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Hypoxia
Flash Presentation
1. Introduction
Hypoxia is a general term used to
describe inadequate oxygenation. Tissue hypoxia may be caused
either by inadequate oxygen content of the blood, defined as
hypoxemia, or by inadequate tissue perfusion, as in low cardiac
output states. In some conditions both may be present.
Hypoxia is a common problem
encountered in surgical practice and there are numerous causes.
Delay in finding and recognizing the cause of the hypoxia may
result in serious morbidity and mortality.
This module will help you to
understand the pathophysiology of the condition and enable you
to develop a differential diagnosis with a view to appropriate
management.
2. Aims
After working through this program
and applying it to your clinical practice you should be able to:
·
rapidly evaluate the
common causes of hypoxia
·
carry out prompt
emergency care
·
arrange appropriate
investigations
·
produce a management
plan
·
be aware of the need for
referral for ventilatory support
·
be aware of the
importance of the clinical and communication skills needed
and best clinical practice.
3. Examples in
Practice
Examples in practice We have
presented you with seven case studies which illustrate
conditions you may commonly come across in your surgical
practice. We suggest you read each of these clinical scenarios
and the accompanying key issues. You will be questioned on these
illustrative cases throughout the chapter.
|
Case 1 - History of respiratory
dysfunction
This 55-year-old obese female
presents with anemia due to a carcinoma of the
cecum. She has smoked 20 cigarettes per day for 30
years, has chronic obstructive airways disease (COAD)
and is judged ASA 3-4 (see ASA categorization). |
Key Issues
Assessment of respiratory
function.
ASA grading.
Effect of anemia on oxygen
carriage.
Optimizing physical state before
operation.
Risk assessment.
Communication with patient and
relatives.
Role of High Dependency Unit (HDU)/
Intensive Therapy Unit (ITU) before operation.
Strategies for prevention of chest
complications. |
|
Case 2 - Dyspnea and restlessness
This 58-year-old female has
presented with septicemia in association with
perforated diverticular disease. She is cold,
perspiring, restless and dyspneic. |
Clinical indicators of systemic
sepsis.
Multi-organ failure.
Management of sepsis.
Ventilatory support.
Referral for Intensive Care. |
|
Case 3 - Hypoxia immediately after
operation
This 70-year-old female returns to
the theatre recovery area following right
hemicolectomy. She is confused, barely arousable and
has shallow respiration. |
Preoperative assessment of
respiratory system.
Role of Recovery and High
Dependency Areas and monitoring of oxygen
saturation.
Effect of anesthetic gases on
alveolar PO2.
Effect of intra-operative drugs on
ventilation.
Pulmonary problems related to
ventilation.
Problems related to central venous
cannulation.
Importance of adequate recovery
before return to ward areas. |
|
Case 4 - Chest pain and Dyspnea
Two days after aorto-bifemoral
arterial graft this 55-year-old male develops chest
pain and marked dyspnea with frothy sputum.
|
Multifocal nature of vascular
disease.
Risk factors for perioperative
myocardial infarction.
Fluid load and cardiac function.
Medical treatment.
Invasive monitoring. |
|
Case 5 - Pyrexia and confusion
This 75-year-old female becomes
pyrexial (fever) and confused four days after trans-hiatal
esophagectomy performed for an advanced carcinoma of
esophagus |
Risk factors for postoperative
pneumonia.
Prevention of respiratory
infection.
Role of physiotherapy.
Bacteriological assessment.
Hospital acquired infections.
Limiting treatment in advanced
cancer.
Communication with patient,
relatives and staff.
Nutrition. |
|
Case 6 - Sudden collapse one week
following surgery
Seven days after total hip
replacement this 65-year-old male suddenly collapses
with chest pain, confusion and dyspnea |
Timing of clinical signs and
symptoms in relation to operation.
Differentiating between myocardial
infarction and pulmonary embolism.
Imaging techniques.
Risk factors for and prophylaxis
of thromboembolism.
Immediate intervention.
Long term effects. |
|
Case 7 - Trauma to chest
The patient is a 35-year-old male
who has fallen from a height, landing on the right
side of his chest and face. His breathing is labored
and he has difficulty opening his mouth.
|
Pre-hospital emergency care.
