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I need to create a scenario in cardiac clinical setting with a patient deterioration with cardiac and respiratory issues and effectively managing it. I will provide an excellent example. can even use the same study in a different way so its not similar to avoid plagiarism. Its my colleague’s I borrowed . We do the same course.
Critical Care Essentials Assignment CAS II
A. Brief clinical history of patient
Patient X is a 99 year-old female who has been in hospital for 2 weeks. Initial presentation to the ward was for increased shortness of breath and decreased exercise tolerance with no associated chest pain. She was diagnosed with bronchiectasis and Type 2 respiratory failure. The patient has a relevant history of asthma, congestive cardiac failure (CCF) and she is a CO2 retainer. The patient was then admitted to the intensive care unit (ICU) for two episodes of acute pulmonary oedema (APO) and acute renal failure (ARF). During this time the patient had an episode of torsades de pointes. After treatment and continuous monitoring, she was well enough to return to the ward for on-going care. The patient had a resuscitation order for MET call measures only, and no CPR. On the ward, the patient became dyspnoeic and anxious after walking with the physiotherapist. On assessment, the patient was alert and orientated but slightly dizzy and very short of breath with visible accessory muscle use. Vital signs were obtained as follows: respiratory rate (RR) 37, oxygen saturation (SpO2) 86%, blood pressure (BP) 97/50, heart rate (HR) 120, and temperature (T) 37.5. There was an audible wheeze with breathing and the patient was on 2L oxygen via nasal specs. An ECG was performed which confirmed rapid atrial fibrillation (RAF). A MET call was done and arterial blood gas (ABG) was taken.
B. Arterial blood gas analysis
Normal arterial blood gas ranges:
pH 7.35-7.45
PaO2 80mmHg-100mmHg
PaCo2 35mmHg-45mmHg
HCO3 22mEq/L-26mEq/L
(Kramer 2009)
Arterial blood gas analysis flowchart:
Questions to ask Patient’s values Analysis
Is the pH acidic or alkalotic? 7.31 The patient’s pH is out of range and below the lower limit of 7.35, therefore the pH is acidic. (Casey 2013)Is the patient hypoxemic? Check PaO2 level 70.5mmHg The PaO2 level is below normal range of 80-100mmHg. This shows that she is hypoxemic because not enough oxygen is diffused into the blood. (Casey 2013)Is there a ventilation/perfusion (V/Q) mismatch?
Check PaCO2 level 57.5mmHg Yes, her PaCO2 is greater than the normal range, which shows a decreased ability to clear carbon dioxide from her blood via the lungs. (Casey 2013)What is the HCO3? 28.6mmHg The bicarbonate, a buffer produced by the kidneys, is greater than the normal range. However, this may be the case of intracellular protein buffers, which may raise the HCO3 slightly, as the renal buffer takes days to become effective. (Casey 2013)What is the driver of patient’s pH? Respiratory The driver of the patient’s acidosis is the respiratory system because the PaCO2 has increased. (Casey 2013)Is there compensation? What system is compensating? Yes, there is some compensation of the intracellular protein and hemoglobin. In order to buffer respiratory acidosis, the intracellular protein response and hemoglobin may help reduce the amount of CO2 in the plasma (Casey 2013)Are other values normal? Most of the critical values are normal.
C. Arterial blood gas interpretation (Appendix 1)
When patients deteriorate in an acute setting, the arterial blood gas (ABG) is one of the first investigations done because it provides a fundamental picture of the patient’s physiological status and what needs to be corrected for healthy function at cellular level (Rogers, Katherine & McCutcheon 2013). Despite the patient’s medical history of chronic respiratory failure and being a CO2 retainer, the arterial blood gas parameters should be within normal range when the patient is stable (McCabe & Wiggins 2010).
Initial ABG results show the patient is hypoxemic and in respiratory acidosis due to low arterial oxygen levels and hypercapnia, respectively. Some compensation is occurring via intracellular protein buffers that slightly increase the bicarbonate ions and the binding of CO2 molecules to hemoglobin to be excreted via the lungs (Casey 2013). The dyspnea she experiences is the compensatory effort to ‘blow off’ carbon dioxide carried by the hemoglobin. The kidneys’ buffer mechanism is a slow process of days, therefore it will not have had much effect on correcting the respiratory acidosis at time of deterioration (McCabe & Wiggins 2010).
With a background of congestive cardiac failure and recent acute pulmonary edema and bronchiectasis, the patient’s lung capacity for gas exchange is reduced even further, leading to acute on chronic exacerbation of COPD (Moore 2013). Therefore, in the events leading up to her deterioration the alveoli may have been compromised by fluid retention that ineffectively ventilate the air sacs for oxygen to be saturated into the alveolar capillaries and results in hypoxemia (Casey 2016). The pulse oximetry indicates a low oxygen saturation (SpO2) of 86% and is supported by the oxygen-hemoglobin dissociation curve where there is a shift to the left as PaO2 correlates to 70mmHg (Booker 2008), and the affinity of hemoglobin to bind with carbon dioxide molecules.
As the patient is already on 2L oxygen, this is the maximum FiO2 of 24% recommended to her due to her altered respiratory drive (Henderson 2008). Her breathing is now driven by the long-term retention of a higher amount of carbon dioxide in her system and a low oxygen level. This is called the hypoxic drive. If a sudden increase in oxygen were given, it may reduce her breathing, which further reduces carbon dioxide removal (Henderson 2008). Thus, oxygen therapy should be carefully titrated or considered before applying more. Some critical values to keep in mind are the potassium and sodium levels, which can further complicate patient status and lead to more fatal arrhythmias.
D. Rhythm strip template
What is the rate? Is it regular or irregular?
