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Rosens > 142. CV Drugs > Flashcards

142. CV Drugs Flashcards

1
Q

Digoxin - where does this med come from?

A

foxglove

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2
Q

Digoxin - 2 CV effects

A

incr force of myocardial contraction to incr CO in HF

decr AV conduction to slow rate in afib

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3
Q

How does digoxin work biochemically?

A

inhibit Na K atpase pumps to incr intracellular na and extracellular K

incr IC na -> extrudes IC ca after systolie so more into SR more powerful contraction

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4
Q

At toxic levels what does dig do?

A

paralyze na k atpase pump so K cannot go into cell and K can rise to concerning levels

block sa node and depress av node, incr sn sa and av node to catechlamines –> slow HR and incr risk av block

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5
Q

digoxin effects on purkinje fibres

A

decr resting potential resulting in slow ph 0 depol and conduction velocity

decr ap duration incr sn of m fibers to electrical stimuli

enhanced automaticity resulting from incr rate ph 4 repol and edealyed after depol

therefore why can get pvc and instability pending toward dysrhytmia

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6
Q

half life elimination of dig

A

36h in urine

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7
Q

digoxin has a __ vol of distrubtion

A

large

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8
Q

sx of chronic dig toxicity

A

nausea, anorexia, and fatigue; but a variety of gastrointestinal, neurologic, and ophthalmic disturbances

Visual disturbances include decreased visual acuity, scotomata, photophobia, and chromatopsia (aberrations of color vision, classically yellow, but may occur in a variety of colors)

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9
Q

chronic poisonijng of digoxin level?

A

6ng/ml (50% mortality level)

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10
Q

Peds and dig - can they tolerate large loads?

A

yes as longb as healthy hearts

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11
Q

Name 8 dysthrymias associated with dig toxicity

A

PVCs, especially bigeminal and multiform AV heart blocks of all degrees
Sinus bradycardia
Sinus tachycardia
SA block or arrest
Atrial fibrillation with slow ventricular response Atrial tachycardia
Junction (escape) rhythm
AV dissociation
Ventricular bigeminy and/or trigeminy Ventricular tachycardia
Ventricular fibrillation

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12
Q

More sp but not pathognomonic dysrhymias assoc with dig toxicity

A

Atrial fibrillation with slow, regular ventricular rate (AV dissociation) Nonparoxysmal junctional tachycardia (rate usually 70–130 beats/min)
Atrial tachycardia with block (atrial rate usually 150–200 beats/min)
Bidirectional ventricular tachycardia

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13
Q

Name 8 factors assoc with incr risk of dig toxicity?

A

Concomitant kidney injury or underlying kidney disease Concomitant or underlying heart disease:
Congenital heart disease Ischemic heart disease Heart failure Myocarditis

Electrolyte disturbances Hyperkalemia Hypokalemia Hypomagnesemia Hypercalcemia

Alkalosis

Hypothyroidism

Sympathomimetic drugs (e.g., cocaine)

Cardiotoxic co-ingestions
Beta-blockers
Calcium channel blockers
Class IA or IC antidysrhythmics (e.g., flecainide) Tricyclic antidepressants

Drug interactions (may increase serum digoxin concentration) Quinidine
Amiodarone Erythromycin Nifedipine

Drug Interactions (may increase serum digoxin concentration and cause synergistic bradycardia)
Verapamil
Diltiazem

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14
Q

Noncardiac sx of cardioactive steroid intox

A

General
Weakness Fatigue Malaise

Gastrointestinal
Nausea and/or vomiting Anorexia
Abdominal pain Diarrhea

Ophthalmologic
Blurred or snowy vision
Photophobia
Chromatopsia (yellow, green, red, brown, blue vision changes) Transient amblyopia, diplopia, scotomata, blindness

Neurologic
Dizziness
Headache
Confusion, disorientation, delirium Visual and/or auditory hallucinations Somnolence
Abnormal dreams
Paresthesias and/or neuralgia Aphasia
Seizure

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15
Q

Acute vs chronic dig poisoning

A

acute: lower mort
brady and avb vs ventr dysrh
typically yo pt
underlying heart dis less common, less morb and mortality

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16
Q

ddx for digoxin toxicity

A

oleaner plant
lily of valey
cerebra odollam
thevetia peruviana
depressajnt drugs
methanol
metformin
ethambutol quinine
antimalaria

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17
Q

Age diff in digoxin intoxication: adult vs ped

A

toxic a lower [] vs asymp at higher
n, fatigue, fisual disturb vs obtundation and emesis
tachydys as common as block and brady vs bradydysrh and blocks more common
allergic rxn fab fragment uncommon vs extremely rare
vd less variable 5-7.5L/kg vs vd more variable 3.5-6l/kg in premie infant, 8-16.3 infants 2-24mo

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18
Q

when to test for. dig [] in concern for toxicity

A

Peak con- centrations after an oral dose of digoxin occur in 1.5 to 2 hours, with a range of 0.5 to 6 hours. Steady-state serum concentrations are not achieved until after alpha distribution, or 6 to 8 hours after a thera- peutic or toxic dose and may be only 20% to 25% of the peak concen- tration.

