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Chris Cards UCC > ACLS > Flashcards

ACLS Flashcards

1
Q

Bradycardia. 3 meds and doses

A
  1. Atropine, 1mg, repeat Q3-5 min, Max 3mg.
  2. Dopamine. 5-20mcg/kg/min. Titrate to response
  3. Epinephrine. 2-10mcg/min Titrate to response.
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2
Q

Bradycardia. Tx. Start with…then progress to…

A

atropine
transcutaneous pacing
dopamine
epi

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3
Q

What do you do with tachycardia and a pulse. Altered. Symptomatic.

A

Synchronized cardioversion unless QRS is narrow then adenosine.

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4
Q

Patient with tachycardia and a pulse with a WIDE QRS. What med and dose?

A

Adenosine.
FIRST Dose 6mg,
SECOND Dose 12mg.
Give rapidly with a 3-way stop cock and 30ml flush from NS Bag.

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5
Q

Arrest. What do you shock?

A

VF/pVT

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6
Q

Arrest. Why give epi?

A

makes heart more receptive to electrical stimulation

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7
Q

Arrest. How many shocks before meds are given?

A

2

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8
Q

Arrest. Asystole/PEA what do you do?

A

Epinephrine, 1mg, flush with 20ml NS, raise that arm.

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9
Q

Arrest. What is the epi ratio?

A

1:10,000.

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10
Q

Arrest. shockable rhythm. you have already given epi. What meds are next?

A

Amiodarone or Lidocaine.

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11
Q

Arrest. First dose of amiodarone?

A

300mg

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12
Q

Arrest. Second dose of amiodarone?

A

150mg

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13
Q

Arrest. What are the joules in order of administration?

A

120j, 150j, 200j

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14
Q

Arrest. What are the doses for lidocaine?

A

FIRST dose: 1-1.5mg/kg
SECOND Dose: 0.5-0.75mg/kg

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15
Q

why lidocaine?

A

Lidocaine is one of several ACLS drugs used to treat cardiac arrest from ventricular tachycardia (VT) and Ventricular Fibrillation (VF). Lidocaine is considered a second-line antiarrhythmic drug aamiodarone is either unavailable or ineffective.

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16
Q

H’s

A

hydrogen (acidosis)
hyper/hypo Kalemia
Hyper/hypo thermia
hypovolemia
hypoxia

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17
Q

T’s

A

tension pneumo
torsades
toxins
thrombo cardiac
thrombo PE

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18
Q

Drugs for Arrest

A

epi
atropine
amiodarone

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19
Q

Drugs for tachycardia

A

adenosine
amiodarone
lidocaine
procainamide
sotalol

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20
Q

Drugs for bradycardia

A

atropine
dopamine
epi

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21
Q

no pulse. first action

A

compressions

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22
Q

how often do you give epi

A

3 min

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23
Q

what does adenosine do?

A

Adenosine is an efficacious diagnostic and therapeutic agent in the acute management of wide complex tachycardias. Its potent negative dromotropic in the AV node, and subsequently the rate of electrical impulses in the heart.) effect terminates supraventricular tachycardias involving the atrioventricular node, allowing differentiation from tachycardias of atrial and ventricular origin.

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24
Q

what is dromotropic?

A

A dromotropic agent is one which affects the conduction speed (in fact the magnitude of delay) in the AV node, and subsequently the rate of electrical impulses in the heart.

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25
Q

What medication is used to differentiate between SVT and VT?

A

Adenosine is safe and effective for differentiating wide-complex supraventricular tachycardia from ventricular tachycardia.

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26
Q

What is the first line drug for ventricular arrhythmias?

A

Typically, amiodarone will be the first-line drug of choice for all ventricular arrhythmias (VT, polymorphic VT, Vfib, etc.)

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27
Q

SVT will typically be managed with what medication?

A

SVT will typically be managed with adenosine

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28
Q

When a person’s pulse falls out of what is considered “normal,” then we say this individual has an

A

arrhythmia.

