Case Presentations

Here you will find cases in which physical examination played a key role in making the diagnosis. Try to work through the cases one step at a time and see if you arrive at the correct diagnosis.


Patient 1: Dyspnea

A middle-age man presents with dyspnea on exertion, orthopnea, and weight gain. His BP is 112/40. This should generate a hypothesis. And you begin to test your hypothesis by evaluating for specific physical findings. What do you notice in this video?

The presence of de Musset’s sign (to-and-fro head bob) is consistent with your hypothesis. So you look for more evidence.

And you find it in the form of Corrigan’s pulse. You continue to evaluate the peripheral pulses and find more evidence to support your hypothesis. 

This should make it easier to appreciate. 

Next you look at the patient’s fingernails. What do you see? 

The patient is having trouble seeing what you see in his nail bed. So you use a light source to help him. 

You continue to evaluate the peripheral pulses, finally reaching his foot: 

Before you even listen to the patient’s heart, your diagnosis has all but been made. And when you listen, you know exactly what to listen for. “The ears can’t hear what the mind doesn’t know” 

You have just diagnosed severe aortic insufficiency with your eyes, your ears, and a Q-tip. 

Patient 2: Fever

A young man is admitted to the hospital with malaise and fever. You examine his hands and find these tender nodules.  

This should generate a hypothesis. 

With your hypothesis in mind, you listen to the patient’s heart. You anticipate what you might hear. “The ears can’t hear what the mind doesn’t know.” 

An additional diagnosis has now been made.


Based on the holosystolic murmur at the apex that you anticipated you would hear, you diagnose the patient with mitral valve endocarditis. Two days later, his heart sounds change. Take a listen. 



Two days later, you no longer hear the pericardial friction rub. In fact, his heart sounds are difficult to hear at all. He develops hypotension and pre-syncope and his neck looks like this: 

This should generate a hypothesis. 

 You confirm your hypothesis with a bedside maneuver (video features a different patient with the same diagnosis): 

You have diagnosed infective endocarditis of the mitral valve with pericardial involvement, evolving to pericardial effusion with cardiac tamponade. All with your eyes and ears. 

Patient 3: Weakness

A middle-aged man walks into your clinic complaining of weakness. You take a moment to observe his gait. What do you notice?

This should generate a hypothesis. 


You reference your framework for weakness and try to determine the location of the lesion to narrow your differential diagnosis. The patient’s gait has already provided a clue (spasticity). 

So you check his reflexes next. 


The hyperreflexia suggests an upper motor neuron lesion. Next, you check for Hoffmann’s sign, which if present, would suggest a cervical lesion.

You have just diagnosed cervical myelopathy. Using only your eyes and a reflex hammer. 

Patient 4: Progressive dyspnea

A middle-aged woman presents with progressive dyspnea. You start with her hands. What do you notice? Does it generate any hypotheses in your mind? 

Could these small erythematous lesions be telangiectasias? Let’s see if they blanch and refill by pressing on one of them.

Indeed, they do, confirming your suspicion. What condition comes to mind? Perhaps you are thinking about hereditary hemorrhagic telangiectasia (HHT). Can it cause dyspnea? Yes, via pulmonary AVMs. What other condition can present with telangiectasias that may involve the lungs? 


Your new hypothesis leads you to examine the hands further, discovering that the patient has a hard time completely straightening her fingers. You ask her to make the universal sign of prayer.

You search her skin for other signs of the condition that is now at the forefront of your mind. What is this hard, white nodule on her elbow? Does it further advance your hypothesis? 

So what about the dyspnea? How does the condition you have in mind affect the lungs? You look for evidence of pulmonary hypertension on exam. You start with the jugular venous pulse. What finding is present? 


Then you auscult the heart. What finding is present? What is your ultimate diagnosis?

This patient has scleroderma with systemic involvement (SSc). Typical cutaneous manifestations include telangiectasias, sclerodactyly (+ Prayer sign), and calcinosis cutis (nodule on her elbow). SSc can cause pulmonary hypertension, leading to Kussmaul’s sign and loud P2. 


A standardized test would provide all of these clues on a silver platter. Any machine can synthesize them and make the diagnosis. The clinician must not only synthesize, but gather these clues at the bedside. Your search must be hypothesis-driven or you might miss them. 


Anticipation is key in medicine. The eyes can’t see what the mind doesn’t know. The ears can’t hear what the mind doesn’t know. 