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19
Q

ideal serum dig [] in HF

A

0.7-1.1ng/ml

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20
Q

serum steady state dig concentration toxicity?

A

concentrations of 1.1 to 3.0 ng/mL are difficult to interpret; that is, concentrations as low as 1.1 ng/mL have been associated with toxicity, and patients with levels up to 3.0 ng/mL can be asymptomatic. The incidence of digoxin-incited dysrhythmia reaches 10% at a con- centration of 1.7 ng/mL and rises to 50% at a concentration of 2.5 ng/ mL.

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21
Q

Management of dig toxicity

A

digifab

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22
Q

Digifab antibodies -risk of allergic reaction in who? what does it look like?

A

asthma

erythema, urticaria, facial edema

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23
Q

Digifab reactions other than allergic - list 3

A

hypokalemia
heart failure exacerbation
increase in VR with afib

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24
Q

List 5 indications for digifab

A
  1. Ventricular dysrhythmias more severe than PVCs
  2. Progressive and hemodynamically significant bradydysrhythmias unrespon-
    sive to atropine
  3. Serum potassium >5.0 mEq/L
  4. Rapidly progressive rhythm disturbances or rising potassium
  5. Co-ingestion of cardiotoxic drugs (for examples, see Box 142.2)
  6. Ingestion of plant known to contain cardioactive steroids plus severe dys-
    rhythmia or potassium >5.0 mEq/L
  7. Acute ingestion of >10 mg or 0.1 mg/kg in a child plus any one of factors 1
    through 6
  8. Steady-state digoxin concentration > 6 ng/mL plus any one of factors 1
    through 6
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25
Q

How to calculate how much digifab you need?

A

body load is amount ingested in mg (total):

total x 0.8 (which is bioavail of dig tablets)

then use this number and divide by 0.5mg bound per vial to determine number of vials

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26
Q

Ex: A toxic-appearing 40-year-old woman has acutely ingested fifty 0.25-mg digoxin tablets. If she needs digifab, how much does she need?

A

Body load = amount ingested
× 0.8 ( bioavailability of digoxin tablets) =
12.5 mg×0.8=10 mg
Dose of digoxin Fab fragments ( in vials) = 10 mg ÷ 0.5 mg bound per vial
= 20 vials

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27
Q

Fab or TVP for bradydysrhythmia second line tx after nonresponse to atropine?

A

fab

tvp higher risk of ventricular dysrhymia

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28
Q

Expected time to response after fab infusion

A

19 mins

can take hours

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29
Q

If the patient is in cardiac arrest, how much fab to give?

A

maximum number of vials of Fab fragments available (up to 10) should be administered undi- luted as an intravenous (IV) bolu

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30
Q

If, in acute or chronic toxicity, the patient is in a life-threatening ventricular dysrhythmia or heart block and the serum digoxin concentration is unknown but the amount of digoxin ingested is known, we recommend full reversal. How is that dosed?

A

one vial of DigiFab contains 40 mg of Fab fragments, which bind 0.5 mg of digoxin (Box 142.5). In the same patient, if the steady-state serum digoxin concentration is known, we recommend full reversal with Fab fragments based upon the digoxin concentration utilizing the formula in Box 142.6. An exception to the above regimens is the case of yellow oleander poisoning, where a high case fatality rate and poor cross-reactivity of Fab fragments with the offending cardioactive steroids necessitates higher dosing. Therefore, with acute yellow oleander poisoning, 20 to 30 vials (if available) are recommended.

31
Q

A toxic-appearing 4-year-old child weighing 20 kg has a digoxin level of 16 ng/mL 8 hours after ingestion of an unknown number of digoxin tablets. How many vials should they get?

A

Dose ( in number of vials) = ( serum digoxin concentration × weight in kg) ÷ 100
= (16×20) ÷100
= approximately 3 vials

32
Q

Ca in a hyperkalemic dig patient - what to do?

A

classic teaching = stone heart:

fab first
then tx per normal hyperkalemia

33
Q

While awaiting fab fragments in dig toxicity if someone is in a tachydysrhytmia, what can you give?

A

phenytoin 100mg bolus q5 min until dhysrh improves or until 18mg/kg reached

lidocaine only if CI to pheny or once at max of same: 1.5mg/kg puhs then infusion 1-4mg/min starting at one and titrate up to response

34
Q

If fab fragments are ineffective, can consider which tx?

