With effective treatment, signs of venous excess (e.g., HJR, NVD) regress. Breathing becomes less labored and skin color normalizes. Jon's heartbeat slowed and the gallop rhythm disappeared. However, diuretics may have serious side effects. For postural hypertension, check for dizziness, weakness, and dropping blood pressure (e.g., greater than 15 mmHg systolic) upon sitting up or standing. To detect irregular beats, count the pulse. Serum electrolytes, muscle cramps, and weakness are found with electrolyte wasting.
Some might elect to use an angiotensin-converting enzyme (ACE) inhibitor in the situation where there is moderate hypertension and a need to block the renin angiotensin cascade which will be triggered with improvement and resultant decreased renal perfusion.
Digoxin improves heart contractility and slows the rate. Both these actions work to increase cardiac output. Because of the need to achieve prompt relief, Jon was given a loading dose followed by a daily replacement dose. Following the loading of digoxin, an ECG would reflect the effects of digoxin. Digoxin may be associated with nonspecific ECG changes (e.g., ST segment depression, shorten QT interval). Its antiarrhythmic action is to slow conduction through the AV node. These properties correlate poorly with the serum concentration. For CHF, a serum concentration of 0.5 to 2.0 ng/mL has been accepted as the therapeutic target; however, a normal serum level may be therapeutic or toxic in a patient, depending upon electrolyte balance (especially potassium and magnesium) and hypoxia. In Jon, serum levels can serve as a guide to a subtherapeutic response or possible toxicity, but clinical judgment is the most essential guide to rational drug therapy.
Digoxin toxicities are multiple and appear insidiously or dramatically. Digoxin can cause all types of arrhythmias because it irritates the atria and ventricles. and blocks the SA/AV nodes. Any time a patient taking digoxin complains of a disturbing symptom, the drug should be considered as a possible iatrogenic agent. A complete cardiac examination (especially noting bradycardia, arrhythmias), an ECG. serum electrolytes and serum digoxin concentration should be evaluated and the digoxin should be withheld pending test results. A serum concentration of digoxin that is within the usual therapeutic range does not exclude digoxin-induced toxicity. Digoxin can also affect the central nervous system (e.g., irritability, confusion. lethargy, headache, yellow-green or halo vision) and the gastrointestinal tract (e.g., anorexia, nausea, vomiting, diarrhea).
In summary, the clinical evaluation of Jon involves improvement of the signs and symptoms caused by the congestive heart failure. The patient should be less dyspneic and less cyanotic. As cardiac pumping action improves, abnormal lungs sounds (e.g., crackles and wheezes) should resolve. On chest x-ray, the cardiac silhouette should decrease, as will hilar vascular markings (see Figure 11.12b). Jon should be able to sleep in a lying position without pillows. Due to the action of the diuretic, hepatojugular reflux and neck vein distention should disappear. The pulse should slow and be checked regularly for changes in rate and rhythm that might reflect digoxin toxicity. Also, with serial cardiac auscultation, the third heart sound (S3) may eventually be inaudible. Over time the ECG should show digoxin effects and resolution of ventricular hypertrophy.
