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39 Cards in this Set

  • Front
  • Back
Which 3 cardiac drugs account for the majority of fatalities?
Digoxin
Verapamil
Propranolol
What is the plant form of digitalis called?
Digitalis purpurea
Foxglove
What are digoxins therapeutic effects?
1 - Increased force of myocardial contraction (useful in CHF)
2 - Decreased AV conduction (useful in AFib)
How does digoxin increase the force of myocardial contraction?
Inhibition of Na/K ATPase causing an increase in intracellular Na and Ca and extracellular K.
Why does K rise in digoxin toxicity?
The Na-K ATPase pump is paralyzed and K cannot be transported intracellularly.
What effect does digoxin have on the SA node?
Therapeutic - increased vagal tone, decreased HR
Toxic - can stop SA node conduction and decreases sympathetic sensitivity
What effect does digoxin have on Purkinje fibers?
Results in increased PVC's
1 - decreased resting potential causing slowed phase 0 depolarization
2 - decreased action potential duration
3 - enhanced automaticity  due to increased phase 4 repolarization
What dysrhythmia do digoxin toxic patients characteristically present with? (Rosen Box 150-1)
Digoxin toxicity con produce virtually any tachyarrhthmia, bradyarrhythmia or conduction block.
More specific ones include: 
-AFib with a slow ventricular rate (AV dissociation)
-Junctional tachycardia (rate 70-130)
-Atrial tachycardia with block (atrial rate 150-200)
-Bidirectional VTach
List factors that put a patient at increased risk of digoxin toxicity (Rosen Box 150-2)
Elderly women
Dumb chemistry
-Electrolyte abnormalities (K/Mg/Ca)
-Alkalosis
Disease
-Hypothyroidism
-Cardiac disease
-Renal insufficiency
Drugs
-Sympathomimetics
-Other cardiac drugs (BB/CCB/TCA/Amiodarone/Captopril)
What are the noncardiac symptoms of digitalis intoxication? (Rosen Box 150-3)
General - weakness, fatigue, malaise
GI - N/V/D/Abd pain
Opthalmic - snowy vision, photophobia, chromatopsia, amblyopia, diplopia
Neurologic - Dizzy, HA, delirium, hallucinations, psychosis, somnolence, paresthesias, aphasia, seizures
Contrast chronic and acute digitalis intoxication
Mortality - chronic higher
Potassium - chronic low-normal, acute normal-high
Dysrhythmia - chronic ventricular, acute brady/blocks
Age - chronic elderly, acute younger
Need for Fab - more often in chronic
Underlying disease - chronic likely, acute less likely
What correlates best with digoxin toxicity?
The steady-state digoxin level (6-8 hours post po ingestion). Levels drawn earlier will read falsely high.
Are activated charcoal, gastric lavage or whole bowel irrigation indicated for acute digoxin OD?
No. There is a good antidote and no proven efficacy of these therapies. Because of significant entero-hepatic circulation this was once thought to be useful, but Digibind is now widely available.
How should hypokalemia be treated in digoxin intoxication?
Acute ingestion - do NOT replace K. It will rise as the Na/K ATPase is blocked
Chronic ingestion - replace K. Oral replacement is safer than IV.
What is stone heart syndrome?
A syndrome described in case studies where giving calcium to a hyperkalemic digoxin OD patient caused their heart to stop. There is poor evidence for this phenomenom. It is reasonable to give Calcium to hyperK digoxin OD patients.
Should hypomagnesemia be corrected in digoxin OD?
Maybe. Consider especially in tachydysrhythmias if significant HypoMg but give slowly (2g over 30 minutes). 
HyperMg can exacerbate toxicity and is a negative inotrope and slows AV conduction.
Should atropine be used in digoxin intoxication?
Worth a shot in brady-arrhythmias
How should a bradycardic patient with digoxin toxicity be paced?
TV pacing has been found to induce tachydysrhythmias. Rosen's advices temporizing with external pacing until Fab takes effect.
Should carotid massage be used to treat digoxin toxicity?
Rosen's says you'll make them go bradycardic or kill them if you try this.
How should a tachydysrhythmia in digatalis toxicity be treated?
Digibind +/- dilantin or lidocaine.
What is Digibind/Fab?
It contains digitalis antibodies derived from sheep immunized with digoxin.
When is Digibind indicated and how fast will it work?
It is indicated in for hyperkalemia (>5.5) and/or hemodynamic compromise related to heart block or dysrhythmia.
Time to onset is 19 minutes with complete resolution taking hours.
What is the dose of Digibind?
Use the formula on the package insert.