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29
Q

The QRS complex represents

A

ventricular depolarization on the EKG

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30
Q

what is WTC

A

wide complex tachycardia

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31
Q

What are some causes of Wide Complex Tach?

A

-Sodium channel blockade
-Hyperkalemia
-Hyper- or hypo-magnesemia
-Supraventricular tachycardia (SVT) with pre-existing or a rate-related bundle branch block (BBB)
-SVT with aberrant conduction
-Atrial fibrillation (Afib) with Wolff-Parkinson-White syndrome (WPWS)
-Mono-morphic ventricular tachycardia (VT)
-Ventricular fibrillation (VFib)
-Polymorphic VT (torsades de pointes)
-Pacemaker mediated tachycardia (PMT)
-Drug overdose and toxicities (i.e., TCA’s, digitalis, cocaine, lithium, diphenhydramine)
-Post-resuscitation (ROSC)
-EKG artifact

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32
Q

Out of all the known causes for wide QRS complex tachycardia, there are two etiologies ? and ? that account for the most cardiac deaths in the U.S.

A

(VT, VF) that account for the most cardiac deaths in the U.S.

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33
Q

What does adenosine do?

A

Adenosine is a purine nucleoside base, most commonly recognized with the molecule adenosine triphosphate, or ATP, and is used thoroughly throughout the entire body in general metabolism.[1] Adenosine’s use as a pharmacological drug works through receptors called purinergic adenosine receptors found throughout the body. Samsel et al. describe four types of adenosine receptors: A1, A2a, A2B, and A3, affecting the immune, nervous, circulatory, respiratory, and urinary systems. Most notably, receptors found in the cardiac atrioventricular (AV) nodal tissue and within the peripheral vasculature are what exhibit clinical manifestations when administering adenosine.[2][3]
Adenosine further classifies as a miscellaneous antiarrhythmic drug outside the Vaughan-Williams classification scheme. It acts on receptors in the cardiac AV node, significantly slowing conduction time.[3] This effect occurs by activation of specific potassium channels, driving potassium outside of cells, and inhibition of calcium influx, disrupting the resting potential of the slow nodal cardiac myocyte. Driving potassium outside of the cell causes hyperpolarization of the resting membrane potential while slowing of calcium influx causes suppression of calcium-dependent action potentials, all requiring a longer time for depolarization to occur and thus slowing down conduction within these cells, which is useful in SVT. SVT is defined as any arrhythmia originating above and including the bundle of His and specifically excludes atrial fibrillation by the ACC/AHA 2015 guidelines.[4] Usually narrow complex, SVT consists of several specific arrhythmias, which at a high rate (greater than 150 beats per minute), is difficult to diagnose. Adenosine has a role in slowing down the heart rate enough to assist in diagnosis. It can also terminate specific reentrant tachycardia involving the AV node, including AV nodal reentrant tachycardia (AVNRT), orthodromic AV reentrant tachycardia (AVRT), and antidromic AVRT, although extreme caution is necessary when administering adenosine for antidromic AVRT as it should be used only if the diagnosis is certain. https://www.ncbi.nlm.nih.gov/books/NBK519049/

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34
Q

Difference between SVT and Sinus Tach?

A

SVT rate will usually be greater than 150 and Sinus tachycardia will be less than 150.

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35
Q

What drug is ideally given through a peripheral intravenous (IV) access initially as a 6 mg dose followed by a 20 mL saline flush for rapid infusion. Subsequent doses start at 12 mg, also followed by 20-mL of saline for rapid infusion.[6]

A

adenosine

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36
Q

Pre-treatment RSI: What med may help prevent rise in ICP and reduce cough reflex? Med and dose. It’s also an amide anesthetic

A

Lidocaine 1.5mg/kg

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37
Q

Pre-treatment RSI
Which med may reduce bronch spasm

A

Lidocaine 1.5mg/kg

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38
Q

Pre-treatment RSI
What opioid receptor Agonist provides a benefit of analgesia and it blunts the effect of catecholamine