Patient 5: Extra Heart Sound

So you hear an extra heart sound. Now what? First: Is the extra sound near S1 or S2? Each scenario is associated with a different differential. Listen to this clip. Is the extra sound here near S1 or S2? 

Not sure you hear three sounds? To orient you, listen to normal S1 and S2. There are two sounds here.


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This is a persistently split S2. (S1 is also split.)

What about the the opening snap? It occurs further from S2 than the split S2, but closer to S2 than the S3 gallop and pericardial knock. It is best heard with the diaphragm and closer to the apex. Take a listen in this patient with severe mitral stenosis: 


What about the the pericardial knock? It occurs outside the range for a split S2 and the OS of mitral stenosis, but not as far from S2 as an S3. It is best heard with the diaphragm over the LLSB/apex. Take a listen in this patient with constrictive pericarditis: 

So back to our patient. What is the extra sound? Orienting yourself to the cardiac cycle is critical. Is the sound near S1 or near S2? How far from S2 is the sound? Is it high- or low-pitched? Is it best heard over the base or apex? 


Our patient has an S3 gallop. 


Never forget importance of history and associated findings. The exam is not practiced in a vacuum. Is pt from a country where rheumatic heart disease is prevalent? Does the patient have sharp and deep X/Y descents indicative of constriction? Other signs of heart failure?

Patient 6: Transient Heart Sound

You hear an extra transient heart sound near S1. Now what? 


Not sure you hear three sounds? Here is normal S1 and S2 to serve as a control.  

There are two sounds. Listen to this clip and then re-listen to the above clip. When you do, you will hear three sounds. Two near where S1 should be, followed by S2. 

So what’s the differential for extra transient sounds near S1?  


Split S1  

S4 gallop  

Ejection click 


Split S1 and S4 gallop can be challenging to distinguish because both are best heard over the APEX area. However, the split S1 sounds are closer together than the S1-S4 interval. And the S4 is best heard with the BELL of the scope. Listen to this split S1: 

Now take a listen to this S4 gallop: 

Notice that the S1-S4 interval is longer compared to the split S1 above. And while we are listening over the same area of the chest (apex), the bell is being used rather than the diaphragm. 

What about the ejection click? It is perhaps the easiest to distinguish because it is often heard over the BASE of the heart – very atypical for the split S1 and S4. The click is best appreciated with the diaphragm of the scope as it is higher pitched. 

So back to our patient. What is the extra sound? 

It is heard over the base of the heart with the diaphragm. This is an ejection click. (It was picked up on routine exam and led to the diagnosis of a severely dilated aortic root.)  

Remember that the exam is never performed in a vacuum. You will also have the benefit of the history and other findings. Does the patient have longstanding HTN (S4)? Does the patient have a giant a wave with an RV heave suggestive of pulmonary hypertension (click)? 


Patient 7: Exertional Dyspnea

A 50-y/o man presents with exertional dyspnea. The two main systems responsible for dyspnea are the heart and the lungs.

The jugular venous pulse can serve as a pivot point. It can take you toward or away from the heart. With this in mind, you evaluate the patient’s neck. What do you notice? 


Not only is the JVP elevated, but it appears to rise with inspiration. This is known as Kussmaul’s sign.

In the above video, you may have also noticed a mark on the patient’s skin, just below the “a wave” in our logo. Here is the mark up close:

What is it? 


You ask the patient when he had radiation therapy to his chest, and he gives you a surprised look. “How did you know?” 


“I haven’t thought about it in 30 years. I had Hodgkin’s lymphoma when I was 17 years old. They shot radiation at my chest. Why does it matter, doc?” 


Next, you listen to the patient’s heart, anticipating what you might hear. “The ears can’t hear what the mind doesn’t know”.



You hear an extra transient sound near S2. Your differential is split S2, S3 gallop, opening snap, and pericardial knock. The location, pitch, distance from S2, and the associated history and JVP findings make this sound most likely to be a pericardial knock. 


You diagnose this patient with radiation-induced constrictive pericarditis. With your eyes and ears. The effects of radiation therapy can show up decades later, when patients have all but forgotten they even had it. 

Patient 8: Heart Failure

A man presents to you with the clinical syndrome of heart failure (weight gain, orthopnea, elevated JVP, etc.). BP is 144/48 mm Hg.

This should generate a hypothesis. Yoo you look for other specific physical findings. What do you notice in this video?