Role of paramedics in acute care
sequence and intubation.
ABC of resuscitation - role of
each in hypoxia.
Management of airway - including
indications for tracheostomy.
Flail chest and need for assisted
ventilation.
Exclusion of other injuries.
Need for chest drains. |
4. What you should think about
4.1 Pathophysiology
If you are to be successful in your
management of hypoxic patients you must have a sound knowledge
of the relevant pathophysiological principles.
Disturbances of oxygen transport
leading to hypoxia may be considered under the following five
headings:
·
reduced alveolar oxygen
tension
·
respiratory failure
·
veno-arterial shunts
·
defective oxygen
transport
·
defective tissue uptake.
..Can you allocate the cases in
section 3 to these categories? Reading the next five sections
should assist you in this task.
4.1.1 Reduced alveolar oxygen tension
Alveolar oxygen tension (PO2) may be
reduced in a variety of circumstances.
During transport by air, cabin
pressure is usually maintained at about the equivalent of 1500 m
above sea level. This will reduce the alveolar PO2 from 104 mmHg at sea level to about
86 mmHg. At altitudes above 4000 m the
markedly reduced inspired oxygen tension may cause the clinical
condition of altitude sickness which may be rapidly fatal. In
clinical practice, alveolar PO2 may be reduced by the presence
of other gases such as nitrous oxide excreted following a
general anesthetic.
Is it safe to transport
critically-ill hypoxic patients by air?
Increasing the FiO2 to 0.25 will
return the alveolar PO2 to normal and therefore oxygen
administration may compensate for the changes due to reduced
pressure. Changes in pressure may have other potentially
dangerous effects. It is essential to insert a chest drain in
any patient who could possibly have a pneumothorax, as
decompression may dramatically increase the volume of air in the
pleural space. “Accurate and rapid identification of respiratory
failure is absolutely vital in patient management - untreated,
it may be rapidly fatal.” A senior surgeon
4.1.2 Respiratory failure
Respiratory failure is defined as an
arterial oxygen tension (PaO2) at sea level of less than 60
mmHg. In type I respiratory failure the arterial carbon dioxide
tension (PaCO2) is less than 50 mmHg and in type II respiratory
failure it is higher than 50 mmHg.
Adequate oxygenation of the blood
depends on an appropriate matching of the ventilation and
perfusion to any area of the lungs. An abnormality of the ratio
of ventilation to perfusion is known as a V/Q mismatch and may
result in hypoxia.
Cyanosis is an indication that at
least 50 g/l of hemoglobin are unsaturated. Peripheral cyanosis
may result from any cause of poor peripheral perfusion (cold,
shock, polycythemia) in addition to hypoxemia, but central
cyanosis (of oral mucous membranes) is indicative of a reduced
PaO2.
Normal arterial blood gases:
|
PaO2 |
75-95 mmHg (PaO2 normally declines
somewhat with age) |
|
PaCO2 |
35-45 mmHg |
|
pH |
7.35-7.45 units |
|
[H+] |
35-45 |
|
[HCO3 -] |
22-28 |
It is essential to know the normal
values of arterial blood gases and be able to interpret the
abnormalities.
Hypercapnia (raised PCO2) may
complicate hypoxia in surgical patients, particularly in the
postoperative period. Think about the mechanism by which the
body compensates for raised PCO2.
When the body retains CO2 a
respiratory acidosis develops. In the first instance, blood pH
is restored by means of the normal physiological buffering
mechanisms. In the longer term, the kidney excretes an increased
amount of H+ into the tubular lumen. This results in correction
of the acidosis by increasing the plasma HCO3 - concentration.
In patients with chronic CO2 retention the plasma HCO3 - may
rise to 35 or higher. This contrasts with the findings in
patients with a metabolic acidosis in whom the HCO3 - is lower
than normal. In patients with acute ventilatory failure the
plasma HCO3 - concentration is usually normal as the renal
compensatory mechanisms are much slower than the respiratory
compensation.
Respiratory failure has five
principal causes:
·
cerebral
·
mechanical
·
airway obstruction
·
abnormalities of
pulmonary vasculature
·
abnormalities of lung
parenchyma.
Cerebral
Which of these categories may be
involved in the development of hypoxia in case 7?
