Cardiovascular Toxicity Dr. Peters (video) Flashcards
(30 cards)
CCBs – know subclasses and drugs in each
Non-dihydropyridine
-Benzothiazepines– Diltiazem
-Phenylalkylamines– Verapamil
Dihydropyridines
-Amlodipine
-Felodipine
-Nicardipine
-Nifedipine
What is the MOA of CCBs and what is the result?
reduction of contractility
ryanodine receptor stops -> Ca doesn’t get to the myocardium
Beta-receptors also stimulate ryanodine receptors (with AMP), so BB has a similar effect as CCB
What does the ryanodine receptor do?
stimulates further movement of Calcium from the sarcoplasmic reticulum to the muscles (skeletal, smooth muscles) -> Ca binds to actin -> muscle contractility
What are the signs and symptoms of CCBs, BBs and both?
CCB:
-Hyperglycemia !!
-metabolic acidosis (bc we block the pyruvate pathway, pyruvate is then converted to lactate)
-pulmonary edema
-ileus
BB:
-Hypoglycemia !!
-Bronchospasm (if non-selective)
both:
-Hypotension
-bradycardia
-arrhythmia
-cardiogenic shock
-AMS
What are the variety of therapies for beta-blockers and CCB toxicities?
-Calcium
-Epinephrine
-Glucagon
-Insulin
Calcium chloride or gluconate – how does it work for these toxicities?
1st line for CCB and BB toxicity (bc both work on Ryanodine receptor
Why is calcium gluconate usually preferred?
causes less necrosis
Atropine – what’s the MOA?
blocks parasympathetic activity to increase heart rate
Vasodilatory shock is better treated with what agent?
Vasopressor therapy
Norepinephrine (more peripheral vasculature vasopressor activity)
What is better for cardiogenic shock?
Vasopressor therapy
Epinephrine
hits both alpha and ß-receptors
more inotropy than NE
What are the adverse effects that limit use of Glucagon?
may increase inotropy and chronotropy
-significant N/V
-need antiemetic (ondansetron and PRN) bc they could aspirate (unprotected airway)
How does Insulin work in CCB and BB overdose?
may increase inotropy and chronotropy
What is the proposed MOA of Insulin for use?
assisting with calcium processing to positively affect contractility and cardiac output without significant impact on BP
How do we prevent hypoglycemia and hypokalemia when using Insulin?
insulin causes K+ shift: get baseline and replenish if needed
get glucose level: if <200 give 25-50g of D50
Why do you concentrate the dextrose in these patients?
so you can give less volume and avoid volume overload
consider concentrating to D50-70 to avoid pulmonary edema
What needs to be monitored with HDIET?
blood glucose every 10-15 min, until stable then hourly (with CCB toxicity may not need insulin bc hyperglycemia)
monitor serum BMP every 2-6hr
maintain
K+ at >2.8 meq/L
Ca2+ at >1.5-2xULN
What is lipid sink therapy and how does it work?
lipids will emulsify the drug and sequester it away
Where is the lipid sink therapy best used in overdose?
works well with lipophilic drugs like propranolol
Hemodialysis – what kinds of drugs are best treated with this modality? (lipid sink therapy)
with overdose of a more hydrophilic drug like atenolol go with hemodialysis, also beneficial with amlodipine
What is the biggest concern for patients with CCB and BB overdose?
contractility
bc of blocking the Ryanodine receptors -> no release of Ca from the sarcoplasmic reticulum to activate the myocardium
What does Digoxin work on within the cardiac membrane?
blocks the Na/K ATP pase
-the Na/Ca starts working instead
(delayed after depolarization leading to variable baseline phase 4)
(leading to re-entrant dysrhythmias)
What is the primary effects of digoxin toxicity?
AV nodal conduction abnormalities -> results in bradycardia (slow HR)
How do serum potassium levels impact patient outcomes of Digoxin toxicity?
it predicts mortality
K <5 = 2%
K: 5-6.4 = 35% mortality
K: >6.4 = 90% mortality
What is the level where Digoxin toxicity can occur?
> 1 ng/ml (therapeutic range is 0.5 - 2 ng/ml)
