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CCFP-EM: Tox, Neuro > Tox: Cardiac Meds > Flashcards

Tox: Cardiac Meds Flashcards

1
Q

Non-cardiac SE of propranolol

A

Can cause delirium in absence of cardiovascular effects, seizures due to lipophilicity

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2
Q

Normal function of beta receptors

A

B1: Cardiac effects (inc HR, contractility, conduction), kidney (inc renin secretion), eyes (inc aqueous humor).

B2: Smooth muscle relaxation (esp lung)

B3: lipolysis in adipose tissue

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3
Q

Symptoms of beta blocker overdose

A

CVD: hypoTN, bradycardia, cardiogenic shock, QRS/QTc prolongation.
Pulm: resp depression, apnea, bronchospasm.
Neuro: AMS, coma, seizures w/ lipophilic agents (propranolol)
Endo: HYPERK, HYPOGLYCEMIA (not always, more likely in kids)

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4
Q

DDx for BB overdose

A

CCB, clonidine, dig toxicity

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5
Q

Tx of BB overdose

A

Decontam:

1) AC if within 1hr
2) Consider GL if presenting within 1hr after ingestion of large quantity of potentially lethal agents that lack effective antidote (e.g. verpamil, diltiazem, propranolol).
3) WBI: if large OD of modified release preparation and patent airway.

Additional Meds for brady/hypoTN:

1) Atropine 1mg IV if bradycardia (repeat up to 3mg)
2) Calcium gluconate: 3-6g
3) Glucagon 1-5mg IV push (max 15 mg)
4) High dose insulin R: 1U/kg IV bolus followed by infusion at 1U/kg/hr (with dextrose)
5) Lipid emulsion as last resort
6) Levophed prn

Non-pharma:
Cardiac pacing, intra-aortic balloon pump, ECMO if pharma fails

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6
Q

Specific additional treatment for propranolol

A

Sodium bicarb as can cause QRS widening due to Na channel blockade

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7
Q

Specific additional treatment for atenolol OD

A

Hemodialysis

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8
Q

Mxn of glucagon in BB/CCB OD

A

bypasses beta-adrenergic receptors to increase cAMP resulting in increased calcium influx into the cell (requires high doses, 5-10mg IV)

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9
Q

Mxn of CCB toxicity

A

Blockade of voltage gated Ca channels –> reduced Ca influx into cells.
In cardiac cells, decreased SA node activity, contractility and slowed AV conduction.

In smooth muscles (periph vasc) -> relaxation and vasodilation.

Panc beta cells –> reduced insulin release.

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10
Q

Agent specific toxicities for: verapamil, diltiazem, dihydropyridines (e.g. nifedipine)

A

Verapamil: Major effect at SA and AV nodes
Diltiazem: Intermediate activity at both cardiac and peripheral vasculature.
DHPs: Major effect on peripheral vasculature.

**Specificity between peripheral vs central cardiovascular effects may be lost in overdose.

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11
Q

Symptoms/exam findings CCB OD

A

CVD: hypoTN, bradycardia, cardiogenic shock. May see QRS widening, QTc prolongation.
Neuro: AMS, seizures, coma, respiratory depression.
Endo: HYPERglycemia.

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12
Q

How can BG levels aid in differentiating CCB and BB OD?

A

BB OD typically euglycemic, CCB OD usually hyperglycemic.

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13
Q

DDx CCB OD

A

BB, digoxin, clonidine OD

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14
Q

GI decontam options for CCB OD

A

GL: only if presenting within 1hr ingestion and lack of effective antidote (verapamil, dilt, propranolol).
AC: If within 1hr presentation and airway protected.
WBI: large overdose of SR preparation and protected airway.

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15
Q

Mgmt of bradycardia and hypoTN in CCB OD

A

Initial: atropine, vasopressors (e.g. levo, epi).
Calcium (inc intracellular Ca/contractility).
Glucagon (may be less successful than with BB toxicity).
High-dose insulin (to inc cardiac output, 1U/kg bolus, then 0.5U/kg infusion with dextrose)

Non-pharma: pacing, intra-aortic balloon pump, ECMO if pharma fails.

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16
Q

What is digoxin/purpose

A

Cardiac glycoside, derived from foxglove.
Used to increase the force of contraction in HFrEF and reduce AV conduction in AF.
Narrow therapeutic window

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17
Q

How is digoxin excreted

A

renally

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18
Q

MOA digoxin

A

inactivates Na/K ATPase on cardiac cell membrane -> increased intracellular Ca, extracellular K.
Increases automaticity.
Reduces conduction through AV node via increased vagal tone.

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19
Q

Compare acute vs chronic dig toxicity

A

Acute:
Severe Na/K ATPase pump inhibition –> hyperK (predictor of poor outcome w/o tx).

