Hypoxia

1
Lecture 6

• Hypoxia
• Hypocapnia
• Hypercapnia
• Asphyxia
• Oxygen therapy
• Drowning
• Effects of increased barometric pressure
• Nitrogen narcosis
• Decompression sickness
• Air embolism
• Oxygen toxicity
• Hyperbaric oxygen therapy
• Acclimatization

2
Hypoxia

• It is the deficiency of O2 at the tissue levels.
  It is also termed anoxia.
• It is divided into 4 categories
• (1) Hypoxic Hypoxia
• - It is also termed anoxic anoxia hypoxemia.
• It is defined as an adequate PO2 in the arterial
  blood.
• The primary causes of HH in diseases are
  hypoventilation, inadequate PO2 in the inspired
  air (such as altitude) or inadequate
  alveolar-capillary transfer (such as shunt or V/Q
  mismatch).

3

• (2) Anemic hypoxia
• - It occurs in which the PaO2 is normal but the
  total O2 content of the blood is reduced because
  of inadequate No. of erythrocytes, deficient or
  abnormal Hb or competition for the Hb molecules
  by CO.
• - It occurs due to lowering the O2-carrying
  capacity of the blood.
• (3) Ischemic hypoxia
• - It is also termed stagnant hypoxia, circulatory
  hypoxia hypoperfusion hyperoxia.
• It occurs in which the BF to a tissue is too low
  that adequate O2, is not delivered to it despite
  a normal PO2 and Hb conc.
• (4) Histotoxic hypoxia
• It occurs in which the quantity of O2 reaching
  the tissues is normal but the cell is unable to
  utilize the O2 because a toxic agent cyanide,
  for example, has interfered with the cells
  metabolic.

4
Hypercapnia

• It means excess CO2 in the body fluids.
• It usually occurs in association with hypoxia
  only when the hypoxia is caused by
  hyperventilation or circulator deficiency.
• Retention of CO2 in the body (hypercapnia)
  initially stimulates respiration.
• Retention of larger amounts produces symptoms due
  to depression of the CNS confusion, diminished
  sensory acuity, and eventually coma with
  respiratory depression and death.
• CO2 is so much more soluble than O2 that
  hypercapnia is rarely a problem in patient with
  pulmonary fibrosis.

5
Hypocapnia

• It is the result of hyperVE.
• During voluntary hyperVE, the PaCO2 falls from 40
  mmHg as low as 15 mmHg while the PAO2 rises to
  120-140 mmHg.
• The consequences of hypocapnia are due to the
  associated respiratory alkalosis, the blood pH
  being ? to 7.5 or 7.6.
• Hypocapnia can cause cerebral vasoconstriction,
  cerebral hypoxia, dizziness, visual disturbances
  and anxiety.

6
Asphyxia

• It is an inability to breath and suffocation.
• The symptoms of Asphyxia includes breathing
  difficulty, rapid pulse, high BP, convulsion,
  paralysis, coma and death.
• The above symptoms of Asphyxia may vary on an
  individual basis for each patient. Only your
  doctor can provide adequate diagnosis of any
  signs or symptoms and whether they are indeed
  Asphyxia symptoms.
• The possible causes of Asphyxia includes
  choking, foreign body, suffocation, toxin fumes,
  CO poisoning, whooping cough, drowning,
  diphtheria, asthma, wound infection, heart
  failure and collapsed lung.
• Treatment of Asphyxia includes First aid to
  remove foreign body, Emergency resuscitation,
  Expired Air Resuscitation (EAR), and
  Cardio-Pulmonary Resuscitation (CPR)

7
Oxygen therapy

• It is used in the treatment of patient with sever
  lung disease who increases the conc of inspired
  O2 or control VE by means of mechanical
  ventilator.
• It is usually very effective in relieving
  hypoxemia, except when this is caused by a shunt
  (BF through unventilated alveoli). In this case
  the added O2 does not have access to the shunted
  blood.
• O2 is now normally administered by small cannulas
  inserted into the nostrils or by means of a
  plastic oronasal mask.
• Giving too much O2 may lead to Pulmonary edema

8
Drowning

• It is suffocation by submersion, usually in
  water.
• Studies of drowned or nearly drowned people show
  that the most important blood gas changes are
  severe hypoxemia combined with hypercapnia and
  respiratory acidosis.
• In 10 of drowning, the first gasp of water
  after losing struggle not to breathe triggers
  laryngospasm, and death results from asphyxia
  without any water in the lungs. In the remaining
  cases, the glottic muscles eventually relax and
  the lung are flooded.
• The immediate goal in the treatment of drowning
  is resuscitation, but long-term treatment must
  take into account the circulatory effects of the
  water in the lungs.

