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92 Cardiovascular observations (III)
Table 4.14 (Continued)
Blood cell Normal test result Normal test result Notes where applicable
(SI units)
Mean corpuscular 80–100 µm
3
80–100 fL
volume (MCV)
Mean corpuscular Hb 27–33 pg/cell 1.70–2.05 fmol/
(MCH) cell
Mean corpuscular 33–37 g Hb/cell 330–370 g/L
Hb concentration
(MCHC)
Monocytes 0–800/µL 0–0.8 × 10
9
/L
Neutrophils 1,800–7,800/µL 1.8–7.8 × 10
9
/L
Platelet count 150–450 × 10
3
/µL 150–450 × 10
9
/L
Reticulocyte count 1–1.5% of total RBC
White cell count 4,500–11,000/µL 4.5–11.0 × 10
9
/L
(WBC)
Test: Erythrocyte sedimentation rate (ESR). This measures the rate at which red cells
form a sediment over one hour. It is an observation of those factors promoting versus
those factors resisting sedimentation. The ERS increases due to inammation, rheumatoid
arthritis, pregnancy, anaemia, infections and some cancers. A reduced ERS occurs in
polycythaemia, leukaemia and sickle-cell anaemia, low plasma protein and congestive
cardiac failure (CCF).
Test: Glycosylated haemoglobin (HbA1c). This measures the average haemoglo-
bin blood glucose level for the three-month period prior to the test. Haemoglobin can
become glycosylated (bound to glucose). The more glucose there is in circulation, the
greater the degree of glycosylation. Because of the limited lifespan of red blood cells and
the fact that they are replaced daily, the test only shows what blood glucose levels were
over the previous three months. It is a useful test for diagnosing diabetes or monitoring
blood glucose levels as part of diabetic control.
Test: Glucose-6-phosphate dehydrogenase (G-6-PD). This is an enzyme present in the
blood that protects red blood cells from the damaging effects of reactive oxygen species
(ROS). These chemicals attack red cells and can cause haemolysis (red cell breakdown),
leading to anaemia (haemolytic anaemia). Sudden onset anaemia or jaundice will prob
-
ably require this test in order to detect any deciency in G-6-PD. Deciency could be due
to a genetic mutation in the G-6-PG gene that can run in families.
Test: Haematocrit (or packed cell volume, PCV). This measures the red cell volume
relative to the total blood volume. This is a guide to assessing anaemia, where the volume
of red cells is likely to decrease due to lower numbers or smaller cells. The haematocrit
will also decrease if the plasma increases. An increase in the red cell volume may occur
in severe dehydration, causing the plasma volume to reduce.
Test: Haemoglobin (Hb) This protein inside red blood cells carries oxygen. Low hae-
moglobin in circulation carries inadequate oxygen causing anaemia, and this may be due
to low red cell numbers or normal numbers carrying reduced haemoglobin. It is a com-
mon test used to assess risk of anaemia, e.g. tiredness, breathless and pallor.
Test: Haemoglobin-binding protein (haptoglobin, HPT). This protein is produced by
the liver and binds with free haemoglobin, i.e. haemoglobin released from the red blood
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Cardiovascular observations (III) 93
cell during red cell breakdown. It prevents haemoglobin destruction while still in circula-
tion, preventing iron loss and protecting the kidneys from free haemoglobin damage. A
large release of haemoglobin, as in haemolytic anaemia, uses up much of the haptoglobin
and the level in the blood becomes low.
Test: Mean corpuscular volume (MCV). This is a calculation of the average volume of
a red blood cell. The formula for this is:
MCV = haematocrit ÷ [RBC]
That is, MCV equals the haematocrit (see haematocrit, earlier) divided by the concentra-
tion of red blood cells.
The volume of red cells can be measured directly. Red cells with high volume are
seen in pernicious anaemia (see vitamin B
12
deciency, page 73), causing macrocytic
(large red cell) anaemia. A low volume of red cells (microcytic) is seen in iron deciency
anaemia.
Test: Mean corpuscular Hb (MCH). This is the average amount of haemoglobin found
in each red blood cell. The formula for this is:
MCH = (10 × haemoglobin) ÷ (red blood cell count)
Low MCH is due to various types of anaemia and iron deciency in the diet. High MCH
may be due to liver disease, some cancers and infections.
