4N.U.R.S.E.S.
Adverse Reactions: Digoxin
For lack of anything sexed up, I thought I'd present something more meat 'n' potatoes; i.e., mnemonics. I make these things all the time, its how I study, so if you find them tedious, well, go ahead and post something else.
The adverse reactions of digoxin are few, but made a good mnemonic. Digibind is the antidote to digoxin; so if your adverse reactions are severe, or your serum dig levels are high, not only may Digibind be indicated, but you may see DIGIBIND:
- D-delirium/depression/dizziness
- I-intestinal upsets: anorexia/diarrhea (and N/V vide infra)
- G-green vision
- I-impared platelets i.e., thrombocytopenia (rare)
- B-bradycardia, blocks 1st, 2nd, 3rd degree
- I-irregular HR: including palpitations, sinus arrhythmia to sinus arrest, ventricular ectopy, and even paradoxical tachycardia
- N-nausea and vomiting
- D-dermatological rash
So remember DIGIBIND; anecdotally, I remember an old, old woman presenting with Dig Toxicity who was tachycardic in the 110-20 range with a summation gallop. This woman was delirious on top of her dementia, with anorexia, GI distress, and curiously tremors, not related to temperature. I believe she did end up receiving digibind. Any body have any information on the summation gallop or its etiology?
Your Colleague,
Christopher.
More Museful Mnemonics
Hello everybody. I really do love mnemonics, so here's a new one for all of us studying for PCCN certification. What is the best, but most underprescribed, class of drugs for heart failure?? ACE inhibitors of course. According to Woods et al. in their Cardiac Nursing Textbook, "These agents are the only drugs used in the treatment of chronic HF that have been shown both to improve symptoms and prolong life." To this day, I cannot understand why my grandmother, the typical class III CHFer, has not been taking these drugs; she and others like her should take them like vitamins. Rather, these patients are simply prescribed more and more diuretics, with more and more renal impairment. So any way, if you can remember
PACE for ACE inhibitor, then you've got a good start.
For the species of the ACE inhibitor family:
PACE - P-Prinivil/Zestril = lisinopril
- A-Accupril = quinapril
- C-captopril = Capoten
- E-enalapril = Vasotec
For the pharmacology of the class:
PACE - P-preload decrease by venodilation; or potassium levels up (both total body and circulating levels)
- A-afterload decrease by blocked angiotensin II
- C-circulation of catecholamines down; or complexity and frequency of of ventricular arrhythmias down
- E-enuresis (i.e., diuresis) by decreased aldosterone
For the adverse reactions:
PACE INH-ibitor
- P-potassium levels high
- A-angioedema/aches (musculoskeletal)
- C-cough/congenital malformations (esp. in 1st trimester)
- E-elevated BUN/Creatinine
- I-insufficiency, renal
- N-neutropenia/nausea & vomiting
- H-hypotension/hepatotoxicity
Ta for now,
Christopher.
pharmacological fancy
How do you describe the coagulation cascade and anticoagulants to a non-medical Buffalonian? Well here's an amusing example:
Conceive an ice floe being carried down the Niagara; you see, clot coagulation is like ice condensation and confluence, and Coumadin and Heparin would then be two ways of preventing icebergs from being projected over the falls, which we may liken to a lesion, hemorrhaging or otherwise. Now, Coumadin indirectly prolongs coagulation time by deforming some vitamin K dependent clotting factors, which would be very like changing the crystic chemical compositon of the great Niagara by adding a saline substance in order to delay freezing; while, on the other hand, Heparin directly intercedes and dams off the coagulation cascade, much like lowering the ice boom in October to obstruct the brash from further navigation down stream. In other words, while Coumadin is slowly but surely modifying the chemical components (vitamin K) of the coagulation cascade, Heparin immediately stands between prothrombin and thrombin. Heparin is easily likened to reason, which would intercede for most when the urge to precipitate oneself by barrel over the falls swelled up (i.e., interceding before I thro[w]m[y]bin-over-the-falls). Further, in order for Coumadin=s powers to take effect, at least six hours and rather several days must pass until those clotting factors, which the drug is involved in the denaturation of, replace the original, unadulterated clotting factors, at which time Heparin will not be necessary.
Until the next,
Your most serious colleague,
Christopher.
Update after Long Lapse
I know some of you continue to stop in occasionally for the news; so you no longer have to be disappointed about not having any. The FTP server, which I spoke of before is indefinitely delayed because I don't have the tech savvy as of yet to carry through all the configurations, despite the almost universal declaration of the simplicity of the endeavour. In other matters, much enthusiasm and care has been aroused by the recent interest on our unit around the PCCN certification. While I didn't attend the review courses, I well understand the pride that this accreditation will bring us. Good luck probationers.
Here is a mnemonic I discovered in my studies of the pathogenesis of atherosclerotic lesions, for some of the most common risk factors thereto. Now you will easily incoporate these risk factors into your patient education.
"C-A-D-D-I-S-H" can stand for the risk factors for CAD or, in general, atherosclerosis.
Historical note: caddish means "of or like a cad; dishonorable; or ungentlemanly." This word comes out of the 18th century for an "ill-bred man, esp. one who behaves in a dishonorable or irresponsible way toward women."
- C-hyper-Cholesterolemia (generally dyslipidemia)
- A-Age
- D-Decreased activity
- D-Diabetes mellitus
- I-Infection (esp., chlymidia pneumoniae)
- S-Smoking
- H-Hypertension
More later, now parting, your colleague,
Christopher