A

Fentanyl at a dose of 1 to 3 mcg/kg over a minute

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39
Q

Pre-treatment RSI
What are the contraindications of fentanyl

A

Decompensated shock and hemodynamically unstable

40
Q

Pre-treatment RSI
Succinylcholine or sux or succs is used for what

A

paralysis. DEPOLARIZING NEURO MUSCULAR BLOCKER, AUTONOMIC (SYMPATHOMIMETIC), SKELETAL MUSCLE RELAXANT,

ACTS IN 60 -90 SEC AND LASTS 3-5 MIN
CAUSES FASICULATION PROGRESSING TO PARALYSIS, INCLUDING PARALYSIS OF DIAPHRAGM
DOSAGE 1.0-1.5 MG/KG IV
PEDS DOSE 1.0-2.0 MG/KG IVP
PREPARE FOR INTUBATION IMMEDIATLEY AFTER ADMINISTRATION, IF INTUBATION IS UNSUCCESSFUL ASSIST VENTILATION.
CONTRAINDICTED IN PTS WITH PMHX OF MALIGNANT HYPERTHERMIA, SKELETAL MUSCLE MYOPATHIES , USE CATIOUSLY IN PEDS, PTS WITH BURNS, AND PTS WITH SIGNS OF RHABDOMYOLOSIS.

41
Q

Pre-treatment RSI: What is fasciculation

A

A fasciculation, or muscle twitch, is a spontaneous, involuntary muscle contraction and relaxation, involving fine muscle fibers. :IN RSI VECURONIUM TO MINIMIZE FASICULATIONS AND DEPOLARIZING EFFECTS OF SUCCS.

42
Q

Pre-treatment RSI: succ Initially causes what

A

Contraction of all the muscles in the body

43
Q

What do inotropes do?

A

increase cardiac contractility

44
Q

What do vasopressors do?

A

induce vasoconstriction increasing MAP

45
Q

What is alpha adrenergic

A

Activation of alpha-1 adrenergic receptors, located in vascular walls, induces significant vasoconstriction. Alpha-1 adrenergic receptors are also present in the heart and can increase the duration of contraction without increased chronotropy. However, clinical significance of this phenomenon is unclear

46
Q

What is beta adrenergic?

A

Beta-1 adrenergic receptors are most common in the heart and mediate increases in inotropy and chronotropy with minimal vasoconstriction. Stimulation of beta-2 adrenergic receptors in blood vessels induces vasodilation.

47
Q

Where are dopamine receptors?

A

— Dopamine receptors are present in the renal, splanchnic (mesenteric), coronary, and cerebral vascular beds; stimulation of these receptors leads to vasodilation. A second subtype of dopamine receptors causes vasoconstriction by inducing norepinephrine release.

48
Q

Delete

A

Some agents increase the sensitivity of the myocardial contractile apparatus to calcium, causing an increase in myofilament tension development and myocardial contractility (eg, pimobendan, levosimendan). These agents have additional pharmacologic properties, such as phosphodiesterase inhibition, which may increase inotropy and vasodilation and contribute significantly to their clinical profile, the details of which are discussed separately.

49
Q

What does angiotensin do?

A

Angiotensin receptors (AT1 and AT2) are G-coupled protein receptors with angiotensin II as their ligand. Angiotensin II is a vasoconstrictor that is part of the renin-aldosterone-angiotensin (RAAS) system. When receptors are stimulated, cytosolic calcium concentration increases to mediate vasoconstrictive effects as well as aldosterone and vasopressin secretion [5].

50
Q

What does dobutaimine do?

A

dobutamine increases cardiac output by beta-1 adrenergic receptor activation; however, it also acts upon beta-2 adrenergic receptors and thus induces vasodilation and can cause hypotension.

51
Q

Pressor administration is done how?