·
Cerebral due to a head
injury and raised intracranial pressure.
·
Airway because of the
facial injury.
·
Mechanical because of a
flail segment.
·
Lung parenchymal because
of pulmonary contusion.
Anything which interferes with the
central control of respiration may cause respiratory failure
(see diagram below).

Possible causes include hypoxia,
hypercapnia, pharmacological agents and conditions causing
cerebral injury.
Morphine is a very useful analgesic
but may have profound respiratory depressant effects. It must be
used in a dose carefully titrated to its optimum clinical effect
in the elderly and in those with impaired hepatic or renal
function. Reduced consciousness with overdosage may predispose
to aspiration pneumonia. The analgesic and respiratory
depressant effects may both be reversed with naloxone.
Remind yourself of the drugs which
affect the respiratory center
In case 3, why was the patient
hypoxic?
Shallow respiration suggests
inadequate reversal of neuromuscular clocking agents (NMBAs),
inadequate recovery from anesthesia or opiate overdose.

Mechanical
Ventilation may be inhibited by any
condition which affects the function of the respiratory muscles,
the mobility of the chest wall or the expansion of the lung.
These may include factors affecting the neuromuscular function
of the respiratory muscles, abnormalities of the chest wall
(flail chest), restricted movements due to pain and space
occupying lesions in the pleural space (pneumo-, hemo- or
hydro-thorax).
At what spinal level will cord
transection cause apnea? Identify on the diagram opposite which
of the three levels indicated would be associated with apnea.
The highest of the three levels
causes apnea as the phrenic nerve arises from spinal segments
C3, 4 and 5. Airway obstruction
Partial airway obstruction increases
the work of breathing and total obstruction rapidly results in
asphyxia. Potential causes include:
·
obstruction in the mouth
or larynx due to trauma, blood, vomitus, foreign body, etc
·
large airway obstruction
due to laryngeal spasm, endotracheal tube misplacement and
compression from space occupying lesions, e.g. retrosternal
goiter
·
small airway obstruction
due to asthma, COPD or inhaled irritant.
In case 7, why did the patient
become so rapidly hypoxic?
He had sustained a facial injury
which produced an airway obstruction and had also sustained a
blunt injury to his chest which could result in hypoventilation
due to pain or flail chest. He could also have a pneumothorax
or hemothorax. Abnormalities of the pulmonary vasculature
Factors which alter the perfusion
pressure and the permeability of the pulmonary circulation will
cause changes in V/Q matching and in the interstitial fluid
volume. These include:
·
pulmonary edema
formation due to heart failure, Adult Respiratory Distress
Syndrome (ARDS) or burns
·
embolism with thrombus
or fat.
The formation of edema is governed
by Starling’s law of capillary function which is demonstrated
here:
kPa x 7.5 = mmHg
A valuable invasive investigation in
the assessment of the cardiac and pulmonary vascular function is
the use of the pulmonary artery flotation catheter (PAFC). This
is used to measure the pulmonary artery pressure and the
pulmonary capillary wedge pressure (PCWP).
The Adult Respiratory Distress Syndrome (ARDS)
This is a condition of rapid onset
which has a number of triggering events and is characterized by
profound hypoxemia, non-cardiogenic pulmonary edema, reduced
pulmonary compliance and right to left shunt (see 4.1.3).
In case 4, what will the patient's
pulmonary capillary wedge pressure be?
His PCWP is likely to be raised
above 15 mmHg. Pulmonary edema due to cardiac failure and ARDS
presents with similar clinical features but must be
differentiated. In pulmonary edema associated with cardiac
failure the pulmonary capillary wedge pressure (PCWP) is greater
than 15 mmHg whereas in ARDS, where the defect is predominantly
due to increased capillary permeability, the pressure is less
than 12 mmHg. The common causes include:
·
Shock of any etiology
·
Trauma including sepsis
head injury
·
Aspiration of gastric
·
Metabolic and contents
hematological disorders.
The pathological features detected
in the lungs vary according to the etiological factors but the
usual findings are:
·
microthrombi in
capillaries
·
endothelial cell
swelling
·
neutrophil accumulation
·
pneumocyte proliferation
·
increased interstitial
fluid volume
·
development of a hyaline
membrane in the capillaries.
