Hypoxia: types & effects, Cyanosis, Hypercapnia,

Dyspnea, Asphyxia

TYPES OF HYPOXIA:

There are 4 types of hypoxia:

1. Hypoxic Hypoxia

2. Anemic Hypoxia

3. Stagnant / Ischemic Hypoxia

4. Histotoxic Hypoxia

HYPOXIC HYPOXIA:

• Decreased arterial partial pressure of oxygen.

• In other types of hypoxia, PO2 is normal.

CAUSES:

• High altitude decreased PO2 in atmospheric air.

• Depression of Respiratory centre (disease / drug).

HYPOXIC HYPOXIA: (continued)

CAUSES:

• Respiratory muscle paralysis.

• Obstructive lung disease (COPD).

• Restrictive lung disease (pulmonary fibrosis, pneumothorax).

• Congenital heart diseases.

Clinical features of Hypoxic Hypoxia:

• Due to decrease arterial PO2 Interstitial cells in peritubular capillaries secrete Erythropoietin polycythemia

• Hypoxia pulm. V.C Pulm. Hypertension Rt. Vent. Hypertrophy Rt. Vent. Failure.

TREATMENT: O2 treatment is most

effective in this type of hypoxia.

ANEMIC HYPOXIA:

• Arterial PO2 is normal but inadequate O2 carrying capacity of blood because of decrease in Hb conc. or due to presence of abnormal Hb like met-Hb or Hb-S or if binding site of Hb for oxygen is not available such as in carbon monoxide poisoning.

• CO is produced due to incomplete combustion of carbon.• Hb has 250 times more affinity to bind with CO as

compared to O2.• Carbon monoxide Hb shifts the oxy-Hb curve to left

O2 dissociation becomes difficult.• CO also inhibits cytochromes.• When there is 70% carbon monoxy Hb in blood death

occurs.• CO is colorless & odourless.• In CO poisoning, skin is cherry red colored.• There is no stim. of resp. centre, because arterial PO2 is

normal.

Treatment:

• Remove the subject from source of exposure.

• 100% oxygen therapy can help.

• Hyper-barric O2 can help (O2 with increased pressure = 2-3 atmospheric pressure)

STAGNANT / ISCHEMIC HYPOXIA:

CAUSES: • Decreased cardiac output / sluggish blood flow due heart

failure, hemorrhage, circulatory shock and venous obstruction.

• Blood remains in tissues for longer time, so tissue extracts increased oxygen from blood more arterio-venous difference of oxygen concentration.

• So PCO2 increases, it facilitates unloading of oxygen from hemoglobin (shifts the oxy-hemoglobin association dissociation curve to right).

HISTOTOXIC HYPOXIA:(poverty amongst plenty)

DEFINITION: Inability of the tissues to utilize oxygen inspite of normal arterial PO2 and oxygen carrying capacity.

CAUSES: • Cyanide poisoning (it inhibits cytochrome oxidases oxidative process

is inhibited). • Narcotic overdosage (it inactivates the enzyme dehydrogenase

inhibition of tissue oxygenation).

• Beri-beri (it is deficiency of thymine co-enzyme which is required for many oxidative reactions).

TREATMENT:• Methylene blue or nitrites. These convert hemoglobin met-

hemoglobin.• Cyanide + met-hemoglobin cyn-met-hemoglobin (non-toxic

compound).

CYANOSIS:

• Definition:

Bluish discoloration of skin & mucus membrane, when conc. of deoxy-Hb in small blood vessels like capillaries is more than 5 g / dl.

Types of Cyanosis:

• Peripheral:• Seen on exposure to

moderate cold & in case of stagnant hypoxia.

• Seen in fingers, outer surface of lips.

• Arterial PO2 remains normal.

• Central:• Seen in case of

Congenital heart diseases & chronic lung disease.

• Mostly Arterial PO2 is below normal (due to hypoxic hypoxia).

Conditions in which Cyanosis does not occur:

• Severe anemia (less than 5 g Hb / dl)

• CO poisoning (masked due to cherry red complexion)

• Met-Hemoglobinemia (chocolate brown discoloration)

DYSPNEA = Air Hunger:

DEFINITION:

• Mental anguish associated with inability to ventilate enough to satisfy the demand for air.