Quincke’s pulse is consistent with your hypothesis, so you look for more evidence in his neck. And you have found it.


You then listen to the patient’s heart in anticipation of hearing a decrescendo diastolic murmur and confirming your suspicions.

But there is no decrescendo diastolic murmur. Further, his echocardiogram is totally normal. There is no aortic valve pathology. There is no systolic dysfunction.

Wide pulse pressure, Quincke’s pulse, and Corrigan’s pulse are not specific for aortic regurgitation. They are physical manifestations of a hyperkinetic state from ANY cause.

The combination of high-output physiology and HF should generate a new hypothesis. You test your hypothesis with right heart catheterization.


You have diagnosed the patient with high-output heart failure. What’s causing it?

Retrospective history reveals the consumption of 3-4 glasses of wine daily. Hypothesis-driven laboratory investigation is pursued.

You have now diagnosed the patient with high-output heart failure secondary to thiamine deficiency (wet beriberi).

Alcohol leads to thiamine deficiency through a variety of mechanisms, including poor diet and decreased absorption of thiamine in the GI tract.

Why is the diagnosis of wet beriberi so critical to make? It is curable. Take a look at BP and PP over time with alcohol cessation and thiamine replacement:

The risk here would have been to diagnose the patient with heart failure with preserved systolic function and then call it a day. “This is a very common diagnosis, take these diuretics and you’ll feel better”.

The observation of the physical findings changed everything.

This patient was cured without need for diuretics or other long-term meds.

The observation of wide pulse pressure and other signs of high-output physiology can provide a pivotal clue to the diagnosis of high-output heart failure, particularly when echo is uninformative.

Patient 9: Rapid Weight Gain

A young man comes to your clinic for evaluation of rapid weight gain. He has heard “diet and exercise” several times before he sees you.

The driver license photo was taken ~9 months prior.

You make some observations, leading you to generate a hypothesis.

Based on your hypothesis, you examine the patient further. And you make several more important observations, increasing the likelihood of your hypothesis.

You remember that skin thickness can be an important sign in this condition, from Lynn Loriaux’s 2017 @NEJM review.

(Examiner’s hand is shown above, patient’s below.)

You now have a clinical syndrome that is consistent with Cushing’s syndrome.

A confirmatory test is your next step.

Urine free cortisol (confirmatory test): 7,960 mcg/24H (!)

You have now confirmed the diagnosis of Cushing’s syndrome. The next question is, is it ACTH-dependent or ACTH-independent?

A plasma ACTH level is necessary to make this determination.

Plasma ACTH level is 496 pg/mL (normal <50)

Where is that ACTH coming from? The pituitary gland (ectopic) or elsewhere (ectopic)?

To determine this, inferior petrosal sinus sampling is necessary.

IPSS shows a ratio <3, confirming an ectopic source of ACTH.

Chest imaging ultimately reveals the presence of a bronchial carcinoid tumor.

You have diagnosed ACTH-dependent Cushing’s syndrome from an ectopic source using only your eyes and hypothesis-driven laboratory and imaging tests.

Patient 10: Ascites

You are rotating on the Procedure Service and your team is asked to perform a routine “therapeutic” paracentesis on a patient with cancer. You walk into the room to meet the patient and this is what you see. This finding should generate a hypothesis.

A “diagnostic” paracentesis wasn’t requested, but the underlying cause of ascites in this case has never been questioned. You consult your framework for ascites: The first question you want to know is whether the process is driven by portal hypertension or not.


Serum albumin is 3.1 g/dL and ascitic fluid album is 0.8 g/dL, yielding a serum-ascites albumin gradient (SAAG) of 2.3 (>1.1), which is consistent with a portal hypertensive process.


Next you wonder if the cause of portal HTN is prehepatic, hepatic, or posthepatic. For this you return to the cornerstone of diagnostic medicine, the history and physical examination. You recall the hypothesis generated by the dilated forehead veins and you evaluate the JVP.

The patient is upright in the video. What do you think right atrial pressure is? High? Low? Normal? It is markedly elevated. Pointing you in the direction of posthepatic causes of portal hypertension.

An echocardiogram is performed, demonstrating severe systolic dysfunction.
You diagnose the patient with HF with reduced systolic function, likely caused by chemotherapeutic agents. While cirrhosis and malignancy are common causes of ascites, other etiologies should always be considered. Heart failure is the cause of ascites in this case.

