The Rationale for Administering Oxygen - Essay Example

?Question Discuss in point form: The key clinical feature of the scenario that lead you to administer oxygen. The scenario’s key clinical featurethat leads to oxygen administration is peripheral cyanosis. Peripheral cyanosis is caused by increased oxygen extraction in the periphery tissues and a decreased local circulation. It occurs in conditions that related to blood stasis and peripheral vasoconstriction, causing peripheral oxygen extraction, such as circulation shock, congestive heart failure, peripheral circulation abnormalities, or exposure to cold temperatures. Peripheral cyanosis is characterized by purple or bluish discoloration of the affected areas and peripheral vasoconstriction (American psychiatrist Association, 234) The physiological rationale for administering oxygen. The physiological rationale for oxygen administration is to prevent cellular hypoxia, which is caused by low Pa02 (Hypoxaemia). It thus prevents potential damage to vital organs that is irreversible. Oxygen administration increases the oxygen tension in the lungs alveoli to the normal levels. This reciprocates for the decreased breathing rate. The increase in oxygen tension boosts the oxygen uptake by the red blood cells in the blood flowing to through blood vessels adjacent to the lung alveoli (Rosdahl & Kowalski 191). The intended outcomes of administering oxygen The intended outcome of administering oxygen is to correct hypoxemia, thus increasing the oxygen partial pressure in the arterial blood. This will increase the oxygen saturation in the body, preventing potential damage to the brain and other vital organs due to the depravation of oxygen. It will also increase the pulse rate of the patient, contributing to him regaining consciousness (Plletti, Groppi & Montagna, 310). Question 2 – On the basis of Vincent’s list of current medication, prior to undertaking any further intervention: What risk factors can you identify that are relevant to the safety of yourself, your partner and Johnny? Peginterferon alfa-2a and Ribavirin are used in the treatment of Hepatitis C. Since Vincent is on medication of these drugs; he is likely to be suffering from Hepatitis C, which is transmitted through body fluids such as blood. Vincent shared a needle with Johnny to inject heroin, meaning that he may have been exposed to blood infected with the disease. It is advisable that I, my partner, and Johnny avoid physical contact with Vincent to prevent the transmission of Hepatitis C. in addition, since Vincent is on medication of fluoxetine, olanzapine, and diazepam, which are used to treat mental disorders, it is an indication that his metal state is unstable. Therefore, it is advisable that I and my partner be on alert as the patient may be uncooperative or show aggressiveness when he regains consciousness (Pugsley, 512). What action(s) will you take on the basis of these considerations? I would dispose the needle that was used to inject heroin while wearing gloves. I would also ensure that no one comes into physical contact with Vincent’s blood or body fluids. Vincent should be taken to hospital to undergo further tests on his mental health. It is recommended that Johnny takes a Hepatitis C test to find out if he has been infected with the disease. It is also advisable that he joins a rehabilitation program. Since Vincent is likely to be suffering from mental disorders, he should be strapped on a stretcher or a bed to avoid aggression when he regains consciousness (Golan et al, 332). Question 3 – Assuming that Vincent is an alcoholic but has no predisposing co-morbidities, discuss the possible reasons why Vincent is more affected than Johnny, noting: Interactions with Vincent’s current medications. Peginterferon alfa-2a and Ribavirin may lead to stomach bleeding. Thus, regular alcohol consumption when on medication of these drugs can increase the patient’s risk of stomach bleeding. In addition, alcohol is a poison and a toxin to the liver. The consumption of alcohol can make liver diseases such as Hepatitis C worse, leading to serious liver damage. Combining fluoxetine, olanzapine, and diazepam with alcohol or any other depressants associated with the central nervous system can lead to increased sedation and respiratory depression that can be potentially dangerous. Particularly, alcohol leads to an increase in the sedative effects of fluoxetine, olanzapine and diazepam, causing a reduction in respiration and heartbeat rate, as well as eventual loss of consciousness (Dahal, Aarts & Smith, 281). The potential impact of Vincent’s alcoholism Alcohol when combined with heroin induces a chemical reaction in the body. It is a depressant for the central nervous system that can intensify the effects of heroin. When used together, alcohol and heroin have an additive effect that leads to both drugs to be even stronger. This can lead to accidental alcohol poisoning or overdose. Alcohol’s action with heroin is synergistic, meaning that is cold result in a cardiopulmonary arrest that is worse than one caused by heroin only. Since Vincent is suffering from Hepatitis C, his liver is likely to be damaged, leading to an impaired ability to digest alcohol (Schuttler& Schwilden, 401). Potential recent changes to Vincent’s lifestyle or drug use habits. Since Vincent is a regular user of heroin and a drinker of alcohol, he is likely to develop more tolerance to the drugs as he abuses them, leading to likelihood that he will abuse even more amounts. In addition, since he takes both alcohol and heroin, this is likely to have caused a deficiency in thiamine, hence that is why he is on thiamine medication. Due to the psychological consequences of drug abuse, Vincent is likely to exhibit changes in lifestyle and behavior. He may lose interest in hobbies and socializing. He may become unmotivated and be negligent, reducing performance in the workplace (Dahal, Aarts & Smith, 393). Question 4 – Describe the mechanism by which an opioid agonist (such as heroin) causes respiratory depression. In your response, consider the: Molecular mechanism of action of opioid agonists. Opioid drugs such as heroin produce their pharmacological actions through the acting of receptors located on neural cell membranes. The opioids presynaptic action of inhibiting the release of neurotransmitter is considered their main effect in the nervous system. There are three types of opioid receptors namely