03 Jun PR INTERVAL IS THE PR INTERVAL NORMAL?
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.
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