Final Exam Flashcards
What is Commotio Cordis?
Commotio Cordis is Ventricular Fibrillation (VF) caused by blunt trauma to the chest in the area of the heart. Extreme agitation of the hearts myocardium creates significant distortion and enough mechanical energy to induce an inappropriate depolarisation, resulting in an unstable dysrhythmia.
What causes Commotio Cordis?
Commotio Cordis is a phenomenon caused by sudden blunt impact to the chest, resulting in death – even though there is no cardiac damage.
In modern times this condition is most commonly caused in sports from an impact to the left side of the chest with a hard ball. The focal distortion of the myocardium causes a sudden VF cardiac arrest in an otherwise structurally normal heart (Tainter and Hughes, 2021).
What is the pathophysiology of Commotio Cordis?
The contact occurs during ventricular repolarisation, during the exact moment of upstroke of the T-Wave before its peak. If the impact occurs any later than this, then it is likely to instead result in a complete heart block, left bundle branch block or ST elevation. This moment of time only makes up approximately 1% of the cardiac cycle, however the relative proportion is increased with a higher heart rate, commensurate with exercise (Tainter and Hughes, 2021).
What is the treatment of Commotio Cordis?
The initial priority of responders should be on managing the cardiac arrest and performing either Advanced, Intermediate or Basic life support, commensurate with the responders clinical skill grade. Dependant on the scenario, it may be prevalent to consider other forms of Traumatic Cardiac Arrest such as Tension Pneumothorax, Cardiac Tamponade, Traumatic Valvular Injury, Pulmonary Laceration, haemorrhagic shock or other extrathoracic injuries dependant on mechanism. (Link, 2012b)
What is Myocarditis?
Myocarditis occurs due to the inflammation of the Cardiac muscle (myocardium). The cause of this inflammatory response is often idiopathic, as around 50% of patients diagnosed with myocarditis have no apparent cause (Mert, Radi and Mert, 2018)
Myocarditis is the inflammation of the cardiac muscle, Pericarditis is the result of inflammation of the pericardium. The pericardium is a double-layered, fibro-elastic sac surrounding the heart. It consists of the epicardium and a parietal layer separated by a pericardial cavity containing, on average, 50 mL of fluid (Dababneh and Siddique, 2020).
What is the cause of Myocarditis?
Patients with an identifiable cause are most commonly due to a viral illness, but bacterial and fungal causes account for approximately 10% of patients diagnosed with myocarditis (Akchar and Kiel, 2020).
Viral illnesses which have been associated with myocarditis include human immunodeficiency virus HIV, enteroviruses, Coxsackie B adenovirus, and hepatitis C.
What are the presentation/symptoms of Myocarditis?
The clinical presentation of patients with acute myocarditis can vary wildly. Patients’ symptoms can range from asymptomatic to mild cardiac discomfort to cardiogenic shock. This range of severity of a patient’s clinical presentation often leads to miss diagnosis (Chang et al 2017).
Common symptoms patients with acute myocarditis may present similarly to patients with heart failure. This includes lower limb oedema and dyspnoea. Other common symptoms include chest pain, and as viral causes account for a large portion of patients with myocarditis, they may describe fever, arthralgia, or fatigue for up to two weeks before the onset of the heart failure symptoms. (Caforio et al. 2013)
Often the pain will be described as a sharp, retrosternal chest pain which is made worse if the patient is supine (relieved when leant forward) or on inspiration. (bmj. 2022) Auscultation often reviles pericardial friction rub, which consists of a rasping sound due to friction between the pericardial layers (Dababneh & Siddique, 2020)
What is the management of Myocarditis?
Both Myocarditis and Pericarditis patients should be offered analgesic pain relief, a comprehensive patient assessment including auscultation and 12 lead ECG to rule out any other differential diagnosis and convey to their ED department for further investigation including blood tests.
“A differential of ST elevations can include early repolarization, which can be seen as an elevated J-point, commonly seen as an initial slur at the beginning of the ST segment. Dababneh and Siddique, 2020”
What is Pneumonia?
Pneumonia in an infection triggered by either bacteria, viruses or fungi which occurs in either one or both of the lungs (John Hopkins Medicine, 2019). It is an acute respiratory infection which affects the lower airway, characterised as the alveoli and distal segment of the bronchial tree (Torres et al, 2021).