Patient 11: Jaundice

This previously healthy woman presents with fatigue and weight gain. We walk into the room to meet her. What findings are present? These findings should generate a hypothesis.
The three primary colors are red, yellow, and blue. Diseases can make skin color shift toward one of the primary colors. 
This patient is tending toward yellow (jaundice). (The eyes are an excellent place to look for icterus in patients with darker skin tone.) We also notice the red lesions on her neck and chest. Here’s a close-up video of a different patient with the same finding:

These lesions are a form of telangiectasia known as spider angiomas – characterized by a central pulsating arteriole that feeds branches that radiate outward, like a spider. Hence the name. We continue our hypothesis-driven approach by examining the hands. Finding?
Palmar erythema describes redness in the thenar and hypothenar areas and the base and pads of the fingers, with sparing of the actual palm area (a bit of a misnomer).
We examine her abdomen next. It is symmetrically distended, generating a hypothesis in our minds. So we perform a specific exam maneuver:

So we have a patient with jaundice, spider angiomas, palmar erythema, and ascites. Retrospective history reveals significant daily alcohol consumption. What is the underlying diagnosis?
We diagnosed Laennec’s cirrhosis with our eyes, ears, hands, and a microscope slide.

Patient 12: Hypoxemia

A young woman presents with progressive dyspnea. You walk into the room and this is what you see. What finding is present?

Central cyanosis indicates the presence of hypoxemia. SPO2 by pulse oximetry is 80%. ABG on room air shows PaO2 of 40 mm Hg and PaCO2 of 30 mm Hg. We reference our framework for hypoxemia to begin the process of narrowing our differential diagnosis.
The first thing we want to know is the A-a gradient. A (from the alveolar gas equation) = 112 mm Hg a (from the ABG) = 40 mm Hg A-a = 112 – 40 = 72 mm Hg. Elevated
Next we revisit the physical examination for more clues. There is profound peripheral cyanosis. But what else do you notice? If you don’t specifically look for this finding you might never notice it. “The eyes can’t see what the mind doesn’t know.”
Clubbing indicates that we are likely dealing with an anatomic shunt.
The patient’s precordial movement shown here is suggestive of an intracardiac shunt. Chest can move in this way when blood travels from a higher pressure chamber to a lower pressure chamber. In this case, from the right to the left.
Our diagnosis is confirmed with an echo with agitated saline contrast. Bubbles appear in the LV within 3 beats. Bubbles are normally filtered by the lungs. They only appear in the L side of the heart if there is an intracardiac (few beats) or intrapulmonary shunt (>5 beats).
We diagnosed an intracardiac shunt with our eyes, a Q-tip, and a few specific hypothesis-driven tests. Physical exam plays a critical role in diagnosis.

Patient 13: Discordant Heart Failure

A 60 y/o man w chronic systolic HF is admitted with increasing dyspnea on exertion, orthopnea, and fatigue. Says his weight hasn’t changed much recently. We perform a quantitative assessment of the jugular venous pulse. Video starts w patient at 60 degrees and then reclines.


The pulse is visible just above the clavicle at 60 degrees. We estimate RA pressure to be mildly elevated at ~12-14 cm H2O (9-10 mm Hg). Are you surprised? Do symptoms seem out of proportion to RA pressure? Next we perform a qualitative assessment. What do you notice?

So right-sided pressures are only mildly elevated. What about the left? How can we tell? Abdominojugular reflux. A sustained rise in JVP >3 cm for more than 10-15 sec while abd pressure is continuously applied is highly suggestive of elevated wedge pressure >15 mm Hg.
Based on the patient’s history and our exam, we predict mildly elevated RA pressure with markedly elevated wedge pressure. Let’s see what right heart catheterization shows.
We are correct. Mean RA pressure only 11 mm Hg but mean wedge pressure 34 mm Hg. Oh and by the way, that Kussmaul’s you observed in his neck? Here’s what it looks like on RHC. See how the RA pressure (bottom tracing) rises and falls with the respiratory cycle?
Why is this interesting? Typically R- and L-sided pressures are concordant in patients with L-sided HF. In this case, there is discordance. Wedge pressure >> RA pressure. This occurs in a minority of HF patients.