Chronic:
Caused by increase in dose or decreased GFR.
Hypokalemia may enhance chronic toxicity (tox at lower dig levels).
Higher overall mortality (generally sicker population at baseline).

20
Q

Symptoms of dig toxicity

A

Onset insidious if chronic.
CVD:
Acute –> more bradycardia, AV blocks.
Chronic –> ventricular dysrhythmias. Bidirectional VT, slow AF, almost any dysrhythmia other than SVT or TdP.
GI: n/v, AN.
Neuro: visual disturbance (scotoma, yellow halos around lights), HA, generalized weakness, AMS.

21
Q

What specific visual changes may be seen with dig toxicity?

A

Scotoma, yellow halos around lights.

22
Q

What ECG finding is fairly specific for cardiac glycoside toxicity (e.g. dig)?

A

Bidirectional VT

23
Q

Diagnosis of dig toxicity

A

Serum concentration may not correlate with symptoms and may take 4-6hrs to reach steady state in acute ingestion.
(so how to dx??)

24
Q

Tx of dig toxicity

A

Supportive.
Ok to use Ca++ if hyperK (previously thought not to).
Brady: atropine, pacing.
Tachydysrhythmias: cardioversion/defib may induce VF/VT. Phenytoin and lidocaine to be safest (phenytoin can increase AV conduction).
DigiFab if indicated.

25
Q

Indications for digoxin antibody

A 
Ventricular dysrhythmias. 
Hemodynamically significant bradycardia unresponsive to standard therapy. 
HyperK >5.5 assoc w/ toxic dig level or presumptive OD. 
Consider for: 
- Pacemaker (may mask dysrhythmia) 
- Dig level >10 in acute ingestion
- Dig level >4 chronic ingestion 
- Adult acute ingestion >10 mg
- Child acute ingestion >4 mg
26
Q

Potential side effects of digibind

A

withdrawal of dig effect (CHF, afib), hypokalemia

27
Q

Timing of onset of effect of digibind

A

~1hr

28
Q

How to give digibind

A

Acute empiric dosing = 10-20 vials.
Chronic adult = 2-4 vials.
Chronic children = 1-2 vials.
Known concentration: #vials = kgx{ng/mL/100]

Give over 30 min unless cardiac arrest in which case you give a bolus dose.

29
Q

How do you monitor dig levels after digibind is given?

A

You don’t. Assays cannot differentiate between free dig and dig that is bound to digifab.

30
Q

Potential complications of ACEi/ARB use

A

angioedema, nonproductive cough, renal insufficiency (from renal artery stenosis)

31
Q

MOA ACEi/ARB

A

ACEi: reduces formation of angiotensin II.
ARB: blocks the receptor for angiotensin II on blood vessels, heart, adrenal cortex.

Blockage of angiotensin II –> decreased aldosterone –> decreased Na/water retention, vasodilation.

32
Q

Symptoms of ACEi/ARB OD

A

mild hypotension, hyperK

33
Q

Tx of ACEi/ARB OD

A

Unlikely to cause significant toxicity.

Tx = supportive.

34
Q

Examples of imidazolines

A

clonidine, oxymetazoline, tetrahydrozoline (optho topical constrictor, nasal decongestants), tizanidine (central muscle realaxant), dexmedetomidine

35
Q

Clonidine MOA/mxn toxicity

A

central presynaptic alpha-2 adrenergic agonist –> decreased sympathetic (NorE) outflow –> hypoTN, bradycardia.
Peripherally, presynaptic alpha2-agonism –> vasoconstriction, paradoxical HTN.

36
Q

Symptoms of clonidine toxicity

A

Looks like opioid OD
CVD: initially, short-lived hyperTN, then progressive hypoTN/bradycardia.
Resp: Hypoventilation.
Neuro: AMS, depression, coma, miosis.

37
Q

DDx of clonidine OD

A

CCB, BB, dig, opioids

38
Q

Tx of clonidine OD

A

Supportive.
Atropine, IVF, possible pressors for hypoTN, bradycardia.
Naloxone may reverse some of the sedation.

39
Q

Examples of vaughn-williams class I antidysrhythmics

A

1A: procainamide, quinidines.
1B: Lidocaine, phenytoin.
1C: Flecainide, propafenone.

40
Q

Receptors affected by class I antidysrhythmics

A

Na channel blockade

41
Q

Examples of class II antidysrhthmics

A

beta blockers

42
Q

Examples class III antidysrhythmics

A

Amiodarone, sotalol

43
Q

Effect of class III antidysrhythmics

A

K+ channel blockade –> prolongation of repolarization. Sotalol also has BB activity.
May cause hypoTN, brady, QTc prolongation.

44
Q

Chronic changes seen with amiodaron toxicity

A

interstitial pneumonitis, grey or bluish skin changes, corneal microdeposits.

45
Q

Example of Class IV antidysrhythmics

A

CCBs

CCFP-EM: Tox, Neuro (34 decks)

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