What medications are used to treat respiratory depression?
If overdose is the cause of respiratory depression, detoxification will be necessary. Doctors often use medications that work against the effects of opioids, such as naloxone (Narcan), methadone (Dolophine), and a combination of buprenorphine and naloxone (Suboxone).
Which respiratory depressants increase the risk of respiratory depression?
Other respiratory depressants, such as propofol, sevoflurane, midazolam, and ethanol, have synergistic effects on respiratory depression when they are combined with opioids (14R). Other conditions increase the risk of respiratory depression, including sleep apnea, pulmonary disease, and other serious medical conditions (3R).
Is there a way to prevent respiratory depression?
It is not possible to prevent all cases of respiratory depression, such as those that are due to accidents or sudden disease. However, other cases are preventable. Ways to reduce the chances of developing the condition include: avoiding sedative medications or taking extra precautions when using them
Can oxygen therapy help respiratory depression?
Oxygen therapy and respiration machines may help treat respiratory depression, depending on its severity. Without treatment, respiratory depression can cause life threatening complications and even death. This article provides an overview of respiratory depression, including its causes, symptoms, and treatments. What is respiratory depression?
What medications can cause respiratory depression?
Substances That Can Cause Respiratory Depression Benzodiazepines, such as Xanax, Valium, Ativan, etc. Barbiturates like Seconal or phenobarbital. Anesthetic or pain-relieving drugs, particularly prescription opioids, such as morphine, Vicodin, OxyContin, fentanyl, etc.
What causes respiratory depression?
Causes of respiratory depression chest wall deformities (interfere with the ability to inhale and exhale) severe obesity (causes the body to work harder to breathe) brain injury (interferes with the brain's ability to control basic functions like breathing) obstructive sleep apnea (collapses airway during sleep)
Do analgesics cause respiratory depression?
Opioid analgesics constitute essential pain therapies that present the lethal side-effect of respiratory depression therefore limiting their effective use in the clinical and at-home settings.
Which class of drug is most likely to cause respiratory depression?
Some health conditions can also cause respiratory depression. Common causes include: overdose of an opiate or opioid, such as morphine, tramadol, heroin, or fentanyl. the use of opioids or anesthetics before, during, or after surgery.
What drugs cause respiratory failure?
Alcohol, cocaine, amphetamines, opiates, and benzodi- azepines are the most commonly abused drugs that may induce events leading to acute respiratory failure.
Does sedation cause respiratory depression?
Loss of airway control and respiratory depression are the most common serious adverse effects associated with sedative drug administration. The greater the degree of sedation, the greater the degree of respiratory depression.
Which opioids cause respiratory depression?
The most frequent cause of overdose death due to opioids is opioid-induced respiratory depression (OIRD). Opioids such as morphine depress the hypoxic ventilatory response in the brainstem by affecting the chemosensitive cells that respond to changes in the partial pressures of carbon dioxide and oxygen in the blood6.
Does midazolam cause respiratory depression?
Warnings. Midazolam, like other CNS depressants, may produce respiratory depression. This is especially likely to occur in patients who are receiving other CNS depressants (opioids, barbiturates) concurrently and in patients with preexisting cardiopulmonary disease.
Does tramadol cause respiratory depression?
Although the risk is less with tramadol than with other opioids, such as morphine, some people who take the medication may develop a breathing problem. This problem, called respiratory depression, causes breathing to become slow and shallow.
Does acetaminophen cause respiratory depression?
Muscle Relaxants: The coadministration of hydrocodone and acetaminophen with muscle relaxants may enhance the neuromuscular blocking action and may induce a higher degree of respiratory depression.
Does codeine depress respiration?
Codeine sulfate causes respiratory depression, in part by a direct effect on the brainstem respiratory centers. Codeine sulfate and other related opioids depress the cough reflex by direct effect on the cough center in the medulla. Codeine sulfate may also cause miosis.
What is respiratory depression?
