Patient history and diagnosis
Discuss about the Acute Respiratory Distress Syndrome.
In this assignment, case of Mr. A will be discussed. In the initial phase of the assignment, his history, diagnosis and presenting condition will be discussed. Diagnostic tests and indicators will also be discussed with special emphasis on the clinical signs and assessment findings. These clinical signs and assessment findings will be related to the physiology. Altered physiology and pathophysiology related to the respiratory failure will be discussed.
Patient Mr. A, had experienced worsening inadequate breathing and shortness of breath since last three years. After performing, clinical and radiographic assessment it was evident that shortness of breath is mainly due to progressive interstitial lung disease and respiratory failure.
He had history of coronary artery disease. He had myocardial infraction before 8 years ago and there is no recent history of angina. Moreover, he was also associated with hypertension and gastroesophageal reflux disease (GERD). He was hospitalized prior to 12 months for the treatment of Pneumonia.
He was smoker for about 20 years, however he quit smoking after diagnosed with cardiovascular conditions. During his job occupation, he used to get exposed to graphite inhalation; however, there is no history of exposure other agents.
Respiratory failure is not a disease as such; however, it is a condition mainly occur due consequences of insufficient breathing. He is exhibiting complications like respiratory depression, hyperthermia, cardiac irregularities and aspiration. Respiratory failure can be categorised into acute and chronic respiratory failure. Acute respiratory failure mainly occurs due to rapid progression of its underlying cause and chronic failure mainly occurs due to progressive and slow progression of its cause. Respiratory failure is associated with two events like oxygenation failure and ventilatory failure. Oxygenation failure is associated with inability to uptake oxygen and ventilation failure is associated with the inability to eliminate carbon dioxide (Vo & Kharasch, 2014; Schneider & Sweberg, 2013).
His shortness of breath is severe and it keeps him awakened after going to sleep. He mentioned that he feels improvement in breathing when he sat upright and he feels suffocation in the lying down position. He mentioned that he is having cough, wheezing and sputum. Initially, healthy patient generally doesn’t get affected by primary hypoxia; however, patient like Mr. A associated with previous cardiopulmonary conditions get affected by hypoxemia and gets further deteriorated (Bausewein & Simon, 2013).
Normal physiology of the respiratory system mainly depends on the three aspects such as : oxygen transfer across the alveolus, oxygen transport to the different tissues of body through blood vessels and elimination of carbon dioxide from the blood into the alveolus and then to the external environment. Impairment of the normal functioning of the respiratory system can lead to respiratory failure. Abnormal functioning of either of these processes can lead to the development of respiratory failure. Hence, central event in the respiratory failure is the impaired gaseous exchange. Alveolar capillary units are the main sites for respiration because gaseous exchange occurs at these sites. At these sites, exchange of oxygen and carbon dioxide occurs between the alveolar gas and blood in the capillaries. After entering into the blood, oxygen binds with the haemoglobin in the blood. Amount of oxygen binding to the haemoglobin depends on the blood partial pressure of oxygen (PaO2). Partial pressure is the measurement of exact quality of oxygen present in the arterial blood (West, 2012). In patients with respiratory failure like Mr A. there is decrease in the PaO2. During respiration, carbon dioxide is mainly transported in three forms like simple carbon dioxide in solution, bicarbonate and in combination with haemoglobin in the form of carbamino compound. Blood flow (perfusion) and ventilation match each other during the normal gaseous exchange of respiration. Hence, alveolar-arterial oxygen tension (PO2) remains stable during normal respiration. However, in patients with respiratory failure there is attenuation of PO2. During normal functioning of respiratory tract also it is not necessary that all the alveoli should get ventilated and perfused. For a specific ventilation, few of the alveoli might not get perfused and for a specific perfusion, few of the alveoli might not get ventilated. Alveoli which are well ventilated; however not properly perfused, have more ventilation-to-perfusion ratio (V/Q). These are dead spaces and termed as high-V/Q units. Alveoli which are well perfused; however not properly ventilated, have less ventilation-to-perfusion ratio (V/Q). These are shunt and termed as low V/Q units. V/Q mismatch and shunt are mainly responsible for the occurrence of hypoxemia. These two mechanisms lead to the development of widened alveolar-arterial PO2 gradient (Lamba et al., 2016). V/Q mismatch occur either due to different pathological events like airway or interstitial lung disease and overperfusion in the presence of normal ventilation. Overperfusion mainly occurs due to pulmonary embolism because blood is usually directed towards normally ventilated region of lungs from the region of obstruction to flow due to pulmonary embolism. In shunt, deoxygenated blood circumvents the alveoli in the ventilated region and get mixed with the oxygenated blood which flows through the ventilated alveoli. It results in the arterial blood contamination. Hypoxemia can be corrected in the V/Q mismatch by administration of 100 % oxygen; however, it can not be corrected in shunt (Oana & Mukherji, 2014).