9
Effects of increased barometric pressure

• The ambient pressure increases by 1 atmos for
  every 10 m of depth in sea water and every 10.4 m
  of depth in fresh water.
• Therefore, at a depth of 31 m (100ft) in the
  ocean, a diver is exposed to a pres of 4 atmos.
• Those who dig underwater tunnels are also exposed
  to the same hazards because the press in the
  chambers in which they work is increased to keep
  out the water.
• The hazards of exposure to ? barometric press
  used to be the concern largely of the specialists
  who cared for deep-sea divers and tunnel workers.
• Examples of the ? barometric press includes O2
  toxicity, N2 narcosis, decompression sickness and
  air embolism (see the table).

10
(No Transcript)
11
Nitrogen narcosis

• N2 narcosis is a condition that occurs in divers
  breathing compressed air. When divers go below
  depths of approx 100 ft, increase in the pp of N2
  produces an altered mental state similar to
  alcohol intoxication.
• N2 narcosis, commonly referred to as "rapture of
  the deep," typically becomes noticeable at 100 ft
  underwater and is incapacitating at 300 ft,
  causing stupor, blindness, unconsciousness, and
  even death.
• N2 narcosis is caused by gases in the body acting
  in a manner described by Dalton's Law of pp. As
  the total gas press ? with ? dive depth, the pp
  of N2 increases and more N2 becomes dissolved in
  the blood. This high N2 conc impairs the
  conduction of nerve impulses and mimics the
  effects of alcohol or narcotics.
• Symptoms of N2 narcosis include giddiness
  euphoria disorientation loss of balance loss
  of manual dexterity slowing of reaction time
  fixation of ideas and impairment of complex
  reasoning.
• The problem of N2 narcosis can be avoided by
  breathing mixture of O2 and helium.

12
Decompression sickness

• As a diver breathing 80 N2 ascends from a dive,
  the elevated PAN2 falls. N2 diffuses from the
  tissues into the lungs along the pp gradient. If
  the return to atmos press (decompression) is
  gradual, no harmful effects are observed but if
  the ascent is rapid, N2 escapes from solution.
  Bubbles form in the tissues and blood, causing
  the ?symptoms of decompression sickness.
• Bubbles in the tissues cause sever pains,
  particularly around joints, and neurologic
  symptoms that include paresthesias and itching.
• Bubbles in the bloodstream, which occure in more
  sever cases, obstruct the arteries to the brain,
  causing major paralysis and respiratory failure.
• Bubbles in the pulmonary capillaries are
  apparently responsible for the dyspnea that
  divers call the chokes. This is characterized
  by serious shortness of breath, often followed by
  sever pulmonary edema and, occasionally, death.
• Bubbles in the coronary artery may cause
  myocardial damage.
• Treatment of this disease is prompt recompression
  in a press chamber, followed by slow
  decompression. Recompression is frequently life
  saving. Recovery is often complete, but there may
  be residual neurologic sequelae due to
  irreversible damage to the nervous sytstem.

13
Air embolism

• An AE, or more generally gas embolism, is a
  medical condition caused by gas bubbles in the
  bloodstream. Small amounts of air often get into
  the blood circulation accidentally during surgery
  and other medical procedures, but AE which shows
  symptoms is relatively rare. Large emboli can be
  rapidly fatal.
• AE can occur whenever a BV is open and a press
  gradient exists favoring entry of gas. Because
  the press in most arteries and veins is greater
  than atmospheric, an air embolus does not always
  happen when a BV is injured. In the veins above
  the heart, such as in the head and neck, the
  press is less than atmos and an injury may let
  air in.
• Trauma to the lung can also cause an AE. This is
  often noticed after the patient is placed on a
  ventilator and air is forced into an injured vein
  causing sudden death.

14

• Symptoms of an AE depend on where the bubbles
  lodge. They range from skin rashes, joint pain,
  visual disturbances, balance disturbances,
  breathing difficulties, extreme fatigue/lack of
  strength, numbness, paralysis, unconsciousness
  and death. If the embolism occurs in the coronary
  arteries of the heart, a heart attack will occur.
  If it lodges in the lungs, a pulmonary embolism
  will occur, resulting in shortness of breath and
  chest pain.
• Gas embolism and decompression sickness are very
  difficult to distinguish, as they have very
  similar symptoms. The treatment for both is the
  same, because they are both the result of gas
  bubbles in the body. In a diving context, the two
  are often called decompression illness.
• Recompression is the only lasting treatment of an
  AE. Normally this is carried out in a
  recmpression chamber.