Test: Mean corpuscular Hb concentration (MCHC). This is the average concentration
of haemoglobin in a given volume of packed red blood cells. The formula is:
MCHC = (haemoglobin × 100) ÷ (haematocrit)
The haemoglobin is divided by the haematocrit (see haematocrit, page 92). High MCHC
may be due to the presence of spherocytosis (red cells with exceptionally high amounts
of haemoglobin) in circulation. Unstable Hb or deciency of vitamin B
12
and folic acid
may be other causes.
Test: Reticulocyte count. Reticulocytes are immature erythrocytes. They would not
usually be released into circulation (from bone marrow) until fully mature. A raised reticu
-
locyte level in circulation indicates that the bone marrow is producing these cells quickly
and releasing them to compensate for low or high levels of red cells, due to anaemia or
bone marrow disorders.
Blood groups (Tables 4.15, 4.16)
There are at least 14 different blood grouping systems known. The only two used in clini-
cal practice are the ABO system (discovered in 1901) and the rhesus (Rh) system (discov-
ered in 1940) (Daniels and Bromilow 2013). The other systems cause mild and transient
reactions. The reactions caused by the ABO and rhesus systems are potentially fatal.
The ABO system is based on the fact that red cells have a combination of two antigens
on their surface: antigens A and B. If the red cells have only antigen A, this is blood group
A; red cells with only antigen B produce blood group B; red cells with antigens A and B
together create blood group AB and those with no A or B antigen present is blood group
O. Antibodies are present in the plasma (see antibodies, page 86), but individuals cannot
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94 Cardiovascular observations (III)
Table 4.15 Blood groups and antigens. The table shows which antigen exists on the red blood cell
(RBC) and which antibody exists in the plasma of each of the four blood types
Blood group Antigen on RBC Antibodies in plasma
A
B
AB
O
A
B
A+B
No antigens
Anti-B (reacts with B antigen)
Anti-A (reacts with A antigen)
No antibodies
Anti-A and anti-B (reacts with both A and B)
Table 4.16 The ABO blood groups compatibility grid. The donor’s red cells (A and B antigens) are
matched with the recipient’s plasma (anti-A and anti-B antibodies) to identify any dan
-
gerous reaction (✗) or no reaction (✓). Recipient AB can take blood from any group
(universal recipient) provided the rhesus factor (not shown) is positive (AB Rh
+
), and
donor O can give blood to any group (universal donor) provided the rhesus factor (not
shown) is negative (O Rh
−
)
Donor blood Recipient blood
A B AB O
Anti-B antibody Anti-A antibody None Anti-A + anti-B antibodies
A ✓ ✗ ✓ ✗
B ✗ ✓ ✓ ✗
AB ✗ ✗ ✓ ✗
O ✓ ✓ ✓ ✓
have the antibodies that react with their own antigen. Instead, they have antibodies that
react with other antigens (Tables 4.15 and 4.16).
The rhesus system involves the RBC surface antigen called the D-factor (the rhesus
factor). If the D-factor is present, the blood is rhesus-positive (Rh
+
), and the plasma has
no anti-D antibody. If the D-factor is absent, the blood is rhesus-negative (Rh
−
), and
the plasma has got anti-D antibody. Any of the four ABO groups can be either Rh
+
or
Rh
−
(i.e. a total of 8 blood groups). The plasma antibodies cannot react with their own
red cells, but transfusion of blood from one person to another creates the conditions
that could cause a reaction, and this must be avoided. Haemolysis (haemo = blood;
lysis = break down) is one type of reaction where red cells are destroyed, haemoglobin
is released and the patient can suffer severe anaemia with jaundice. Agglutination is
another type of reaction where red cells clump together in large lumps that can block
smaller vessels, such as the arterioles within the kidneys, causing kidney failure. These
reactions happen due to mismatched transfusions, and careful checking is required to
prevent this (Table 4.16).
Blood tests in development
• A blood test that can determine the presence or not of a myocardial infarction (MI)
quicker than the current troponin tests (see page 70) could be available. The test gives
results in about 20 minutes, and unlike troponins it does not need repeating some hours
later. It rapidly excludes a lot of patients who present with non-cardiac chest pain and
who could then be sent home. It identies the presence of any cardiac myosin-binding
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Cardiovascular observations (III) 95
protein C (cMyC), which is raised earlier and higher in the blood following a myocar-
dial infarction than the troponins (see troponin tests, page 70).
