Drugs that don't fit in the Vaughn-Williams classification system Flashcards
Nifedipine
Drug class
Use
Blocks L-type Calcium channels
but not used for dysrhythmias
Use: Hypertension, angina
Ziconotide
Pros
treats severe, chronic pain
No significant respiratory depression or loss of motor coordination
No euphoria associated with opioid analgesics
No development of tolerance
No withdrawal symptoms
Not addictive
Ziconotide
Cons
-intrathecal delivery
narrow therapeutic window
severe but reversible psychiatric symptoms - cognitive impairment, hallucinations, changes in mood+consciousness
Digoxin groups and what they’re like
- Aglycone group - determines pharmacodynamic properties
- Lactone group - intermediate solubility
- steroid nucleus - lipid soluble
- sugar resides: water soluble and determine pharamacokinetic properties
How digoxin works
Blocks Na+/K+ ATPase
-positive inotropic effect i.e. ↑Heart rate
Digoxin for whom and how it may help
Patients in sinus rhythm that remain symptomatic despite taking an ACE inhibitor and a diuretic
- ↑exercise tolerance
- helps symptoms
- ↓need for hospitalisation
Digoxin effects on cardiac rate and rhythm
at therapeutic doses
↑vagus nerve activity:
- Slows SA node firing rate
- Slows AV node conduction velocity
- improves filling and pumping
Digoxin effects on cardiac rate and rhythm at toxic doses
Dysrhymias
↑sympathetic tone
Inhibition of Na+/K+ ATPase causes membrane to be closer to threshold for depolarisation, so more APs firing, more ectopic beats and more after-depolarisations
Signs of digoxin toxicity
Nausea and vomiting
sight disturbances
ventricular tachyarrhythmias
Treatment of digoxin toxicity
4 steps
- Stop digoxin
- Correct hypokalaemia via giving KCl and/or NaCl or KCl and glucose IV infusion
- Propranolol or phenytoin to control arrhymias
- digoxin-specific antibody fragments IV infusion
Uses of adenosine
suppression of:
- PSVT
- Ventricular tachycardia associated with Wolff-Parkinson-White syndrome
- supraventricular tachyarrthymias that may occur during general anaesthesia
Adenosine method of actions
Activates (GPCR) A1-purinoceptors on cardiac myocytes
-oepns K+Ach channel causing hyperpolarisation
This inhibits VSCC from opening so ↓AP duration, ↓slope of pacemaker potentials
-lower discharge rate of SA node
-lower conduction
-↑refractory period in AV note
decreased excitability
Physiochemical properties of Adenosine
purine nucleoside (+neurotransmitter) half life= 10 secs hence not oral effects of rapid bolus dose last 20-30 secs Rapid uptake and metabolism by RBCs-beneficial for treatment of SVT
Adenosine unwanted effects
when to avoid
- Bradycardia - hence avoid in sick sinus syndrome and heart block
- facial flushing
- chest pain
- bronchoconstriction - avoid in asthma