Stress Response and Health Breakdown

Answer

Stress Response and Health Breakdown

Part A

Bill’s respiratory functions changed in response to the exacerbation of asthma. The pulmonary function changes could be observed in his mechanics of breathing, and intrapulmonary pressure. The unresolved stress on the breathing system also altered the V/Q ratio with some associated physical factors. Bill’s signs and symptoms indicated a severe adult asthma exacerbation.

The mechanics of breathing were adjusted to meet the demand for oxygen and CO₂ elimination from tissues despite the constriction of the airways. Bill showed the features of strained mechanics of breathing during the clinical assessment in the emergency department. Bill experienced a noted use of accessory muscles of respiration. Breathing at rest should be quiet and performed unconsciously (Bacharier and Guilbert 2012 p. 290). Accessory muscles are just supposed to assist in respiration during normal breathing. According to Leatherman (2015), use of accessory muscles as the primary drive for respiration is pathologic indicating a respiratory distress. Asthma causes constriction of the airway so that inadequate air reaches the lungs and therefore, less oxygen would perfuse to tissues. The chemoreceptors in the aortic arch will be stimulated by the reduction in oxygen level and in turn impulses sent to the brain to stimulate the accessory muscles of respiration (Goldenberg and Hare 2014). The accessory muscles would include sternocleidomastoid and the scalene that would contract to reduce the pleural pressure so that the lungs can expand to increase airflow during inspiration Porpodis, Zarogoulidis, Spyratos, Domvri, Kioumis, Angelis, and Zarogoulidis, (2014 p. 153). These accessory muscles are recruited to preserve the tidal volume of the lungs because the recoil of the lungs cannot expel air (Yamauchi, Kohyama, Jo, and Nagase 2012 p. 260). Bill must breathe harder so that more amount of oxygen reaches the lungs. The extent of use of the accessory muscles could be evaluated by palpation of the sternocleidomastoid and the scalene muscles to check the progress of the care plan.

Bill had a remarked increase in his respiratory rate of 36 breathes per minute. A respiratory rate of more than 30 breathes per minute is a sign of a severe asthma attack in an adult. The increased respiratory rate is a compensatory mechanism for the low oxygen levels in the body during the asthmatic exacerbation (Jolley, Luo, Steier, Rafferty, Polkey, and Moxham 2015 p. 360). The reduction in airflow during the asthmatic attack reduced the amount of oxygen available in the blood, a condition termed as hypoxemia. The body in turn initiates compensatory mechanisms to get enough oxygen to the vital organs such as the brain, heart, lungs, and kidneys. Therefore, the respiratory rate increases to increase the amount of oxygen reaching the body through the lungs during inspiration. Bill must breathe faster so that more oxygen can reach the lungs per minute. The frequency of inspiration increases so that the normal concentration of oxygen in the blood can be maintained (Schivo, Zeki, Kenyon, and Albertson 2012 p. 36). However, there is a potential risk of excessive removal of CO₂ from the tissues. Bill was at a risk of developing hypocapnia and respiratory alkalosis due to the increased rate of removal of CO₂ from the body (Goldenberg and Hare 2014 p. 196). Therefore, Bill should be intubated to reduce the fatigue from the use of accessory muscles of respiration and the risk of alkalosis that could reduce his mentation. 

There were also adjustments in Bill’s intrapulmonary pressure to increase the amount of air reaching the lungs. Asthma is one of the obstructive respiratory diseases that only reduces airflow to the lungs but does not interfere with the elasticity of the lungs like other restrictive diseases. The increased strain in breathing and involvement of the accessory muscles of respiration would immensely increase the negative intrapleural pressure (Pauwels, Buist, Calverley, Jenkins, and Hurd 2012 p. 1266). Therefore, the lung will expand and the intrapulmonary pressure would reduce so that more pressure difference is created between the lungs and the atmosphere. The increased negative pressure predisposed Bill to a pleural effusion. However, the observation only persists for a while because asthma mainly obstructs expiration (Doeing and Solway 2013 p. 834). Therefore, the lungs will become hyper-inflated. Consequently, the increased volume of the lungs will increase the intrapulmonary pressure, a mechanism termed as dynamic hyperinflation of the lungs. The dynamic hyperinflation would be beneficial as it would allow more gaseous exchange between the lungs and blood in pulmonary capillaries (Yamauchi, Kohyama, Jo, and Nagase 2012 p. 268). Asthma increased the work of breathing due to the dynamic hyperinflation that increases the minute volume that can maintain adequate ventilation. 

