The objective of this essay is to critically analyse the pathophysiology and the management of a case study patient currently having an asthma attack. This will be achieved by exploring the normal physiology and role of homeostasis, and the pathophysiology of the human body during an asthma attack. In addition, the pharmacodynamics of medications will also be explained alongside the treatment plan available to a paramedic, and further care in the community following hospital discharge.
To understand the complications, the pathophysiology, of the patient; first it is essential to understand the normal physiology. The air that the human body needs to survive is compromised of a variety of molecules of which only twenty percent is oxygen (O2). It is important for the body to have O2 and to understand why, it necessary to explain the process of energy creation.
Cells within the body need energy which is liberated from adenosine triphosphate (ATP) to maintain their shape, function and be able to produce chemical reactions within (Scott and Fong, 2016). Without ATP cells are unable to function and simply die. ATP is predominately manufactured using glucose from the carbohydrates eaten. As the glucose is chemically broken down within the body it is essentially stripped free of electrons. These electrons, which are negatively charged, are moved to a series of proteins, known as the electron transport chain which is embedded in a specialised organelle called the mitochondria. They then travel from one protein to the next creating a flow of electrons forcing proteins to create a chemical pump, in simplest form. This is electricity within a cell. These proteins pump hydrogen ions (H+) from one section of the mitochondria to another. Eventually a higher number of H+ are contained into an area of the mitochondria needing to flow into the second compartment that is low in H+. As this happens, another molecule known as adenosine diphosphate (ADP) receives an enzyme creating more ATP (Tortora and Derrickson, 2014). O2 is needed to remove these electrons in order for the cycle to continue.
O2 is extremely electronegative because of it’s atomic structure, meaning that it has a high attraction towards electrons. Each molecule of O2 will pick up four electrons and four H+ forming two molecules of water. Once O2 removes the electrons from the end of the chain, more electrons can keep on flowing leading to the recharging of more ATP (Tortora and Derrickson, 2014).
Another key role of respiration is the maintenance of correct blood pH. Acidosis is the increase of pH in the blood; that is an increase of H+, whereas alkalosis is the increase of pH in the blood; a decrease of H+. The body can adjust to try and balance the pH in the blood as part of homeostasis. Normal blood pH is between 7.35-7.45 (Martin, 2010). Homeostasis is achieved with use of specific chemoreceptors within the arteries which are highly sensitive to subtle molecular changes in the blood. Where there is a build up of H+ ions; therefore acidosis, these chemoreceptors send a message to the respiratory regulation centre to increase breathing effort and rate in order to attempt to exhale more carbon dioxide (CO2), taking on more O2, thus rectifying the acid base balance rapidly. If there are too little H+ within the blood; therefore alkalosis, the body is able to adjust accordingly with use of kidneys and using the bicarbonate buffering system. The balancing of the pH of the blood is hugely important as Bohr, Hasselbalch and Keogh (1904) stated that, “haemoglobin's oxygen binding affinity is inversely related both to acidity and to the concentration of carbon dioxide”. That is that an increase of blood CO2, thus a decrease in pH, will cause haemoglobin proteins to release their load of O2. In parallel, decreased of blood CO2, creates an increase in blood pH thus haemoglobin picking up more O2.
The process in which air is drawn from the atmosphere into alveoli within the lungs is known as pulmonary ventilation (Cohen, 2015) or external respiration. This is achieved because of alternating pressure differences created by contraction and relaxation of respiratory muscles (Tortora and Derrickson, 2014: 856). O2 rich air travels through the nose where it is warmed and moistened, travels via the nasopharynx and oropharynx into the trachea via the larynx. The trachea divides into two smaller airways known as bronchi, the right and left bronchus. These bronchus pass into each lung, right and left respectively, where they divide into many bronchioles each leading to alveolar ducts which end in the alveoli. Surrounding the alveoli are capillaries separated by two thin membranes of epithelial cells; capillary and alveolar wall (Cohen, 2015) where the exchange of gases through diffusion between the alveoli and the blood in the pulmonary capillaries (Tortora and Derrickson, 2014) takes place.
Internal respiration takes place within cells around the body regarding the exchange of O2 and CO2. The O2 has diffused from the alveoli into the blood as previously described, the increased amount of O2 within the blood diffuses the O2 into the tissue cells. At the same time, cells build up a higher CO2 concentration more so the concentration in the blood (Scott and Fong, 2016). This is due to cell function. In turn, this causes diffusion to take place exchanging O2 and CO2 within all cells in the body. The deoxygenated blood then takes the CO2 in the form of bicarbonate ions (HCO-3) back to the lungs where they are exhaled (Scott and Fong, 2016) thus correcting pH, restoring homeostasis.
Asthma is a chronic widespread inflammatory and narrowing of the bronchiolar airways (Martin, 2010). It is distinguished by recurrent obstruction to airflow, causing limited airflow into the lungs, hyper responsiveness of the airway smooth muscle (ASM), inflammation of the bronchi, and secretion of oedema within the bronchiolar airway (Battista and Yassin, 2013).
