HYPOXIA AND

ASPHYXIA
Dr . Sreekala P.L
Department of Periodontics
Vokkaligara Sangha Dental College
Bangalore
 Contents
 Definition
 Classification
1. Hypoxic hypoxia and its management
2. Anaemic hypoxia and its management
3. Stagnant hypoxia and its management
4. Histotoxic hypoxia and its management
 O2 status in various hypoxias
 Asphyxia-local and general
 HYPOXIA
 Hypoxia is defined as “State of reduced
oxygen supply to the tissues”.

 Less oxygen in blood is called hypoxaemia

 Classification
Based on pathogenesis
1. Hypoxic Hypoxia(anoxic anoxia)
Po2 of arterial blood is reduced
2. Anaemic Hypoxia
Arterial Po2 is normal but the amount of Hb to carry o2 is
reduced
3. Stagnant or Ischaemic Hypoxia
Normal Hb and arterial Po2 but blood flow to the tissue is low
, so low O2 is delivered.
4. Histotoxic Hypoxia
Amount of O2 delivered is normal but because of the action
of a toxic agent tissue cannot make use of the O2 supplied to
them
 Hypoxic hypoxia
Can be due to
 Low PO2 of the inspired air- Usually seen in
high altitude
 Decreased ventilation-respiratory paralysis,
asthma, emphysema, airway obstruction
 Defective transfer of O2 due to problems in
respiratory membrane-pulmonary edema
 Presence of shunt through which deoxygenated
blood bypasses pulmonary capillaries
 Effects
 Decreased O2 content in the arterial and venous
blood

Tissue hypoxia
 Less O2 to the brain

 Mental confusion, Impaired judgement

(PO2<20mm Hg loss of consciousness in 10-20
secs and death in 4-5mints)
 Delayed effects of high altitude
 Develops 8-24 hrs after arrival and lasts 4-8 days
 Head ache , irritability, insomnia, breathlessness, nausea
and vomiting
 Due to cerebral oedema
 Low PO2

 Arteriolar dilatation
cerebral auto regulation not compensate
 Increased capillary pressure

 Transudation of fluid to brain (cerebral oedema)

 Compensatory
changes(Acclimatisation)
 Occours if hypoxia is gradual and persistent
1. Respiratory stimulation (aims to increase
arterial O2)

CO2 wash out

Alkalosis and alkaline urine

2.Rise of BP,polycythemia and increased Hb
conc
3.Increased 2,3 DPG content of the red cells and
shift of O2 dissociation curve to right.
4. Erythropoietin levels increases on assent to
high altitude
5. Increase in mitochondria and myoglobin
 Management
 Prompt O2 therapy (c/c cases associated with
hypercapnia, O2 with care)
 Removal of the cause(in high altitude illness-
descent to lower height)
 Diuretic -acetazolamide
 Anaemic hypoxia
 Can be due to
1. Low Hb concentration of blood
 RBC Hb conc low . O2 content of blood low.
PaO2 normal(due to O2 dissolved in plasma)
2. CO poisoning
 CO combines irreversibly with Hb and O2
cannot bind
 Can lead to CNS depression ,myocardial
ischemia etc
 Management
 Acute cases-Hyperbaric O2 therapy
 Chronic cases –O2 inhalation

Attempts to increase erythropoietin production

 Stagnant hypoxia
 Reduction of blood velocity

 Blood stays in capillaries for long time

 O2 in blood exhausted,but demand of tissues

continues

 Hypoxia of tissues (arterio venous difference of O2 in

this condition is very high)
Occours in
 Heart failure

 Venous obstruction

 Cardiogenic shock
 Histotoxic hypoxia
 Most dangerous type
 Due to the inhibition of enzymes required for
utilization of O2 especially cytochrome oxidase
 Commonly due to cyanide poisoning
 Normal O2 status of arterial blood but tissues
cannot use O2 and suffer
 Arterio venous difference of O2 is almost zero
 Blood is bright red in colour
 Management

 Using methelene blue or nitrates

Hb

 Methemoglobin
CYANIDE

 Cyanmethemoglobin (nontoxic)
O2 status in various hypoxias
 ASPHYXIA
 Condition characterized by decreased O2 and increased
CO2 in the body
 Asphyxia = Hypoxia +Hypercapnia
 2 types
 Local asphyxia
 Obstruction of blood supply to a particular region
 Local changes due to hypoxia , hypercapnia and
accumulation of metabolites
 Area becomes congested ,edematous , blue and painful
 General asphyxia – involves whole body
 Can be acute or chronic
 Acute general asphyxia
 By strangulation resulting in acute tracheal
obstruction or in the person subjected to an
atmosphere with less O2 and more CO2
 Hypercapnia respiratory effort
 Hypoxia develops, anaerobic metabolism takes
place with production of lactic acid
 All these leads stimulate respiration vigorously
 Further progresses CO2 narcosis and
convulsion can occour
 BP, heart rate and catecholamine release is
increased and blood PH drops
 Finally there is central depression ,fall of BP
and death
 Stage 1 (duration 1 mt)
Violent respiratory effect due to hypercapnia
and unconsciousness due to hypoxia
 Stage 11 (duration 1 mt)

Hypoxia sympathetic sharp rise of

stimulation BP and HR
 Ventricular fibrillation, involuntary micturition
and defecation
 Hypercapnia Convulsion
 Stage 111 (duration 3 mts)
Gasping respiration, loss of reflexes ,pupillary dilation
, fall of BP, Bradycardia, cardiac arrest and death due
to progressive brain damage

 Chronic general asphyxia

 Seen in c/c lung diseases like c/c bronchitis,
emphysema etc.
 Decreased alveolar ventilation resulting in gradual
increase in CO2 content in body with hypoxia
 If artificial respiration is not started ,cardiac
arrest occours in 4-5 minutes