Asthma increases the resistance of the airways to airflow. The obstruction of airflow would reduce the forced expiratory volume below normal. The measurements of expiratory airflow are remarkably reduced during an asthmatic attack. According to Yamauchi, Kohyama, Jo, and Nagase (2012), FEV₁, FEV₁/FVC, and PEF reduce when the airflow is obstructed (p. 260). The forced expiratory volume reduced due to the obstruction of gasses escaping from the lungs. Asthma causes FEV₁ to reduce to less than the normal value of 80% (Yamauchi, Kohyama, Jo, and Nagase 2012 p. 260). Additionally, his forced expiratory flow between 25-75%, forced vital capacity, and inspiratory capacity would be low (Yamauchi, Kohyama, Jo, and Nagase 2012 p. 260). The residual volume, total lung capacity, and functional residual capacity would also be low (Goldenberg and Hare 2014 p. 196). The increased work of expiration would limit the amount of airflow out of the lungs. Air trapping due to hyperinflation is very common in asthmatics and the volume of air in the lungs increases markedly due to the increased resistance to the flow of the expired gasses (Elbehairy, Ciavaglia, Webb, Guenette, Jensen, Mourad, and O'Donnell 2015 p. 1384). The compliance of the lungs also reduces during asthmatic attacks due to the increased workload of expanding the lungs Roca, Verduri, Corbetta, Clini, Fabbri, and Beghé, (2013 p. 514). The increased workload could be attributed to the dynamic hyperinflation and the increased resistance to the flow of air to the lungs. Therefore, the lungs will expand less under pressure; a complication whose consequence is reduced movement of atmospheric air to the lungs and removal of CO₂ from the lungs.

The reduced amount of airflow to the lungs would affect the V/Q ratio of Bill and increases V/Q mismatches. Asthma is one of the Chronic Obstructive Pulmonary Diseases that cause widespread obstruction of the airways that leads to the development of extensive regions within the alveolar units that are dead spaces (Wells, Washko, Han, Abbas, Nath, Mamary, and Dransfield 2012 p. 916). These dead spaces have profoundly reduced ventilation while the blood flow is maintained (Goldenberg and Hare 2014 p. 195). Therefore, a reduction in ventilation with persistent perfusion would be observed in Bill’s case. The mismatch changes the composition of blood gas. Therefore, asthma that leads to extreme V/Q mismatches can be a life-threatening infection considered as an emergency.

Part B

Bill also experienced hemodynamic changes because of the effects of airflow obstruction on the chemical composition of the blood. Obstruction of breathing usually coexists with cardiovascular effects (Wise, Anzueto, Cotton, Dahl, Devins, Disse, and Calverley 2013 p. 1498). The first recognizable cardiovascular effect was an increase in his blood pressure to 142/88mmHg. The normal average systolic pressure is 120mmHg and the normal average diastolic pressure is 60mmHg (Wells, Washko, Han, Abbas, Nath, Mamary, and Dransfield 2012). The increased blood pressure was a compensatory mechanism for the low concentration of oxygen in the blood. Asthma is associated with both hypertension and hypotension depending on the severity of the asthmatic attack (Yamauchi, Kohyama, Jo, and Nagase 2012). In a case where blood pressure drops because of acute asthma, the emergency department must act promptly because the cardiac muscles are not receiving enough oxygen even to pump blood. However, Bill had his blood pressure elevated due to the asthmatic attack. This elevation shows that his breathing was not compromised to a very severe extent when compared to patients who develop hypotension due to cardiopulmonary arrest following the asthmatic attack. The aortic arch chemoreceptors would detect the low levels of oxygen concentration and stimulate the myocardium to contract harder at an increased frequency (Yamauchi, Kohyama, Jo, and Nagase 2012). Consequently, there would be positive inotropic, dromotropic, and chronotropic effects because the heart must now pump more blood faster to reach all the tissues so that the less oxygen distributes very fast (Ludviksdottir, Diamant, Alving, Bjermer, and Malinovschi 2012). Blood pressure is expressed as directly proportional to cardiac output and total peripheral resistance. Therefore, regardless of the constant peripheral resistance during the asthma exacerbation, the increased cardiac output due to increased heart rate and myocardium contractility would automatically increase the blood pressure.

The increased heart rate also explains the increase in cardiac output that increases blood pressure. Bill had a heart rate of 150 beats per minute in the emergency department. The normal average heart rate is approximately 70 beats per minute (Barzilai and Jacob 2015 p. 5). The increase in heart rate is a complex compensatory mechanism for both hypoxemia and dynamic hyperinflation. Hypoxemia leads to the stimulation of the ventricular muscles to contract faster so that more blood can be circulated per minute. Additionally, dynamic hyperinflation leads to the more negative intrathoracic pressure that impairs systolic emptying by increasing the left ventricular after-load. Hyperinflation also increases the blood pressure of the pulmonary arteries thereby increasing right ventricular afterload further (Porpodis, Zarogoulidis, Spyratos, Domvri, Kioumis, Angelis, and Zarogoulidis 2014 p. 155). Cardiac muscles contract according to their initial stretch and increased afterload would stretch the cardiac muscle fibers. Therefore, the contractility would increase. The increased heart rate would increase cardiac output and more blood would be pumped to the body per unit time. However, these changes can lead to persistently lower systolic blood pressure and therefore, reducing tissue perfusion. The reduced tissue perfusion can then lead to cyanosis due to the high concentration of deoxyhemoglobin. 