What is the pathophysiology of Pneumonia
Pneumonia can be contracted from a virus, bacteria or fungus and studies have suggested there may be up to 30 different causes of pneumonia infection (John Hopkins Medicine, 2019). Initially, pathogens enter the nasopharynx through the nostrils by either direct or indirect contact with an individual who is already infected, aerosols or droplets (Torres et al, 2019)
Eventually, inhalation results in the pathogen being transported to the lower airway where infection can occur (Torres et al, 2019). Under normal physiological conditions, the lungs contain a multitude of bacteria which are important to normal lung function (Torres et al, 2019). However, when a pathogen enters the lungs and begins to replicate, this disrupts the normal lung flora which ultimately damages the tissues lining the lungs, triggering 2 mechanisms; a protective mechanism and a tissue repair mechanism (Torres et al, 2019). The protective mechanism causes the epithelial cells of the lungs to begin to produce secretory products, forming a mucus barrier in order to try to protect the lung tissue from further damage, which causes the changes in lung sounds heard on auscultation (Torres et al, 2019). In addition, the death of the tissue cells of the lung as a result of damage to them triggers an inflammatory response in the lung tissue in order to facilitate the immune response to remove the pathogen (Torres et al, 2019). In order to prevent excessive inflammation which may inhibit adequate gas exchange in the lungs, the cells also secrete anti-inflammatory agents (Torres et al, 2019).
What is the assessment for Pneumonia?
Due to the fact many of the symptoms of pneumonia are non-specific, clinicians should ensure they conduct a thorough history take and assessment of the patient and use their clinical judgement to decide an appropriate pathway for the patient (NICE, 2021). Clinicians should consider the symptoms characteristic of pneumonia such as a productive cough with green or yellow sputum, fever, tachycardia, tachypnea, diaphoresis and pleuritic chest pain (Torres et al, 2019)(John Hopkins Medicine, 2019)(JRCALC, 2020). Clinicians should also consider the onset, duration and severity of symptoms which the patient presents with (NICE, 2021). For every patient, a full set of observations should be conducted along with a respiratory assessment including auscultation of the chest (NICE, 2021). It may also be pertinent to conduct a cardiovascular assessment to rule out other causes due to the lack of specificity of the symptoms. As per NICE guidelines (2021), clinicians should conduct a CRB-65 score on all patients with pneumonia to assess risk of mortality and, as per JRCALC guidelines (2019), a NEWS score in order to determine risk of sepsis.
Management for Pneumonia?
The management of patients suffering from pneumonia will very much depend on the severity of their condition, any risk factors which they suffer from, and their ability to self manage the condition at home. For those individuals who have both a low NEWS score and CRB-65 score, it may be appropriate for them to self manage their condition at home, provided there are no red flag symptoms present (JRCALC, 2019). These patients should be given self care advice, for example ensure good fluid intake and rest, and if appropriate their GP contacted to arrange antibiotics (NICE, 2021). However, for patients with a high NEWS score or any red flag symptoms present, conveyance to hospital should be advised and any reversible causes managed.
What is Cocaine?
Cocaine is a stimulant which affects the sympathetic nervous system by inhibiting reuptake of norepinephrine, dopamine, and serotonin by interacting with each transporter, leading to exaggerated, prolonged sympathetic nervous system activity (Vongpatanasin et al 1999)
There is a large body of evidence which has shown that the use/abuse of cocaine is associated with an increased risk of several cardiovascular complication including hypertension, arrythmias, myocardial infarction, atherosclerosis, coronary spasm and if used chronically coronary artery disease. (Kim and Park, 2019)
What is the pathophysiology of Cocaine to the cardiovascular system?
Cocaine use has also been shown to block both sodium and potassium channels particularly when combined with alcohol use (Schwartz, Rezkalla and Kloner, 2010). This effect can be witnessed as the effects of cocaine on the potassium channel blockade results in prolonged QT interval and ventricular tachyarrhythmia. (O’Leary, 2002). These physiological changes are further exacerbated by the consumption of both cocaine and alcohol.
The mechanism of cocaine and its connection to causing myocardial infarction is multifaceted and therefore complicated. Cocaine causes a sympathetic nervous response of tachycardia, hypertension and increase myocardial contractibility (Mouhaffel et al., 1995), This results in an increased oxygen demand of the cardiac cells. This increased oxygen demand and the other physiological effects of cocaine such as vasoconstriction and platelet adherence results in an imbalance between oxygen supply and increased demand. This imbalance can result in myocardial infarction. (Kim and Park, 2019)
What is morphine sulphate?
