ACLS Flashcards
(116 cards)
1
Q
Bradycardia. 3 meds and doses
A
- Atropine, 1mg, repeat Q3-5 min, Max 3mg.
- Dopamine. 5-20mcg/kg/min. Titrate to response
- Epinephrine. 2-10mcg/min Titrate to response.
2
Q
Bradycardia. Tx. Start with…then progress to…
A
atropine
transcutaneous pacing
dopamine
epi
3
Q
What do you do with tachycardia and a pulse. Altered. Symptomatic.
A
Synchronized cardioversion unless QRS is narrow then adenosine.
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.
5
Q
Arrest. What do you shock?
A
VF/pVT
6
Q
Arrest. Why give epi?
A
makes heart more receptive to electrical stimulation
7
Q
Arrest. How many shocks before meds are given?
A
2
8
Q
Arrest. Asystole/PEA what do you do?
A
Epinephrine, 1mg, flush with 20ml NS, raise that arm.
9
Q
Arrest. What is the epi ratio?
A
1:10,000.
10
Q
Arrest. shockable rhythm. you have already given epi. What meds are next?
A
Amiodarone or Lidocaine.
11
Q
Arrest. First dose of amiodarone?
A
300mg
12
Q
Arrest. Second dose of amiodarone?
A
150mg
13
Q
Arrest. What are the joules in order of administration?
A
120j, 150j, 200j
14
Q
Arrest. What are the doses for lidocaine?
A
FIRST dose: 1-1.5mg/kg
SECOND Dose: 0.5-0.75mg/kg
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.
16
Q
H’s
A
hydrogen (acidosis)
hyper/hypo Kalemia
Hyper/hypo thermia
hypovolemia
hypoxia
17
Q
T’s
A
tension pneumo
torsades
toxins
thrombo cardiac
thrombo PE
18
Q
Drugs for Arrest
A
epi
atropine
amiodarone
19
Q
Drugs for tachycardia
A
adenosine
amiodarone
lidocaine
procainamide
sotalol
20
Q
Drugs for bradycardia
A
atropine
dopamine
epi
21
Q
no pulse. first action
A
compressions
22
Q
how often do you give epi
A
3 min
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.
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.
25
What medication is used to differentiate between SVT and VT?
Adenosine is safe and effective for differentiating wide-complex supraventricular tachycardia from ventricular tachycardia.
26
What is the first line drug for ventricular arrhythmias?
Typically, amiodarone will be the first-line drug of choice for all ventricular arrhythmias (VT, polymorphic VT, Vfib, etc.)
27
SVT will typically be managed with what medication?
SVT will typically be managed with adenosine
28
When a person’s pulse falls out of what is considered “normal,” then we say this individual has an
arrhythmia.
29
The QRS complex represents
ventricular depolarization on the EKG
30
what is WTC
wide complex tachycardia
31
What are some causes of Wide Complex Tach?
-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
32
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.
(VT, VF) that account for the most cardiac deaths in the U.S.
33
What does adenosine do?
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/
34
Difference between SVT and Sinus Tach?
SVT rate will usually be greater than 150 and Sinus tachycardia will be less than 150.
35
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]
adenosine
36
Pre-treatment RSI: What med may help prevent rise in ICP and reduce cough reflex? Med and dose. It's also an amide anesthetic
Lidocaine 1.5mg/kg
37
Pre-treatment RSI
Which med may reduce bronch spasm
Lidocaine 1.5mg/kg
38
Pre-treatment RSI
What opioid receptor Agonist provides a benefit of analgesia and it blunts the effect of catecholamine
Fentanyl at a dose of 1 to 3 mcg/kg over a minute
39
Pre-treatment RSI
What are the contraindications of fentanyl
Decompensated shock and hemodynamically unstable
40
Pre-treatment RSI
Succinylcholine or sux or succs is used for what
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
Pre-treatment RSI: What is fasciculation
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
Pre-treatment RSI: succ Initially causes what
Contraction of all the muscles in the body
43
What do inotropes do?
increase cardiac contractility
44
What do vasopressors do?
induce vasoconstriction increasing MAP
45
What is alpha adrenergic
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
What is beta adrenergic?
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
Where are dopamine receptors?
— 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
Delete
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
What does angiotensin do?
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
What does dobutaimine do?
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
Pressor administration is done how?