Does this matter? It goes back to the Starling curve. Top graph is a typical HF patient. Diuresis can improve cardiac function. Bottom graph is our patient. The curve is shallow. Diuresis will achieve little.
There is still some room to fully optimize RA pressure with diuresis here. But the focus should be on afterload in these patients with L>>R discordance. And, if available and appropriate, workup for advanced HF therapies (inotropes, LVAD, transplant) should commence.
We used history and physical exam to diagnose discordant L>>R filling pressures, an atypical scenario in HF patients. This has implications for treatment. Reference used: Drazner et al. J Heart Lung Transplant. 1999;18: 1126 –1132 

Patient 14: Migratory Arthritis

A 26 y/o woman presents with migratory arthritis. Started with a red and hot foot/ankle. Then went to the knee. Overuse, she was told. When ice/rest did not help, she went to the hospital. An arthrocentesis procedure was performed.
20K white blood cells but no organisms. She was taken for a washout procedure for presumed septic arthritis. And when the knee didn’t improve, she was taken for another one. And when she still didn’t improve, she was transferred to our hospital

We consult our framework for arthritis.

Inflammatory arthritis is suggested by the cardinal physical findings of inflammation: erythema (rubor), warmth (calor), pain (dolor), and swelling (tumor). As seen in this elbow joint from another patient:
Our patient has inflammatory arthritis. Next we think about the number of joints that are involved.

There are 2 joints involved, putting us in the category of oligoarticular arthritis, which helps to focus our differential diagnosis. Now we can seek hypothesis-driven information from the history and the exam.
One of our hypotheses leads us to examine her fingernails. What is this finding?
We were looking for nail bed pitting but instead find what looks like a drop of oil. Ah, the oil drop sign. So we perform a full skin examine and the following findings were hiding on the nape of the neck (had to lift up her hair to see it) and the back of her ear.

There are several spondyloarthritides, among them psoriatic arthritis. Patient was started on methotrexate and etanercept, with subsequent resolution of symptoms.
This patient went through several unnecessary surgical procedures. Physical exam plays a critical role in diagnosis.

Patient 15: Hyperpigmentation

A 44 y/o man is admitted with acute abdominal pain, nausea, vomiting, and diarrhea. HR 130, BP 90/52. You walk into the room to meet the patient. What do you notice? This should generate at least one hypothesis.
You ask the patient for an old photograph for comparison. His wife pulls out her phone and produces this picture (B) taken about 10 years prior. Pt reports darkening of skin over an 8 year period (for which he saw several clinicians). What conditions are you considering?
Let’s consider the hypotension. Physical examination is critical in determining which “category” of hypotension we are dealing with. How can physical exam help

In this case, JVP is low and extremities are warm.

This pattern is characteristic of distributive hypotension. Do any of the conditions listed there match your initial hypothesis?

A confirmatory test is your next step. Serum cortisol is 4.4 ug/dL 60 minutes after a 250 ug injection of ACTH. (Normal adrenal function is established when serum cortisol level is >18 ug/dL after ACTH stimulation.)
You have now confirmed the diagnosis of adrenal insufficiency. The next question is, is it ACTH-dependent or ACTH-independent? A plasma ACTH level is necessary to make this determination. But based on your physical exam, you already know the answer.
Plasma ACTH level (drawn prior to the stim test) is 872 pg/mL (reference range 10-60 pg/mL).
ACTH stimulates melanocortin-1 receptor in the skin –> hyperpigmentation. It usually occurs first in areas of skin under pressure, such as the knuckles or elbows, as in this case below. How long has she been feeling ill? The fingernails provide a clue.
Back to our patient. He has primary adrenal insufficiency, most likely isolated autoimmune adrenalitis.
Adrenal crisis is usually triggered by acute illness (in this case bacterial colitis). Many of the symptoms/signs can be mistakenly attributed to the acute illness that triggers the adrenal crisis, causing the diagnosis to be missed.
This patient went 8 years without a diagnosis. We can all learn from that. Next time we see hyperpigmentation we will consider adrenal insufficiency.

Patient 16: Chronic Diarrhea with heart problem

A 55 y/o man presents for evaluation of chronic diarrhea. We walk into the room to meet him. We have an opportunity to make an “augenblick” diagnosis – one that can be made in the blink of an eye.

We listen to his heart to help confirm our hypothesis (best with headphones). There is a holosystolic murmur over the LLSB. Notice that the intensity of the murmur seems to vary in a regular cycle? It gets louder/quieter/louder/quieter. What is the significance of this?