Morphine sulphate is an alkaloid (nitrogen compound) of opium and acts as an analgesic for severe pain (DrugBank, 2018). Morphine sulphate acts as an agonist of the µ-receptor (opioid receptor) which causes analgesic effect, respiratory depression, euphoria, inhibition of gastric motility and dependence. It is also a competitive agonist of the ĸ-receptor which causes spinal analgesia, miosis (pupil constriction) and sedation. Mast cell degranulation, induced by morphine sulphate, provokes a histamine release as an immune response which causes vasodilation (Zhang et al. 2018) (Afshari et al. 2009). The chemoreceptor trigger zone (CTZ) within the postrema of the medulla is stimulated by morphine sulphate and as a result induces nausea and vomiting (Smith et al. 2012).
Contraindications of morphine sulphate
It is important to consider the contraindications and cautions of morphine sulphate when administration is indicated. Morphine sulphate must not be administered to children under 1, patients in respiratory depression (<10 breaths per minute in adults), actual hypotension of <90 systolic in adults, head injury with <GCS 9/15 and known hypersensitivity (JRCALC, 2021).
Cautions to consider with morphine sulphate
The cautions of morphine sulphate must be considered when administering the drug along with how achieving the desired effect of the drug will differ depending on the patient it is being administered to, the route it is administered and the pharmacokinetics of the drug. Patients with severe renal or hepatic impairment should receive a smaller dose as functions of the kidneys and liver are reduced, therefore metabolism and excretion are affected (JRCALC, 2021). Administering of morphine sulphate to pregnant patients must be with minimal doses during pregnancy and breastfeeding patients as neonates may suffer with dependency/withdrawal and where Nitrous Oxide is unavailable in labour pains due to respiratory depression in the neonate immediately following delivery (JRCALC, 2021). Morphine sulphate administration may lengthen labour as strength and duration of contractions decreases (EMC, 2020). Respiratory depression is a common effect/side effect of morphine sulphate, which should be considered before administering to patients with respiratory conditions and chest injuries (JRCALC, 2021). Respiratory depression should also be considered as an unwanted side effect in head injury patients with suspected elevated intercranial pressure. Inadequate expulsion of carbon dioxide from the blood as a result of respiratory depression will cause an increase in arterial pressure which will further increase intercranial pressure (JRCALC, 2021) (de Nadal et al. 2021). Alcohol intoxication and other CNS depressants or sedatives such as benzodiazepams may be compounded with morphine sulphate administration (JRCALC, 2021). Morphine sulphate may be indicated for patient’s suffering with sickle cell disease in crisis, however studies show an association between morphine administration and acute chest syndrome (ACS) (Birken et al. 2013), therefore the clinician should consider following ACS monitoring following administration. Finally, the clinician should weigh up the benefits versus the drawbacks of morphine sulphate administration for opiate addicts and the potential for tolerance, dependency and relapse to opiate/morphine use (EMC, 2020).
What is Aortic Stenosis?
Stenosis is the narrowing or constriction of the diameter of a bodily passage or orifice (Merriam-Webster, 2022) which, when applied to aortic stenosis, refers to the aortic valve. Blood flow from the left ventricle is restricted due the aortic valve not opening properly and causing an increase in pressure within the left ventricle in order to pump the ventricular load out and into the aorta (Waugh and Grant, 2018, pp.132–133) (Sverdlov et al., 2011). This increased pressurised blood flow can be heard with heart auscultation and is known as a murmur. Failure of the valve to close following ventricular constriction will allow the blood meant for the aorta to flow back into the ventricle and consequently lead to higher pressure within the left atrium and associated valves, this is known as incompetence (Waugh and Grant, 2018, pp.132–133).
What are the causes of Aortic Stenosis?
Aortic valve stenosis has two main causes, an early cause due to progressive fibrosis and a later cause due to calcification of the valve. Fibrosis is the development of fibrous tissue as a reparative response to injury or damage (scarring). This fibrous tissue is created by fibroblast cells depositing collagen and an enzyme called lysyl oxidases which increase the size/number of bonds between the collagen fibres which stiffens the bonds (Wells, 2022). This means the fibrous tissue or scar tissue is stiffer than the cells it has replaced and does not allow for the constant, smooth opening and closing of the aortic valve. Calcification can occur due to hypercalcaemia or tissue injury. Calcium is regulated by the parathyroid hormone (PTH) which induces uptake of calcium from the renal tubules and intestines when calcium is low. When the PTH cannot be regulated e.g. as a result of hyperparathyroidism it will keep inducing uptake of calcium which causes hypercalcaemia. Calcium also aids in tissue repair, hence why calcification will occur following tissue injury, particularly recurring tissue injury e.g. as a result of heart failure, hypertension (Wilson, 2016).