·
accumulation of
proteinaceous fluid in alveoli
These features are produced by an
increased pulmonary vascular resistance and increased capillary
permeability. The accumulated neutrophils release proteases
which further increase the permeability of the capillary,
resulting in exudate of protein rich fluids.
Other contributory factors include
endotoxin, prostaglandins, leukotrienes, activated complement,
oxygen free radicals released from leucocytes and neurogenic
effects.
The patient therefore develops areas
of lung which are ventilated but not perfused and other areas
which are perfused but not ventilated. This causes major changes
in the V/Q ratio. The increased interstitial fluid volume acts
as a diffusion barrier and reduces pulmonary compliance.
In case 2, why is she hypoxic?
Septicemia has caused the pathological changes described above
resulting in ARDS.
Inhalation injury
Airway burns produce serious
respiratory problems due to a combination of thermal injury and
inhaled toxins.
Pulmonary embolism (PE)
Embolism of the pulmonary
circulation with thrombus results in a major alteration in the
V/Q match and may precipitate right heart failure.
Fat embolism
Fat embolism is more common in young
men with femoral shaft fractures but may occur even in the
absence of bony injury. It occurs in 2-22% of patients with long
bone fractures.
There are two theories about the
pathology of fat embolism. The first suggests a release of
marrow content into venous sinuses in the medullary cavity of
the bone with subsequent embolization. The second suggests that
the etiology is related to an increase in circulating free fatty
acids which are toxic to endothelial cells. Defective hepatic
function due to hypovolemic shock may exacerbate the effects by
reducing the capacity for fatty acid clearance.
Lung parenchymal disease
Parenchymal disease may result in
reduced lung compliance, V/Q mismatch or a barrier to diffusion.
Causes include:
·
pneumonia and aspiration
of enteral contents (especially with esophageal disease and
intestinal obstruction)
·
lymphangitis
carcinomatosa
·
pre-existing lung
disease such as emphysema, sarcoidosis and pulmonary
fibrosis.
The diagnosis of ‘pneumonia’ in
surgical patients can be controversial. Pneumonia is generally
accepted to be diagnosed in a patient with pyrexia, pulmonary
abnormalities on chest X-ray, and a positive sputum culture.
However, many postoperative patients have pyrexia and positive
sputum culture due to upper airway contamination. The pulmonary
fields on X-ray may be abnormal because of atelectasis rather
than infection. Definitive diagnosis may, therefore, be
difficult and many patients may have the diagnosis of pneumonia
made in error.
In case 5, why did the patient
develop postoperative pneumonia?
She may have pre-existing lung
disease. Because she has cancer and is malnourished, she may be
immunosuppressed and have diminished respiratory muscular
strength. She may be hypoventilating because of pain or opiate
overdose and may have suffered aspiration of enteral contents.
“Pneumonia is commonly unrecognized in the elderly who are at
risk of aspiration and who are very susceptible to opiate
overdose. The diagnosis may only be made when the patient is
moribund.” A senior surgeon
4.1.3 Veno-arterial shunting
A right to left shunt results in
venous blood passing into the arterial circulation without being
oxygenated. This may have a profound effect on the PaO2 and
increasing the inspired oxygen concentration (FiO2) will not
fully correct the reduced PaO2. This is because the shunted
blood is not exposed to the raised oxygen tension. The small
right to left shunt in normal individuals through the bronchial
circulation is sufficient to reduce the PO2 of 104 mmHg in the
pulmonary vein to 95 mmHg in the systemic arterial circulation.
Many of the conditions described under respiratory failure exert
their effects by producing a physiological shunt. There are
however some significant pathological anatomical shunts of which
the best recognized is that produced by the congenital cardiac
anomaly - the Tetralogy of Fallot.
4.1.4 Defective oxygen transport
The transport of oxygen is dependent
on the oxygen carrying capacity of the blood and on blood flow.