A

ecmo

35
Q

Beta blocker function overall

A

block catecholamines like epi at beta adr receptors to prevent incr inotropy, conduction and HR

beta 2: vascular sm relax, liver glycogenolysis and gluconeo, lung/bronchodilation, adipose tissue release FFA, uterus sm relaxation

36
Q

Symptoms of a beta blocker OD

A

bradycardia
hypotension
altered LOC
apnea

HYPOGLYC rare adults, mc kids

propranolol can cause seizure

37
Q

Which beta blockers imapir sa and av node function, as well as ventricular conduction showing qrs widening?

A

propranolol
nadolol
betaxolol
acebutlolol

38
Q

Labetalol and carvedilol additionally block which receptor, causing which sx?

A

hypotension
distrib shock

block alpha 1

39
Q

Beta blocker toxicity time to onset (generally)?

A

within 30 mins

apparent within 6 hours - can last up to 24h

40
Q

Beta blocker special features if OD sotalol?

A

qt. prolongation
torsades

41
Q

Name 5 dialyzable beta blockers?

A

nadolol
timolol
sotalol
atenolol
acetbuolol

42
Q

DDX beta blocker OD?

A

clonidine and tizanidine or imid- azoline receptor agonists such as tetrahydrozoline and oxymetazoline may also cause this constellation of symptoms.

odium channel poisoning with QRS widening can occur, suggesting other antidysrhythmic drugs or cyclic antidepressants. The differential diagnoses also include sedative-hypnotic drug overdose, hypoglycemic drug ingestion, opioid overdose, CNS injury or infec- tion, various endocrine and metabolic disorders, sepsis, and acute myocardial infarction.

43
Q

Diagnostic testing in a beta blocker overdose

A

ecg
bg
med hx

44
Q

Management of a beta blocker overdose

A

abc
IVF
o2 as needed for hypoxia

atropine if HR <50
IV ca
glucagon 3-10mg IV bolus or 0.05mg/kg child then infusion if responds well 3-5mg/hour
high dose insulin R 1 U/kg/hr titrated up by 2 U/kg/hr every 10 minutes (up to a maximum of 10 U/kg/hr) with 25g glucose unless bg >20
bicarb boluses til qrs narrows

then NE itrate to MAP of 60, second line VP

intralipid: initial bolus of 1.5 mL/ kg of 20% lipid solution given over 2 to 3 minutes, followed imme- diately by an infusion of 0.25 mL/kg/min. If a response occurs at this infusion rate, the infusion dose may be decreased to 0.025 mL/ kg/min (1/10th the initial rate) to sustain lipemic serum for a lon- ger period of time

ecmo

45
Q

sequential approach to bb poisoning

A

IV bolus andrepeat
symptomatic brady with atropine x3 up to total 3mg
hypotension ongoin, give cagluc infused over 10 mins
glucagon 5mg bolus to bridge to HDI: with one amp d50, then 1u/kg insulin R
-start glucose 25g/hour
incr insulin by 2 units q10 mins until hypotension resolves or until max 10
still hypotensive NE

+/- tvp
+/- vasopressin
ECMO or intralipid

46
Q

Phase 1 tx of beta blocker

A

Activated charcoal as indicated Isotonic fluid bolus 20–40 mL/kg Atropine
Calcium
Glucagon

47
Q

Phase 2 tx beta blocker

A

Place central & arterial lines HDI infusion Norepinephrine
Vasopressin
3rd agent based on type of shock Pacemaker for bradycardia

48
Q

Phase 3 tx beta blocker OD

A

IFE
ECMO
Other mechanical devices if ECMO not available

49
Q

Phase 1 CCB toxicity tx

A

Activated charcoal as indicated Isotonic fluid bolus 20–40 mL/kg Atropine
Calcium

50
Q

phase 2 ccb od tx

A

Place central & arterial lines HDI infusion Norepinephrine
Vasopressin
3rd agent based on type of shock Pacemaker for bradycardia

51
Q

phase 3 ccb od tx

A

IFE
Methylene blue
ECMO
Other mechanical devices if ECMO not available

52
Q

which bb od pt need to be adm?

A

Patients with sec- ond or third-degree AV heart block, hypotension not responding to IV fluid administration, or who have hemodynamically significant dysrhythmias should be admitted to an intensive care unit.

53
Q

CCB function

A

block L type ca channels in myocardium and vascular sm so get peripheral vasodilation
reduce contractility
depres sa nod activity
slow av node

54
Q

ccb onset of toxicity vs longest time to onset

A

Onset of action and toxicity may occur as early as 30 minutes after ingestion. In contrast, the poisoning from sustained-release ver- apamil may not manifest for 12 hours or more. High protein binding and Vd greater than 1 to 2 L/kg make hemodialysis or hemoperfusion ineffective with calcium antagonists.