Summary. Respiratory depression, or hypoventilation, happens when the lungs do not effectively exchange the gases oxygen and carbon dioxide. It can lead to complications, such as respiratory acidosis, and, without treatment, it can be fatal. Causes include medical conditions that affect the brain, such as a stroke, ...
Who should seek medical attention for respiratory depression?
Anyone who suspects respiratory depression or notices several of the typical symptoms should seek medical attention immediately.
How many breaths per minute is normal for a person with respiratory depression?
A common symptom of respiratory depression is taking breaths that are slower and shallower than normal. In most cases, breathing rates are as low as 8–10 breaths per minute. The normal breathing rate of a healthy adult is 12–20 breath s per minute.
Can breathing machines cause respiratory depression?
In mild cases, the person may not notice any symptoms. In other cases, they may have slow and shallow breathing. Oxygen therapy and respiration machines may help treat respiratory depression, depending on its severity.
Can oxygen therapy help with respiratory depression?
Oxygen therapy and respiration machines may help treat respiratory depression, depending on its severity. Without treatment, respiratory depression can cause life threatening complications and even death. This article provides an overview of respiratory depression, including its causes, symptoms, and treatments.
What is respiratory depression?
Respiratory depression is a dose-dependent side effect of opioid use. It generally occurs after administration of high doses of opioids in opioid-naïve individuals.
Does buprenorphine cause pulmonary edema?
Non-cardiogenic pulmonary edema has been reported after a single dose of buprenorphine [17 ].
Can buprenorphine cause respiratory depression?
Respiratory depression can occur with buprenorphine. It is not often a clinical problem, except in older and weaker subjects, in whom it can be fatal [13 ]. When it occurs it is often prolonged and can be particularly difficult to reverse [ 14]. Norbuprenorphine, a metabolite of buprenorphine via CYP3A4 causes dose-dependent respiratory depression, perhaps mediated by opioid receptors in the lung rather than the brain, and is ten times more potent than buprenorphine [15 ].
Can you use naloxone for respiratory depression?
Naloxone should not be used unless there is respiratory depression (sedation alone is not an indication for the use of naloxone). When indicated it should be administered in a diluted solution and titrated in small increments to avoid precipitating severe pain and withdrawal symptoms. In the postoperative situation this approach can allow maintenance of analgesia. It is usually possible to start with 0.1 mg every 2—5 min until reversal of the symptoms occur. In patients with an ongoing need for analgesia the opioid involved should be reduced or temporarily discontinued and treatment changed to a different opioid if necessary. The patient should be monitored as naloxone has an elimination half-life of 30 min and respiratory depression may recur. Repeat administration or a continuous intravenous or subcutaneous infusion may be required.
Is respiratory depression a symptom of opioid naiveness?
Respiratory depression is a well-known and widely recognized opioid effect and the literature does not help establish a rate for the effect. The effect is dose dependent and highly sensitive to risk factors. Respiratory depression is more likely to occur during acute rather than chronic pain treatment because (1) patients are often opioid naive and (2) other respiratory depressant drugs (hypnotics and anxiolytics) are often used concomitantly. Some degree of respiratory depression is an inevitable consequence of opioid use in opioid naive patients, even at low doses. Mild respiratory depression may warrant supplementary oxygen, but is otherwise clinically unimportant. Serious respiratory depression can cause hypoxic brain injury, even death, making it the most serious adverse effect of acute opioid therapy. The effect can usually be avoided by using safe dosing protocols and appropriate monitoring.
Is pain a depressant?
Pain is an effective antagonist to the respiratory depressant effects of opioids. Abolition of pain in patients on opioid medication has resulted in respiratory depression ( Hanks et al 1981, Wells et al 1984 ).
Can opioids be used in conjunction with other respiratory depressants?
However, when opioids are used in high dosages to provide surgical analgesia (such as fentanyl infusions at 20 μg/kg per hour or higher) or when they are used in conjunction with other respiratory depressant drugs (such as thiopental, propofol, or the inhaled anesthetics), assisted or controlled ventilation may be required.
