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Pharmacotherapy 4271 > CV Medication Toxicity (Final) > Flashcards

CV Medication Toxicity (Final) Flashcards

1
Q

this is a type of hemodynamic instability, where SBP > 180 or DBP > 120. there is no organ damage. there is a risk here of the long term adverse effects of uncontrolled HTN

A

hypetension urgency

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2
Q

what is the treatment for hypertension urgency

A

initiating, reinititing or intensifying oral anyihypertensive medications

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3
Q

true or false: aggressive lowering of BP occurs in hypertensive urgency

A

FALSE!!!! - overly aggressive BP lowering places patients at risk for ischemic complications

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4
Q

this is a type of hemodynamic instability, where SBP > 180 or DBP > 120 (DBP especially looked at here!). associated with end organ damage, such as AKI, retinal hemorrhage, hemorrhagic stroke, encephalopathy, heart failure, rupture of aneurysm.

this hemodynamic instability requires ICU admission for IV antihypertensives

A

HTN emergency

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5
Q

true or false: aggressive lowering of BP occurs in hypertensive emergency

A

true!! - acute target organ disease is present, the benefit of rapid BP lowering with IV antihypertensives generally outweighs the risk of potential ischemic complications

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6
Q

what is a benefit of IV infusions for antihypertensive medications in HTN emergency

A

allow dose titration:
- titrate up quickly for rapid control
- if BP decreases too much can decrease infusion to minimize S/E

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7
Q

what is the main purpose of IV medications used for HTN emergency

A

vasodilation (decreases BP) or adrenergic inhibition (inhibits epi/NE, therefore decreases BP/HR)

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8
Q

this is a type of hemodynamic instability; usually characterized by SBP < 90 or MAP < 70; clinically defined as a blood pressure that is inadequate to perfuse organs

A

hypotension

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9
Q

what is used to tx hypotension

A

fluids, vasopressors & specific antidotes

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10
Q

what is the tx used for acute heart failure

A

main aspect is stabilization!! - oxygen, diuretics, fluid restriction
(may also use beta-blockers, ACEI/ARB)

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11
Q

what are some examples of conduction abnormalities

A

AV block, bradycardia

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12
Q

what is the tx used for conduction abnormalities

A

atropine, symptoms treatment (e.g. hypotension) & specific antidotes

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13
Q

what HR threshold is considered tachycardia

A

> 100 bpm

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14
Q

this subtype of tachycardia is found above the ventricles. it can progress to hypotension, chest pain, asystole

A

supra ventricular tachycardia

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15
Q

what is the tx used for supra ventricular tachycardia

A

beta-blocker, cardioverison

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16
Q

this subtype of tachycardia can be life threatening if it is sustained

A

ventricular tachycardia

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17
Q

what is the tx used for ventricular tachycardia

A

depends on sxs
beta-blockers, cardioversion, implantable device

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18
Q

are DHP or non-DHP more toxic at higher levels? why?

A

non-DHP (e.g. verapamil & diltiazem) because they act directly on the heart whereas DHP act peripherally

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19
Q

true or false: ALL CCB’s work on L-type calcium channels

A

true - each CCB has a different affinity for these receptors which dictates its clinical effect

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20
Q

this class of CCB’s has an inhibitory effect on the SA/AV node and they decrease conduction, HR, CO and BP

A

non-DHP

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21
Q

this non-DHP CCB has the most profound effect on the SA/AV node

A

verapamil

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22
Q

this class of CCBs promote peripheral vasodilation and has the greatest affinity for peripheral vascular smooth muscle, therefore decreases SVR (may get reflex tachycardia)

A

DHP

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23
Q

true or false: CCB’s are not well absorbed PO

A

false - well absorbed PO but undergo extensive 1st pass metabolism

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24
Q

true or false: CCB’s are renally excreted

A

true

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25
Q

true or false: based on the distribution kinetics of CCB’s, dialysis can be used to reverse CCB toxicity

A

false - CCBs are highly protein bound, therefore dialysis cannot be used as a life saving measure with CCBs toxicity because proteins are big, which the drug is bound to and can’t be removed by dialysis

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26
Q

what are the two hallmark clinical manifestations of CV toxicity

A

bradycardia and hypotension

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27
Q

what are some other cardiovascular clinical manifestations of CV toxicity

A

decreased LOC due to decreased blood flow and AV block, arrhythmias

28
Q

this, which is not directly related to cardiovascular manifestations, is a clinical manifestation of CV toxicity; this manifestations can help distinguish between beta-blocker and CCB toxicity

A

hyperglycaemia
- due to surpassed insulin release from pancreas -> insulin release is dependant on Ca influx via L-type channels (associated with CCBs)

29
Q

what is used in a diagnostic evaluation of a patient with CV toxicity

A
  • history
  • EKG
  • blood work (glucose, electrolytes, Cr, BUN and oxygen sat)
30
Q

what is the management for a patient experiencing CCB CV toxicity

A
  • ABC’s (airway, breathing, circulation)
  • GI decontamination (1g/kg of activated charcoal, even if asymptomatic)
31
Q

what is the timeline for when a patient can be given activated charcoal if they are experiencing CCB CV toxicity

A

present in 1-2 hours, because medication will still be in GI tract

32
Q

this management option should be given to a patient if they are hypotensive. caution should be taken in patients with heart failure, acute respiratory distress syndrome (ARDS) and chronic kidney disease

A

fluids

33
Q

this management option is the drug of choice for symptomatic bradycardia, as is increases the HR by increasing SA and AV node conduction. This option is not effective in severe CCB positioning due to peripheral CCB effects

