CV Medication Toxicity (Final) Flashcards
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
hypetension urgency
what is the treatment for hypertension urgency
initiating, reinititing or intensifying oral anyihypertensive medications
true or false: aggressive lowering of BP occurs in hypertensive urgency
FALSE!!!! - overly aggressive BP lowering places patients at risk for ischemic complications
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
HTN emergency
true or false: aggressive lowering of BP occurs in hypertensive emergency
true!! - acute target organ disease is present, the benefit of rapid BP lowering with IV antihypertensives generally outweighs the risk of potential ischemic complications
what is a benefit of IV infusions for antihypertensive medications in HTN emergency
allow dose titration:
- titrate up quickly for rapid control
- if BP decreases too much can decrease infusion to minimize S/E
what is the main purpose of IV medications used for HTN emergency
vasodilation (decreases BP) or adrenergic inhibition (inhibits epi/NE, therefore decreases BP/HR)
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
hypotension
what is used to tx hypotension
fluids, vasopressors & specific antidotes
what is the tx used for acute heart failure
main aspect is stabilization!! - oxygen, diuretics, fluid restriction
(may also use beta-blockers, ACEI/ARB)
what are some examples of conduction abnormalities
AV block, bradycardia
what is the tx used for conduction abnormalities
atropine, symptoms treatment (e.g. hypotension) & specific antidotes
what HR threshold is considered tachycardia
> 100 bpm
this subtype of tachycardia is found above the ventricles. it can progress to hypotension, chest pain, asystole
supra ventricular tachycardia
what is the tx used for supra ventricular tachycardia
beta-blocker, cardioverison
this subtype of tachycardia can be life threatening if it is sustained
ventricular tachycardia
what is the tx used for ventricular tachycardia
depends on sxs
beta-blockers, cardioversion, implantable device
are DHP or non-DHP more toxic at higher levels? why?
non-DHP (e.g. verapamil & diltiazem) because they act directly on the heart whereas DHP act peripherally
true or false: ALL CCB’s work on L-type calcium channels
true - each CCB has a different affinity for these receptors which dictates its clinical effect
this class of CCB’s has an inhibitory effect on the SA/AV node and they decrease conduction, HR, CO and BP
non-DHP
this non-DHP CCB has the most profound effect on the SA/AV node
verapamil
this class of CCBs promote peripheral vasodilation and has the greatest affinity for peripheral vascular smooth muscle, therefore decreases SVR (may get reflex tachycardia)
DHP
true or false: CCB’s are not well absorbed PO
false - well absorbed PO but undergo extensive 1st pass metabolism
true or false: CCB’s are renally excreted
true
true or false: based on the distribution kinetics of CCB’s, dialysis can be used to reverse CCB toxicity
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
what are the two hallmark clinical manifestations of CV toxicity
bradycardia and hypotension
what are some other cardiovascular clinical manifestations of CV toxicity
decreased LOC due to decreased blood flow and AV block, arrhythmias
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
hyperglycaemia
- due to surpassed insulin release from pancreas -> insulin release is dependant on Ca influx via L-type channels (associated with CCBs)
what is used in a diagnostic evaluation of a patient with CV toxicity
- history
- EKG
- blood work (glucose, electrolytes, Cr, BUN and oxygen sat)
what is the management for a patient experiencing CCB CV toxicity
- ABC’s (airway, breathing, circulation)
- GI decontamination (1g/kg of activated charcoal, even if asymptomatic)
what is the timeline for when a patient can be given activated charcoal if they are experiencing CCB CV toxicity
present in 1-2 hours, because medication will still be in GI tract
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
fluids
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
atropine
what is the management for CCB toxicity
*list in order
- fluids
- atropine
- calcium
- glucagon
- insulin
- vasopressors
true or false: calcium channel blockers reduce calcium ion influx into the cell through type L channels therefore reducing contractility
true
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
true
true or false: calcium is used as a management therapy for CCB toxicity in severe patients
false - non severe
this type of calcium has to be given as a bigger volume, therefore this may be an issue in patients with heart failure
calcium glutinate
this type of calcium is very concentrated therefore would need to be given in a central line
CaCl2
what type of toxicity needs to be ruled out BEFORE giving calcium to a patient with a suspected CCB toxicity
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
what are some adverse effects of calcium being administered for CCB toxicity
- hypercalcemia (obvi)
- hypophosphatemia
- vomiting
- flushing
- constipation (obvi)
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
glucagon
what are some adverse effects of glucagon
-n/v
- hyperglycaemia
true or false: if a patent is life threatening, high dose insulin is a part of initial treatment
true
this should be given with high dose insulin; is it not required if the patients blood glucose level is > 16 mmol/L
dextrose
what are some adverse effects of high dose insulin
- hypoglycaemia
- hypokalemia due to K+ shift
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
vasopressors
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
beta blockers
which beta blocker has high lipid solubility - therefore has a higher risk of crossing the BBB
propanolol and carvediolol
true or false: lipid soluble beta blockers accumulate in renal function
false - water soluble
this medication can cause a K channel blockade, which can prolong QT, cause torsades de pointes and ventricular arrhythmias and CV toxicity
sotalol
this type of effects are usually seen with lipophilic agents such as propranolol in CV toxicity . e.g. delirium, coma and seizures
CNS effects
true or false: respiratory depression is common in CV toxicity
false - rare unless patient has pre-existing asthma or COPD
vasodilation - more pronounced hypotension is commonly seen with this beta blocker due to its alpha activity
carvedilol
what is the management for beta-blocker toxicity
*list in order
- fluids
- atropine
- glucagon
- calcium
- insulin - if above fail
- vasopressors
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
digoxin
what patients are predisposed to digoxin toxicity
- comorbidites
- concomitant medications
- low potassium
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
chronic
does this describe acute or chronic digoxin toxicity:
- N/V abdominal pain
- lethargic, weak due to decreased CO
may be asymptomatic
acute
true or false: if the patient has no GI symptoms after several hours of digoxin toxicity, they are not likely to develop severe toxicity
true
what electrolyte abnormalities are usually seen with digoxin toxicity
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
what is a cardiac manifestation of digoxin toxicity
bradydysrhythmias
- heart is firing out of sequence but not rapidly
is acute or chronic digoxin toxicity usually responsive to atropine
acute
what is used to make a diagnosis of digoxin toxicity
- bradydysrhythmias
- serum digoxin levels
- blood work (electrolytes, SCr, EKG)
what are some treatment options for digoxin toxicity
- GI decontamination (activated charcoal)
- symptomatic treatment (correct electrolyte abnormalities)
- Digibind
true or false: digoxin has a greater affinity for Digibind than its target receptors
true
what are the indications for Digibind, that may indicate a digoxin toxicity
- severe toxicity/arrhytmias
- no response to atropine
- K > 5 mmol/L
- Dig conc > 12.8 nmol/L at steady state
- large ingestions