What is respiratory depression?
Respiratory depression (also referred to as respiratory suppression or respiratory insufficiency) is a decline in the ability of a person to inhale and exhale. It can be a common side effect of drugs that suppress functions of the central nervous system.
What is moderate respiratory suppression?
Moderate respiratory suppression: At this level, individuals are typically taking higher doses of these drugs. The person becomes aware that their breathing rate has slowed down. Typically, the respiratory suppression that occurs at this level is noticeable but not uncomfortable, such that individuals are typically only taking one to two breaths less per minute than they normally do. This level of respiratory suppression is associated with mild sedation and does not lead to an individual struggling with their breathing, gasping for air, or having any shortness of breath.
What is the term for a person who experiences a significant decline in their inhalations and exhalations as?
Substance-induced respiratory suppression/depression occurs when an individual experiences a significant decline in their inhalations and exhalations as a result of using some drug or medication.
What happens when you take a high dose of central nervous system depressants?
Severe respiratory suppression: Severe respiratory suppression occurs when individuals take high doses of central nervous system depressants that can present a potential danger to their health. The individual’s breathing rate is noticeably slower, and they may begin to get the sensation that they are not adequately moving air in and out of their lungs. For many of these individuals, their respiration rate becomes a focus of their attention. Individuals may gasp for air, fall short of breath, begin to experience anxiety or confusion, and be heavily sedated. When this level of respiratory suppression is maintained, individuals can suffer issues with hypoxia, a significant decrease or lack of oxygen to the brain and other organs that can produce significant tissue damage.
How do depressants affect the central nervous system?
Central nervous system depressants induce respiratory suppression and respiratory failure by attaching to the receptor sites in the brain stem in areas that are responsible for the control of automatic life-sustaining functions, such as heart rate and breathing.
Can central nervous system depressants be reduced?
Individuals who use central nervous system depressant drugs illicitly can only reduce their use of the drugs in order to control these effects.
Is respiratory depression a drug or alcohol?
The level of respiratory depression that occurs with the use of drugs or alcohol is dose-dependent.
What to do if a patient complains of respiratory depression?
If a patient comes in complaining of the symptoms associated with respiratory depression it's important for the nurse to recognize the symptoms and ask detailed questions to see if the patient has any risk factors (causes) associated with hypoventilation. Further treatment greatly depends on the cause of hypoventilation.
What is the best treatment for hypoventilation?
The most effective treatments aside from treating the problem causing the hypoventilation is supportive therapy with supplemental oxygen and or CPAP or BiPAP (machines which use pressure to keep airways open).
What to do if a patient is groggy and has a decreased level of consciousness?
If a patient comes in with a decreased level of consciousness (the patient might be poorly responsive, overly groggy, or totally unconscious), one the first steps may be to administer a medication to reverse the effects of opioid medications, such as naloxone, to see if it causes the patient to become more alert. If a patient comes in complaining of the symptoms associated with respiratory depression it's important for the nurse to recognize the symptoms and ask detailed questions to see if the patient has any risk factors (causes) associated with hypoventilation.
Can narcotics cause hypoventilation?
Hypoventilation caused by narcotic overdose can be treated with medication to reverse the effects of narcotics, such as naloxone. In cases of airway diseases such as COPD, the lifetime use of inhaled corticosteroids and other meds may be needed to treat airway disease.
Can mountain sickness be resolved?
Finally, chronic mountain sickness can resolve if the patient leaves high altitudes and stays at sea level. Lesson Summary. When someone has hypoventilation, also known as respiratory depression, they don't have enough tidal volume to generate an adequate exhalation of CO2 resulting in impaired gas exchange.
What is respiratory depression?
Respiratory depression, also known as hypoventilation or hypoventilatory syndrome, is the abnormal retention of carbon dioxide in the blood due to the poor exchange of carbon dioxide and oxygen within the lungs. Slow and shallow breathing characterizes this breathing disorder, ...
Does hypoventilation lower carbon dioxide?