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
How does atropine work
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
Brady dopamine rate
Dopamine 5-20 mcg/kg/min, max 50 mcg/kg/min
54
Brady epi rate
Epinephrine 2-10 mcg/min (~0.03-0.2 mcg/kg/min, max 1 mcg/kg/min)
55
Brady isoproterenol rate
Isoproterenol 2-10 mcg/min
56
Delete
Dobutamine 2-20 mcg/kg/min, max 40 mcg/kg/min
57
Within the VT/VF pulseless arrest algorithm what is the first and second dose of Amiodarone
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
What is the maximum dose of amiodarone in 24 hour period
2.2 grams
59
XXXX is only used after defibrillation (or cardioversion) and epinephrine (first line medication) fail to convert VT/VF.
amiodarone
60
which medication is direct IV push during cardiac arrest and infused during bradycardia
epinephrine
61
During Cardiac arrest how often and much epi
1mg Q3-5min
62
what is IV infusion concentration for epinephrine for bradycardia
1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 micrograms/min (titrated to effect).
63
what does EPi do to the heart and why is that bad
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
what is the primary drug used in the cardiac arrest algorithm?
epi- a vasopressor
65
What does epi bind to
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
what does amiodarone treat
supraventricular arrhythmias and ventricular arrhythmias
67
Do you dilute amiodarone for IVP?
nope, but you do for an infusion
68
When do you dilute amiodarone?
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
which medication can be absorbed by the IV tubing
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
when do you use lidocaine?
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
Lidocaine indications for ACLS
* 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
s/e of lidocaine?
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
What is the initial dose of lidocaine for cardiac arrest?
* 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
What is the single dose for atropine?
1mg q3-5m. max total dosage is 3mg
75
what is the first line medication for bradycardia?
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
what is a concern of atropine
Use atropine cautiously in the presence of myocardial ischemia and hypoxia because it increases oxygen demand on the heart and can worsen ischemia.
77
what is the max cumulative dose of atropine
3mg
78
what are the second line drugs for bradycardia
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
how do you give dopamine
infusion
80
dopamine is a XXX
beta agonist
81
How do you mix dopamine for an infusion for bradycardia?
* 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
How do you mix epinephrine for an infusion for bradycardia?
* 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
what is the goal when treating bradycardia
The goal of therapy is to improve the patient’s clinical status rather than target an exact heart rate.
84
what is the primary drug for treatment of stable narrow-complex SVT?
Adenosine
85
Which medication is slammed fast and chased with 20mls NS
adenosine
86
which medication interrupts reentry pathways through the the AV node and restores sinus rhythm in pts with SVT
adenosine
87
why is adenosine absorbed so fast
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
how many times can you give adenosine?
they say 2x
89
what is the first dose of adenosine?
6mg, the second is 12mg
90
what is the second dose of adenosine?
12mg
91
how long to wait between doses of adenosine
2 minutes
92
what are Some side effects of adenosine administration
flushing, chest pain/tightness, brief asystole or bradycardia.
93
when shouldn't you give adenosine?
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
95
96
97
Temp range for targeted temp management
32-36 for 23 hours
98
AVPU?
Airway
Verbal
Pain
Unresponsive
99
For stroke : door to drug
60min
100
For stroke: onset to tPa or a CCU bed time
3 hours
101
For stroke: onset to tPa or a CCU bed time
3 hours
102
For stroke: head trauma or previous stroke within how many months
3
103
For STEMI: 2mm of elevation in which lead
V2 - V3
104
What are the lateral leads
1 and aVL
105
What are the anterior leads
V1 v2 v3 v4
106
Lidocaine blocks what channels
Sodium
107
Amiodarone blocks what channels
Mostly potassium, weakly sodium, and calcium channels
108
What ACLS drug requires a filter
Amiodarone 0.22 micron filter and special tubing
109
What ACLS drug requires a filter
Amiodarone 0.22 micron filter and special tubing
110
What ACLS drug requires D5W not NS
Amiodarone
111
Which ACLS drug should be given via central line
Dopamine because it is destructive to tissue
112
Which ACLS med shortens QT interval
Magnesium and it stabilizes membrane potentials
113
What is the second line drug and infusion rate for symptomatic bradycardia
Dopamine 2-10mcg/kg/min
114
Second degree type 2
Some Ps don’t have QRSs
115
Second degree type 1
Longer longer longer drop is a weinkie bop
116
Over how long do you give Mg sulfate
2gm over 10 minutes
