Hypoxia

Anemic hypoxia REF: Ganong’s physiology 22nd edition, chapter 37, Fundamentals of Human Physiology by Lauralee Sherwood page 371

Repeat form December 2009

See APPENDIX-42 for “TYPES OF HYPDXIA”

Anemic hypoxia REF: Ganong’s physiology 22^nd edition, chapter 37, Fundamentals of Human Physiology by Lauralee Sherwood page 371

See APPENDIX-16 for “Types of hypoxia” Indirect repeat from June 2008, June 2010

“Approximately 5 g/dL of unoxygenated hemoglobin in the capillaries generates the dark blue color appreciated clinically as cyanosis. For this reason, patients who are anemic maybe hypoxemic without showing any cyanosis”

The presence of cyanosis is influenced by several factors, including site of observation, pH, temperature, and concentrations of adult and fetal hemoglobins. Cyanosis appears when the absolute concentration of reduced hemoglobin in arterial blood is greater than 4-5 g/dL. Because this amount of reduced arterial hemoglobin is necessary to produce cyanosis, a low hemoglobin concentration requires an arterial saturation of 60% to produce approximately 4 g/dL of deoxyhemoglobin and cyanosis.

Ref: Ganong’s physiology 22nd edition, chapter 37, Fundamentals of Human Physiology by Lauralee Sherwood, Page 371; Pediatric Hospital Medicine: Textbook of Inpatient Management By Ronald M. Perkin, Dale A. Newton, M.D., James D. Swift, M.D., 2007, Page 80

• Hypoxemia (sometimes termed hypoxic hypoxia), in which the PO2 of the arterial blood is reduced.
• Anemic hypoxia, in which the arterial PO2 is normal but the amount of hemoglobin available to carry O2 is reduced.
• Ischemic or stagnant hypoxia, in which the blood flow to a tissue is so low that adequate O2 is not delivered to it despite a normal PO2 and hemoglobin concentration.
• Histotoxic hypoxia, in which the amount of O2 delivered to a tissue is adequate but, because of the action of a toxic agent, the tissue cells cannot make use of the O2 supplied to them.

• Hypoxic hypoxia, in which the PO2 of the arterial blood is reduced.
• Anemic hypoxia, in which the arterial PO2 is normal but the amount of hemoglobin available to carry O2 is reduced.
• Ischemic or stagnant hypoxia, in which the blood flow to a tissue is so low that adequate O2 is not delivered to it despite a normal PO2 and hemoglobin concentration.
• Histotoxic hypoxia, in which the amount of O2 delivered to a tissue is adequate but, because of the action of a toxic agent, the tissue cells cannot make use of the O2 supplied to them.

B i.e. Anemic hypoxia

D i.e. L O₂ content in arterial blood

A i.e. Arterial PO₂.

C i.e. Hb

Arterial hypoxemia is defined as an arterial Poe (partial pressure of oxygen) less than 80 mmHg, who is breathing room air at sea level. And because the partial pressure of a gas is determined by the soluble fraction of gas and not by the amount carried chemically bound to hemoglobin – the Hb does not determine P02 and hypoxemia does not depend on Hb levelQ.

– In CO poisoning effective hemoglobin that can carry 0₂ decreasesQ (because CO occupies Hb binding site) since P02 or arterial blood O₂ remains normalQ, peripheral chemoreceptors are not stimulated and hyperventilation is not seen. In hypoxia, with the reduction of PO₂ cerebral blood flow increases (d/t vaso dilatation)Q to maintain O₂ delivery in the brain.

The cerebral cortex can tolerate acute hypoxia for 5-10 min at 28°0:2, 20 min at 20°C, and 50 min at 50°C.

–  Hypoxic ischemia almost invariably involve hippocampus. The hippocampal CA1 neurons are vulnerable to even brief episodes of hypoxic ischemia.

Hypoxemia & Hypoxia

–   Hypoxemia means low arterial oxygen tension in blood (i.e. low Pao2). Arterial hypoxemia is defined as an arterial partial pressure of O₂ (i.e. Pao₂) < 80 mmHg in an adult who is breathing room air at sea level.

