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PHM 702- Toxicology > BB and CCB Toxicity > Flashcards

BB and CCB Toxicity Flashcards

1
Q

Clinical manifestation of BB toxicity

A

hypotension
bradycardia
dysrhythmias (prolonged QRS and QTc intervals)
hypoglycemia
seizures
respiratory depression and apnea
coma

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2
Q

Clinical manifestation of CCB toxicity: what are the hallmark symptoms

A

hypotension and bradycardia, hyperglycemia

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3
Q

Clinical manifestation of CCB toxicity: lack of perfusion to the CNS can cause what?

A

Fatigue, dizziness, lightheadedness

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4
Q

A severe CCB OD can cause what?

A

Syncope, coma, sudden death, ARDS

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5
Q

Diagnostic tests for BB and CCB toxicity

A

12-lead ECG
Continuous cardiac and hemodynamic monitoring
Chest x-ray and oxygen saturation
BMP with serum glucose, magnesium, calcium
Digoxin level (to rule out digoxin toxicity)
Thyroid function tests
Cardiac enzymes
Lactate

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6
Q

BB and CCB OD treatment: GI decontamination treatment options

A

AC, MDAC, gastric lavage, WBI

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7
Q

What GI decontamination technique should you use for patients who OD’ed on SR CCBs and beta-blockers?

A

AC

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8
Q

What should you do to patients who OD’ed on CCBs or BBs before administering AC?

A

Protect their airway to prevent aspiration!

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9
Q

BB and CCB OD treatment: if the patient is hypotensive

A

Any crystalloid fluid 10-20ml/kg, repeat PRN

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10
Q

What kinds of BB and CCB OD patients won’t respond to IV crystalloids?

A

Patients who are severely poisoned

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11
Q

BB and CCB OD treatment: bradycardia

A

Atropine 0.5-1mg IV push q2-3mins, MDD 3mg

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12
Q

What kinds of BB and CCB OD patients won’t respond to atropine?

A

Patients who are severely poisoned

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13
Q

BB and CCB OD treatment: calcium

A

Calcium chloride 10% 10-20ml, or calcium gluconate 30-60ml over 10 minutes administered q10min x2 doses, then q20-60min PRN

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14
Q

What is the purpose of administering calcium in a CCB or BB OD and what are the effects?

A

Increase extracellular calcium → improves hypotension, reverses negative inotropy, and impaired conduction

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15
Q

When to NOT give calcium in CCB or BB OD treatment and what it can cause if you do

A

If digoxin toxicity is also suspected; it can cause stone heart phenomenon

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16
Q

When to administer calcium first

A

CCB OD

(can give glucagon after if it fails)

17
Q

When to administer glucagon first

A

BB OD

(can give calcium after if it fails)

18
Q

BB and CCB OD treatment: glucagon

A

3-5mg IV over 1-2 minutes, may repeat with 4-10mg after 5 minutes with no improvement in hemodynamics

19
Q

What is the purpose of administering glucagon in a CCB or BB OD and what are the effects?

A

Has inotropic and chronotropic effects; is able to bypass beta-adrenergic receptors and activates adenylate cyclase in myocardium

20
Q

When can glucagon infusions be considered?

A

If an effect is achieved with glucagon administration

21
Q

Reason glucagon infusions aren’t used often

A

ADEs

22
Q

ADEs of glucagon infusion

A

vomiting, hyperglycemia

23
Q

If you decide to proceed with a glucagon drip, what dose do you start with?

A

The starting rate is based on the dose the patient responded to

24
Q

What ADE is expected with glucagon infusions and what do you have to do to manage the patient’s hemodynamics?

A

Tachyphylaxis is expected; you may need higher doses or other interventions

25
Q

When to use IV lipid emulsion in a CCB or BB OD

A

If all other treatments fail

26
Q

Cornerstone of CCB and BB OD treatment

A

HDI

27
Q

Downside of HDI

A

It has a delayed onset of action of 15-40 minutes

28
Q

What do you give while you wait for HDI to start working?

A

The other treatments (calcium, glucagon, crystalloid fluids, atropine, etc.)

29
Q

MoA of HDI

A

impairs sodium-calcium antiporter resulting in an increase of intracellular calcium → increases calcium in the sarcoplasmic reticulum → increases cardiac contractility

30
Q

Bolus dose of HDI

A

1 unit/kg IV push with 0.5mg/kg of dextrose unless blood glucose is greater than 300mg/dl

31
Q

Continuous infusion dose of HDI

A

1 unit/kg/hr titrated to effect in combination with dextrose infusion at 0.5g/kg/hr

32
Q

Monitoring for HDI

A

BG q30min for first 4 hours, and then q hour after

33
Q

More frequent monitoring of BG when using HDI is necessary in what disease state?

A

Renal failure

34
Q

ADEs of HDI

A

hypoglycemia, hypokalemia

35
Q

Adjunctive hemodynamic support in a CCB or BB OD

A

Inotropes and vasopressors
Cardiac pacing
Intraaortic balloon pump
Extracorporeal membrane oxygenation

PHM 702- Toxicology (12 decks)

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