Respiratory anatomy illustrations

Figure 4.1 Lung markings – anterior view.

Figure 4.2 Lung markings – posterior view.

Useful lung markings*
Apex	Anterior – 2.5 cm above clavicles
	Posterior – T1
Lower borders	Anterior – sixth rib
	Posterior – T10/11
	Mid-axilla – eighth rib
Tracheal bifurcation	Anterior – manubriosternal junction
Tracheal bifurcation	Posterior – T4
Right horizontal fissure	Anterior – fourth rib (above the nipple)
Oblique fissures	Anterior – sixth rib (below the nipple)
	Posterior – T2/3
Left diaphragm	Anterior – sixth rib
	Posterior – T10
	Mid-axilla – eighth rib
Right diaphragm	Anterior – fifth rib
	Posterior – T9
	Mid-axilla – eighth rib

* These lung markings are approximate and can vary between individuals.

Figure 4.3 Anterior view of bronchial tree.

Figure 4.4 Bronchopulmonary segments – right lateral view.

Figure 4.5 Bronchopulmonary segments – left lateral view.

Respiratory volumes and capacities

Figure 4.6 Respiratory volumes and capacities. Average volumes in healthy adult male.

Chest X-rays

Figure 4.7 A Normal PA chest X-ray (from Pryor & Prasad 2008); B structures normally visible on X-ray.

Analysing chest X-rays

Adopt a systematic approach when analysing X-rays (). You should check the following:

Auscultation

Auscultation should be conducted in a systematic manner, comparing the same area on the left and right side while visualizing the underlying lung structures. Ideally patients should be sitting upright and be asked to breathe through the mouth to reduce nose turbulence.

Breath sounds

Normal

More prominent at the top of the lungs and centrally, with the volume decreasing towards the bases and periphery. Expiration is shorter and quieter than inspiration and follows inspiration without a pause.

Abnormal (bronchial breathing)

Diminished

Breath sounds will be reduced if air entry is compromised by either an obstruction or a decrease in airflow. Caused by pneumothorax, pleural effusion, emphysema, collapse with occluded bronchus, atelectasis, inability to breathe deeply, obesity.

Added sounds

Wheeze

Caused by air being forced through narrowed or compressed airways. Described as either high or low pitched and monophonic (single note) or polyphonic (where several airways may be obstructed). Airway narrowing can be caused by bronchospasm, mucosal oedema or sputum retention. An expiratory wheeze with prolonged expiration is usually indicative of bronchospasm, while a low-pitched wheeze throughout inspiration and expiration is normally caused by secretions.

Pleural rub

If the pleural surfaces are inflamed or infected they become rough and rub together, creating a creaking or grating sound. Heard equally during inspiration and expiration.

Voice sounds

In normal lung tissue, voice sounds are indistinct and unintelligible. When there is consolidation, sound is transmitted more clearly and loudly and speech can be distinguished. Voice sounds can be diminished in the presence of emphysema, pneumothorax and pleural effusion. They can be heard through a stethoscope (vocal resonance) or felt by hand (vocal fremitus).To test voice sounds patients can be asked to say or whisper ‘99’ repeatedly.

Percussion note

Elicited by placing the middle finger of one hand firmly in the space between the ribs and tapping the distal phalanx sharply with the middle finger of the other hand.

The pitch of the note is determined by whether the lungs contain air, solid or fluid and will either sound normal, resonant, dull or stony dull.

Interpreting blood gas values

Arterial blood analysis	Reference ranges in adults
ph	7.35−7.45 pH
PaO₂	10.7–13.3 kPa (80–100 mmHg)
PaCO₂	4.7–6.0 kPa (35–45 mmHg)
HCO₃⁻	22–26 mmol/L
Base excess	−2 to +2

Assessing acid–base disorders

Assessing acid–base disorders involves examining the pH, PaCO₂ and HCO₃⁻:

• pH – a low pH (<7.4) indicates a tendency towards acidosis, a high pH (>7.4) indicates a tendency towards alkalosis.