“In hemorrhaging patients it is
essential to replace volume rapidly but the oxygen carrying
capacity of the circulating fluid must not be forgotten.” A
consultant anesthetist

Oxygen dissociation curve
Oxygen carriage
The oxygen carrying capacity of the
blood is related to the hemoglobin concentration, as 97% of the
oxygen is carried bound to hemoglobin. One gram of hemoglobin
carries 1.34 ml of oxygen when fully saturated and therefore in
a normal person with a hemoglobin of 150 g/l there will be 200
ml carried by every liter of blood. In normal individuals the
hemoglobin is over 97% saturated in the arterial circulation and
therefore the amount of oxygen carried is directly related to
the hemoglobin concentration. Clearly patients who are anemic
will tolerate desaturation less well. The uptake and release of
oxygen by hemoglobin is governed by the oxygen dissociation
curve as shown opposite.
The oxygen dissociation curve is
shifted to the right by an increase in the temperature and the
concentrations of hydrogen ions, carbon dioxide and 2-3 DPG (diphosphoglycerate),
an enzyme facilitating oxygen transport in red blood cells. This
enables the hemoglobin to give up more oxygen in metabolically
active tissues.
Oxygen carriage may be abnormal in
patients with abnormal hemoglobin as in the congenital
hemoglobinopathies.
Is the Hb dissociation curve of
transfused blood shifted to the right or the left?
The curve is shifted to the left by
a reduced 2-3 DPG content which makes it less able to give up
oxygen in the tissues. It is debatable whether this is
clinically significant. It takes about 24 hours for the 2-3 DPG
concentrations to be replenished. Blood flow
Blood flow is governed by three
components:
·
perfusion pressure
(related to cardiac output)
·
peripheral resistance
(related to the diameter of the vessels)
·
viscosity of the blood
(related to the content of cells and the components of the
plasma).
|
The following curve shows the
relationship between the hematocrit (a measure of
whole blood viscosity) and the delivery of oxygen to
the tissues.  |
For the next five patients you see
with major hemorrhage, note the initial hematocrit and the
hematocrit following resuscitation to see how accurately the
loss has been estimated and replaced.
In case 1, at what level of hematocrit would you expect the patient's oxygen delivery to
deteriorate?
It appears from the curve that
oxygen delivery begins to fall as the hematocrit drops below
30%. However the delivery may still be adequate down to 25-30%
provided there are not significantly increased demands and
cardiac function is adequate. The normal hematocrit is higher
than that at which the curve reaches its peak and this is an
inbuilt safety measure. Obviously if you operate on someone
whose hematocrit is at the peak of the curve the oxygen delivery
will fall as soon as you lose any blood.
4.1.5 Defective tissue
oxygen uptake
Defective tissue utilization of
oxygen may be due to two factors:
·
A diffusion barrier
around the capillary preventing oxygen diffusion to the
cell. This occurs in septic shock where there is an
increased capillary permeability and accumulation of protein
rich fluid in the interstitial space.
·
Poisoning of
intracellular enzymes (cyanide).
4.2 Differential diagnosis
You should now have an understanding
of the pathophysiology of hypoxia and this will enable you to
produce a differential diagnosis. The differential diagnosis is
related to the clinical scenario in which the patient presents.
The following are common scenarios.
Which of the example patients are
likely to have a reduced blood flow?
|
Case 2 -
due to
reduced perfusion in sepsis. |
Case 6 -
due to
reduced output after pulmonary embolism. |
|
Case 3 -
due to
inadequate replacement during operation. |
Case 7 -
due to
hypovolemic shock. |
|
Case 4 -
due to
cardiac failure. |
|
4.2.1
Preoperative hypoxia
·
smoking
·
lung disease such as
COPD, atelectasis and infection
·
pulmonary edema due to
cardiac failure or ARDS
·
pleural disease such as
effusion, empyema or pneumothorax
·
ventilatory failure from
drugs or neurological disease
·
anemia.
4.2.2 Postoperative hypoxia
Immediately after operation
·
inadequate recovery from
drugs used during anaesthesia
·
pneumothorax (thoracotomy
or insertion of central venous line)
·
pulmonary collapse
(inadequate ventilation)
·
aspiration of intestinal
content pain.
Within 72 hours of operation
·
pulmonary infection or
collapse and aspiration
·
pulmonary edema
(overload, heart failure or ARDS)
·
hypoventilation due to
morphine overdose, stroke or pain hypotension due to
hypovolemia or myocardial infarction
·
septicemia
More than three days after operation
·
pulmonary embolism
·
pulmonary infection
·
stroke
·
septicemia.
