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Transcript of Definition
Interference either with the mechanism or function of respiration , leading to lack of tissue oxygenation i.e hypoxia
defective oxygenation of blood in lungs . due to :
( e.g high altitudes ) or presence of
( N2 , CO2 ) or
instead of air ( drowning )
Mechanical interference to the passage of air into the respiratory tract by
a. closure of external respiratory orifices :
- Accidental, as in falling of houses & falling in sands ( accidental smothering )
- Violence,as in manual smothring .
b. Causes in the neck :
: closure of the air passage by impaction of foreign bodies as in choking or pathological by tumor or laryngeal edema .
c.Causes in bronchopulmonary tree :
- Severe bronchiolar obstruction as in status asthmatics .
- Severe lung pathology : collapse , consolidation , hemorrhage , edema , pneumothorax & hemothorax .
Interference with the mechanism of respiration
a. Central (
Paralysis of respiratory center
- Mechanical : by trauma or hemorrhage .
- Toxic : endogenous as uremia or exogenous as narcotics .
- Electrical : electrocution
b. Peripheral (
Interference with respiratory movement
s ) :
- Pathological : as in poliomyelitis .
- Bacterial : as in tetanus .
- Toxic : as in strychnine & curare .
- Electrical : electrocution .
- Status epileptics .
- Mechanical : as in traumatic asphyxia
it's due to decrease of oxygen carrying capacity of the blood . resulting from :
a. Lack of functioning hemoglobin, as in CO poisoning or methemoglobinemia .
b. Hemoglobin deficiency, as in hemorrhage or hemolysis .
It's due to impaired circulation of oxygenated blood as in shock or congestive heart failure .
It's due to impaired use of available oxygen by tissues .
as in paralysis of tissue respiratory enzymes ( cytochrome oxidase ) in cyanide poisoning
Stages ( C/P ) of asphyxia
A) Stage of dyspnea :
B) Stage of convulsions :
C) Stage of apnea :
D) Final stage :
1- ( ↑PCO2 & ↓PO2 ) → stimulation of respiratory & vasomotor centers →
2- ↑ reduced HB ≥ 5gm/100ml blood →
a. ↑ rate & depth of respiration →
rapid , regular & forcible respiration
→ ↑ intra alveolar pressure → alveolar rupture . (
b. Release of adrenaline →
↑ pulse & BP.
1- Further ↑ PCO2 & ↓ PO2 → stimulation of :
a. Respiratory center → Respiration ( spasmodic & labored )
b. Vasomotor center → ↑ adrenaline release + generalized VC → ↑ ABP , VBP and capillary pressure , so :
↑ VBP → Congestion & edema
Rupture of unsupported capillaries and small venules → petechial hemorrhage .
N.B : Petechial Hemorrhages are called Tardiue spots when found under serous membranes
c. Convulsions (++ of motor areas)
2- Cyanosis → deeper .
More ↑ PCO2 & ↓ PO2 → severe Brain anoxia → loss of Consciousness & paralysis of most centers →
a. depression in resp. center → shallow , slow , irregular followed by gasping respiration
b. ↓ convulsions .
c. ↓ BP & HR
d. Loss of consciousness .
e. lost reflexes & Flaccid Muscles
f.incontinence of urine & feaces .
a. complete loss of consciousness
b. complete respiratory paralysis →Cheyne stokes resp.
c. Heart continues to beat for few mins .
d. Dilated pupils .
e. Terminal vomiting may be present .
N.B : Death occurs in 4-5 mins in typical asphyxia.
Diagnosis of asphyxia :
No specific reliable signs so it depends on :
■ Circumstantial evedince
■ Complete autopsy
■ Full toxicological examination
■ General signs of asphyxia
General signs of asphyxia
Classic signs of asphyxia include :
petechial hemorrhage , congestion , edema , cyanosis , engorgement of right heart & fluidity of the blood .
a. The increase in venous pressure associated with asphyxia causes
generalized organ congestion +/- oedema
b. The blood is very dark (
c. There is usually
dilatation and engorgement
of the right side of the heart .
d. The lungs are
congested and oedematous
e. there may be
in serous membranes (pleurae, pericardium), meninges and thymus.
f. With asphyxia there will be hypoxia/ anoxia and hypercarbia.
- The hypercarbia will cause increased secretion of fibrinolysin by the vascular endothelium.
The fibrinolysin will cause:
(i) increased fluidity of blood
(ii) neck veins and right heart distended with blood
(iii) increased hypostatic blood
The “classical” features of asphyxia at autopsy
may not be seen
in some deaths which appear to have occurred in an “asphyxia setting" because of:
Vagal inhibition (vagal reflex cardiac arrest)
: This may occur in any kind of asphyxial death but notably occurs in strangulation (especially the manual type). Violent stimulation of the parasympathetic nervous system (via the vagus nerve) slows the heart rate and leads to abrupt cardiac arrest. Vagal inhibition may be caused by compression of the vagus in the neck, compression of the larynx, a blow to the abdomen, the shock of cold water on the skin in sudden immersion etc.
: It must be noted that asphyxial signs are very striking in
fresh bodies only
. They disappear progressively with the passage of time and as a result of putrefaction.
: closure of the air passages by external pressure on the neck as in hanging , strangulation , & throttling .
a. The anoxia will cause capillary dilatation resulting in increased blood in the tissues. This results in
b. The anoxia also caused increase in the capillary permeability resulting in transudation of plasma from the vessels to the tissues. This results in the
→especially the face .
d. The blood will contain increased levels of reduced haemoglobin and this accounts for bluish discoloration (
) seen both externally ( lips , ears , finger nails ) and internally . The
areas will be show deep blue discoloration soon after death.
, due to rupture of small venules due to an acute rise in venous pressure. They occur most commonly in areas where the vessels are least supported – in this case the face – especially the eyelids, the conjunctivae and sclera.
of urine , semen & feces .