This results in lower levels of carbon dioxide in the blood, which is the opposite of hypoventilation, during which your body cannot effectively remove carbon dioxide.
Can medications cause respiratory depression?
Large doses of certain medications and substances can also cause respiratory depression or increase the risk of it. Some medications can lead to hypoventilation as a side effect.
Can respiratory depression cause death?
Treatment is important if you have been diagnosed with respiratory depression. If left untreated, hypoventilation can lead to life-threatening health complications including death.
Drugs used to treat Respiratory Depression
The following list of medications are in some way related to, or used in the treatment of this condition.
Further information
Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.
What drugs depress ventilation?
In current medical practice, the most important group of drugs that depress ventilation are opioids, which include both the natural derivatives from the poppy plant, Papaver somniferum(opiates such as morphine), and (semi)synthetic opioids ( the fenylpiperidines such as fentanyl, sufentanil, alfentanil, and remifentanil and others such as buprenorphine, oxycodone, and methadone) [3]. Opioids are used to treat acute and chronic pain (inside and outside of the hospital setting) and play an important role in palliative care. In patients receiving high-dose opioids in the community for the treatment of non-malignant pain, inadvertent overdose or addiction is a major cause of morbidity and mortality [4]. Furthermore, these prescription opioids often change hands, resulting in misuse and abuse outside of the medical setting with casualties from overdose or dangerous drug combinations (for example, opioids combined with sedatives, alcohol). Currently, more individuals die from prescription opioids than from illicit drugs (for example, heroin and cocaine). In the US, the number of prescription opioid overdose deaths increased from 4,400 in 1999 (12 individuals per day) to 16,000 in 2010 (44 individuals per day) [5]. Over this same period, there were similar increases in opioid sales (more than 4 million Americans per year receive long-acting or prolonged-release opioids for treatment of chronic pain) and admissions in opioid-abuse treatment centers (>400%) [5]. The rise in opioid prescriptions in the US is partly related to the increased awareness of clinicians to diagnose and treat chronic pain, to the increase in the number of opioid formulations being marketed, and to the pressure from the industry on physicians to prescribe opioids [6]. Although we have a good idea of the number of individuals who die from prescription opioids, the number of near-fatal events remains unknown. Our educated guess is that non-fatal respiratory events from prescription opioids exceed fatal events by at least a factor of 100. In agreement with the data from the community, parenteral opioids in the clinical setting are considered a major and independent risk factor for development of cardiorespiratory arrest [7–9].
Which system controls respiratory depression?
The ventilatory control system and opioid-induced respiratory depression. Humans are critically dependent on the cardiorespiratory control system for adequate uptake of oxygen and removal of CO2via the lungs [1]. Ventilation is controlled by two systems: the chemical or metabolic control of breathing and the behavioral control system.
What are the three classes of stimulants that are used to treat OIRD?
Three drug classes will be discussed: potassium channel blockers, ampakines, and 5-hydroxytryptamine (serotonin, 5HT) receptor agonists.
What is the effect of opioids on respiratory neurons?
Opioid-induced respiratory depression (OIRD) is potentially life threatening and the cause of substantial morbidity and mortality. One possible way of prevention of OIRD is by adding a respiratory ...
How to prevent OIRD?
In light of the above, an import question is how to prevent OIRD. Various solutions come to mind. One possibility is to develop analgesics that rely on their analgesic effect by acting at opioidergic and non-opioidergic pathways simultaneously. One such drug is tapentadol [15], which is an MOR agonist (with a weaker affinity for the MOR than morphine) and noradrenaline re-uptake inhibitor. Tapentadol produces potent analgesia due to analgesic synergy from its two mechanisms of action. Theoretically, tapentadol would produce limited respiratory depression. However, no studies on the respiratory effects of tapentadol are currently available. Another possibility would be to add a respiratory stimulant to the opioid, which through activation of non-opioidergic pathways will excite breathing and consequently offset OIRD. It is important that these adjuvants not affect analgesia. Respiratory stimulants used in the last four or five decades include CO2, doxapram, almitrine, acetazolamide, theophylline, and caffeine. Whereas some of these are still in use today, none has been developed to treat OIRD and most come with side effects that limit their clinical use [16]. Currently, novel drugs are being developed or investigated (or both) to treat OIRD specifically [1]. These agents will be discussed below.