A

Vasopressors and inotropic agents should be administered through an appropriately positioned central venous catheter, if available. This facilitates more rapid delivery of the agent to the heart for systemic distribution and eliminates the risk of peripheral extravasation. When a patient does not have a central venous catheter, vasopressors and inotropic agents can be administered through an appropriately positioned peripheral intravenous catheter temporarily, until a central venous catheter is inserted

52
Q

How does atropine work

A

Atropine works by poisoning the vagus nerve, thereby removing parasympathetic inputs to the heart. This works beautifully for vagally-mediated bradycardia (e.g. vagal reflexes, cholinergic drugs). However, it fails for bradycardias caused by other mechanisms (e.g. heart block beyond the AV node). Overall, atropine is completely effective in only 28% of patients with symptomatic bradycardia (Brady 1999).

53
Q

Brady dopamine rate

A

Dopamine 5-20 mcg/kg/min, max 50 mcg/kg/min
Dobutamine 2-20 mcg/kg/min, max 40 mcg/kg/min
Epinephrine 2-10 mcg/min (~0.03-0.2 mcg/kg/min, max 1 mcg/kg/min)
Isoproterenol 2-10 mcg/min

54
Q

Brady epi rate

A

Dopamine 5-20 mcg/kg/min, max 50 mcg/kg/min
Dobutamine 2-20 mcg/kg/min, max 40 mcg/kg/min
Epinephrine 2-10 mcg/min (~0.03-0.2 mcg/kg/min, max 1 mcg/kg/min)
Isoproterenol 2-10 mcg/min

55
Q

Brady isoproterenol rate

A

Isoproterenol 2-10 mcg/min

56
Q

Brady dobutamine rate

A

Dobutamine 2-20 mcg/kg/min, max 40 mcg/kg/min

57
Q

Within the VT/VF pulseless arrest algorithm what is the first and second dose of Amiodarone

A

300mg IV/IO push → (if no conversion) 150 mg IV/IO push → (after conversion) Infusion #1 360 mg IV over 6 hours (1mg/min) → Infusion #2 540 mg IV over 18 hours (0.5mg/min)

58
Q

What is the maximum dose of amiodarone in 24 hour period

A

2.2 grams

59
Q

XXXX is only used after defibrillation (or cardioversion) and epinephrine (first line medication) fail to convert VT/VF.

A

amiodarone

60
Q

which medication is direct IV push during cardiac arrest and infused during bradycardia

A

epinephrine

61
Q

During Cardiac arrest how often and much epi

A

1mg Q3-5min

62
Q

what is IV infusion concentration for epinephrine for bradycardia

A

1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 micrograms/min (titrated to effect).

63
Q

what does EPi do to the heart and why is that bad

A

Epinephrine should be used with caution in patients suffering from myocardial infarction since epinephrine increases heart rate and raises blood pressure. This increase in HR and BP can increase myocardial oxygen demand and worsen ischemia.

64
Q

what is the primary drug used in the cardiac arrest algorithm?

A

epi- a vasopressor

65
Q

What does epi bind to

A

binds to beta-1-adrenergic receptors of the heart. This indirectly improves cardiac output by:
* Increasing heart rate
* Increasing heart muscle contractility
* Increasing conductivity through the AV node

66
Q

what does amiodarone treat

A

supraventricular arrhythmias and ventricular arrhythmias

67
Q

Do you dilute amiodarone for IVP?

A

nope, but you do for an infusion

68
Q

When do you dilute amiodarone?

A

To prepare Amiodarone for an IV infusion, mix with D5W and give through an in-line filter. Alternatively, it is NOT necessary to dilute amiodarone for IV push administration and a filter is not necessary.

69
Q

which medication can be absorbed by the IV tubing

A

amiodarone. When infusions exceed 2 hours, amiodarone can absorb into the plastic used for standard IV bags. This will change the medication concentration. Therefore, when an infusion exceeds 2 hours use a glass or polyolefin bottle for the administration container.

70
Q

when do you use lidocaine?