What are the symptoms of Aortic stenosis?
Symptoms of aortic stenosis (AS) may be managed with the use of ACE inhibitors and ARB’s which prevent the narrowing of vessels, however the current treatment for AS is an aortic valve replacement. Symptoms of AS include dyspnoea, angina (without the presence of coronary artery disease), arrythmias, chest pain, dizziness, peripheral oedema and fatigue (American Heart Association, 2016) (Sverdlov et al., 2011). Recognition of AS, pre-hospitally, is dependent on presenting symptoms, history (AS has an association with other cardiac conditions) and a helpful diagnostic aid in the use of auscultation of heart sounds. When auscultating for aortic valve murmurs ensure the patient is sat leaning forward and the bell of the stethoscope placed on the right side of the 2nd intercostal space. The sound of AS murmur is described as diamond shaped where the sound will crescendo (go up in pitch) and then decrescendo (go down in pitch) following a typical ‘ba bum’ heart sound (ba bum (cres decres) ba bum (cres decres) etc) (HowToGastro, 2017). It is good to know that the peak of the murmur, where crescendo ends and decrescendo begins, will get further away from the ‘ba bum’ with more severe stenosis.
What is COPD?
Chronic obstructive pulmonary disease (COPD) is a blanket term used for a group of diseases which result in poorly reversible obstruction to the airway (MacNee, 2016). It is a common and largely preventable disease which results in abnormal inflammation of the airway due to exposure to an environmental stimulus (MacNee, 2016).
Pathophysiology of COPD
As mentioned before, COPD results in the chronic inflammation of the lungs, due to long term exposure to harmful particulates and gases (MacNee, 2016). COPD describes a number of different conditions, including chronic bronchitis, which results in an excess of mucous secretion, emphysema, which causes destruction of the lung tissue, and bronchiolitis, which prevents the normal repair mechanisms of the body from occurring causing inflammation of the lung tissue (MacNee, 2016). The development of COPD is predominantly caused by the prolonged exposure to a harmful environmental agent, such as cigarette smoke, which results in chronic inflammation of the lung tissue (MacNee, 2016). The prolonged exposure to an environmental agent results in increased numbers of neutrophils, macrophages and T cells within the lungs (MacNee, 2016). The increased number of T cells causes damage to the walls of the alveoli, due to their toxicity, whereas both macrophages and neutrophils secrete inflammatory mediators and proteases, resulting in an increase in sputum production in the lung (MacNee, 2016). The increased sputum production eventually results in the hypersecretion of mucus, which causes the characteristic productive cough seen in many COPD sufferers (MacNee, 2016). This in combination with inflammation in smaller airways results in narrowing and blockage of these airways which causes air trapping and therefore hyperinflation of the lungs (Macnee, 2016). The inflammation also results in damage to the tissue of the alveoli, eventually resulting in alveolar collapse, further trapping air (Macnee, 2016). All of these factors prevent adequate ventilation from occurring to the lungs, which ultimately causes poor gas exchange (MacNee, 2016).
Systemic effects of COPD
Due to the lungs loss of ability to adequately conduct gas exchange, COPD impacts not only the respiratory system but also a range of other systems within the body. The cardiovascular system is severely impacted by the presence of COPD, and the risk of developing cardiovascular disease is three times higher in individuals who suffer from COPD (Augusti, 2005). It is thought this is due to the persistent inflammation present in COPD patients, which damages both the heart and blood vessels (Augusti, 2005). The presence of severe COPD can also result in a condition known as cor pulmonale due to the presence of pulmonary hypertension in COPD sufferers (MacNee, 2016) The increased pressure in the pulmonary circulation results in increased strain on the right side of the heart, which causes right ventricular hypertrophy and eventually, right sided heart failure (MacNee, 2016).
COPD also impacts significantly on the musculoskeletal system, due to decreased exercise tolerance as a result of poor ventilation of the lungs (Augusti, 2005). This results in wastage of the skeletal muscle which can result in weight loss, and also wastage of the bone due to sedentary lifestyles, resulting in osteoporosis (Augusti, 2005). The increased work of breathing observed in COPD patients is also thought to cause an increase in their baseline metabolic rate, which exacerbates the weight loss observed (Augusti, 2005).
