Therapeutics I Exam IV (A.fib + Stroke + Antiarrhythmics) Flashcards
A. Fib, Stroke, and Antiarrhythmics
1
Q
Advanced cardiac life support (ACLS) is used in the urgent treatment of what 5 things?
A
- Cardiac arrest
- Pulseless electrical activity/asystole
- Ventricular fibrillation/ Pulselessness ventricular tachycardia
- Post-cardiac arrest
- Opioid emergency
2
Q
What guidelines are used to determine to need for ACLS?
A
2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC)
3
Q
What is the definition of a medical emergency?
A
Any situation in which an individual’s life is acutely threatened due to illness or medical complications as evidenced by alterations of vital signs requiring immediate attention.
4
Q
What are the predictors for better outcomes with ACLS following a medical emergency?
A
Immediate CPR initiation, cardiac cause behind the emergency, young age, witnessed arrest, In-hospital cardiac arrest (IHCA), short duration or arrest, and shockable arrest.
5
Q
What are the predictors of worse outcomes with ACLS following a medical emergency?
A
Greater than 3-6 minutes before CPR initiation, pulmonary cause behind the emergency, preexisting comorbid conditions, non-witness arrest, out-of-hospital cardiac arrest (OHCA), long duration of arrest, non-shockable arrest, and cancer.
6
Q
What are the two drivers for out-of-hospital cardiac arrest (OHCA)?
A
- Lay rescuer cardiopulmonary resuscitation (CPR)
- Use of external automated defibrillator (AED)
7
Q
What is the definition of a cardiopulmonary arrest?
A
Loss of organ perfusion resulting from loss of functional myocardial contraction (pulselessness).
8
Q
Cardiopulmonary arrest is the loss of organ perfusion resulting from the loss of __________________ myocardial contraction.
A
Functional
9
Q
T or F: Pulse is generated by electrical potential not blood flow.
A
False. Pulse is generated by blood flow and not electrical potential.
10
Q
T or F: Coronary perfusion pressure is central to surviving cardiac arrest.
A
True
11
Q
Deoxygenated blood from the body travels through the ______ _______ into the ________ atria.
A
Vena Cava
Right
12
Q
Deoxygenated blood from the right ventricle is pumped through the _________ ________ into the lungs to be oxygenated.
A
Pulmonary artery
13
Q
Oxygenated blood from the lungs travels back to the heart via the ________ _________.
A
Pulmonary vein
14
Q
Oxygenated blood from the pulmonary vein enters the left atria and it pumped to the rest of the body via the __________.
A
Aorta
15
Q
T or F: The electrical signals of the heart can be working (ie producing an EKG) without the heart actually contracting. This is called pulseless electrical activity and it is a shockable rhythm.
A
False. This is the correct description of what PEA is but it is not a shockable rhythm. PEA and asystole are not shockable rhythms, focus on reversing Hs and Ts!
16
Q
The electrical signals of the heart can be working (ie producing an EKG) without the heart actually contracting. This is called pulseless electrical activity and it is a ________ rhythm.
A
Non-shockable
17
Q
The P wave on an EKG represents what?
A
Atrial depolarization
18
Q
The T wave on an EKG represents what?
A
Ventricular repolarization
19
Q
The QRS complex on an EKG represents what?
A
Ventricular depolarization (atrial repolarization also occurs here but the ventricular force is so powerful there is no visual of the atrial action)
20
Q
What is ventricular fibrillation (VFib)?
A
This is when there are rapid, uncoordinated, and fluttering contractions of the ventricles with normal atrial contraction. VFib inhibits isolated ventricular contractions and blood flow to the body.
21
Q
What is pulseless ventricular tachycardia (pVT)?
A
Super fast beats from the ventricles which does not allow blood to fill up in the ventricles leading to decreased cardiac output.
22
Q
What is pulseless electrical activity (PEA)?
A
This is when there is electrical activity occurring in the heart as seen in an EKG but the heart is not actually moving.
23
Q
What is asystole?
A
This is a complete stand still of the heart pumping and the electrical activity as seen in an EKG.
24
Q
T or F: PEA (Pulseless Electrical Acitivty) can be any rhythm, there is just no heart rate accompanying it.
A
True
25
What is the most common type of arrest?
Asystole (39%)
26
What is the general approach to a cardiac arrest?
C- Circulation absent (no pulse) : initiate CPR
A- Airway establishment
B- Breathing artificially in non-breathing persons
D- Defibrillate immediately if pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VFib)
27
What are the two shockable rhythms discussed?
Pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VFib)
28
CPR should go at a pace of _______ beats per min.
100-120
29
T or F: Allowing for the chest to fully recoil during CPR is not important.
False. Letting the chest fully recoil is crucial in allowing the ventricles to fill properly and supply the body.