55
Q

Clinical features of ccb toxicity

A

hypot
bradycardia
av block, smus arresrt, av dissoc, junctiona rhythm, asystole
qrs widening may not be seen early on
edema including pulmonary edema

56
Q

BG - hyperglycemia in bb or ccb toxicity?

A

ccb!
secondary to insulin inhibition

57
Q

What is a hail mary med for ccb toxicity?

A

methylene blue
vasoncstrictor - inhibits enzyme og guanylyl cyclase resulting in cBMP to incr SVR

58
Q

dose methylene blue for ccb od?

A

1-2mg/kg bolus of 1% methylene blue followed by infusion of 1mg/kg up to 6h

59
Q

Clonidine mech of action

A

central acting alpha 2 ag and imidazoline agonist

binds to presync alpha 2 adr to inhibit neurons causing decr NE releaes

60
Q

what conditions does clonidine tx

A

hypertension
adhd
pheo
withdrawal from opioids , etoh and nicotine

61
Q

clonidine sx

A

brady- cardia, hypotension, decreased mental status, miosis, and occasionally hypothermia.

62
Q

ddx clonidine od

A

antihypertensive medications (e.g., guanabenz, α- methyldopa), ADHD medications (e.g., guanfacine), muscle relaxers (e.g., tizanidine), and topical vasoconstrictors in dermatologic (e.g., brimonidine),62 ocular, and nasal settings (e.g., tetrahydrozoline, oxymetazoline, and naphazoline

63
Q

clonidine od management

A

bolus IVF for hypotension
less concern pulmonary edema than bb or ccb od
ne for map >60

?naloxone? trial 0.2 –> 0.4 –> 10mg bolus

64
Q

clonidine peak effect and half life

A

2-4 hours
half life 5-13h

65
Q

Example of nitrates causing toxicity

action

A

ntg
isosorbide mononitrate
dinatrate

vasodil - typ. veins but higher dose arteries

66
Q

what are poppers

A

alkyl nitrites (amyl, butyl, isobutyl, or ethyl nitrite)

sexual pleasure prolonging

67
Q

how does methemoglobinemia work?

A

nitrites and nitrates have oxidizing power of fe2+ to fe3+ which incapable of carrying o2 and shifts ox dissoc curve L - functional anemia impairing ability to o2 deliver

68
Q

methemoglobinemia: clinical features

A

hypotension
reflex tachy
headache
cyanosis
venipuncture choc brown blood
nonsp sx fatigue, dyspnea, weakness, dizzy, drowsy, syncope, coma, seizure, death

69
Q

DDx methemoglobinemia:

A

diuretics, angiotensin-converting enzyme (ACE) inhibitors, and dihydropyridine calcium channel blockers, as well as oxidative phosphorylation uncouplers such as cyanide and carbon monoxide. Non-toxicologic conditions capable of mimicking nitrate poisoning include sepsis and anaphylaxis. The differential diagnosis of methemoglobinemia includes hypoxia, as well as other hemoglobinop- athies such as sulfhemoglobinemia.

70
Q

diagnosis methemoglobinemia

A

o2 challenge
cooximetery for percent methemoglobin
if confirm get hemoglobin []
if anemic a smaller am of methemoglobin may be sign

71
Q

Pulse ox readings and methemoglobinemia - how does this work?

A

pulse oximeters function by read- ing the absorbance of light at wavelengths of 660 and 940 nm, which are selected to separate oxy and deoxyhemoglobin. Methemoglobin absorbs light at both these wavelengths more than either oxy or deoxy- hemoglobin. This results in unreliable pulse oximetry that typically reads near 85%, regardless of the patient’s oxygenation status.

72
Q

Management of nitratev posioning

A

supine pos ivf
removal ofending agent

73
Q

nitrate are CI in which concomittent ddrgu use and why?

A

erectile dysfunction, such as sildenafil (Viagra) or tadalafil (Cialis). These drugs inhibit type 5 phosphodiesterase, relaxing vascular smooth muscle, which can prolong and intensify the vasodilating effects of nitrates causing severe hypotension. If blood pressure does not normalize with IV fluids and cessation of the nitrate infusion, norepinephrine should be cautiously titrated to a MAP of 60 mm Hg, beginning at 0.1 mcg/kg/min.

74
Q

Tx for methemoglobinemia

A

supplemental o2
ivf
iv methyelne blue as oxidizing agent in presence of NADPH methemoglobin reductase, reduced to leukomethylen blue –> reduces methemeoglobin back to hemoglobin

IV 1-2mg/kg of 1% metyhlene blue
repeat 1hr if cyanosis not resolved

if >7mg/kg methylene blue just makes methemoglobin worse so don’t do that

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