Surface anatomy – know your landmarks!

Surface anatomy is key to examination, especially when it comes to percussion and auscultation. Here are some of the major landmarks to guide your examinations:


  • The apex of the heart is in the mid-clavicular line, 5th intercostal space. This is where the tricuspid valve is best auscultated
  • The mitral valve should be auscultated at the lower left sternal edge, medial to the apex in the 5th intercostal space
  • The pulmonary valve can auscultated just lateral to the sternum in the left 2nd intercostal space
  • The aortic valve should be auscultated just lateral to the sternum in the right 2nd intercostal space

Lung borders:

  • The apices of the lungs extend 3cm above the mid clavicular point
  • In quiet respiration, the inferior margin of the lungs are:
    • T6 (midclavicular)
    • T8 (midaxillary)
    • T10 posteriorly (median plane)
  • Pleura surface markings two ribs lower

Lung Fissures: 

  • Oblique fissure – T3 to 6th costochondral junction
  • Horizontal fissure – from the oblique fissure in the mid-axillary line to the 4th costal cartilage


  • Marked on left side of the back, with its long axis corresponding with that of 10th rib
  • Upper border corresponds to upper border of 9th rib & lower border to lower border of 11th rib


  • The upper surface of the liver is percussed at the level of the fifth intercostal space
  • Lower border is the costal margin


  • Posteriorly: T11-L3 (Right lower than left)

Why look for JVP in an abdominal exam?

Looking for a raised jugular venous pressure is normally reserved for cardiac and respiratory examinations. A raised JVP is a sign of venous hypertension and most commonly manifests in the context of heart failure when the right side of the heart is unable to cope with venous return from the systemic circulation. The subsequent back-up manifests in a visible internal jugular vein.

However, it is also worth looking for an elevated JVP in an abdominal exam for both common and rare causes:

  1. Portopulmonary hypertension. This is the simultaneous co-existance of high blood pressure in both the portal circulation and the pulmonary circulation. It is a complication of liver cirrhosis and occurs in up to 4% of cirrhotic patients.
  2. Carcinoid of the gastrointestinal tract. This is caused by neuroendocrine tumours arising from enterochromaffin cells of luminal epithelia throughout the gut
  3. Congestive hepatopathy. Also called cardiac cirrhosis, this is deranged liver function in the setting of right heart failure. Increased pressure in the hepatic veins (secondary to right heart failure) causes necrosis of the liver lobules. This post’s image demonstrates the congested and fibrotic change that occurs histologically in congestive hepatopathy.

Quick tip: palpating for a liver edge

The upper surface of the liver is at the level of the fifth intercostal space on the right side and the lower border is at the costal margin. Therefore in healthy adults you often cannot palpate a liver edge.

The liver should always be palpated on inspiration to maximise the potential for a normal or pathological liver edge to be felt. Because the liver is situated just under the diaphragm, the liver will move inferiorly on inspiration as the diaphragm contracts and moves down itself.

Always palpate from the right iliac fossa up to the costal margin. Place your hand lightly on the patient’s abdomen and ask your patient to take deep breaths in and out. Palpate more firmly as your patient breathes in and attempt to feel the liver edge.

Quick tip: percussion

When percussing, most of us will percuss twice in the same spot before moving across the chest or abdomen. Remember to ensure that on the second tap, you remember to immediately lift your percussing finger off at the end, just like you did for the first tap. If you don’t, the first and second notes will not elicit the same resonance or dullness. Specifically, you will get a relatively more dull percussion note is your percussing finger is left down longer.

AAA – Expansile or pulsatile?

During an abdominal exam, you routinely feel for an abdominal aorta and whether or not it is aneurysmal. This is done by placing the finger tips of each hand parallel to the outer margins of aorta. This allows you to differentiate between an expansile and pulsatile aneurysm.

An expansile AAA will expand and contract, causing your fingers to be separated with each expansion and return with each contraction. With a pulsatile AAA, you will feel the pulse during systole but your fingers will not be separated apart as the AAA does not expand and contract. Don’t forget that the aorta is an artery and being pulsatile is normal. We are only worried if the aorta’s diameter becomes more than 5.5cm and is therefore classified as an AAA. You should also consider that a pulsatile abdominal mass isn’t necessarily the aorta itself, rather another structure that is transmitting the pulses from the aorta, such as lymph nodes.