Finally, COPD has also been shown to have significant impacts on the nervous system (Gestel and Steir, 2010). Hyperinflation of the lungs causes an increase in intrathoracic pressure in COPD patients which causes chronic stimulation of the cardiac baroreceptors (Gestel and Steir, 2010). COPD patients also suffer from chronic hypoxaemia which stimulates the chemoreceptors in the body (Gestel and Steir, 2010). Stimulation of both of these results in increased sympathetic stimulation in COPD patients at rest and decreased sensitivity of these receptors due to chronic stimulation (Gestel and Steir, 2010).
Assessment and management of COPD
When managing a patient suffering from COPD, clinicians should conduct a full set of observations and a thorough respiratory assessment, including auscultation of the chest (ΝICE, 2021). Patients with COPD most commonly present with dyspnea, particularly on exertion, a persistent productive cough, crackles or wheeze on auscultation and oxygen saturations between 88-92%. (NICE, 2021). When attending patients who suffer from COPD, clinicians should consider whether their symptoms are a result of an acute exacerbation of their condition. Signs and symptoms of an acute exacerbation of COPD include increased breathlessness relative to their normal baseline, chest tightness, acute confusion, cyanosis or peripheral oedema (NICE, 2021).
The management of COPD patients will depend significantly on the severity of their symptoms and their ability to manage their condition at home (NICE, 2021). If a patient appears to be presenting with an acute exacerbation of COPD, clinicians should administer salbutamol and ipratropium bromide through a nebuliser, being mindful to ensure 6 minutes on, 6 minutes off the nebuliser in order to prevent hypercapnia (JRCALC, 2020). If patients do not respond appropriately, paramedics should aim to cannulate and administer intravenous hydrocortisone, however this can also be administered intramuscularly if necessary (JRCALC, 2020. Patients who respond well to this administration should then be conveyed to hospital for further assessment, as well as patients who have been administered ipratropium bromide, or patients who are failing to appropriately manage their condition at home, or have other red flag symptoms present (JRCALC, 2020). For any patient suffering from extreme breathing difficulty, signs of exhaustion, persistent severe hypoxia or cyanosis, a time critical transfer should be conducted to the nearest emergency department (JRCALC, 2020). For patients who present with no red flags and are able to self-manage their condition, worsening advice and appropriate self care advice should be given and, if necessary, their GP contacted.
The impact of morphine on the respiratory system.
One side effect of morphine is that it is known to cause respiratory depression (JRCALC, 2019). Studies have shown that the administration of intravenous morphine results in a decrease in the rate of ventilation as well as the level of inspiratory air flow, meaning that less oxygen reaches the lungs for gas exchange (Bachmutsky et al, 2020). This is because morphine binds to the μ-receptors, which are found on neurones in both the pre-Bötzinger complex and the parabrachial nucleus (Bachmutsky et al, 2020). Genetic animal studies have shown that these two centres in the brain are the primary drivers of both respiratory rate and depth, therefore the inhibition of the activity of these regions by morphine results in respiratory depression (Bachmutsky et al, 2020). In addition to this, μ-receptors are also found on peripheral chemoreceptors, meaning morphine is also able to bind to and inhibit the action of these (Murphy and Barrett, 2022). It is thought that the peripheral chemoreceptors are responsible for 80% of ventilatory drive when hypoxia is detected, therefore the inhibition of these chemoreceptors also reduces the bodies ability to respond to hypoxic states, preventing the increase of respiratory rate to increase oxygen intake (Murphy and Barrett, 2022).
The impact of morphine on the cardiovascular system
The administration of morphine also results in impacts on the cardiovascular system, resulting in both hypotension and bradycardia (Caspi and Aronson, 2020). This is again partially due to morphine binding with μ-receptors, resulting in relaxation of the smooth muscle found in the walls of blood vessels (Caspi and Aronson, 2020). However, the predominant cause of vasodilation and bradycardia in morphine administration is due to the fact that morphine stimulates histamine release (Behzadi, Jouker and Beik, 2018).
Histamine then binds to both the H1 and H2 receptors found in the smooth muscle, which causes further relaxation of the smooth muscle and, as a result, causes vasodilation (Ebeigbe and Olufunke, 2014). Vasodilation causes the blood pressure to decrease, resulting in hypotension (Shanazari et al, 2011).
Histamine also binds to H3 receptors in the heart which are important for the maintenance of cardiovascular function, and therefore it has been suggested that this is the cause of bradycardia in morphine administration (Ebeigbe and Olufunke, 2014), in combination with the fact that morphine administration results in sympathetic stimulation (Caspi and Aronson, 2020).
