There is a lot of focus and puzzles on hypoxic drive in the modern society. What is hypoxic drive and what are the processes that facilitate it? Hypoxia refers to a condition where there is lack of oxygen in a part of the body or the entire body. In this condition, the patient’s body utilizes oxygen chemoreceptors rather than carbon dioxide to regulate the respiratory cycle (Greaves et al. 120). This essay discusses biochemical, physiological, epidemiological, and clinical evidence to support hypoxic drive in the chronic hypercapnia patient (Galvagno 58).
Macro and micro neural circuity involved in respiratoty/ventilator drives and pattern generation
Rhythmic respiratory movements originate from neutral activity. Specialized organized micro and macro-circuits in the brainstem generate the neutral activity. There is a spatial and dynamic hierarchy of interacting circuits in the respiratory network, which controls a number of aspects of pattern formation and respiratory rhythm. The neurons that control ventilation comprise of the dorsal respiratory group, pontine respiratory group (PRG), and the ventral respiratory groups (VRG). The PRG control the respiratory phase timing, respiration, and integration of the flexes. The parabrachial nucleus sends information from medullary neurons to the hypothalamus, amygdala, and other suprapontine structures (Smith et al. 3). The DRG is the relay station for afferents from peripheral respiratory chemoreceptors and mechanoreceptors. The neurons are part of a central pattern generator network that controls the periodic activity of spinal and bulbar motor neutrons innervating the respiratory muscles. The maintenance and generation of normal respiratory ventilation and rhythm needs a tonic “drive” which as a result maintains respiratory neuron excitability (Hamid et al. 237). The drive originate from peripheral and central chemoreceptors or arousal sytems sensitive to changes in PaCO2, PAO2 or both and from inputs from metabolic mechanisms.
Neurotransmitter receptors bind the neurotransmitter to postsynaptic cells by opening the receptor channels. This process combined with the generation of postsynaptic potentials needs biochemical work. The biochemical work is important to synthesize the neurotransmitters, transport the neurotransmitter-filled vesicles, and to close and open the ion channels in the membranes. Additionally, the biochemical processes are required to release the neurotransmitters into the synaptic cleft and to bind the vesicles to the upper surface of the axon terminal. However, the postsynaptic potential reduces as it moves from the synapse to the axon hill. The reduction in potential results in attenuation that occurs in the postsynaptic cell. Furthermore, it also occurs due to spreading of the potential in different directions. Biochemical processes are important to generate an action potential when postsynaptic potentials overcome the cell action potential (Simms 209).
Biochemical and physiological processes involved in a vascular response to blood chemistry.
Variations in the concentration of gases found in the atmosphere have a significant influence on human physiology. This is evident as changes in pulmonary function, neurologic, and metabolism processes. Peripheral and central chemoreceptors detect the changes in PaO2, pH, and PaCO2 in the blood leading to a ventilator response. To respond to the above changes, there is decreased cerebral blood flow and increased cerebral vasoconstriction, general vasoconstriction of gut and renal blood vessels, and decrease in retinal blood flow. On the other hand, biochemical response entails margination where leukocytes accumulate in the affected area, secondly, there is adhesion where platelets become sticky; forming a clot and fibrin forms a latticework. During the same process, cytokines controls the leukocytes to fight infection and travel into the interstitial spaces. There is also the process of chemotaxis where the cells migrate in the direction away from a chemical signal. Lastly, under biological process, the leukocytes attach to the pathogens and destroy them (Cowen 32).
Additionally, in understanding hypoxic drive, there is a need to look at the physiological and biochemical processes involved in compensatory responses to hypoxemia, hypoxia, and hypercapnia. Hypoxia is a situation where there is a lack of oxygen in body tissues or oxygen starvation that can result because of some reasons. Hypoxemia precedes hypoxia, and it refers to a situation where there is decreased the concentration of oxygen in the tissues (Calton et al. 1). Suppose there is an inadequate delivery of oxygen to the cells. There will be a shift of hydrogen to pyruvic acid. The shift converts it to lactic acid and compensate for hypoxia, hypoxemia, and hypercapnia. The lactic acid accumulates in the blood and tissues and shows that there is insufficient mitochondrion oxygenation because of inadequate blood flow, hypoxemia or a mixture of the two.
Consequently, the anaerobic metabolism releases little amounts of energy. Chemoreceptor in the carotid body detects hypoxia in the human body. This response regulates ventilation rate below and neuron activity accelerating the receptors increases instantly. The increases overrun signals from central chemoreceptors in the hypothalamus, which increases the pO2 (Wilkins 240). The response to hypoxia is vasodilation by enlarging the blood vessels and as a result allows greater perfusion in the tissues.
Furthermore, response to hypoxia in the lungs is vasoconstriction. Although there is some potential physiologic mechanic for hypoxemia, however, patients with COPD the popular one is V/Q mismatch. Other physiological responses include precise responses. During complete responses, some chemosensory systems instantly regulate perfusion and pulmonary ventilation as well as regulate blood circulation to utilize the supply of oxygen to metabolizing tissues. These responses depend on the neuroepithelial bodies and the chemoreceptor carotid bodies in the arterial circulation. Similarly, pulmonary vasculature vessels shrink to stop blood away from the poorly ventilated region. Another response is through neuroepithelial and carotid bodies that sense changes through airway neuroepithelial bodies in inspired oxygen. The carotid bodies monitor arterial oxygen levels and respond to the decreased oxygen supply. The carotid bodies initiate an activity in chemosensory fibers that produce cardiorespiratory adjustments when exposed to low pO2 (Michiels 3).
How does hypoxic drive and respiratory drive react towards (ROS)? Hypoxia, as mentioned above, refers to a scarcity of oxygen in the body or part of the body. When oxygen is scarce, mitochondria expel out reactive oxygen species (ROS) that alarm the cell to respond to the shortage. Similarly, respiratory complex II produces ROS. Additionally, the respiratory complex II also contributes to the high rate of production of ROS through the mitochondria. Why is there need for mitochondria? The mitochondrion is required to activate hypoxia-reactive pathways that aid to restore oxygen levels. Stabilization of the hypoxia-inducible factor (HIF)-1 activates the hypoxia-reactive pathways. HIF regulate physiological responses to hypoxia. Additionally, mitochondrial expel ATP, consume oxygen, and produce ROS. Similarly, hypoxia increases ROS through movement of electrons from ubisemiquinone to molecular oxygen. The movement occurs at the Qo section of complex III of the mitochondrial electron transfer chain. Hypoxia-inducible factor (HIF)-1 induces some genes which include vascular endothelial growth factor and erythropoietin. Hypoxic drive triggers many gene products to assist sustain the supply of oxygen to the tissues and enhance survival of cells when there is severe oxygen. Erythropoietin (Epo) 1 and tyrosine hydroxylase. Tyrosine hydroxylase synthesizes neurotransmitter dopamine, erythropoietin (Epo) 1 increases the proliferation of erythrocase and angiognic stimulates the growth of new capillaries. Glucose transporters Glut1 and Glut3 and glycolytic enhance survival during hypoxia. In sum then, cells detect decrease in oxygen and trigger stabilization of (HIF)-1 (Chandel et al.)
Works cited
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