Air entry and breath sounds, are they the same?

No. And next time you hear a doctor reporting ‘good air entry’, you have a responsibility to slap them on the wrist and correct them. Let me explain why.

When you examine a patient, you report what you can hear and what you can see. You can then make inferences about what you have found. You cannot find sepsis on examination, but you can find signs of infection and tachycardia, tachypnoea or aberrant body temperature which together would make you think of sepsis.

The same is true here: you cannot hear air entry into the lungs because beyond the main bronchi, air flow is laminar and you cannot hear laminar air flow on auscultation. What you can hear is turbulent air movement in the trachea and bronchi and we tend to assume this air will enter the lungs. However, in certain pathologies such as in airway obstruction or collapsed lung, this may not be the case.

So let’s think about breath sounds. A breath sound is the sound of turbulent air in the large airways transmitting through the chest to the diaphragm of the stethoscope. Although you cannot hear laminar air flow, the lung parenchyma and air moving through the lower airways carry the sound of turbulent air from the upper airways. So with normal breath sounds it is likely that there is good air entry as nothing is interrupting the transmission of sound waves.

A normal breath sound is called a vesicular breath sound. As someone breathes in and turbulent airflow increases, the breath sound will get increasingly loud as sound is transmitted through the lung parenchyma. During expiration, air is expelled but beyond the first third of expiration, the sound of turbulent air flow is not transmitted to the lower airways and therefore we cannot hear it.

If part of a lung collapses, there is no lung parenchyma to carry the sound waves from the large airways to the diaphragm of your stethoscope. The breath sounds will therefore be reduced or absent.

Conversely, if there is fluid in the lungs (for example with consolidation in pneumonia), breath sounds will be increased. Why? Because sound waves are transmitted more effectively in liquids than gases. We now call this a bronchial breath sound – the same sound that you will hear if you place your stethoscope over the trachea. These are harsher sounds with a more discernible gap between inspiration and expiration than in vesicular breath sounds. This gap is emblematic of when turbulent air flow from inspiration ends, and before it begins during expiration. This gap is still there is vesicular breath sounds it is smoothly dissipated by the elastic recoil of the lower airways. The trachea does not have the same expansibility and recoil.

So why is this important? If there is reduced air entry into the lungs due to an airway obstruction, you will certainly hear reduced breath sounds (the sound of turbulent air flow cannot be transmitted). But the opposite is not necessarily true. You may have reduced breath sounds but air entry into the lungs may be normal. For example, breath sounds may be absent or reduced in pleural effusions or chest wall swelling. The air is reaching the lungs just fine but you effectively have a wall blocking sound from travelling from the distal lung fields to the diaphragm of the stethoscope. Likewise, in patients who are very thin, breath sounds might be louder for the opposite reason.

So next time you hear someone say air entry, ask what they really mean.

What is colic?

Colic is a form of pain, characterised by intense episodes that start and stop abruptly. It occurs when a muscular tube contracts against an obstruction from within the lumen.

The frequency of the fluctuations in pain can help us determine the anatomical location of the obstruction.

  • Renal: The smooth-muscle layer in the distal one third of the ureters contracts at a frequency of 3 per minute.
    • Thus, renal colic is characterised by extreme loin pain with frequent fluctuations in intensity.
  • Biliary: Neither the cystic duct nor the common bile duct has peristaltic motility however, the post-prandial gall bladder will contract at a frequency of 3 per hour.
    • Thus, biliary colic is characterised by intense, spasmodic pain every 10-20 minutes until a steady state of dull, aching pain in the upper right quadrant after approximately one hour.
  • Gastrointestinal: Perstalsis in the gut varies along its length (stomach 3/min, duodenum 12/min, ileum 9/min) but contractions last a few minutes per 10-20cm segment.
    • Thus, bowel colic tends to be cramping in nature and lasts 2-3 minutes. This is a true colic as there is no pain between episodes.