The nurse identifies an electrolyte imbalance, an elevated pulse rate, and a weight gain of 4.4 lbs (2 kg) in 24 hours for a client with chronic kidney disease. Which intervention should the nurse include in the plan of care?

Heart failure in older adults involves the heart’s inability to maintain cardiac output, leading to pulmonary and systemic venous congestion. When the left ventricle fails, fluid backs up into the lungs, causing interstitial edema and crackles. This shift in fluid dynamics results in impaired gas exchange and orthopnea, necessitating immediate repositioning and pharmacological intervention to reduce preload and improve respiratory efficiency.

Rationale:

A. Administering the prescribed furosemide is a vital pharmacological intervention to treat the underlying fluid overload. As a loop diuretic, it inhibits sodium reabsorption, causing rapid diuresis that reduces circulatory volume and pulmonary congestion. This action directly addresses the cause of the crackles and pedal edema by shifting fluid out of the tissues.

B. Raising the head of the bed to the Fowler’s position is the initial priority to alleviate orthopnea. This position allows the abdominal contents to move downward, reducing pressure on the diaphragmatic muscle and increasing thoracic capacity. By optimizing lung expansion, the nurse provides immediate, non-invasive relief to the patient’s respiratory distress before other interventions.

C. Providing oxygen per nasal cannula addresses the hypoxemia indicated by the saturation of 93%. Supplemental oxygen increases the concentration of oxygen in the alveoli, facilitating better diffusion across the fluid-filled membranes of the lungs. Correcting the oxygen deficit is a critical secondary step to prevent myocardial strain and cellular hypoxia in the elderly client.

D. Monitoring urinary output is the final step used to evaluate the effectiveness of the diuretic therapy. The nurse must track the volume and concentration of urine to ensure the kidneys are responding to the medication and that fluid balance is being restored. This assessment provides the objective data needed to guide further treatment and ensure patient safety.

Brief introduction:

Electroconvulsive therapy induces a controlled generalized seizure to modulate neurotransmitter sensitivity and neuroplasticity. The procedure triggers a profound autonomic surge, causing transient hypertension and tachycardia, which necessitates careful screening for physiological vulnerabilities to prevent cerebral herniation or myocardial infarction during the induced convulsion.

Rationale:

A. Severe pulmonary disease is a contraindication because the procedure requires general anesthesia and neuromuscular blockade. Patients with compromised lung function are at high risk for prolonged apnea or respiratory failure when given succinylcholine, as they cannot maintain adequate arterial oxygenation during the post-ictal period.

B. A history of migraine headaches is not a contraindication for receiving this neurostimulation treatment. While patients may experience a post-procedure headache due to the seizure activity, this is a manageable side effect that does not pose a structural risk to the brain or interfere with the therapy.

C. Cardiovascular disease poses a significant risk due to the hemodynamic stress of the procedure. The initial parasympathetic bradycardia followed by sympathetic-mediated tachycardia and hypertension can precipitate cardiac arrhythmias or ischemia in patients with unstable angina, valvular defects, or poorly controlled congestive heart failure.

D. A personality disorder is a psychiatric diagnosis that may coexist with depression but does not impact physiological safety. While ECT is specifically indicated for major depression, the presence of a personality disorder does not present any biochemical contraindications or physical dangers related to the electrical stimulus.

E. A history of recent stroke is a critical contraindication because it suggests vascular fragility and altered intracranial pressure. The seizure-induced increase in cerebral blood flow can lead to hemorrhage or secondary injury in brain tissue that has not yet healed from a recent ischemic event.