3 factors that develop the sensation of dyspnea:

1) Abnormality of respiratory gases in body fluids (mainly hypercapnia & partly hypoxia)

2) Work of ventilation by respiratory muscles

3) State of Mind (neurogenic / emotional dyspnea)

Abnormality of respiratory gases

• A person may become very dyspneic due to excess rise of CO2 in body fluids.

Work of ventilation

• Sometimes the levels of CO2 & O2 are normal but to achieve this normality of respiratory gases, a person has to breathe forcefully feeling of dyspnea.

Neurogenic / Emotional dyspnea

• Respiratory functions may be normal but still dyspnea may be experienced due to abnormal state of mind.

• More enhanced in people who are claustrophobic (fear of not being able to receive a sufficient quantity of air e.g., small or crowded places).

HYPERCAPNIA:

DEFINITION:

• Excess CO2 in body fluids.

(Hypercapnia + Hypoxia):

Only when hypoxia is caused by hypoventilation or circulatory deficiency.

Causes of hypoxia in the absence of hypercapnia:

Hypoxia caused by:

too little oxygen in the air,

too little Hb,

poisoning of oxidative enzymes

Causes of hypoxia in the absence of serious hypercapnia:

• In hypoxia due to poor diffusion through the pulmonary Membrane or tissues (serious hypercapnia does not occur because CO2 diffuses 20 times as rapidly as O2).

• If hypercapnia begin to occur simultaneously stimulate pulm. Vent. correction of hypercapnia but not necessarily hypoxia.

Causes of hypoxia + hypercapnia (simultaneously):

• In hypoxia due to hypoventilation, CO2 transfer between alveoli & atmosphere is affected as much as is oxygen transfer.

• In circulatory deficiency decreased blood flow decreased removal of CO2 from the tissues tissue hypercapnia + hypoxia.

• But transport capacity of blood for CO2 is more than 3 times that for O2, so resulting tissue hypercapnia in much less than tissue hypoxia.

Severe Dyspnea:

• When alveolar PCO2 rises above about 60-75 mm Hg air hunger / dyspnea becomes severe.

• If PCO2 rises to 80-100 mm Hg lethargy, +/- semicomatose

• If PCO2 rises to 120 to 150 mm Hg + / - anesthesia & death

• At such high PCO2 Resp. Centre is depressed rather than stimulated vicious circle:

1. MORE CO2

2. FURTHER DECREASE IN RESPIRATION

3. MORE CO2 Respiratory death

VICIOUS CIRCLE

ASPHYXIA:

DEFINITION:

Simultanoeus acute hypoxia & hypercapnia.

CAUSES:

• Acute airway obstruction

• When a person is forced to re-breathe his own air in a confined space.

Mechanism:• During asphyxia hypoxia + hypercapnia =

hypercarbia strong stimulation of respiratory centre & violent inspiratory efforts heart rate increases, BP increases, CATS increase from adrenal medulla (increase in nor-epinephrine > epinephrine) unconsciousness, convulsions & decrease in respiratory rate death.

O2 THERAPY: (3 ways)

• 1) O2 mask on nose

• 2) Intra-nasal tube

• 3) O2 tent (newborn)

When O2 is given for longer period toxic effects.

100% O2 treatment for over 8 hrs:

Features of airway irritation

sore throat

substernal distress

nasal congestion

coughing

100% O2 treatment for 24-48 hrs:

Toxic effects start like lung damage,

decreased ability of alveolar

macrophages to kill bacteria,

decrease in surfactant secretion,

cyst formation in lung may occur,

Retrolental fibroplasia in infants kept in

O2 tents for long.

Cause of toxic effects of oxygen:

• Formation of certain ions:

• Super-oxide ions (O2 -)

• Hydrogen peroxide (H2O2)

Prevention of toxic effects of oxygen:

• By anti-oxidants like vitamin E.

Benefit of Oxygen therapy:

• Helpful in some types of hypoxia.

• Most helpful in hypoxic hypoxia.

• May be helpful in cyanide or CO poisoning

• May be helpful in case of Gas Gangrene.

• No use in Anemic & Ischemic (stagnant) hypoxia.