You are seeing a patient with suspected pneumonia. Your attending hears crackles but you do not hear them. Later the radiograph shows pneumonia right where the attending heard crackles. What can you do to improve your pulmonary examination?


Sit up and take a deep breath might be bad advice?


Increase signal

Sensitivity for auscultation of crackles is increased in the supine position. Should you always listen supine? No. That is hard to do because anterior is less helpful and posterior requires you to squeeze the stethoscope behind their supine back. But be aware it is an option if you need to increase the sensitivity for the physical examination.


You can make crackles more easily discerned by varying your exam. If it sounded too quiet have them take a deeper breath.


Decrease noise

Should they always take a deep breath? No. That can increase other noise if they make upper respiratory noises. Have the patient take a “full and quiet” breath. That might be best for minimizing noise and maximizing signal.


Take Home Points:

-“Sit up and take a deep breath” is not the only way to do a lung examination

-Increase signal by auscultating the supine back

-Decrease noise by asking the patient to breathe deeply, but quietly



An elderly patient presents with cough and shortness of breath. The resident says the lung examination is normal and the chest x-ray is negative and wants to send the patient home. But you hear crackles posteriorly at the right base. And the oxygen saturation is 94%. And the patient looks ill. What do you do?


If your practice is to use chest radiograph as the gold standard for pneumonia (following IDSA guidelines – Mandell 2007) then you might be missing pneumonia. In medicine we tend (alas) to assume our reference standards are disease-defining until we compare them against something else.


Against CT scan, chest radiograph is probably about 75% sensitive and specific for pneumonia. Often the literature does not give exact numbers but false negatives and false positives are extensively documented. Where sensitivity is reported, it can be as low as 44%.(Self Am J Emergency Medicine 2013 – from a datebase of PE workups) A more representative finding for sensitivity is 77% (Ye PLoS One 2015). Good, but not perfect. Other studies show significant false positive rates (Clasessens Am J Resp Crit Care Med 2015). Specificity is probably also about 75% but we do not yet have a precise estimate of that. And of course there are significant differences between a supine 1 view chest radiograph in an altered patient and a 2 view standing radiograph with tidal volume inspiration.


Your overall accuracy is not doomed by limited tests. Your accuracy depends on how well you formulate Bayesian “prior probability” BEFORE applying results of tests. Of course, if you don’t want to do that there is always pulmonary ultrasound, with 95% sensitivity (Ye PLoS One 2015). But let’s talk bedside medicine.


The classical clinical signs of pneumonia are:




-asymmetric breath sounds


-progression of symptoms after 3-5 days


Steven McGee’s Evidence-Based Physical Diagnosis has an excellent chapter on this topic. It essentially supports the classical findings but reminds us of their limitations too.


Back to the case. You have a moderate clinical suspicion and you are aware that the gold standard is flawed. Do you order an ultrasound? CT? Do you start empiric antibiotics? Do you recommend next day follow-up? In this case you desire to admit the patient because she appears ill. But the utilization case manager and hospitalist argue that the admission does not meet Interqual criteria. They say it is impossible for a patient to have pneumonia without a positive chest x-ray and besides, the patient does not even have a fever (oral temperature).


You palpate the temperature at the neck with the back of your hand and leave it there for 5 seconds, and feel a tingle – this is a fever. The RN confirms the rectal temperature is 103. You perform a bedside ultrasound and find mild hepatization and a few air bronchograms in the area where you heard crackles. They do not accept the legitimacy of that test, despite the literature.


You order a CT scan and the radiologist confirms a moderate size consolidation, interpreted as pneumonia, at the exact area where you heard crackles hours before.



-Chest x-ray has limitations in sensitivity and specificity for pneumonia (probably about 75% for each)

-If you do a thorough physical examination with attention to heart rate, oxygenation, and auscultation then the CXR is probably adequate for most patients.

-When you need more information, consider pulmonary ultrasound, or CT scan of the chest.


A patient a history of COPD presents with shortness of breath. Physical examination shows pursed lip breathing, prolonged exhalation, recruitment of accessory muscles, etc. COPD exacerbation, right?


Hold on. Have a COPD patient jog around the parking lot and they will look just the same. Anything that causes shortness of breath in a COPD patient will accentuate the physical signs of COPD. All those signs mean is that they are either having to breath harder, or deal with secretions.


The GOLD criteria for COPD emphasize a change in sputum character or quantity or dyspnea. A viral URI can do that. So can PE, metabolic acidosis, CHF, etc.