The augmentation of the murmur during inspiration is known as Carvallo’s sign, and indicates that the abnormal heart sound is coming from the R-side of the heart. Here is a more dramatic example in a different patient with tricuspid stenosis:

Our patient has tricuspid regurgitation. We’ve made a diagnosis, but does it end there? No. We must now determine the cause of the TR. Similar to the “diagnosis” of anemia. . .we don’t stop there, we must determine the underlying cause. So what is the cause of TR here?
Let’s get back to the chief complaint of diarrhea. Is there a tie-in with tricuspid regurgitation? We consult our framework for diarrhea:
The diarrhea is chronic and non-bloody, making infectious (and other inflammatory) causes less likely.
ImageAdditional history reveals that the diarrhea occurs up to 15 times per day, and persists even during periods when he does not eat. These features suggest a secretory cause.

ImageIs there a cause of secretory diarrhea in the framework that can be associated with tricuspid valve regurgitation? Yes there is.

ImageVasoactive substances released by carcinoid tumors can damage the heart valves, leading to stenosis and/or regurgitation. Left-sided valves are spared in most cases because the lungs inactivate the vasoactive substances before they reach the left side of the heart.

Octreotide scan shows areas of normal radiotracer uptake (bladder, kidneys, spleen), but there is a focus of increased uptake in the region of the small intestine (the primary tumor site), and multiple globular foci of increased uptake in the liver (mets).
First, we diagnosed TR with our eyes only. An augenblick diagnosis. Next, we used the diarrhea framework to identify a connection to TR, leading to hypothesis-driven confirmation.

Patient 17: Dyspnea and high arches

A young man presents with dyspnea. We start with his hands. My hand is gloved in the second photo (for frame of reference, I can palm a basketball). Our patient has a finding that should generate a hypothesis.


Our hypothesis takes us to the patient’s mouth.


A high-arched palate. Otherwise note as an “ogival” arch. These arches are pointed at the top and are a key feature of Gothic architecture, beginning in the 12th century.

Here is a real example. I took this photo of an arrowslit inside a famous castle in Syria (Qala’at al-Hosn or Krak des Chevaliers) when I visited in 2010. There is an ogival arch right above the slit.



Here we see more “standard” arches in and around Damascus. Left, a monastery/church in Sednaya, a city near Damascus where Aramaic is still spoken. Right, Roman ruins thousands of years old. But our patient’s palate doesn’t look like these arches. He has an ogival palate.


Now we must ask, how can Marfan’s syndrome lead to dyspnea? Before we auscultate, we anticipate what the heart will sound like. “The ears can’t hear what the mind doesn’t know.” Take a listen. (Best with headphones.)

He has a systolic murmur and a diastolic murmur. Classic for aortic insufficiency (the systolic component is like a “flow” murmur related to the large SV generated by the extra end-diastolic volume). So we revisit the hands. What finding is present in this video?
With our eyes and ears only (and with the benefit of a brief tour through Syria), we diagnosed this patient with Marfan’s syndrome complicated by aortic valve insufficiency. I hope you enjoyed the journey.

Patient 18: Old man with a masked face

This patient presents for evaluation after family noticed he’s been “slowing down” recently. We walk in to meet him. How old do you think he is? Perhaps there is already a clue to the underlying diagnosis.

After speaking with him, our clues are starting to add up.
We take a look at his hands to further test our hypothesis. (The hands are often a rich source of diagnostic information.)
A classic finding is present. We move on to evaluate his gait, anticipating what we might see. And we see it

A classic freezing and festinating gait is observed. As the French say, marche à petits pas (“walking in little steps”). The patient has difficulty getting started, as if the feet are glued to the floor. We diagnosed Parkinson’s disease with our eyes only.
By the way, this patient is older than 70 years. The expressionless “masked facies” of Parkinson’s can possibly make patients appear younger than they are.

Patient 19: Chest pain, joint pain, erythematous nodules and the Silk Road.

A young Lebanese man presents with several days of chest pain. Let’s remind ourselves where Lebanon is on the map. It may prove valuable “down the road”.


Now let’s deal with his chest pain. It can be helpful to think of chest pain as either cardiac or noncardiac in nature. The history and exam will point you down one “road” or the other



Our patient’s pain is substernal, sharp, and worsens when he breaths deeply. We auscult the heart with a hypothesis in mind, anticipating what we might hear. “The ears can’t hear what the mind doesn’t know”.

(Best with headphones or good speakers.)

