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36 CASE 36


A 28-year-old man is brought to the emergency department complaining of headache, vertigo, dizziness, and confusion.


It was a cold winter evening. The patient lives alone in a rural area and was using a kerosene heater to heat his house. He was found by a neighbor walking outside the house without a jacket. There was an odor of kerosene and some smoke in the house.



PHYSICAL EXAMINATION



VS: T 35°C, P 90/min, R 22/min, BP 120/90 mm Hg

PE: The patient remains confused and complains of chest pain and weakness.


LABORATORY STUDIES



Arterial blood gases: PO2 95 mm Hg, PCO2 40 mm Hg, pH 7.4

Mixed venous blood gases: PO2 22 mm Hg, PCO2 43 mm Hg, pH 7.37

Carboxyhemoglobin level: 40%

Hematocrit: 42%

Arterial O2 content: Estimated at 12 mL O2/dL blood


DIAGNOSIS


Carbon monoxide poisoning



PATHOPHYSIOLOGY OF KEY SYMPTOMS


The major symptoms for this patient are due to central nervous system hypoxia. The hypoxia is caused by the defect in oxygen delivery to the brain from the low arterial blood oxygen content.


Oxygen is transported in the blood through two separate mechanisms. Oxygen dissolves in the plasma of the blood in proportion to the oxygen partial pressure. Normal alveolar PO2 is around 100 mm Hg, and, assuming no abnormalities in diffusion, the Po2 of the blood in the pulmonary capillary is also around 100 mm Hg. Blood in the pulmonary vein has a slightly lower PO2 because of venous admixture from relatively oxygen depleted blood from the bronchial circulation. Therefore, normal arterial PO2 is 95 to 100 mm Hg.


The amount of oxygen that can be dissolved in the plasma is not sufficient to support life.


Hemoglobin contained within the red blood cells is the primary oxygen transport mechanism, accounting for approximately 98% of the oxygen dissolved in arterial blood. Each hemoglobin protein can bind up to four oxygen molecules. The shape of the oxygen-hemoglobin dissociation curve reflects the very high affinity of hemoglobin for oxygen. At a normal arterial PO2 of 100 mm Hg, the oxygen binding sites on hemoglobin are 98% saturated. At a normal venous PO2 of 40 mm Hg, the oxygen binding sites on hemoglobin are still 75% saturated (see Fig. 33-1).


The arterial oxygen content, therefore, is a function primarily of the amount of oxygen bound to hemoglobin. A drop in hematocrit, or a chemical change in hemoglobin that interferes with oxygen binding, can result in a decrease in the amount of oxygen bound to hemoglobin without interfering with the amount of oxygen dissolved in the plasma. Carbon monoxide binds to hemoglobin with an affinity 200 times greater than that of oxygen. Carboxyhemoglobin can no longer bind oxygen and, consequently, diminishes the total blood oxygen content.


The arterial PO2 in this patient is normal, because the dissolved oxygen content came into equilibrium with the oxygen partial pressure of the alveoli. The aortic body and carotid body chemoreceptors sense the dissolved oxygen content, and, consequently, there is no ventilatory stimulus from hypoxia in this patient.


Mixed venous blood gas, however, shows a marked hypoxia. A small amount of dissolved oxygen in the plasma is not sufficient to support metabolism. In the systemic capillaries, oxygen is extracted from the plasma and then from the oxygen stores’ remaining functional hemoglobin molecules. The hypoxia in the mixed venous blood gas sample indicates that the tissues, including the central nervous system, are hypoxic. Central nervous system chemoreceptors only respond to CO2/pH, and, consequently, there is no central chemoreceptor stimulation of ventilation in this patient. The defect in oxygen delivery also impairs oxygen utilization in the mitochondria and, thus, the body does not generate as much CO2 from metabolism as is normal.


Because the defect is in the hemoglobin-carrying capacity and not hemoglobin percent saturation, an increase in ventilation would not lead to an increase in arterial blood oxygen content. The hemoglobin that is capable of binding oxygen is close to 100% saturated at a normal alveolar minute ventilation rate.


Restoration of oxygen delivery to the brain will result in a diminishing of this patient’s symptoms. The defect in oxygen-carrying capacity, however, represents a significant barrier. Breathing 100% oxygen would increase fivefold the amount of oxygen dissolved in the plasma. This increase alone, however, would not be sufficient to support metabolism. Patients with severe carbon monoxide poisoning, where carboxyhemoglobin levels exceed 70%, are treated in a hyperbaric oxygen chamber. At the higher total barometric pressure, the dissolved oxygen can be sufficient to support basal metabolism.


Given time, carbon monoxide will disassociate from hemoglobin and hemoglobin-carrying capability can be restored. Alternatively, transfusion can be used to introduce normal hemoglobin into the patient to enhance the blood oxygen-carrying capacity.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 36

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