The physiology of the respiratory system
Inhalation capability mainly depends on the neurological system which stimulates respiratory muscles. Diaphragm contraction results in the reduction in the intrathoracic pressure and aid flow of gas in the lungs. Exhalation depends on the patient airways and lung parenchyma with optimum elastic recoil which can be helpful in the holding bronchioles open. Ventilatory failure mainly occurs due to the depression of the respiratory centre (Hillman et al., 2014).
Depression of the respiratory system occurs due to drugs like narcotics. Inspiratory muscle weakness is also responsible for the ventilatory failure. Weak ventilatory muscle and pulmonary hyperinflation which is also called as pulmonary oedema are mainly responsible for the inefficiency of diaphragm and altered position. Signal to the muscles for breathing is carried by nerves. In respiratory failure these nerves get paralysed by conditions like infection which lead to development of sepsis. Spinal cord injury can also lead to respiratory failure because all the muscles including respiratory muscles, below the level of injury get damaged. It can lead to mechanical disadvantage for hyperinflation. These aspects are responsible for the occurrence of hypoxia (Howard, 2016).
Main function of respiratory system to maintain optimum exchange of oxygen and carbon dioxide between the blood and atmospheric air. Normal functioning of the respiratory system depends on the integrated functioning of multiple systems. Along with trigger from the nervous system, different systems like integrity of the airways, lung structure, and blood vessels within the lungs need to work in coordination for effective breathing. Alteration in the functioning of either of these systems can lead to respiratory failure. Patients with hypoperfusion following cardiogenic, hypovolemic, or septic shock exhibit respiratory failure (Chiumello, 2017).
Due to shortness of breath, lung breaths in less amount of oxygen, hence it can lead to the less gaseous exchange at capillary wall and alveolar wall interface. Alteration in this gaseous exchange is mainly responsible for the respiratory failure. Due to failure of this gaseous exchange, all the organs would receive less amount of oxygen and there would be increase in the metabolic demands of oxygen. Body’s acid-base stabilization also get disturbed. Respiratory failure lead to ventilation-perfusion mismatch. Ventilation-perfusion mismatch is primarily responsible for the occurrence of poor lung ventilation and optimum pulmonary blood flow. There is occurrence of regional vasoconstriction of pulmonary capillaries, however it doesn’t stop complete blood flow completely. It results in the leaving of blood from the lungs without containing adequate oxygen (Matalon & Sznajder, 2012).
Altered physiology and pathophysiology related to respiratory failure
Failure of this gaseous exchange can lead to development of severe hypoxemia in this patient. It can also lead to development of anoxia and tissue asphyxia. Respiratory failure can lead to fluid filling in the alveolar spaces, alveolar spaces collapse, no blood flow to the alveolar tissues due to pulmonary embolism, loss of pulmonary tissue due to emphysema, trauma, fibrosis.
Build-up of fluid in the lung is responsible for the development of pulmonary oedema and it leads to shortness of breathing. Pulmonary oedema mainly occurs due to augmentation of the hydrostatic pressure in the pulmonary capillaries mainly due to the left ventricular failure. Due to this oedema, it become difficult for the lung to expand and perform optimum function of breathing (Murray, 2011). In respiratory failure, there is also occurrence of thickening of alveolar membrane and fluid guild up in alveolar membrane which can lead to impaired gaseous exchange due to pneumonia. It is evident that in Mr. A also suffered through pneumonia. Impaired gaseous exchange lead to chronic hypoxia and it lead to augmentation of red blood cells which is called as erythrocytosis.
Impaired gaseous exchange lead to accumulation of carbon dioxide in the arterial blood. Carbon dioxide accumulation results in the increase in amount of carbonic acid in the tissues. It results in the respiratory acidosis. Renal system play role to compensate increased carbonic acid by retaining bicarbonate ion. Reduced oxygenation of the arterial blood lead to breathing through carotid bodies and results in dyspnea (Kacmarek et al., 2016).
Patients like Mr. A respond to hypoxaemia by breathing at the faster rate which is called as tachypnea. Tachypnea lead to minute ventilation, increase in PaO2 and decrease in the PaCO2. Parts of the lung which are ventilated but not perfused are called as dead spaces. During tachypnea, these dead spaces can be fixed. In cases on patients with abnormalities in the respiratory system, there can be increased load on breathing during tachypnea. Hypoxaemia can produce varied respiratory and cardiovascular problems. Chronic hypoxaemia can result in the right heart failure due to long duration existence of pulmonary resistance (Hinski, 2014). Diagnostic tests like ABG, chest X ray and complete blood count (CBC) need to be conducted in Mr. A. ABG results can be interpreted in terms of metabolic acidosis and respiratory alkalosis. Both these conditions occur mainly due to excessive minute ventilations.