There are many possible causes of an acute asthma attack, for example; allergens, respiratory tract infections (RTI), medicines, climate, genetics, and exercise. These are either known as an extrinsic (allergy) or intrinsic (non allergic) cause (Battista and Yassin, 2013). The most common cause of an asthma attack, like hay fever and anaphylaxis, is caused by the same basic process through the presence of an allergen. One or more of these stimuli can cause the bronchial airways undergo structural and physiological changes (Doeing and Solway, 2013).
Allergens react with respiratory mucosa within the bronchioles triggering a Immuglobulin-E (IgE)-mediated mast cell response. The response of these mast cells is to degranulate and to release various pro inflammatory mediators such as histamines and prostaglandins which then attract and recruit more inflammatory response cells (Busse and Lemanske, 2001). These cells secrete more mediators; thus more pro inflammatory response cells, amplifying the inflammatory response causing narrowing the airway by bronchospasm or bronchoconstriction (Neal, 2009). The initial stage of the exposure to a stimuli, and resultant bronchoconstriction, is know as an immediate-phase response which can be effectively controlled by bronchodilators such as salbutamol (Battista and Yassin, 2013). If the O2 is not able to enter the body through external respirations and then internal respirations due to the worsening bronchoconstriction, the electrons within the mitochondria seize to flow, the protein pump wont work and therefore H+ cannot get forced into the other compartment of the mitochondria and the electrons are not collected, more cannot enter the electron transport chain. Thus, ATP cannot be remade and if these ions can’t get into that secondary compartment, they can’t flow back through the ATP synthase to recharge more ATP. If ATP is not made, the cells don't have energy to do work. If cells can’t do work, they eventually die. If left without treatment to this point, the patient will be in a late-phase response (Battista and Yassin, 2013). This late-phase consists of further bronchospasm, vasodilation, oedema, and excess mucous excretion caused by the inflammatory mediators. At this late-phase stage anti-inflammatory drug intervention is needed (Battista and Yassin, 2013).
Due to this restricted air flow in and out of the lungs and subsequent inhibited O2 transfer within the alveoli; the body has to increase its effort of breathing by rate and the position it is in for adequate internal ventilations. This can be seen within the case studies ‘general impression’ and ‘breathing’ assessment. The position of the patient is in a ‘tripod’ to open up the lungs. Furthering this assessment in ‘breathing’, it is shown that the patient is having to use accessory muscles; Arnold et al. (2011) states that, “…accessory muscle use… [is] …any visible use of the scalene, sternocleidomastoid-suprasternal, intercostal or subcostal muscles”. By employing accessory muscles, the body is able to use further force in order to open up the thoracic cavity thus creating a larger volume and lower pressure of air within than the air outside the body, thus forcing air into the lungs applying Boyle’s Law (BBC.co.uk, n.d.). Boyle's Law describes the inverse relationship between the pressure and volume of a fixed amount of gas at a constant temperature.
The patient appears to be in a late-phase stage which is shown in a reduced SpO2 at 87% and the reduced GCS. This indicates, as briefly touched upon, that the patients airways are compromised reducing O2 intake, therefore reducing O2 rich haemoglobin proteins that are unable to fully achieve internal respirations to the brain tissue causing a reduction in brain function and thus confusion. In-turn, the heart is working harder to increase the O2 delivery raising the hearts beats per minute and the body directing blood into the core where is it most needed for survival. This is all reflected within the patients observations.
To effectively combat the cause of disruption to homeostasis within the body, a paramedic has a range of pharmacological treatments available. These are O2, bronchodilators, antimuscarinic bronchodilators, Glucocorticoid steroids and adrenaline.
O2 is the first choice available to a clinician in the event of an acute severe or life-threatening asthma episode. As well as previously described about O2, given in high flow dose increases alveolar O2 tension and decreases the work of breathing that is necessary to maintain homeostasis (Battista and Yassin, 2013). O2 is given depending on patient saturations e.g. in the patient presenting eighty-seven percent O2 saturations, according to the Joint Royal Colleges Ambulance Liaison Committee (2016) guidelines it is recommended to give five to ten litres of O2 through a simple face mask aiming to achieve the normal ninety-four percent or more saturations.
Bronchodilators like Salbutamol are a β2-adrenoreceptor agonist. The ASMs do not have a sympathetic nervous supply but contain β2-adrenoreceptors that react to the circulating adrenaline, this resulting in relaxing of ASM and bronchodilation (Battista and Yassin, 2013). Salbutamol is a short acting medication and is used to relieve bronchospasm. If given by nebuliser its smooth muscle relaxing action, combined with the moistening effect by the driven nebuliser, can quickly relieve bronchospasm (Joint Royal Colleges Ambulance Liaison Committee, 2016). In the instance of asthma salbutamol is given when normal inhaler therapy has failed. Side effects can include tremor, tachycardia, palpitations, headaches, feeling of tension, peripheral vasodilation, muscle cramps and a rash. Tachycardia is produced as β2-adrenoreceptor antagonists have some β1-stimulating properties (Battista and Yassin, 2013). β1-cells are found in cardiac tissue. According to the Joint Royal Colleges Ambulance Liaison Committee (2016) guidelines, for the respective patient an adult dose of salbutamol through a nebuliser, powered by O2 at six to eight litres, would be an initial does of five milligrams (mg). This can be repeated after five minutes with no maximum dose. However, if the side effects become significant, such as tachycardia and palpitations, repeat doses should be ceased (Joint Royal Colleges Ambulance Liaison Committee, 2016).
