Shock for the Tox-medic

tox-skullA strong understanding of the shock state and anaerobic metabolism is essential to the understanding of several mechanisms of toxicity within the tox-medic’s scope of care. Many toxic substances inflict harm by disrupting the aerobic metabolism pathway in some way, creating a kind of shortcut or back door to hypoperfusion and shock.

Before we can discuss these mechanisms, a brief overview of aerobic versus anaerobic metabolism is warranted.

In normal aerobic metabolism, the body uses oxygen in combination with glucose or other nutrients to synthesize adenosine triphosphate (ATP). This ATP is vital fuel for cellular processes, including the function of the sodium potassium pumps which maintain the necessary ionic concentration gradients across the cell membrane—a high concentration of sodium (Na+) outside the cell, with a high concentration of potassium (K+) inside the cell. When aerobic metabolism takes place, there is an abundance of ATP to fuel these pumps, and normal ion concentrations are maintained.

This aerobic metabolism relies on a chain of events within the mitochondria collectively known as oxidative phosphorylation (OXPHOS). Very briefly, OXPHOS transports electrons along a series of proteins known as the electron transport chain, and combines them with oxygen to store energy as ATP. When we talk about aerobic metabolism, we are specifically referring to OXPHOS, as it is the only process that uses oxygen to create ATP. It is responsible for the vast majority of cellular production of ATP, netting approximately 32-36 ATP per molecule of glucose.

It should be noted that the electron transport chain contains several “links,” and if it is disrupted at any point, aerobic ATP synthesis will fail even when oxygen and nutrients are present at the cellular level.

The electron transport chain
The electron transport chain

OXPHOS, and thus aerobic metabolism, is only the final step in the process of cellular respiration. The process begins with glycolysis and the TCA cycle (also known as the Krebs or citric acid cycle). Amino acids and fatty acids can also fuel the TCA cycle through other processes. None of these preliminary processes require oxygen, and are thus anaerobic. However, this anaerobic metabolism only produces a fraction of the ATP generated by OXPHOS –a net gain of only 2 ATP per metabolized glucose molecule.

The energy deficit created by anaerobic metabolism quickly leads to failure of the Na+/K+ pumps. With failure of these pumps comes an influx of Na+ into the cell along its concentration gradient, increasing the oncotic pull within the cell (you probably know this as “water follows sodium”). This leads to swelling of the structures of the cell and eventual cell lysis. Meanwhile, the outflow of K+ along its concentration gradient contributes to a metabolic acidosis which is compounded by the production of lactate from anaerobic metabolism. This is an additional pathway to cellular death. If the process of aerobic metabolism cannot be restored quickly, cellular death leads to irreversible tissue and organ damage and, ultimately, death.

Here is an excellent series of videos explaining cellular respiration in greater detail, for those interested.

In future articles we will explore how carbon monoxide poisoning, methemoglobinemia, and cyanide and hydrogen sulfide toxicity, among others, disrupt OXPHOS and shunt the body into anaerobic metabolism. We will also examine treatment methodologies and how we can restore normal cellular respiration.

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