Is it fast or slow?
Is there a pattern?
Is there a P wave? Is it within normal parameters?
Is it inverted?
PR interval Is the PR interval normal?
Is there a QRS wave? Is it within normal parameters?
Is it inverted?
Is there a T wave? Is it within normal parameters?
Is it inverted?
Is the ST segment normal? Is there inversion or elevation?
What is the rhythm?
(Woodrow 2009)
E. Rhythm strip interpretation (Appendix 2)
What is the rate? 125 beats per minute
Is there a P wave? Some interference with the ECG makes it difficult to detect existing P waves but globally there is no P wave present.
PR interval Absence of P waves makes PR interval unpredictable.
Is there a QRS wave? Yes, there is a QRS wave that is within parameters of three small squares, and it is not inverted. It is a normal QRS wave.
Is there a T wave? Yes, there is a T wave. It is slightly peaked but within the normal limit of 5mm (one large square), and it is not inverted. This is a normal T wave.
Is the ST segment normal? A bit difficult to interpret due to interference, but the ST segment seems to fall at baseline with no inversion now elevation. This is normal.
What is the rhythm? With the absence of P waves and the irregularly fast heart rate, this rhythm is atrial fibrillation.
Acute rapid atrial fibrillation can be triggered by illness and risk factors of comorbidities such as pulmonary disease and congestive cardiac failure (Nottingham 2010). Patient X has this history and on top of the recent diagnosis of bronchiectasis, her heart has been overloaded and thus brings on this fast rhythm. Her low BP is due to the fast and irregular heart rate, which reduces ventricular blood filling and cardiac output (Nottingham 2010). This in turn decreases blood perfusion to the brain, which may cause dizziness.
F. Rationale for key treatment
The patient’s hypoxemia and rapid atrial fibrillation (RAF) were the main concerns to be treated. The RAF could have been a contributing factor to further decrease perfusion in the lungs, hence reducing oxygen molecule delivery (Casey 2013). Calming the patient and allowing her to rest with supplemental oxygen at 2L via nasal cannula helped reassure her. The patient’s oxygen was increased to 3L for a short period to maintain SpO2 at the acceptable minimum of 88%, then titrated back to 2L. This is consistent with the recommendations in Moore’s article where the oxygen is not a high concentration (>35%) and the safe range of oxygen saturation is 88%-92% for respiratory patients with a hypoxic drive (2013).
The patient was given intravenous digoxin to control the heart rate and bring it down to 60-100 beats per minute to increase time for ventricular filling (Arrigo, Bettex & Rudiger 2014). She was already on anticoagulant therapy, and this reduced her risk of a thrombus in her heart due to the inadequate pumping of the atria (Nottingham 2010). Another issue was hypotension. According to Arrigo, Bettex and Rudiger (2014), antiarrhythmic drugs have dilative effects on blood vessels which can exacerbate low blood pressure. A bolus dose of 250 mls of intravenous normal saline was given and she was consistently monitored for signs of fluid overload. The patient was also on telemetry to monitor heart rate and rhythm, and observations were increased to fifteen minutely.
In conjunction, nebulizers were given to the patient to help dilate her airways for better ventilation. Salbutamol was not considered as it would have exacerbated her palpitations, so ipratropium was given for its quick effect and lesser cardiovascular side effects (Nazir & Erbland 2009).
Appendix 1
Appendix 2
References
Arrigo, M, Bettex, D & Rudiger, A 2014, ‘Management of Atrial Fibrillation in Critically Ill Patients’, Critical Care Research and Practice, vol. 2014, p. 10.
Booker, R 2008, ‘Pulse oximetry…art & science clinical skills: 43 [corrected] [published erratum appears in NURS STAND 2009 Apr 1-7;23(30):33]’, Nursing Standard, vol. 22, no. 30, pp. 39-41.
Casey, G 2013, ‘Interpreting arterial blood gases’, Kai Tiaki Nursing New Zealand, vol. 19, no. 6, pp. 20-24.
Casey, G 2016, ‘COPD: obstructed lungs’, Kai Tiaki Nursing New Zealand, vol. 22, no. 5, pp. 20-24.
Henderson, Y 2008, ‘Delivering oxygen therapy to acutely breathless adults…clinical skills: 48 [corrected] [published erratum appears in NURS STAND 2008 Dec 3-Dec 9;23(13):33]’, Nursing Standard, vol. 22, no. 35, pp. 46-48.
Kramer, BJ 2009, ‘Arterial blood gases’, RN, vol. 72, no. 4, pp. 22-24.
McCabe, C & Wiggins, J 2010, ‘Differential diagnosis of respiratory diseases part 2’, Practice Nurse, vol. 40, no. 2, pp. 33-41.
Moore, D 2013, ‘Preventing acute hypercapnic respiratory failure in COPD patients’, Nursing Standard, vol. 27, no. 47, pp. 35-41.
Nazir, SA & Erbland, ML 2009, ‘Chronic obstructive pulmonary disease: an update on diagnosis and management issues in older adults’, Drugs & Aging, vol. 26, no. 10, pp. 813-831.
Nottingham, F 2010, ‘Diagnosis and treatment of atrial fibrillation in the acute care setting’, Journal of the American Academy of Nurse Practitioners, vol. 22, no. 6, pp. 280-287.
Rogers, A, Katherine, M & McCutcheon, K 2013, ‘Understanding arterial blood gases’, Journal of Perioperative Practice, vol. 23, no. 9, pp. 191-197.
Woodrow, P 2009, ‘An introduction to electrocardiogram interpretation: part 1’, Nursing Standard, vol. 24, no. 12, pp. 50-58.