The pleuritic nature of the pain and the 3-component pericardial friction rub are key features that tell us we are dealing with a cardiac cause of chest pain.

The quality of the pain does not sound like angina, but let’s look at his EKG to help us rule out ACS and confirm our hypothesis. We anticipate what we might see. “The eyes can’t see what the mind doesn’t know”.



Indeed, diffuse ST elevation, diffuse PR depression, and PR elevation in aVR are consistent with our hypothesis of acute pericarditis.


But why does our patient have pericarditis? Let’s review the main causes.



Additional hypothesis-driven history reveals joint pain and stiffness, especially in the morning. This points us toward a rheumatologic cause of pericarditis (connective tissue disease).Image

The skin and mucosa can be rich sources of clues to particular rheumatologic conditions. We start with the lower extremities and find these tender erythematous nodules on both shins.Image

We ask the patient if he has any other painful spots on his body. He pulls down on his lower lip and shows us this painful lesion, which he says shows up from time to time in his mouth and on his scrotum and penis.


Let’s come back to Lebanon. It is a country in the Levant, with Syria to the north and east, Palestine to the south, and the Mediterranean Sea to the west.


The territory of modern-day Lebanon was part of an ancient network of trade routes, known as the Silk Road, which extended from eastern Asia to the Mediterranean.



Silk Road disease, AKA Behçet’s disease, is a form of systemic vasculitis. It is more common in peoples whose ancestors inhabited the lands around the ancient Silk Road, including Lebanon. The pericardium is the most common site of cardiac involvement in Behçet’s disease.


We diagnosed Behçet’s with our eyes and ears and a little help from geography and ancient history. Genetic ancestry – and its imperfect surrogate terms – can provide an important clue to diagnosis. 


Patient 20: Dyspnea with Hypotension

A middle-aged man presents with acute sudden-onset dyspnea and hypotension. He is sitting upright. What do you notice? Let’s see if we can figure out the cause of hypotension.

First. What are the 4 basic mechanisms of hypotension? Hypotension can be hypovolemic, cardiogenic, distributive, or obstructive.
Hypovolemic hypotension occurs as a result of decreased hydrostatic pressure within blood vessels, and decreased cardiac preload with an associated decrease in cardiac output. It is characterized by decreased CVP (primary issue), decreased CO, and increased SVR (choice C).Image

What are the causes of hypovolemic hypotension?Image

Cardiogenic hypotension occurs as a result of pump failure with an associated decrease in cardiac output. It is characterized by increased CVP, decreased CO (primary issue), and increased SVR (choice A).Image

What are the causes of cardiogenic hypotension?Image

Distributive hypotension occurs as a result of pathologic peripheral vasodilation with an associated decrease in SVR. It is characterized by decreased CVP, increased CO, and decreased SVR (primary issue) (choice B).Image

What are the causes of distributive hypotension?Image

Obstructive hypotension occurs as a result of decreased cardiac filling with an associated decrease in both preload and cardiac output. It is characterized by increased CVP (primary issue), decreased CO, and increased SVR (choice A).Image

What are the causes of obstructive hypotension?Image

Physical examination is critical in the evaluation of hypotension. Our surrogate for CVP is the JVP; our surrogate for CO is the strength of the peripheral pulse; and the surrogate for SVR is warm/cool extremities. Here is Quincke’s pulse in a patient with septic shock.
Back to our patient. His extremities are cool to the touch. What did you notice in the neck? JVP is elevated. This immediately cuts our differential diagnosis in half.Image

Our patient could have either cardiogenic or obstructive hypotension. Let’s go a little deeper. What do you notice in this video of our patient? (Turn sound up.)

Contrary to popular belief, Kussmaul’s sign does not occur in pure cardiac tamponade. It can occur in constrictive pericarditis (or effusive-constrictive pericarditis) but the sudden-onset of symptoms points away from this. Cardiogenic hypotension it is. But from what?
Is there a clue in the neck veins? You bet there is. Let’s look at the original video. Which component of the waveform stands out to you?

The giant a wave, as well as Kussmaul’s sign in the other video, lead us to causes of RV failure. And so does our patient’s RV heave, shown below.

As we ponder the causes of sudden-onset RV failure, we begin to narrow our focus. And we anticipate what we might hear when we listen to the heart. (Sound up.) “The ears can’t hear what the mind doesn’t know.”