A

atropine

34
Q

what is the management for CCB toxicity
*list in order

A
  1. fluids
  2. atropine
  3. calcium
  4. glucagon
  5. insulin
  6. vasopressors
35
Q

true or false: calcium channel blockers reduce calcium ion influx into the cell through type L channels therefore reducing contractility

A

true

36
Q

true or false: giving a patient calcium as an antidote for CCB toxicity will cause a concentration gradient which will allow for an influx of calcium and therefore stimulation of actin and myosin thus increased contractility

A

true

37
Q

true or false: calcium is used as a management therapy for CCB toxicity in severe patients

A

false - non severe

38
Q

this type of calcium has to be given as a bigger volume, therefore this may be an issue in patients with heart failure

A

calcium glutinate

39
Q

this type of calcium is very concentrated therefore would need to be given in a central line

A

CaCl2

40
Q

what type of toxicity needs to be ruled out BEFORE giving calcium to a patient with a suspected CCB toxicity

A

DIGOXIN TOXICITY
- digoxin increases contractility of heart by affecting the SA/AV node, the same as calcium. therefore, if we give a patient with digoxin toxicity calcium, we will worsen the digoxin toxicity

41
Q

what are some adverse effects of calcium being administered for CCB toxicity

A
  • hypercalcemia (obvi)
  • hypophosphatemia
  • vomiting
  • flushing
  • constipation (obvi)
42
Q

this management option is unique as it acts a pure beta agonist with no peripheral vasodilator effects. it is the treatment of choice in beta-blocker toxicity because it bypasses the receptor and activates adenylate cyclase which causes an influx of calcium into the cells and causes increased contractility

A

glucagon

43
Q

what are some adverse effects of glucagon

A

-n/v
- hyperglycaemia

44
Q

true or false: if a patent is life threatening, high dose insulin is a part of initial treatment

A

true

45
Q

this should be given with high dose insulin; is it not required if the patients blood glucose level is > 16 mmol/L

A

dextrose

46
Q

what are some adverse effects of high dose insulin

A
  • hypoglycaemia
  • hypokalemia due to K+ shift
47
Q

this management option is last line and only used if the patient is so hypotensive they are at risk of death. e.g. norepinephrine, epinephrine, dobutamine, dopamine and vasopressin

A

vasopressors

48
Q

these competitively antagonize the effects of catecholamines on beta receptors and blunt th echronotropic and inotropic response to catecholamines; also help to slow the SA and AV node conduction

A

beta blockers

49
Q

which beta blocker has high lipid solubility - therefore has a higher risk of crossing the BBB

A

propanolol and carvediolol

50
Q

true or false: lipid soluble beta blockers accumulate in renal function

A

false - water soluble

51
Q

this medication can cause a K channel blockade, which can prolong QT, cause torsades de pointes and ventricular arrhythmias and CV toxicity

A

sotalol

52
Q

this type of effects are usually seen with lipophilic agents such as propranolol in CV toxicity . e.g. delirium, coma and seizures

A

CNS effects

53
Q

true or false: respiratory depression is common in CV toxicity

A

false - rare unless patient has pre-existing asthma or COPD

54
Q

vasodilation - more pronounced hypotension is commonly seen with this beta blocker due to its alpha activity

A

carvedilol

55
Q

what is the management for beta-blocker toxicity
*list in order

A
  1. fluids
  2. atropine
  3. glucagon
  4. calcium
  5. insulin - if above fail
  6. vasopressors
56
Q

this medication can be seen in patient with CHF and sometimes AFib; it increases the force if contraction of the heart by increasing cytosolic calcium. decreases the rate of conduction through SA and AV node so it can be used for AFib; has a narrow therapeutic index

A

digoxin

57
Q

what patients are predisposed to digoxin toxicity

A
  • comorbidites
  • concomitant medications
  • low potassium
58
Q

does this describe acute or chronic digoxin toxicity:
- slow-developing, non-specific sxs
- loss of appetite, N/V, weight loss
- drowsiness, delirium, confusion, disorientation
- photophobia, GREEN YELLOW HALOS

A

chronic

59
Q

does this describe acute or chronic digoxin toxicity:
- N/V abdominal pain
- lethargic, weak due to decreased CO
may be asymptomatic

A

acute

60
Q

true or false: if the patient has no GI symptoms after several hours of digoxin toxicity, they are not likely to develop severe toxicity

A

true

61
Q

what electrolyte abnormalities are usually seen with digoxin toxicity

A

hyperkalemia - marker for increased mortality
- digoxin inhibits the Na-K ATPase pump which inhibits K from entering the cells therefore it all stays in the serum

62
Q

what is a cardiac manifestation of digoxin toxicity

A

bradydysrhythmias
- heart is firing out of sequence but not rapidly

63
Q

is acute or chronic digoxin toxicity usually responsive to atropine

A

acute

64
Q

what is used to make a diagnosis of digoxin toxicity

A
  • bradydysrhythmias
  • serum digoxin levels
  • blood work (electrolytes, SCr, EKG)
65
Q

what are some treatment options for digoxin toxicity

A
  • GI decontamination (activated charcoal)
  • symptomatic treatment (correct electrolyte abnormalities)
  • Digibind
66
Q

true or false: digoxin has a greater affinity for Digibind than its target receptors

A

true

67
Q

what are the indications for Digibind, that may indicate a digoxin toxicity

A
  • severe toxicity/arrhytmias
  • no response to atropine
  • K > 5 mmol/L
  • Dig conc > 12.8 nmol/L at steady state
  • large ingestions

Pharmacotherapy 4271 (29 decks)

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