hypoxia and hypercapnia

1. HYPOXIAAND HYPERCAPNIA :
PATHOLOGY AND
PATHOPHYSIOLOGY
MODERATOR-
Dr. Mazher Maqusood
Professor and HOD
Pulmonary medicine
TMMC & RC
Presenter -
Dr. Sagar Jain
Junior Resident
Pulmonary medicine
TMMC & RC

2. INTRODUCTION
 Hypoxia is defined as insufficient O2 to carry out
normal metabolic functions; hypoxia often occurs
when the PaO2 is less than 60 mm Hg.
 There are four major categories of hypoxia.
 Hypoxic hypoxia
 Anemic hypoxia
 Hypoperfusion hypoxia
 Histotoxic hypoxia

4. Hypoxic Hypoxia

5.  The first, hypoxic hypoxia, is the most common.
 The six main pulmonary conditions associated with
hypoxic hypoxia—
 Anatomical shunt
 Physiological shunt,
 Decreased FiO2
 V
̇ /Q
̇ mismatching
 Diffusion abnormalities

6. Anatomical Shunts
 Two alveoli are ventilated, each of which is supplied
by blood from the heart.
 When ventilation is uniform, half the inspired gas goes
to each alveolus, and when perfusion is uniform, half
the cardiac output goes to each alveolus.
 In this normal unit, the ventilation/perfusion ratio in
each of the alveoli is the same and is equal to 1. The
alveoli are perfused by mixed venous blood that is
deoxygenated and contains increased PaCO2.

7.  PAO2 is higher than mixed venous O2, and this provides a
gradient for movement of O2 into blood. In contrast, mixed
venous CO2 is greater than PAO2, and this provides a
gradient for movement of CO2 into the alveolus.
 In this ideal model, alveolar-arterial O2 values do not differ.
 The blood that bypasses the gas-exchange unit is thus
shunted, and because the blood is deoxygenated, this type
of bypass is called a Right-to-Left shunt.

8.  The effect of this right-to-left shunt is to mix deoxygenated blood with
oxygenated blood, and it results in varying degrees of arterial hypoxemia.
 The blood that bypasses the gas-exchanging units is never exposed to the
enriched O2, and thus it continues to be deoxygenated.
 The PO2 in the blood that is not being shunted increases and it mixes with
the deoxygenated blood.
 If the hypoxemia is severe, the increased respiratory drive secondary to
the hypoxemia increases the ventilation and can decrease PaCO2 to below
the normal range.

10. Physiological Shunts
 A physiological shunt (also known as venous admixture)
can develop when ventilation to lung units is absent in
the presence of continuing perfusion.
 In this situation, in the two–lung unit model, all the
ventilation goes to the other lung unit, whereas
perfusion is equally distributed between both lung units.
 The lung unit without ventilation but with perfusion has
a V
̇ /Q
̇ ratio of 0.

12.  The effect of a physiological shunt on oxygenation
is similar to the effect of an anatomical shunt; that
is, deoxygenated blood bypasses a gas-exchanging
unit and admixes with arterial blood.
 Clinically, atelectasis (which is obstruction to ventilation
of a gas-exchanging unit with subsequent loss of volume)
is an example of a situation in
which the lung region has a V
̇ /Q
̇ of 0.
 Causes of atelectasis include mucous plugs, airway edema,
foreign bodies, and tumors in the airway

13. Low Ventilation/Perfusion
 Mismatching between ventilation and perfusion is the
most frequent cause of arterial hypoxemia in individuals
with respiratory disorders.
 Both the arterial O2 content and CO2 content are
abnormal in the blood that has come from the unit
with the decreased ventilation (V
̇ /Q
̇ , <1).
 The unit with the increased ventilation (V
̇ /Q
̇ , >1) has a
lower CO2 content and a higher O2 content because it is
being overventilated.

15.  The alveolar-arterial O2 gradient (AaDO2) is increased
because the relative over ventilation of one unit does
not fully compensate (either by the addition of extra or
by the removal of extra CO2) for under ventilation of
the other unit.

16. Alveolar Hypoventilation
 The PAO2 is determined by a balance between the rate
of O2 uptake and the rate of O2 replenishment by
ventilation.
 Oxygen uptake depends on blood flow through the lung
and the metabolic demands of the tissues. If ventilation
decreases, PAO2 decreases, and PaO2 subsequently
decreases.

17.  In addition, VA and PACO2 are directly but inversely
related. When ventilation is halved, the PACO2
doubles and thus so does the PaCO2.
 Ventilation insufficient to maintain normal levels of
CO2 is called hypoventilation.
 Hypoventilation always decreases PaO2 and increases
PaCO2.

18.  One of the hallmarks of hypoventilation is a normal
AaDO2. Hypoventilation reduces PAO2, which in turn
results in a decrease in PaO2.
 Because gas exchange is normal, the AaO2 remains
normal. Hypoventilation accompanies diseases
associated with muscle weakness and is
associated with drugs that reduce the respiratory
drive.

