esophagus.
Yes, this is one of the highest yield study tools for IMGs preparing for Step 1 and especially Step 2 CK. Hearing the sounds while reading about the mechanism cements the pattern faster than any flashcard. We recommend pairing audio practice with the visual timing chart in this blog so you learn the shape and the sound together.
Our UIT program is built around the same reasoning approach you saw in this blog: concepts first, integration across systems, and clinically oriented thinking that mirrors how attendings teach. We pair each IMG with mentors who have matched into US residency and we provide structured frameworks, NBME style assessments, and one on one guidance. Many IMGs find that murmurs go from their weakest cardiology topic to their strongest within a few weeks of starting our curriculum.
Murmurs become easy once you understand blood flow physics. That is not a slogan. It is the rule that has guided every IMG we have trained from “I always fail murmur questions” to “murmurs are now my favorite topic.” The path is simple: stop memorizing, start reasoning. Read each vignette through the three layer framework we taught you. Apply the maneuver logic. Recognize the buzzwords as clues, not as answers.
If you closed this blog feeling like the heart is no longer a black box, we did our job. If you want the same reasoning approach applied to every system on Step 1, that is exactly what we built at UIT.
IMG HELPING HANDS – UIT STEP 1 PROGRAM
UIT is the flagship Step 1 program by IMG Helping Hands. We teach concept-driven reasoning across systems, NBME-aligned practice, and one-on-one mentorship with matched IMG mentors.
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IMG Helping Hands • Concept-first Step 1 prep for IMGs
Articles published by IMG Helping Hands are prepared by our team using information from direct experience, publicly available resources, and educational references. AI tools may be used to assist with drafting, proofreading, and formatting; however, all content undergoes review and approval before publication.
The information provided is intended for educational purposes only. Requirements, policies, and processes may change over time. Readers should consult official sources for the most current information.
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