Assessment and diagnosis include physical examination, vital signs, chest X-ray, ABG and pulmonary function test.
|
Assessment |
Rationale |
|
30 breaths per minute. Shallow breathing. |
These symptoms observed in patients with respiratory failure. Mr. A has tachypnoea and dyspnoea due to shortness of breath as a result there is declined lung capacity and difficulty in breathing (Kinkade & Long, 2016) |
|
ABG – Metabolic acidosis and respiratory alkalosis with probable respiratory compensation. PaO2 – 70 mmHg PaCO2 – 60 mmHg |
It occurs due to decrease in the oxygen saturation and increase in the carbon dioxide saturation. Lung starts breathing faster rate to compensate deficiency of oxygen. pH or acid content can be measured in this test which indicates oxygen and carbon dioxide level in blood (Byrne et al., 2014). |
|
Chest examination – Reduced AE with crackles. Auscultated coarse crackles observed at right lower lobe of his lung. |
Chest examination usually demonstrates inspiratory crackles and breathing sounds. Observed course crackles in him are louder and longer duration. It mainly occurs due to gas bubbles through the accumulated fluid due to pulmonary oedema (Ware, 2014) |
|
Chest radiography |
Chest radiography exhibits augmented interstitial markings due to intestinal lung disease. Acute alveolar damage and bilateral airspace infiltrates are evident in radiography. Bilateral airspace infiltrates reflect air space opacification which mainly occurs due to reduction in the lung parenchyma which results in the pulmonary vessels obstruction (Ware, 2014) |
|
Pulmonary function test FEV < 40 % ; FVC < 60 % ; FEV1 < 45% ; FEV1/FVC > 80% |
Pulmonary function testing using spirometry can be useful in identifying severity of respiratory system impairment. In respiratory failure, there can be obstruction for the inhaled and exhaled air due to blocking of airway due to pulmonary oedema. Forced expiratory volume (FEV) determines volume of air exhaled at the end first second after forced expiration. More than 80 % is considered as the normal value for FEV1. Forced vital capacity (FVC) determines the vital capacity after maximally forced expiratory effort. More than 80 % is considered as the normal value for FVC. FEV1/FVC determines percentage of FVC expired in one second. FEV1/FVC ratio less than 70 % considered as normal (Shiner & Steier, 2012) |
References:
Bausewein C & Simon ST. (2013). Shortness of breath and cough in patients in palliative care. Deutsches Ärzteblatt International, 110(33-34), pp. 563-71.
Byrne AL, Bennett M, Chatterji R, Symons R, Pace NL, & Thomas PS. (2014). Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology, 19(2), pp. 168-175.
Chiumello D. (2017). Acute Respiratory Distress Syndrome. Springer.
Hillman D, Singh B, McArdle N & Eastwood P. (2014). Relationships between ventilatory impairment, sleep hypoventilation and type 2 respiratory failure. Respirology, 19(8), pp. 1106-16.
Hinski ST. (2014). Respiratory Care Clinical Competency Lab Manual. Elsevier Health Sciences
Howard RS. (2016). Respiratory failure because of neuromuscular disease. Current Opinion in Neurology, 29(5), pp. 592-601.
Lamba TS, Sharara RS, Singh AC & Balaan M. (2016). Pathophysiology and Classification of Respiratory Failure. Critical Care Nursing Quarterly, 39(2), pp. 85-93.
Kacmarek RM, Stoller JK & Al Heuer. (2016). Egan’s Fundamentals of Respiratory Care. Elsevier Health Sciences.
Kinkade S & Long NA. (2016). Acute Bronchitis. American Family Physician, 94(7), pp. 560-565.
Matalon S & Sznajder JI. (2012). Acute Respiratory Distress Syndrome: Cellular and Molecular Mechanisms and Clinical Management. Springer Science & Business Media.
Murray JF. (2011). Pulmonary edema: pathophysiology and diagnosis. International Journal of Tuberculosis and Lung Disease, 15(2), pp. 155-60
Oana S & Mukherji J. (2014). Acute and chronic respiratory failure. Handbook of Clinical Neurology, 119, pp. 273-88.
Patadia, M.O., Murrill, L.L., Corey, J. (2014). Asthma: symptoms and presentation. Otolaryngologic Clinics of North America, 47(1), pp. 23-32.
Schneider J & Sweberg T. (2013). Acute respiratory failure. Critical Care Clinics, 29(2), pp. 167-83.
Shiner RJ & Steier J. (2012). Lung Function Tests Made Easy. Elsevier Health Sciences.
Vo P & Kharasch VS. (2014). Respiratory failure. Pediatrics in Review, 35(11), pp. 476-84.
Ware, LB. (2014). Acute Respiratory Distress Syndrome, An Issue of Clinics in Chest Medicine. Elsevier Health Sciences.
West JB. (2012). Respiratory Physiology: The Essentials. Lippincott Williams & Wilkins.
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