1 - empirical - history, symptoms, life threat --> 10 vials over 30 minutes. Cardiac arrest - 20 vials IV bolus.
2 - calculate - for each 1mg of digoxin ingested give 2 vials (78mg)
3 - calculate - base dose on the steady-state serum digoxin level after 6-8 hours
How do BB work?
They competitively inhibit endogonous beta-adrenergic agents at the beta receptor preventing cAMP formation.
What are beta1 effects?
Inotropy (contraction), dromotropy (conduction) & chronotropy (heart rate).
What are beta2 effects
Vascular - vasodilation
Hepatic - glycogenolysis, gluconeogenesis
Lung - bronchodilation
Adipose - FA release
Uterus - relaxation
What are the relevant pharmacodynamics of BBs?
D - Vd >1 (more in tissue than serum, hard to dialyze)
What are the symptoms of BB OD? (Rosen Box 150-8)
Cardiovascular
-Bradycardia (SA and AV node function depressed, QRS widens)
-Hypotension
-VT/VF
Respiratory
-Respiratory insufficiency
-Bronchospasm (uncommon)
Neurological
-Unsconsciousness
-Seizures (only propranolol)
-Hypoglycemia (more common in children)
Are activated charcoal, gastric lavage or whole bowel irrigation indicated for BB/CCB OD?
Worth a try
-Activated charcoal, multidose if enterohepatic circulation (unproven)
-Gastric lavage or whole bowel irrigation are equally unproven but can be considered
How should BB OD be treated?
-IV fluids for hypotension
-Trial of atropine for bradycardia
-Trial of Glucagon for hypotension (50mcg/kg IV loading dose then 1-10mg/h IV infusion)
-Sodium bicarbonate for QRS widening (slow push)
-High dose insulin (0.5-1U/kg/h) for hypotension with titrated dextrose infusion
-Pressors for hypotension - no consensus, but I'd start high and titrate rapidly with epi (10-50mcg/m
-Trial of calcium (1-2g over 5-10 minutes
-Pacing
-Consider intralipid
-Consider hemodialysis
-Consider balloon-pump
-Consider ECMO
How does glucagon work in a BB/CCB OD?
It is able to bypass the B-blocker receptor to activate cAMP
CCB's have an effect downstream from cAMP so it's unclear how it would work in these cases. However, there is some evidence that it does.
How does high-dose insulin therapy work in BB/CCB OD?
Somehow, it increases inotropy by getting glucose into the cell while improving tissue perfusion and coronary blood flow
How do CCB work?
By blocking the slow calcium channels in the myocardium and vascular smooth muscle they affect the heart and vasculature.
Heart - decreased contractility, depressed SA activity, decreased AV conduction
Vasculature - coronary and peripheral vasodilation
How are CCB classified?
Dihydropyridine - more vasculature, less heart (amlodipine, felodipine, nifedipine)
Nondihydropyridine - more heart, less vasculature (verapamil & diltiazam)
What are the relevant pharmacodynamics of CCBs?
A - slower absorption of SR preparations
D - Vd generally >1 so hemodialysis is not very effective. ++ protein binding
What are the symptoms of CCB OD? (Rosens Box 150-10)
Cardio - hypotension, bradycardia, sinus arrest, AV block, AV dissociation, junctional rhythm, asystole
Pulmonary - respiratory depression, pulmonary edema, ARDS
Gastrointestinal - N/V, bowel infaction - rare
Neurologic - lethargy, confusion, slurred speech, stroke/seizure - rare
Metabolic - lactic acidosis, hyperglycemia, hyperkalemia
Dermatologic - flushing, diaphoresis, pallor, cyanosis
How should a CCB OD be treated?
-IV fluids for hypotension
-Calcium for blockade - give 10-20mL of 10% CaCl3 slow push over 5-10 minutes then 5-10mL/h infusion (bring no higher than 14mg/dL as this is severe hypercalcemia)
-Atropine for bradycardia
-High dose catecholamine - high and rapidly titrated epinephrine or isoproterenol
-High dose insulin/glucose (0.5-1U/kg/h) for hypotension with titrated dextrose infusion
-Glucagon (50mcg/kg IV loading dose then 1-10mg/h IV infusion)
-Pacing
-Consider intralipid
-Consider dialysis
-Consider balloon pump
-Consider ECMO
In what situation can iatrogenic methemoglobinemia occur?
Patients with glucose-6-phosphate dehydrogenase deficiency can get this complication when exposed to nitrites. Their blood looks chocolate brown and skin looks blue (although they are clinically okay)
What is the treatment for methemoglobinemia?
IV methylene blue - usually only needed if methemoglobin approaches 30% or patient is symptomatic.