• Several blood tests are based on the detection of cell-free DNA (cfDNA) in blood
plasma. DNA fragments from these dead cells are constantly being discharged into the
blood. It is now possible to collect these fragments in a sample of blood and analyse
this DNA. Several examples are:
1 cfDNA in the maternal blood from the unborn foetus during the early stages of preg-
nancy can be checked for the presence of Down’s syndrome (trisomy-21)
2 cfDNA from tumours or foreign organisms can be found and analysed to detect new
growths or infections
3 cfDNA from transplanted organs can be checked in the recipient blood to identify
any signs of organ rejection, when the cfDNA would rise
4 cfDNA in the blood may soon be able to detect the death of pancreatic islet cells
before symptoms of diabetes occur.
These tests are now available. One of the problems has been identifying what organ or
tissue the cfDNA comes from, but already a system identifying the methylation of DNA
(the attachment of methyl groups to the DNA) has been devised since methylation varies
for different organs.
Tests to detect the presence of biomarkers for brain-derived proteins in circulation that
are released in brain injury or diseases such as Alzheimer disease (AD). Neurolament
light (NFL) rises sharply in blood plasma after brain injury and be a blood biomarker
for the presence of several chronic neurodegeneration disorders, including AD, in those
with a history of head injury. In a separate test, the relative amounts of the various beta-
amyloid proteins present in the brain can now be assessed from the beta-amyloid found
in the blood. The blood results correlate well with beta-amyloid found in brain scans.
Key points
• The total blood volume in circulation is 5,000 ml (5 L).
• The blood cells are erythrocytes (red blood cells), leucocytes (white blood cells) and
thrombocytes (platelets).
• Blood cells have a limited lifespan and are replaced by new cells from bone marrow.
• Plasma transports many substances and a lot of these can be tested for.
• Plasma proteins are mostly albumin and globulin, with others in smaller quantities,
including some hormones, enzymes, clotting factors and antibodies.
• Plasma proteins are mostly produced in the liver.
• Blood group A has antigen A on the RBCs and anti-B antibodies in the plasma. Blood
group B has antigen B with anti-A antibodies in the plasma. Blood group AB has anti-
gens A and B and no anti-A or anti-B antibodies, and blood group O has no A or B
antigen and anti-A and anti-B antibodies in the plasma.
• The rhesus factor (D-factor) is present in rhesus-positive (Rh
+
), the plasma having no
anti-D antibody. The D-factor is absent in rhesus-negative (Rh
−
), the plasma having
anti-D antibody.
Notes
1 The symptoms of beriberi are fatigue, poor appetite, weight loss, diarrhoea, muscle wasting,
oedema, paralysis and heart failure (Table 7.3, page 142).
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96 Cardiovascular observations (III)
2 The four D’s of pellagra are diarrhoea, dermatitis, dementia and death (Table 7.3, page 142).
3 Early symptoms of scurvy are weakness and tiredness, and later sore gums, bleeding and anaemia
(Table 7.3, page 142).
4 Rickets causes soft, bent bones in children with vitamin D deciency. Osteomalacia is the adult
equivalent, causing easy fractures and bone pain. The difference is due to the fact that rickets is
the disease in bone that is still growing, while osteomalacia is the disease in fully mature bones.
5 Note that the capital H is the chemical symbol for hydrogen (since acidity is all about hydrogen
ion concentration), so it becomes meaningless to write a small h. Because hydrogen is H and not
PH, it important to write a small p (p stands for potential). So, PH, Ph and ph are all wrong and
meaningless. It must always be pH (potential hydrogen), even at the start of a sentence (see also
acid-base measurement of urine, Chapter 8, and Figure 8.14).
References
Bain B. (2017) A Beginner’s Guide to Blood Cells (3rd edition). Wiley-Blackwell, Hoboken, NJ.
Basten G. (2013) Blood Results in Clinical Practice. M&K Update, Keswick.
Blann A. and Ahmed N. (2014) Blood Science: Principles and Pathology. Wiley-Blackwell, Hobo-
ken, NJ.
Blows W.T. (2022) The Biological Basis of Mental Health (4th edition). Routledge, Abingdon, UK
and New York.
Caironi P. and Gattinoni L. (2009) The clinical use of albumin: The point of view of a specialist in
intensive care. Blood Transfusion, 7(4): 259–267. http://doi.org/10.2450/2009.0002-09
Daniels G. and Bromilow I. (2013) Essential Guide to Blood Groups (3rd edition). Wiley-Blackwell,
Hoboken, NJ.
Rennie J.M. and Kendall G.S. (2013) A Manual of Neonatal Intensive Care (5th edition). CRC Press,
Boca Raton, FL.