15
Oxygen toxicity

• OT or OT syndrome is severe hyperoxia caused by
  breathing O2 at elevated pp. The high conc of O2
  damages cells.
• Hyperoxia is excess O2 in body tissues or higher
  than normal pp of O2. Hyperoxia is caused by
  breathing air at pressures greater than normal
  atmos press or by breathing nitrox or O2 at
  normal atmos press for a prolonged period of
  time.
• The OT syndrome may occur
• - as a diving disorder, when divers breathe
  any breathing gas at the high press of depth,
• - as a potential complication of mechanical VE
  with pure O2, where it is called the respiratory
  lung syndrome.
• - OT is not a major factor in hyperVE, as some
  people believe. The problems caused by hyperVE
  are due to ? CO2 within the blood. With or
  without hyperVE, it is impossible to develop OT
  breathing air at typical surface atmos press.

16

• In humans, there are several types of O2
  toxicity
• - CNS OT is manifested as convulsions, which
  although not lethal themselves, can cause
  drowning of divers or lethal pressure damage
  during a rapid ascent.
• - The likelihood of this type of accident is
  directly proportional to the pp of O2 in the
  breathing gas and to the duration of exposure.
• - Pulmonary OT is caused by exposure over 16 hrs
  to pp of 0.5 bar or more. The damage to the lungs
  may be irreversible. This is rare complication in
  divers, but may be of concern in intensive care
  patients needing high-inspired oxygen
  concentrations.
• - Rethinopathic OT causes damage to the retina.
  Oxygen may be a contributing factor for the
  disorder called retenopathy of prematurity.

17
Hyperbaric O2 therapy

• The intense oxidizing properties of high-press O2
  (hyperbaric O2) can have valuable therapeutic
  effects in several important clinical conditions.
  Therefore, large press tanks are now available in
  many medical centers into which patients can be
  placed and treated with hyperbaric O2.
• The most useful use of hyperbaric O2 has been for
  treatment of gas gangrene, because the organism
  cannot live in a high PO2 environment. The
  organism is called clostridial, which best grow
  under anaerobic conditions.
• A hyperbaric chamber is also useful for treating
  decompression sickness, arterial gas embolism, CO
  poisoning, osteomyelitis and myocardial
  infarction.

18
Major means of acclimatization

• Mountain climbers have found that when they
  ascend a mountain slowly, over a period of days
  rather than the period of hours, they breathe
  much more deeply and therefore can withstand for
  lower atmos O2 conc than when they ascend
  rapidly. This is called acclimatization.
• HyperVE is an ? in VE.
• Figure show the changes in PAO2 and PACO2 that
  occur in acclimatized subjects and also in
  subjects acutely exposed to a low barometric
  press.
• The cause of hyperVE is hypoxic stimulation of
  the peripheral chemoreceptors. The resulting low
  PaCO2 and alkalosis of the CSF and blood tend to
  inhibit this ? in VE activity. This is a
  suggestion, however, the cause of the sustained
  hyperVE is still not fully understood.
• Polycythemia is another feature of
  acclimatization of high altitude is an ? in the
  RBC conc of the blood. The resulting rise in Hb
  conc and therefore O2-carrying capacity, means
  that, although the PaO2 and O2 saturation are
  diminished, the O2 content of the arterial blood
  may be normal or even above normal.
• Polycythemia tends to maintain the PO2 of mixed
  venous blood as shown in the figure.
• The stimulus for the ? production of RBCs is
  tissue hypoxia, which release erythropoiten from
  the kidney, which in turn stimulates the bone
  marrow. Polycythemia is also seen in many
  patients with chronic hypoxemia caused by lung or
  heart disease.

19

• Other features of acclimatization includes
• - A shift to the right of the O2 dissociation
  curve, which result in a better unloading of O2
  in the venous blood at a given PO2.
• - ? the conc of capillaries in the peripheral
  muscles because the muscle fiber become smaller.
  There are also ? in some oxidative enzyme inside
  the cells. The maximum breathing capacity ?
  because the air is less dense and this makes
  possible the very high VE (upto 200 l/min) which
  occur on exercise. The maximum O2 uptake,
  however, declines rapidly above 4500m.
• - Pulmonary vasoconstriction which occurs at high
  altitude as a result of alveolar hypoxia.
• - Pulmonary hypertension which occasionally
  associated with high altitude pulmonary edema.
  Typically a climber or skier who has ascended to
  high altitude, perhaps without an adequate period
  of acclimatization, develops shortness of breath
  and may cough up pink, frothy sputum. The
  treatment is to move the patient to a lower
  altitude and to give O2 if this is available.

20
(No Transcript)
21
(No Transcript)
22
(No Transcript)
23
(No Transcript)