This is why I recommend thinking of COPD as a diagnosis of exclusion. If there are copious secretions then maybe that tells you the origin of the problem. But if it is just shortness of breath, then work it up the same way you would work up any patient with shortness of breath.



-Think of COPD as a diagnosis of exclusion- consider other causes like CHF, pneumonia, pulmonary embolism

-Be especially vigilant in the COPD patient who presents with shortness of breath and no change in secretions


A 5 week old presents with nasal congestion and difficulty breathing. RSV bronchiolitis is ultimately diagnosed. Can the patient go home?

Not every infant with bronchiolitis can be admitted. But the ED provider must be aware that the dreaded complication of apnea tends to occur in patients who are under 2-3 months old.

The studies on apnea from bronchiolitis are heterogeneous and the results are mixed. For example the incidence of apnea in newborns varies from <1% to 24% (Ralston J Pediatrics 2009).

One study of all bronchiolitis patients under one year of age found that all the apnea occurred in patients under 10 weeks of age, and 73% in those under 1 month of adjusted age (adjusting for prematurity).(Ricart Ped Infect Dis J 2014) Numerous studies show similar clustering in the newborn period.( Pruikkonen 2014, Arms 2008)

Take Home Points:

-Apnea in RSV is more likely in those under 2-3 months of age or who were premature


Why do some critically ill patients, when they are laid flat for intubation, either get worse or sometimes even go into cardiac arrest?

Patients with CHF, COPD, and morbid obesity are considered susceptible. I am not sure what I have read in the literature is correct in explaining it. I suspect that anyone who lays flat has more air trapping. This can crowd out venous return. In a patient on the brink of dying, impairing venous return might put them over that brink.

An interesting corollary of this idea is that patients with high autoPEEP on a ventilator can be placed in the upright position and this significantly reduces their autoPEEP.

So in summary, supine positioning appears to exacerbate auto-PEEP, and in the peri-arrest state can precipitate cardiac arrest apparently through crowding out venous return

Take Home Points

-Supine positioning causes autoPEEP

-In the patient with a respiratory life threat, keep the patient upright as long as possible.

-Consider 30 degrees elevation (reverse Trendelenburg) for intubating patients thought to have potential for arrest during intubation

-In the ventilated patient who develops auto-PEEP, use reverse Trendelenburg or upright posture as a treatment

Head-Elevated Patient Positioning Decreases Complications of Emergent Tracheal Intubation in the Ward and Intensive Care Unit.

Khandelwal N, Khorsand S, Mitchell SH, Joffe AM.

Anesth Analg. 2016 Apr;122(4):1101-7


Pulmonary hypertension is known for being difficult to diagnose, but there are some physical signs that may offer a clue:

  1. Giant A waves in the jugular venous pulse.
  2. Loud P2
  3. a parasternal heave at the left lower sternal border

1) Giant A waves in the jugular venous pulse can be a sign of pulmonary hypertension.  The A stands for atrial systole, and is present just before the carotid impulse.  Paul Wood, a famous cardiologist and teacher from the 20th century, recorded in 1957 a 20 minute video introducing this topic. (accessed July 26, 2011).  Jugular waveform analysis is somewhat of a lost art, being ignored in most modern studies, despite the fact that in Dr. Wood’s cases the sign is easily discerned.  To my knowledge the sensitivity is not known.

2) A loud P2 in some cases can be discerned at the bedside in the emergency department.  Physiologic splitting happens on inspiration, and A2 (aortic sound) comes first, followed by P2 (pulmonic sound). A loud P2 is thought to be 38%-57% sensitive for pulmonary hypertension(Pilatis 2000, Sompradeekul 2010).  Audio samples are encouraged, and an example is found at (accessed July 26, 2011).  This is best heard with the diaphragm in the pulmonic area with the patient leaning forward.

3) A parasternal heave is recognized by placing the palm on the patient’s parasternal area, with the elbow locked.  An impulse upward is considered a heave.  It was estimated as having 38% sensitivity for pulmonary hypertension (Pilatis 2000).

Historical signs of physical diagnosis sometimes are sometimes ignored for low sensitivity. However, these signs present with varying degrees of intensity, and certainly it behooves us to be prepared so that we can recognize those presentations that are discernible.

Take home points:

Physical signs of pulmonary hypertension include giant A waves, a loud P2,  and a parasternal heave.