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5 Respiratory observations
• Introduction
• Respiratory physiology
• The neurophysiology of respiration
• Observations of breathing
• ABCDE assessment
• Childhood breathing
• Drugs affecting the respiratory system
• Key points
• Notes
• References
Introduction
Although we need oxygen (O
2
) from the air, oxygen is not the main driving force of
breathing. The need to remove carbon (C) from the body is the primary drive. Oxygen is
required for this process, by combining with waste carbon (CO
2
) and removing it from the
body. CO
2
(carbon dioxide) is the by-product of tissue energy production (Chapter 1, Fig-
ure 1.3, page 4). It is excreted via the lungs, having been transported there by the blood.
Observations of respiration are a means of assessing the efciency of this process and
detecting any abnormalities. Carbon dioxide is both benecial and harmful, depending
on the quantity present. Constant volumes of this gas in both the tissues and the blood are
essential to maintain the driving force for breathing. Too much carbon dioxide in the cells
would cause life threatening problems with energy production. Oxygen has a smaller
role in maintaining the respiratory drive. Its main role is to combine with the two waste
products of cellular metabolism, hydrogen and carbon and remove these from the body:
• Two hydrogens (2H) combine with oxygen (O) to form water (H
2
O), which is excreted
through the lungs and skin.
• One carbon (C) combines with oxygen (O
2
) to form CO
2
, which is excreted through the
lungs.
DOI: 10.4324/9781003389118-5
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98 Respiratory observations
Air passes from the atmosphere into the lungs through the airway, which consists of the
nasal and oral openings, the pharynx, the larynx (often called the voice box), the trachea
(sometimes called the windpipe), both left and right bronchi, multiple bronchioles and
the tiny air sacs (called alveoli) at the end (Figure 5.1). Most of the airway is lined with
mucous membrane that produces mucin (mucous). Mucous membrane warms incoming
air to body temperature, particularly within the nose, adds moisture to it so it will not dry
out the alveoli, and traps unwanted pollutants which stick to the mucous. Tiny hairlike
cellular extensions (called cilia) then beat in an upward motion to ‘sweep’ the mucous
and pollutants out of the lungs towards the throat, where they will be swallowed. This is
called the muco-ciliary escalator. Beneath the mucous membrane, in most of the airway,
is a smooth muscle layer. In the bronchi, this smooth muscle can contract (causing a nar-
rowing of the airway, called bronchoconstriction) or relax (causing a widening of the air-
way, called bronchodilation). The narrowest part of the upper airway, the glottis, is within
the larynx. This is where the vocal cords are stretched across the airway to produce sound.
Some parts of the upper airway wall, especially the trachea and bronchi, are reinforced
with stiff cartilage rings to prevent airway collapse.
Right
Left
lung
lung
Diaphragm
Nasal
cavity
Oral
cavity
with tongue
Pharynx
Larynx
Trachea
Figure 5.1 T he respiratory tract includes the nasal and oral cavities, the pharynx and larynx (voice
box) and the trachea which divides at the lower end into left and right bronchi, one for
each lung.
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Respiratory observations 99
Respiratory physiology
Respiration means the exchange of the gases oxygen and carbon dioxide. There are two
places where these gases are exchanged with the blood, i.e. in the lungs (external respi-
ration) and in the tissues (internal respiration). Breathing is the act of getting air into and
out of the lungs.
The alveoli are minute air sacs that make up the bulk of lung tissue and provide the
location for gas exchange (external respiration). There are three gas exchange compart-
ments: (1) the air within the alveoli (called alveolar air); (2) the blood and (3) the tissues
of the alveolar wall (Figure 5.2).
While the air and blood are constantly being changed, the tissues provide a con-
stant close yet distinct barrier between the two. Gases move across this barrier, driven
by the concentration gradient. Substances will ow from a high concentration to a low
concentration, a movement referred to as diffusion. This is dened as the movement of
substances such as gases or liquids from the point of greatest concentration to areas of
lower concentration. This equals out the concentration so no gradient exists and move-
ment stops. In respiration, diffusion refers to the movement of oxygen and carbon dioxide
during external and internal respiration.
In the lungs, the gradient – and therefore gas ow – is maintained, i.e. equalisation of
concentration is prevented. During breathing, oxygen is moving into the blood but is kept
in a higher concentration in the alveoli than in the blood by the continued addition of
new oxygen from the air. Carbon dioxide is moving into the lungs from the blood, but the
concentration of this gas in the alveoli is kept lower than in the blood by the continued
Alveolus
(air)
O
2
CO
2
Pulmonary
capillary
Inter
stitial
fluid
T
ype I
al
veolar cell
T
ype II
al
veolar cell
Figure 5.2 Microscopic view of the lung showing an alveolus containing air, with walls of type I and
type II cells, a pulmonary capillary containing blood and interstitial uid between the
capillary and the alveolus. The direction of gas movement is shown.