The cardiovascular effects of asthma are experienced due to the stimulation of particular adrenergic receptors. It is important to understand the roles of these receptors in asthma exacerbation to understand the pharmacodynamics of medications administered to the asthmatic patients. The heart has both sympathetic and parasympathetic stimulation (Barzilai and Jacob 2015 p. 4). It is the adrenergic receptors that are responsible for the increase in heart rate, blood pressure, and cardiac output. The heart rate was increased following the stimulation of the β₁-adrenoceptors of the myocardium. The Β_1-agonist like epinephrine became bound to the receptor and lead to a cascade that increases the heart rate, action potential conduction velocity, and the myocardial contractility (Barzilai and Jacob 2015 p. 5). Some epinephrine was also bound to the β₂-adrenoceptors that became remarkable down-regulated. Therefore, it would be important to consider the effects of stimulation of these receptors when administering medications to ease breathing. Most asthmatic attacks are treated with β-agonists that can as well stimulate the heart increasing further the cardiac output (Morales, Jackson, Lipworth, Donnan, and Guthrie 2014). The progressive stimulation of the cardiac muscles can greatly reduce the ventricular filling time thereby reducing the stroke volume. This situation can lead to the permanent cardiac arrest and therefore, must be treated with urgency.

Part C

Bill’s arterial blood gas composition also changed due to the changes in ventilation during the asthma exacerbation. Low oxygen concentration could be adduced in the emergency department assessment. His SpO2 was 88% and this is lower than the normal range of 90-100% (Louie, Morrissey, Kenyon, Albertson, and Avdalovic 2012). Bill also had respiratory acidosis as can be adduced from the acidic pH of his blood of 7.25. The normal blood pH ranges from 7.35 to 7.45. The acidity is due to the impaired removal of CO₂ following the obstruction of expiratory airflow (Nievas and Anand 2013 p. 91). CO₂ levels accumulated in his blood and led to the increase in acidity of the blood. The accumulation of CO₂ was further affirmed by its elevated partial pressure of 55mmHg while the normal range is from 35-45mmHg. The low saturation of oxygen of 88% was due to the reduced amount of oxygen reaching the lungs. However, the amount of bases in the blood remained within the normal range.

The analysis of the components of Bill's blood would be important in evaluating the severity of the cardiopulmonary distress, his acid-base balance, and the amount of oxygen in the blood. The acid-base balance was affected due to the incapability of the lungs to blow off CO₂ from the body. Therefore, the partial pressure of CO₂ rose due to its retention in the blood. According to Holgate (2011), the excess C0₂ in the blood reacts with water to form weak carbonic acid and thus, H⁺ dissociates from water molecules. This dissociation raises the concentration of hydrogen in the blood and therefore, lowering the arteriolar pH.  Despite the progressive increase in a number of hydrogen ions, there are several buffering systems that work towards increasing the pH of the blood. In the case of Bill, the acidosis is due to a respiratory failure and therefore, there would be less emphasis on the respiratory compensatory mechanisms. However, other buffering systems such as proteins, phosphate buffers, and the kidney would play indispensable roles in regulating excess hydrogen ions in the blood.

The excess acidity was compensated through the buffer systems, renal mechanisms, and other regulatory mechanisms. It was important to maintain his blood pH for hemostasis and enzymatic functions. The role of the bicarbonate buffering system would be ineffective due to the compromised respiratory functions. According to Rogers and McCutcheon, (2015), proteins can bind excess hydrogen ions when in acidic medium and release the hydrogen ions when the pH increases (p. 48). The protein buffering system is effective in both extracellular and intracellular fluids. The key proteins that could regulate Bill’s pH were hemoglobin in the erythrocytes, plasma proteins, and specific amino acids. Another vital buffer system that compensated the respiratory acidosis in Bill was the renal buffering mechanisms. As such, there was an increased secretion of hydrogen carbonate molecules in the kidney to neutralize the excess acidity. The kidney would excrete hydrogen ions and re-absorb more hydrogen carbonates (Roca, Verduri, Corbetta, Clini, Fabbri, and Beghé 2013). The function of phosphates as buffer focuses on the role of the dihydrogen phosphate. This molecule can bind extra hydrogen ions to regulate acidity because the valency of phosphate is 3. The phosphate system would have more of its effects in the renal tubules where its concentration is highest.

The changes in the blood composition would also correlate to the shifts in the oxyhemoglobin curve that favors oxygen delivery to tissues. Johansen, Johansen, and Dahl (2014) argue that increased CO₂ retention increases respiratory alkalosis that shifts the oxyhemoglobin curve to the right. The factors that shift the curve to the right are hypercapnia, hyperthermia, acidosis, and high amount of 2, 3-Diphosphoglycerate. A shift of the curve to the right indicates increased oxygen delivery to the tissues. According to Melén and Pershagen, (2012), the actual shift of the curve to the left might compromise oxygen delivery to the tissues. The curve shifts to the left due to the hypercapnia that compounds the respiratory acidosis Schivo, Zeki, Kenyon, and Albertson (2012 p. 36). Similar changes are also observed in the pressure gradients of respiratory gasses. The partial pressure of oxygen reduces due to the obstructed airflow. The gasses become less soluble due to their reduced partial pressures. Therefore, oxygen delivery to the tissues was compromised and Bill should be put on an artificial ventilator.