A

Lidocaine may be considered a suitable antiarrhythmic that can be used to treat cardiac arrest from VT/VF.
Lidocaine is now included in the AHA Cardiac Arrest diagram along with amiodarone. Emphasis should not be on the use of medications and it is the AHA recommendation to place more emphasis on high quality CPR and early defibrillation.

71
Q

Lidocaine indications for ACLS

A
  • In ACLS, Lidocaine is used intravenously for the treatment of ventricular arrhythmias. (VT/VF)
  • It is also useful for the treatment of stable monomorphic VT with preserved ventricular function and for stable polymorphic VT with preserved left ventricular function, normal QT interval, and correction of any electrolyte imbalances.
72
Q

s/e of lidocaine?

A

Lidocaine should be used with caution due to negative cardiovascular effects which include hypotension, bradycardia, arrhythmias, and/or cardiac arrest. Some of these side effects may be due to hypoxemia secondary to respiratory depression.

73
Q

What is the initial dose of lidocaine for cardiac arrest?

A
  • Initial dose: 1 to 1.5 mg/kg IV/IO
  • For refractory VF may give additional 0.5 to 0.75 mg/kg IV push, repeat in 5 to 10 minutes; maximum 3 doses or total of 3mg/kg
74
Q

What is the single dose for atropine?

A

1mg q3-5m. max total dosage is 3mg

75
Q

what is the first line medication for bradycardia?

A

atropine. atropine blocks the effects of the vagus nerve on the heart. When the vagus nerve is blocked, the SA node increases its rate of electrical discharge and this, in turn, results in the increased HR.

76
Q

what is a concern of atropine

A

Use atropine cautiously in the presence of myocardial ischemia and hypoxia because it increases oxygen demand on the heart and can worsen ischemia.

77
Q

what is the max cumulative dose of atropine

A

3mg

78
Q

what are the second line drugs for bradycardia

A

Epinephrine and dopamine are second-line drugs for symptomatic bradycardia. They are both used as infusions in the bradycardia algorithm if atropine is ineffective.

79
Q

how do you give dopamine

A

infusion

80
Q

dopamine is a XXX

A

beta agonist

81
Q

How do you mix dopamine for an infusion for bradycardia?

A
  • Dopamine 400 mg is mixed with 250 ml NS. Begin the dopamine infusion at 5 to 20 mcg/kg/min and titrate to the patient’s response.
82
Q

How do you mix epinephrine for an infusion for bradycardia?

A
  • 1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 mcg/min and titrate to the patient’s response.
83
Q

what is the goal when treating bradycardia

A

The goal of therapy is to improve the patient’s clinical status rather than target an exact heart rate.

84
Q

what is the primary drug for treatment of stable narrow-complex SVT?

A

Adenosine

85
Q

Which medication is slammed fast and chased with 20mls NS

A

adenosine

86
Q

which medication interrupts reentry pathways through the the AV node and restores sinus rhythm in pts with SVT

A

adenosine

87
Q

why is adenosine absorbed so fast

A

When injected into the body, adenosine is rapidly absorbed by red blood cells and blood vessel endothelial cells and metabolized for natural uses throughout the body. In light of this adenosine should be administered by RAPID intravenous bolus so that a significant bolus of adenosine reaches the heart before it is metabolized.

88
Q

how many times can you give adenosine?

A

they say 2x

89
Q

what is the first dose of adenosine?

A

6mg, the second is 12mg

90
Q

what is the second dose of adenosine?

A

12mg

91
Q

how long to wait between doses of adenosine

A

2 minutes

92
Q

what are Some side effects of adenosine administration

A

flushing, chest pain/tightness, brief asystole or bradycardia.

93
Q

when shouldn’t you give adenosine?

A

Make sure that adenosine is not used for irregular, polymorphic wide-complex tachycardia and unstable VT. Use in these cases may cause clinical deterioration.

94
Q
A
95
Q
A
96
Q
A

Chris Cards UCC (2 decks)

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