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100 Respiratory observations
removal of CO
2
from the alveoli by breathing. The act of breathing itself ensures that these
concentration gradients are maintained, and therefore these gases will continue to ow in
and out of the lungs and blood (Figure 5.2).
Mechanics of breathing
Breathing is a mechanical process that involves the movement of muscles within the chest
wall and diaphragm. These movements control lung expansion and contraction because
the lungs are held tightly against the chest wall by a slight negative pressure (or vacuum,
i.e. −4 mmHg). This vacuum exists between the membrane attached to the outer surface
of the lungs (the visceral layer of the pleura) and the membrane attached to the inner
surface of the chest wall (the parietal layer of the pleura), causing these two surfaces to
stick close together (Figure 5.3).
The negative intrapleural pressure is 4 mmHg lower than the atmospheric pressure
outside the chest wall and inside the lungs. As the chest wall moves the lungs must go
along with it. If this vacuum is compromised the lungs and chest wall will separate, i.e.
complete or partial lung collapse, or atelectasis. It could be air that gets into this space (a
pneumothorax) or water from blood plasma (a hydrothorax) or whole blood (a haemo-
thorax) or any combination of these, e.g. a haemopneumothorax. The lungs would fail to
respond to chest wall movements, making breathing very difcult and painful.
The muscle of the chest wall operates the ribs, which during inspiration are moved
upwards and outwards, expanding the volume (or space) within the chest two-dimen-
sionally from front to back and side to side. Contraction of the diaphragm at the same
time causes it to atten (at rest it is normally slightly dome-shaped), increasing the chest
volume in the third dimension (i.e. from top to bottom). The lungs are stretched outwards
in all directions, causing the air pressure inside the lungs to drop below atmospheric
Trachea
Chest wall
Left
lung
PP PC
Diaphragm
PCVP
Right
lung
Chest wall
Figure 5.3 The lungs and the pleural membrane. PC: pleural cavity containing the negative (suc-
tion) pressure; PP: parietal layer of the pleural membrane attached to the chest wall and
diaphragm; VP: visceral layer of the pleural membrane attached to the lung surface.
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Respiratory observations 101
Air
A
Air B
Figure 5.4 Inspir ation and expiration. (A) During inspiration, the chest wall moves upwards and
outwards, and the diaphragm attens, causing the lungs to be stretched in all directions.
The resulting increase in the volume inside the lungs causes the pressure to fall, and air
is drawn in to ll the space. (B) During expiration, the return of the lungs and diaphragm
decreases the lung space, forcing the pressure up, and air is blown out.
pressure, thus creating a partial vacuum within the lungs that must be instantly lled by
air taken in from the atmosphere (inhalation or inspiration). The reverse is also true, when
the respiratory muscles relax, allowing the ribs and diaphragm to return to their previous
normal position. This squeezes the lungs, increasing the pressure inside the lungs above
atmospheric pressure, which then forces the air back out into the atmosphere (exhalation
or expiration; Figure 5.4).
The cycle of diaphragmatic movements starts with contraction of its muscle com-
ponent, which attens the normal dome shape. This pushes down the abdominal con-
tents, notably the liver which lies immediately below the diaphragm. Relaxation of
the diaphragm results in its return to a domed shape, aided by the liver and other
abdominal contents pushing back. Pressure from within the abdomen aids expiration,
and this is the reason why, in some positions, abdominal movements can be seen dur-
ing breathing.
The relationship between volume and pressure seen in the lungs is expressed in Boyle’s
law, where the pressure inside the lungs falls if the volume increases at a constant tem-
perature (as in inhalation), or the pressure rises if the volume decreases at a constant tem-
perature (as in exhalation). The muscles used during normal breathing are primary, since
they act all the time. Sometimes additional effort must be made to breathe, e.g. immedi-
ately after exercise, and secondary (or accessory) muscles are used to assist in chest wall
movement. These standby muscles of breathing include some of the muscles of the neck
and shoulders. The most efcient position for the use of these muscles is upright, leaning
slightly forward, with arms raised to a horizontal position. Severely breathless patients
will adopt this position to aid their breathing if they are able to do so.
Air volumes
The volume of air we take in with each breath is the tidal volume, i.e. the air moving in
and out of the lungs. This volume is about 500 ml in adults (Figure 5.5). The 500 ml can
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