• PaCO₂ – an increase in PaCO₂ leads to acidosis, a decrease to alkalosis.

• HCO₃⁻ – an increase in HCO₃⁻ leads to alkalosis, a decrease to acidosis.

Assessment

1. Establish whether the patient’s pH is acidotic, alkalotic or normal.

2. If the pH is acidotic establish whether this is due to:

–increased PaCO₂ – indicating respiratory acidosis

–decreased HCO₃⁻ – indicating metabolic acidosis.

3. If the pH is alkalotic establish whether this is due to:

– decreased PaCO₂ – indicating respiratory alkalosis

– increased HCO₃⁻ – indicating metabolic alkalosis.

4. If the pH is within normal range the original abnormality can be identified by comparing the pH to the PaCO₂ and the HCO₃⁻. If the pH is below 7.4 (tending towards acid) then the component that correlates with acidosis (increased PaCO₂ or decreased HCO₃⁻) is the cause and the other is the compensation. Likewise, if the pH is above 7.4 (tending towards alkaline) the component that correlates with alkalosis (decreased PaCO₂ or increased HCO₃⁻) is the cause and the other is the compensation.

Simple acid–base disorders

Base excess

Allows assessment of the metabolic component of acid–base disturbances and therefore the degree of renal compensation that has occurred. A base deficit (less than −2) indicates a metabolic acidosis and a base excess (greater than +2) correlates with metabolic alkalosis.

Respiratory failure

Broadly defined as an inability of the respiratory system to maintain blood gas values within normal ranges. There are two types:

Type I (hypoxaemic respiratory failure)

A decreased PaO₂ (hypoxaemia) with a normal or slightly reduced PaCO₂ due to inadequate gas exchange. Causes include pneumonia, emphysema, fibrosing alveolitis, severe asthma and adult respiratory distress syndrome.

Defined as PaO₂<8 kPa (60 mmHg).

Type II (ventilatory failure)

A decreased PaO₂ with an increased PaCO₂ (hypercapnia) caused by hypoventilation. Causes include neuromuscular disorders (e.g. muscular dystrophy, Guillain–Barré), lung diseases (e.g. asthma, COPD), drug-related respiratory drive depression and injuries to the chest wall.

Defined as PaO₂<8 kPa (60 mmHg), PaCO₂>6.7 kPa (50 mmHg).

Arterial blood gas classification of respiratory failure

Nasal cannula

The following values are approximate as the patient’s flow rates, ability to breathe through the nose, type of cannula and build-up of nasal mucus may all affect the amount of oxygen received. As a general rule the FiO₂ is raised by 3–4% for each litre of oxygen.

To convert litres of O₂ to FiO₂
RA≈ 21% FiO₂
1 L/min ≈ 24% FiO₂
2 L/min ≈ 28% FiO₂
3 L/min ≈ 32% FiO₂
4 L/min ≈ 36% FiO₂
5 L/min ≈ 40% FiO₂
6 L/min ≈ 44% FiO₂

RA=room air.

> 6 L/min has little effect on FiO₂ and may lead to irritation and drying of the nasal mucosa.

Sputum analysis (Middleton & Middleton 2008, with permission)

	Description	Causes
Saliva	Clear watery fluid
Mucoid	Opalescent or white	Chronic bronchitis without infection, asthma
Muco- purulent	Slightly discoloured, but not frank pus	Bronchiectasis, cystic fibrosis, pneumonia
Purulent	Thick, viscous: – yellow – dark green/brown – rusty – redcurrant jelly	Haemophilus Pseudomonas Pneumococcus, Mycoplasma Klebsiella
Frothy	Pink or white	Pulmonary oedema
Haemoptysis	Ranging from blood specks to frank blood, old blood (dark brown)	Infection (tuberculosis, bronchiectasis), infarction, carcinoma, vasculitis, trauma, also coagulation disorders, cardiac disease
Black	Black specks in mucoid secretions	Smoke inhalation (fires, tobacco, heroin), coal dust