Antimuscarinic bronchodilators, such as Ipratropium Bromide, are another class of medication used in the treatment of an asthmatic attack. It is indicated in acute severe or life-threatening asthma and acute asthma unresponsive to salbutamol. Like Salbutamol, Ipratropium Bromide offers short-term relief and uses nebulisation in the same fashion. It can be used at the same time as Salbutamol. Salbutamol generally works quicker and more effectively than Ipratropium Bromide (Joint Royal Colleges Ambulance Liaison Committee, 2016). Parasympathetic vagal fibres provide bronchoconstrictor tone to the ASM and are activated by reflex from an irritant detected within the airway walls. Antimuscarinic medications work by blocking muscarinic receptors, especially the M3 subtype, which responds to the parasympathetic bronchoconstrictor tone (Battista and Yassin, 2013). This stops further bronchoconstriction effectively keeping ASM dilated. Ipratropium Bromide should be used with caution with patients who have glaucoma. The initial and maximum dose is five hundred micrograms (mcg) (Joint Royal Colleges Ambulance Liaison Committee, 2016).
Paramedics have use of a glucocorticoid steroid known as hydrocortisone. These glucocorticoids depress the inflammatory response specifically within bronchial mucosa and thus lessen bronchial hyper-responsiveness suppressing the immune response (Neal, 2009) (Joint Royal Colleges Ambulance Liaison Committee, 2016). Due to these actions, they are useful in the treatment in acute severe or life-threatening asthma among other life threatening conditions. Hydrocortisone is administered as one dose of one hundred mg intravenously slowly over two minutes to avoid a burning or itching sensation in the groin (Joint Royal Colleges Ambulance Liaison Committee, 2016).
Adrenaline is the final drug a paramedic has as a pharmacological treatment. This is the last course of drug action available in the event of failing ventilations and continued deterioration despite nebuliser therapy. Adrenaline is a sympathomimetic that stimulates both alpha- and beta-adrenergic receptors (BNF, 2016) increasing both heart rate and contractility in (β1); peripheral vasodilation (β2) or vasoconstriction (ɑ). It also reverses allergic manifestations and relieves bronchospasm in acute severe asthma (Joint Royal Colleges Ambulance Liaison Committee, 2016). Horn and Hansten (2009) state that caution should be exercised in patients taking beta blockers due to profound hypertension as adrenaline wont be able to effect β2 cells due to the blockers causing vasoconstriction. In the case of severe asthma, adrenaline is administered intramuscularly at a dose of five-hundred mcg repeating doses every five minutes, with no maximum dose (Joint Royal Colleges Ambulance Liaison Committee, 2016).
Within the Joint Royal Colleges Ambulance Liaison Committee (2016) guidelines there is an asthma algorithm tool (pp. 23 of the pocket book) to aid in the treatment of asthma at varying severities. It follows a set plan which can help a clinician assess the severity of the current asthmatic episode and follow the treatment plan using the most appropriate medications available. Due to inadequate external ventilation, will be experiencing blood acidosis due to the build up of H+ ions. In an attempt to regain a balance of homeostasis the patients body will try and ‘blow off’ CO2. The first treatment considered would be O2. This is an attempt to increase O2 saturation and improve alveolar O2 tension and decrease work of breathing and reverse acidosis. Due to own inhalers failing, salbutamol and ipratropium would be given simultaneously to provide the best short-term relief possible stimulating the ASM to dilate and remain dilated. If no improvement, a clinician would move onto hydrocortisone in an attempt to depress the inflammatory response and the hyper-responsiveness of the bronchial airways. Salbutamol would be repeated as described previously. Finally, adrenaline would be given in an attempt to reverse bronchospasm if deemed necessary. Failing the above, a ’T’ piece, the bag-valve-mask and nebulisation can be used to force air into the lungs in an attempt to restore homeostasis. However, the patient appears, from initial assessment, to be within the acute severe asthma criteria in which homeostasis would be able to be restored. The patient within the assignment would be taken to hospital for further treatment. This is because of their current presentation and previous medical history. They had a similar asthmatic episode which resulted in hospitalisation and three days prior of minor attacks. It would be unwise to treat and leave the patient at home as there is a high chance of further episodes occurring. It is important to deliver the right care, at the right time.
Following hospital admission within hospital NICE (2013) outline the ongoing care a patient would receive to prevent further deterioration or a relapse. NICE (2013) states that, “Those who received treatment in hospital or through out-of-hours services for an acute exacerbation of asthma who are followed up by their own GP practice within 2 working days of treatment”. Medication for the patient would be reevaluated and a consult would take place to make sure the patient is compliant with medications predominantly to prevent readmissions and recurrences of episodes.