19. Diffusion Abnormalities
 Abnormalities in diffusion of O2 across the alveolar-
capillary barrier could potentially result in arterial hypoxia.
 Equilibration between alveolar and capillary O2 and CO2
content occurs rapidly: in a fraction of the time that it takes
for.
 Diffusion equilibrium almost always occurs in
normal people, even during exercise, when the transit
time of red blood cells through the lung increases.

20.  An increased AaDO2 attributable to incomplete
diffusion (diffusion disequilibrium) has been
observed in normal persons only during exercise at
high altitude (≥10,000 feet).
 Alveolar capillary block, or thickening of the air-
blood barrier, is an uncommon cause of hypoxemia.
Even when the alveolar wall is thickened, there is
usually sufficient time for gas diffusion unless the red
blood cell transit time is increased.

21. Anemic hypoxia

22.  A second category is anemic hypoxia, which is caused by a
decrease in the amount of functioning hemoglobin as a
result of too little hemoglobin, abnormal hemoglobin, or
interference with the chemical combination of oxygen and
hemoglobin (e.g., carbon monoxide poisoning).
 Here at rest hypoxia is not severe as, in anemia there is
more 2,3 DPG which releases oxygen from Hb.
 During exercise more O2 demand by tissues as more O2 is
consumed so severe hypoxia develops.

23. Hypoperfusion hypoxia
 The third category is hypoperfusion hypoxia, which
results from low blood flow (e.g., decreased cardiac
output) and reduced oxygen delivery to the tissues.
 Causes
 CCF
 Circulatory failure
 Hemorrhage
 Shock
 Venous Obstruction

24.  Due to slow speed of blood flow or Stagnation
blood stays for long in tissues.
 Venous PO2 is less and accumulation of CO2 in
tissues shift the curve to right, so more O2 is
released to tissue.

25. Histotoxic hypoxia
 Histotoxic hypoxia, the fourth category of hypoxia,
occurs when the cellular machinery that uses oxygen to
produce energy is poisoned, as in cyanide poisoning.
 In this situation, arterial and venous PO2 are
normal or increased because oxygen is not being
utilized.

26. Causes
 Cyanide poisioning- cyanide blocks the action of
cytochrome oxidase enzyme completely so tissue cant
utilize oxygen
 Vit B deficiency of Beri – Beri.

27. Effects
 On Respiration- all except anemic hypoxia stimulates
peripheral chemoreceptors and thus increases respiration
 On CVS- increase in HR and BP
 Anorexia, Nausea and vomiting
 On CNS - Depressed metal activity, drowsiness,
disoriented, headache and coma.
 Reduced work capacity of muscles.

29. Hypercapnia

30. Hypercapnia Pathology
 Increased CO2 in the body can be caused by metabolic
compensation or respiratory failure.
 A CNS (central nervous system) injury such as
Guillain-Barré syndrome or traumatic brain injury can
lead to a reduced respiratory drive.
 Reduced respiratory rate leads low tidal volume and
hypoventilation. Causing poor gas exchange in the
alveoli.

31.  This causes a retention of CO2 and therefore
hypercapnia or type 2 respiratory failure.
 Type II (hypercapnic) respiratory failure When the
Paco2 rises due to alveola hypoventilation.

32. Mechanisms of Hypercapnia
 Two major mechanisms account for the development of
hypercapnia (elevated PCO2): hypoventilation and
wasted, or increased, dead space ventilation.
 As noted previously, alveolar ventilation and alveolar
CO2 are inversely related.
 When ventilation is halved, PACO2 and PaCO2 double.

33.  Hypoventilation always decreases PaO2 and increases
PaCO2 and thereby results in a hypoxemia that responds
to an enriched source of O2.
 Dead space ventilation is wasted, or increased, when
pulmonary blood flow is interrupted in the presence of
normal ventilation. This is most often caused by a
pulmonary embolus that obstructs blood flow.
 The embolus halts blood flow to pulmonary areas with
normal ventilation (V
̇ /Q
̇ = ∞).

34.  In this situation, the ventilation is wasted because it fails to
oxygenate any of the mixed venous blood.
 The ventilation to the perfused regions of the lung is less
than ideal (i.e., there is relative “hypoventilation” to this
area because in this situation, it receives all the pulmonary
blood flow with “normal” ventilation).
 If compensation does not occur, PaCO2 increases and PaO2
decreases. Compensation after a pulmonary embolus, however,
begins almost immediately; local bronchoconstriction occurs,
and the distribution of ventilation shifts to the areas being
perfused.

35. EFFECTS OF HYPERCAPNEA
1. Effects on Respiration
During hypercapnia, respiratory centres are
stimulated excessively. It leads to dyspnea.
2. Effects on Blood
The pH of blood reduces and blood becomes
acidic.
3. Effects on Cardiovascular System
Hypercapnea is associated with tachycardia and
and increased blood pressure. There is flushing of
skin due to peripheral vasodilatation.

36. 4. Effects on Central Nervous System
During Hypercapnia, the nervous is also affected
resulting in Headache, depression and laziness.
These symptoms are followed by muscle rigidity,
fine tremors and generalised convulsion. Finally
giddiness and loss of consciousness occur.

37. Thank