What is Bronchiectasis?
Bronchiectasis is defined as permanent and abnormal widening of the bronchi (King, 2009). This is the result of an initial infectious agent entering the lungs and triggering a mucociliary response in order to expel the offending agent. Neutrophils, lymphocytes and macrophages are released into the affected bronchi as an inflammatory response, of which, the neutrophils alter the epithelium (surrounding tissue) of the cilia. The cilia are fibres within the bronchi that move microbes and debris out of the airway. This alteration causes a change in the cilia beat frequency and mucous gland hypersecretion which are detrimental to mucociliary clearance (Delmotte and Sanderson, 2006) (Bronchiectasis.com, 2022).
Due to poor mucociliary clearance and infectious agents within the mucous the bronchi and lungs are highly susceptible to repeat infections which restart the process. This eventually leads to fibrosis of the bronchial muscle which stiffens it and decreases mucociliary clearance further, repeating the process again and displaying ‘Cole’s vicious cycle’, this constant presence of mucous and fibrous bronchi causes airway obstruction which worsens over time (King, 2009) (Bronchiectasis.com, 2022).
What is cystic fibrosis?
Cystic fibrosis is a life-threatening genetic disorder that leads to a build up of mucous secretions in multiple systems/organs, commonly the gastrointestinal tract, pulmonary system and genitourinary tract (Brown, White and Tobin, 2017). This disorder is caused by a mutation of the CF transmembrane conductance regulator (CFTR) which is responsible for regulation of sodium and chloride in and out of cells in order to attract water to thin surrounding mucous in order to ease its expulsion (Cystic Fibrosis Foundation, 2022). When the CFTR fails it causes a build-up of thickened mucous throughout the body and ion deficiency, which when coupled with compromised mucociliary clearance such as in bronchiectasis, allows for bacterial colonisation which induces recurrent inflammatory responses (Brown, White and Tobin, 2017). Cystic fibrosis coupled with bronchiectasis will lead to Cole’s vicious cycle, however, cystic fibrosis tends to affect the gastrointestinal tract before other systems.
Meconium ileus is present in up to 20% of infants with cystic fibrosis and occurs due to the inability of the meconium (infant faeces) to pass the ileum due to sticky mucous secretions within the GI tract (Parikh, Ibrahim and Ahlawat, 2020). These secretions commonly cause bronchiectasis, sterility and pancreatic dysfunction which leads to cystic fibrosis related diabetes (Brown, White and Tobin, 2017).
How does naloxone work?
Naloxone is a competitive opioid antagonist which has a high affinity to the μ-opioid receptor. It has been used since the 1960s (Anon, 2019) for its reversal of opioid effects. Naloxone works by reversing the depression of the central nervous system and respiratory system when caused by opioids (Jordan and Morrisonponce, 2019). Naloxone counteracts the depressive effects of opioids by having a higher uptake rate/ affinity for the μ-opioid receptors.
Respiratory efforts are produced by the medullary respiratory rhythm generators and are controlled by various sites in the lower brainstem (Bötzinger complex and parabrachial nucleus) (Ikeda et al., 2016) (Bachmutsky et al, 2020). These signals are then output as motor activity in the premotor efferent networks in the brainstem and spinal cord. (Ikeda et al., 2016). Opioids have a depressive effect on these areas, this results in respiratory depression with both rate and depth of respiratory effort (Jordan and Morrisonponce, 2019). Therefore, preventing opioids from binding to these receptors results in normal respiration in patients which have been given a dose of naloxone.
The administration of naloxone also has a secondary side effect on the cardiovascular system which can often reverse the patient’s hypotension and or bradycardia due to its blocking μ-opioid receptors and pro-rhythmogenic effects of naloxone (Hunter, 2005). When opioids bind to the μ-receptors it can result in the relaxation of smooth muscle found in the walls of blood vessels as well as the relieves of histamine shown to dilatate blood vessels. (Caspi and Aronson, 2020) this reduction in ventricular tone results in reduced blood flow and blood pressure.
Naloxone has very few side effects and is only contraindicated in Neonates born to opioid addicted mothers can suffer from serious withdrawal effects (JRCALC 2021). Caution should be used when administering naloxone to a suspected opioid overdose as often can often result in aggression, nausea, vomiting, diarrhea, abdominal pain, and rhinorrhoea as patients may suffer from acute opioid withdrawal. (Jordan and Morrisonponce, 2019)