·
myocardial infarction
(MI)
4.2.3 Hypoxia following trauma
On arrival in the Accident and
Emergency Department (A&E)
·
airway obstruction due
to trauma, vomitus, blood, burns etc.
·
head, chest wall,
pulmonary, bronchial and cardiac injury
·
cerebral injury
·
pneumothorax/hemothorax
·
hypovolemia.
Following resuscitation
·
injury to lung or heart
·
ARDS and infection
·
embolism (fat or
thrombus)
·
myocardial infarction.
Consider the seven example cases.
Can you allocate them to any of these diagnostic categories?
|
Case 1 -
Anemia and
COPD |
Case 5 -
Pulmonary
infection or ARDS from septicemia due to anastomotic
leak |
|
Case 2 -
Pulmonary
edema, ARDS. |
Case 6 -
Pulmonary
embolism or myocardial infarction |
|
Case 3 -
Inadequate
recovery from anesthetic drugs. |
Case 7 -
Cerebral
injury, airway obstruction, flail chest, pulmonary
contusion |
|
Case 4 -
Pulmonary
edema, heart failure. |
|
For the next ten patients with
hypoxia that you see, try to put them into one of the diagnostic
categories. Include examples of the various clinical scenarios
in your portfolio.
5.What you should do
When you are presented with a
patient with hypoxia you should consider the situation with
regard to the different categories described in section 4.2.
This will then give you a working differential diagnosis with
which to target your investigations.
5.1 Assessment of the hypoxic patient
Assessment of the patient involves
the standard routine of history, examination and investigation.
5.1.1 History
In a preoperative patient a careful
history of any pulmonary or cardiac problems is essential.
Exercise tolerance is probably the most useful indicator of
cardio-respiratory fitness. A history of smoking is a major risk
factor for respiratory and cardiovascular disease. Cough,
purulent sputum, wheeze and hemoptysis are important symptoms
and ankle edema may be an indication of cardiac failure.
Previous venous thrombo-embolism is a significant concern in
patients undergoing major surgery and recent myocardial
infarction (less than three months) considerably increases the
risk of re-infarction.
Take a careful drug history,
including the frequency of use of inhalers for example. Note
details of any previous operations.
In trauma patients it is vital to
gain some impression of the mechanism of the injury and the
severity of the injuring force.
“I find that frequently the
patient’s drug history gives me a better indication of the
severity of the respiratory condition than their symptoms.” A
senior clinician
5.1.2 Examination
A careful examination is fundamental
to the care of any patient and may well give some indication of
the cause of hypoxia. In the preoperative situation this will
usually be identified by a low oxygen saturation detected by
saturation monitor.
Oxygen saturation monitors are
routinely used to monitor patients in theatre and in the post
operative period. The monitor is applied to a finger (or ear
lobe or other appendage) and functions on a colorimetric
assessment of the hemoglobin. It is unreliable in the absence of
pulsatile flow, e.g. in patients who are cold or shocked. Most
monitors will display an error warning in this situation.
Make a list of the conditions which
may cause a false reading of oxygen saturation on the pulse
oximeter.
·
poorly calibrated
for saturations below 80%
·
diathermy
·
motion
·
intravenous dyes
(transient)
·
bilirubin (small
in practice)
|
·
skin pigmentation
(small in practice)
·
light
·
poor perfusion
·
carboxy-/met-
hemoglobin
·
nail polish!
|
The following features should be
carefully assessed.
·
Airway - obstructing
lesions, vomitus, blood, foreign bodies.
·
Assess for evidence of
chronic lung disease (finger clubbing, cyanosis, etc).
·
Respiratory pattern:
o
rapid panting
respiration using accessory muscles with emphysema, pneumonia,
pulmonary contusion, ARDS
o
pursed lips and wheeze
with obstructive lung disease
o
rapid respiration with
frothy sputum in cardiac failure
o
slow and shallow in CNS
depression
o
struggling, shallow
breathing with neurological problems, neuromuscular blockade,
pulmonary collapse and pain.
·
Chest examination:
o
reduced movement with
neuromuscular problems and pain
o
hyperinflation with
emphysema
o