–  Hypoxia is O₂ deficinecy at the tissue level to carry out normal metabolic functions and often occurs when Pao₂ is less than 60 mmHg. Anoxia means no O₂ at all left in the tissue.

-Hypercapnia is an increase in partial pressure of arterial CO₂ (Paco₂) above the normal range (40 + 2 mmHg) and hypocapnia is abnormally low Paco₂ (< 35 mmHg).

C i.e. Histotoxic-anoxia

Answer is D (All of the above):

The four basic mechanisms of hypoxemia are a decrease in inspired P0₂ (Decreased Fi0₂), hypoventilation (as in Myaesthenia gravis), VQ mismatch (as in pulmonary emboli) and shunting.

Ans. D i.e. Anemic hypoxia

Anemic hypoxia

• It is a state in which the arterial partial pressure of oxygen is normal, but total oxygen content of the blood is reduced due to a decreased ability for hemoglobin to carry oxygen.
• Anemic hypoxia occurs in chronic anemia and carbon monoxide poisoning.

Ans. C i.e. Stagnant hypoxia

Central cyanosis

• Often due to a circulatory or ventilatory problem that leads to poor blood oxygenatio in the lungs.

It develops when arterial saturation drops to 85% or 75% (in dark-skinned individuals).

Central cyanosis may be due to the following causes

Central Nervous System (impairing normal ventilation):

• Intracranial hemorrhage,
• Drug overdose (Heroin)

–           Respiratory System:

• Pneumonia,
• Bronchilitis,
• Pulmonary hypertension

–           Cardiac Disorders:

• Congenital heart disease: TOF, Right to left shunts

Blood:

• Methemoglobinemia,
• Polycythemia

Others: High altitude

Peripheral cyanosis

• Peripheral cyanosis is the blue tint in fingers or extremities, due to inadequate circulation.
• The blood reaching the extremities is not oxygen rich and when viewed through the skin a combination of factors can lead to the appearance of a blue colour.

All factors contributing to central cyanosis can also cause peripheral symptoms to appear, however peripheral cyanosis can be observed without there being heart or lung failures.

Peripheral cyanosis may be due to the following causes:

–  All common causes of central cyanosis

Reduced cardiac output (e.g. heart failure, hypovolemia)

– Cold exposure

– Arterial obstruction (e.g. peripheral vascular disease, Raynaud phenomenon)

– Venous obstruction (e.g. DVT)

Differential cyanosis

• Differential cyanosis is the bluish coloration of the lower but not the upper extremity and the head.
• This is seen in patients with a patent ductus arteriosus .
• Patients with a large ductus develop progressive pulmonary vascular disease, and pressure overload of the right ventricle occurs.
• As soon as pulmonary pressure exceeds aortic pressure, shunt reversal (right-to-left shunt) occurs.
• The upper extremity remains pink because the brachiocephalic trunk, left common carotid trunk and the left subclavian trunk is given off proximal to the PDA.

Ans. C: Anaemic hypoxia

When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin

Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin.

The affinity between carbon monoxide and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.

CO binds to hemoglobin, producing carboxyhemoglobin (COHb), which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.

This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.

Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left.

Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes anemic hypoxic.

Carbon monoxide binds to hemoglobin (reducing oxygen transportation), myoglobin (decreasing its oxygen storage capacity), and mitochondrial cytochrome oxidase (inhibiting cellular respiration).

Hallmark pathological change following CO poisoning is bilateral necrosis of the pallidum.

Hemoglobin acquires a bright red color when converted to carboxyhemoglobin, so a casualty of CO poisoning is described as looking pink-cheeked and healthy.

The main medical treatment for carbon monoxide poisoning is breathing 100% oxygen.

Ans. D: Blocks Cytochrome enzyme P- 450

The cyanide ion halts cellular respiration by inhibiting an enzyme in mitochondria called cytochrome c oxidase.

Ans. A : Oxygen

Long term home oxygen therapy improves survival in selected patients with COPD complicated by severe hypoxemia (arterial Pa02 less than 8.0 kPa/ 55 mmHg)

Ans. Histotoxic anoxia

Ans. Anemic hypoxia

Ans. CO poisoning

Ans. is ‘d’ i.e., Shock

Ans. is ‘d’ i.e., Cyanide poisoning