How to reduce postoperative respiratory depression?
Some elements of anesthetic management directed at opioid-sparing suggested by enhanced recovery after major surgery [43] protocols could be useful. Pre-emptive treatment with acetaminophen, a low-cost and widely studied drug, can reduce the need for opiates, which in turn could reduce rates of opioid-induced respiratory depression [43].
What are the complications of respiratory muscle relaxers?
Inadequate recovery of respiratory muscles related to residual effects of muscle relaxants, and depressed respiratory drive by opioids, can lead to complications associated with severe hypoxemia, hypercarbia, cardiovascular complications, or death.
What happens to respiratory physiology after anesthesia?
The recovery following anesthesia and surgery is complex, marked by the readjustment of altered organ physiology. Substantial dysfunction of respiratory physiology occurs following even the most straightforward general anesthetic, in part related to the effects of perioperative medications and mechanical ventilation. Accordingly, during the early phase of anesthetic recovery, potentially life-threatening respiratory complications are not uncommon (e.g., hypoxemia, hypoventilation, airway obstruction [8], and residual neuromuscular blockade resulting in respiratory failure [9]).
Is gabapentinol a respiratory med?
Based on this emerging data, in December 2019, the FDA issued a warning on gabapentinoids usage and respiratory complications [7], increasing the recommended level of respiratory vigilance in patients with chronic use of this medication. Anesthetic management may improve recovery and reduce PACU complications.
Does gabapentin cause respiratory depression?
The association between preoperative gabapentin and respiratory depression was an unexpected finding in several studies [17,18,33-37]. Toxicology literature suggests that ingestion of even large doses of gabapentin or pregabalin results in sedation, but not respiratory arrest [33-36]. Also, meta-analyses of preoperative gabapentin and pregabalin found an increased risk of postoperative sedation, but not respiratory depression [38,39]. However, randomized prospective trials and the resultant meta-analyses are known to underreport risk from real-world use [40-42]. In regards to the safety of gabapentinoids and its perioperative use, a prospective clinical trial evaluated the analgesic effect of perioperative pregabalin, remifentanil, and their combination. The trial found that pregabalin and remifentanil have an additive analgesic effect but also a substantial synergistic impact on respiratory drive [18]. A large population-based study from Toronto analyzed deaths among patients with non-malignant pain treated with chronic opioids and matched these cases using a 4:1 matching design with subjects similarly treated with chronic opioids for non-malignant pain, found associations with concomitant use of gabapentin and an increased risk of death. A follow-up study from that group found a similar relationship with pregabalin [17,37]. At the Mayo Clinic, it was found that home use of gabapentinoids had a dose-dependent association with naloxone administration in the wards, with an odds ratio of 2.64 [95% CI 1.31–5.35] for low-dose home use and 8.29 [95% CI 3.04–22.64] for high-dose home use. Maintenance of chronic gabapentinoids into the perioperative period was observed to be associated with an overall six-fold increased risk for naloxone administration, with a dose-dependent effect: odds ratio was 2.64 [95% CI 1.31, 5.35] and 8.29 [95% CI 3.04, 22.64] for low dose (300 mg) and high dose (600 mg) of gabapentinoids use, respectively, p≤ 0.001 [4]. This effect was reflected in increased postoperative rapid response team activation, with an increased risk (odds ratio of 1.60 [95% CI 1.17–2.20]) of activation in patients who have preoperatively received gabapentin as a part of the enhanced recovery after surgery and anesthesia (ERAS) protocol [5]. Based on this emerging data, in December 2019, the FDA issued a warning on gabapentinoids usage and respiratory complications [7], increasing the recommended level of respiratory vigilance in patients with chronic use of this medication.