S2 is split. And the second of the two sounds (P2) is louder than the first (A2). This patient has an acute pulmonary embolism.

Patient 21: Chest Pain, Dyspnea



A 75-year-old woman presents with chest pain and dyspnea. What do you notice about her neck veins?
The jugular venous pulse is dynamic, with impressive X and Y descents, as well as Kussmaul’s sign (rise in JVP with inspiration). These findings are critical because the two main systems involved in dyspnea are the heart and lungs.



The abnormalities of the jugular venous pulse point us in the direction of the heart. A simple and cost-free bedside assessment allows us to focus our attention on the heart.
Now we listen to the heart. What do you hear? (For the best listening experience use headphones or good computer speakers.)
There is a 3-component pericardial friction rub. Telling us the patient has acute pericarditis. Sharp/deep X/Y descents in the venous waveform is known as the W sign, and in combination with Kussmaul’s sign, is indicative of pericardial constriction.

Acute pericarditis and constrictive pericarditis are different clinical entities but can co-occur: 1. Effusive-constrictive dz 2. Subacute pericardial constriction, which is a form of transient constrictive pericarditis (caused by acute edema rather than scarring/fibrosis).
Our patient was treated with NSAIDs and colchicine with resolution of symptoms, resolution of signs of pericardial constriction (confirming subacute constrictive pericarditis), and marked improvement in inflammatory markers.
Despite a thorough workup, a specific cause of the acute pericarditis with subacute pericardial constriction could not be determined. Idiopathic, as they say. In most cases, idiopathic acute pericarditis is probably caused by unidentified viruses.

Patient 22: Hematuria with skin lesions


A young man presents with hematuria and is found to have these painful skin lesions on physical exam.
In a patient with hematuria, the first question I always ask is as follows: what is the source of that blood? Is it glomerular or non-glomerular?
How can we tell if the bleeding is glomerular or not? We have to evaluate the urine sediment. But the eyes can’t see what the mind doesn’t know. So what are we looking for? (Images courtesy of

What is the shape of the RBCs? Normal shape (isomorphic)? Or are they abnormal in shape (dysmorphic) because they have squeezed through an inflamed glomerulus? If we look closely some of these RBCs are indeed dysmorphic (purple arrows). Blue arrows point to isomorphic RBCs.
When those RBCs squeeze through the glomerulus they end up in the tubules, where they can form casts. Check out what

found below. That’s an RBC cast ! Another clue that our bleeding source is glomerular.


Our patient has hematuria of glomerular origin.
I like to approach GN serologically.
But instead of just ordering all of those labs simultaneously at a high cost, history and physical exam should guide that workup. Let’s revisit the exam. What is this skin lesion? Image
Our derm colleagues come by and confidently diagnose ecthyma. What organism most commonly causes echythma? Streptococcus. Can we connect the dots now? Our hypothesis drives us to order serum complement levels and ASO titers.
And we have our diagnosis.

Patient 23: Nose and gum bleed with skin rash


A young woman presents with bleeding from her nose and gums and the following skin rash.
Petechiae are pinpoint hemorrhages <2 mm in size, purpura are 2 mm to 1 cm, and ecchymoses are >1 cm. Our patient has all three. These lesions are the result of extravasation of blood from the vasculature into skin/mucosa and do not blanch, as shown in this video:
A platelet disorder could explain these symptoms and physical findings. But is the platelet issue qualitative (platelets are normal in number but abnormal in function) or quantitative (platelets are normal in function, but abnormal in number)?Image

A CBC can sort us out.
Now that we know we are dealing with thrombocytopenia, our next question is… are platelets not being produced appropriately, or are they being destroyed?
Well there’s a test for that too. Immature platelets = newly released platelets. The immature platelet fraction is like an RBC reticulocyte count. If low/normal, there is decreased platelet production; if elevated, there is increased platelet destruction.
The elevated immature platelet fraction tells us we are dealing with a process causing platelet destruction. The bone marrow is responding appropriately and cranking out platelets, it just can’t keep up.
So what’s our diagnosis?
The degree of thrombocytopenia (1!) narrows our differential to TMA and HIT. The absence of concomitant hemolytic anemia points us to the right diagnosis:


ITP is an acquired d/o characterized by autoantibody-mediated platelet destruction. It can be primary or secondary (eg, SLE). In adults, it’s often a chronic condition. In our case, @Bloodman  recommended steroids + IVIG and our patient’s platelet count has recovered nicely.