m, d, and k, with all of them coupled via G-proteins to intracellular mechanisms. Opioids mechanisms of action take place in two sites, the postsynaptic neuron, and the presynatic nerve terminal. The opioids postsynaptic action is inhibitory while the presynaptic action is inhibiting the release of neurotransmitter, with this being considered their major effect in the nervous system. However, an opioids final effect in the brain is the result of its postsynaptic effects, as well as its action on both excitatory and inhibitory neurons at multiple presynaptic sites (Barrie & May, 329). Pathophysiology of opioid-induced respiratory depression The need to breath is determined by the medulla mainly through PCO2’s (carbon dioxide partial pressure) levels that are detected by chemo receptors that are located in the carotid arteries. The pulmonary musculature (intercostals and diaphragm) is stimulated by the medulla to breathe faster, deeper and more rhythmically in times of accumulation of PCO2. This facilitates increase in oxygenation and at the same time a drop in PCO2 levels. PO2 (Partial pressure of oxygen) chemoreceptor system is a back up mechanism that stimulates ventilation. However, since this system is less sensitive than the PACO2 system, it initiates breathing only when PO2 is depressed significantly. In the presence of opioids, the brain is unaware of rising levels of PCO2, leading to the under stimulation of the lung musculature. This leads to respiratory depression that can vary from severe to mild, depending on the presence of concurrent diseases and the particular agent or agents involved (Rosdahl & Kowalski 271). Question 5 – Discuss in detail: The pharmacodynamic rationale for administering naloxone. Naloxolone is a morphine derivative that is semi synthetic and a specific opioid antagonist, which acts at opioid receptors competitively. It has a high affinity for the receptor sites of opioids, thus displacing both partial antagonists and opioid agonists. Naloxone does not counteract central depression that may occur due to non-opioids, and has no morphine like properties present in other opioid antagonists. If there are no opioids or opioid agonistic effects present, naloxone exhibits no pharmacologic activity. In addition, since it does not aggravate the respiratory depression that may be caused by other substances, it can applied for differential diagnosis. It neither causes mental or physical dependence, nor does it produce tolerance. Naloxone administration enhances physical dependence symptoms in the case of opioid dependence (Dahal, Aarts & Smith, 513). The mechanism of action of naloxone. Naloxone antagonizes the effects of opioids by competing for the kappa, mu, and sigma opiate receptor sites in the central nervous system, having a greater affinity for the mu receptor. When administered intravenously, naloxone’s onset of action is about two minutes, with this onset slightly less rapid when administered intramuscularly or subcutaneously. The action duration depends on the method of administration and the dose. A more prolonged effect is produced by intramuscular administration than by intravenous method. As naloxone’s onset of action is less than that some opiates, the opiates effects may be felt as the naloxone effects returns (Golan et al, 332). The pharmacological considerations of current approaches to narcotic overdose recommending; Partial reversal For opioid depression’s partial reversal, small doses of naloxone are in most cases sufficient, wit the dose being titrated in accordance to the response of the patient. In the case of the initial respiratory depression reversal, naloxone is injected intravenously in does of 0.1 to 0.2mg at intervals of 2 to 3 minutes until the desired reversal degree is achieved. Repeat doses may be needed at intervals of one or two hours depending on the dose amount, time interval since last administration, and type of dose, whether long or short acting. Longer lasting effect has been produced by supplemental intramuscular doses (Dahal, Aarts & Smith, 291). Rapid, full reversal Should the respiratory rate of the patient fail to improve following the partial reversal, an increase to a 15mg naloxone dose may be administered. However, such a depression is unlikely to be caused by opioid intoxication, but rather other diagnosis which should be considered. A patient may require between 4 and 6 hours of observation after a Rapid, full reversal, prior to being discharged (Rosdahl & Kowalski 271). Question 6 – Discuss your considerations regarding whether it is safe to leave Vincent in his home? In your response consider: The likely pharmacological impact of Vincent’s drug use The potential need for further medical treatment and or tests. As much as naloxone and oxygen would overcome the acute problems facing Vincent, administering him with a naloxone drip and oxygen is not enough. In addition, he is not only suffering from hypoxia and heroin overdose, but also hepatitis C and addiction to alcohol. Thus, he has to be taken to a hospital where he can undergo more tests. His return to consciousness following naloxone administration was merely an emergency procedure aimed at treating the overdose and stabilizing him (Golan et al, 392). References American Psychiatrist Association. American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders: Compendium 2006. New York: American Psychiatric Pub Barrie, J & May, G. 2006. Diagnosis of drug overdose by rapid reversal with naloxone. Emergency Medical Journal. 23(11), pp874–875. Dahal, A., Aarts, L., & Smith, T.W. 2010. Incidence, Reversal, and Prevention of Opioid-induced Respiratory Depression. Anesthesiology. 112(1), pp 226-38. Golan, G., Tashjian, A.H., Armstrong, E.J., & Armstrong, A. 2011. Principles of Pharmacology: The Pathophysiology Basis of Drug Therapy. New York: Lippincott Williams & Wilkins Plletti, A., Groppi, A. & Montagna, M. 1999. The role of alcohol abuse in the etiology of heroin-related deaths: Evidence for pharmacokinetic interactions between heroin and alcohol. Journal of Analytical Toxicology. 23(7), pp 570-576. Pugsley, M.K. (2002). The diverse molecular mechanisms responsible for the actions of opioids on the cardiovascular system. Pharmacology & Therapeutics. 93 (1), PP 51–75 Rosdahl, C.B. & Kowalski, M.T. 2007. Textbook of Basic Nursing. New York: Lippincott Williams & Wilkins Schuttler, J & Schwilden, H. Modern Anesthetics. New York: Springer. Read More