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:

Heart:

  • 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

Spleen:

  • 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

Liver:

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

Kidneys:

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

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.

What causes clubbing?

Nail clubbing is one of the first things we look for when examining patients, but just like C-reactive protein in a blood test, it is a non specific sign of disease that often won’t help narrow your differential. To name just a few, it is associated with forms of heart, lung, gastrointestinal, and thyroid disease. But what causes clubbing? The most widely accepted theory is the ‘Platelet Theory’.

Megakaryocytes are large bone marrow derived cells released into the circulation that give rise to platelets but also a series of growth factors. A significant proportion of megakaryocytes reside in the lungs but during inflammation, megakaryocytes migrate from the lungs to the peripheries and become trapped in nail bed capillaries where they deposit their growth factors such as PDGF and VEGF. This leads to connective tissue proliferation and the characteristic thickening of the distal phalanx, increased nail curvature, and reduction of the angle between the nail and the cuticle.

What about non inflammatory disease? In congenital heart disease, a right to left shunt will cause megakaryocytes to bypass the pulmonary circulation into the systemic circulation where they will also be trapped in capillaries in the nail beds.

Why does systolic blood pressure drop with inspiration?

Breathe in.

As you do, the expansion of your chest reduces the pressure in the thorax below atmospheric pressure.

This has two effects on the heart:

  1. Reduced pressure on the Vena Cava, means more venous return to the right side of the heart
  2. Increased capacity of the pulmonary arteries (as they are pulled open), reduced venous return to the left side of the heart

This imbalance of heart filling compromises left ventricular capacity. The resultant reduction in stroke volume causes a reduction in systolic blood pressure by <10mmHg.

Given:

Cardiac Output = Stroke Volume x Heart Rate

Cardiac output is maintained by a baroreceptor-mediated increase in sympathetic outflow to the heart resulting in an increased pulse rate.

Breathe out.