30
When someone is presenting with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VFib), the focus is now on _______ __________.
Early defibrillation
31
When someone presents with asystole or pulseless electrical activity (nonshockable rhythms), the focus is now on __________ ________.
Reversible causes (5Hs and 5Ts)
32
What are the potential causes of pulseless electrical arrest (non-shockable rhythm)?
5Hs and 5Ts
Hs- Hypovolemia, hypoxia, H+ ions (acidosis), hypo/hyperkalemia, and hypothermia
Ts- Toxins, Tamponade, tension pneumothorax, thrombosis (pulmonary), thrombosis (MI)
33
T or F: You can only give shock to a heart that is still moving.
True! There is no 'frankensteining' a heart back to life.
34
What is the preferred defibrillation set-up and dose?
Biphasic and 200 joules (total 400 J)
35
What does biphasic mean in terms of defibrillation devices?
The current is delivered from one pad to the other and then reverses.
36
What are the two common causes of pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VFib)?
Acute coronary ischemia and myocardial infarction
37
If a person presents with a shockable rhythm (ie: pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VFib), always start with ______________ and then add medications.
Defibrillation (continue every 3-5 minutes)
38
What were the three medications discussed commonly used in adjunct with a defibrillator in a patient presenting with a shockable rhythm (ie: pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VFib)?
Epinephrine, amiodarone, or lidocaine
39
Every round of CPR given during a code should be a minimum of _____ minutes.
2 minutes
40
What is the MOA of epinephrine?
Stimulates alpha-1 and beta receptors. Via alpha-1 agonism, it vasoontricts the vessels allowing for increase BP, coronary perfusion, and cerebral perfusion. Via beta agonism, it increases cardiac output via increasing heart rate and contractility.
41
Epinephrine should be given every ______-______ minutes during a code blue.
3-5 minutes
42
What is the code blue dosing for epinephrine?
1 mg Q3-5minutes
43
T or F: Epinephrine can increase the return of spontaneous circulation (ROSC) and survival in patients.
True!
44
When should epinephrine be given in the cases of non-shockable rhythms like asystole or pulseless electrical activity?
ASAP!! These are non-shockable rhythms so no AED is needed.
45
When should epinephrine be given in the cases of shockable rhythm like VFib or pVT?
Give epinephrine are the first debfillrillation fails.
46
What are the 4 common adverse effects associated with epinephrine use?
Myocardial Ischemia
Ventricular Arrhythmias
Premature Ventricular Contractions (PVCs)
Aggravate or cause post-resuscitation supra ventricular tachycardia (SVT)
47
T or F: Epinephrine does not mix well with sodium bicarbonate therefore should be flushed after each dose.
True
48
T or F: Epinephrine is indicated in all arrest scenarios.
True. I know this is an absolute but it actually is true that epinephrine is indicated for every arrest event.
49
What medication used to be used in code scenarios but was found to be less efficacious compared to epinephrine?
Vasopressin
50
If a person fails CPR, shocks, epinephrine, amiodarone, and lidocaine, they are considered the have ____________ VFib or pVT?
Refractory
51
How is refractory VFib or pVT treated?
1. Could use double defibrillation meaning the joules are increased in the shock
2. Could use esmolol 0.5 mg/kg bolus followed by infusion
(Neither are high priority due to low evidence)
52
If antiarrhythmics are needed in a code blue during VFib or pVT, what two medications should be picked?
Amiodarone or lidocaine
53
T or F: Amiodarone and lidocaine administration shows improved survival to hospital admission and at hospital discharge.
False. Amiodarone and lidocaine improved survival to hospital admission but not till hospital discharge.
54
What is the MOA of amiodarone?
It is a class III anti-arrhythmic that delays the repolarization by prolonging the action potential and refractory period via Na+ and K+ channel blockades.
55
What is the dosing for amiodarone in a code blue scenario?
300 mg rapid IV bolus (in 20mL D5W)
if additional dose is needed:
150 mg rapid V bolus
56
T or F: Amiodarone is always an IV push medication even in situations that are not ACLS.
False. Only push amiodarone when in an ACLS event.
57
In non-ACLS situations, why is amiodarone not given IV push?
If a person has a pulse, pushing the medication will result in severe hypotension due to its polysorbate 80 diluent component.
58
What is the MOA for lidocaine?
It is a Class 1b anti-arrhythmic. It suppresses automaticity of conduction tissue by blocking Na+ channels therefore increasing the threshold of ventricle/Purkinje system/ventricular depolarization.
Lidocaine employs WEAK binding/affinity for SODIUM ion channels ONLY.
59
What is the dosing for lidocaine in a code blue scenario?
1-1.5 mg/kg IV push
If more needed, can repeat 0.5-0.75 mg/kg once
60
If a person obtains return of spontaneous circulation after recieving doses of amiodarone or lidocaine, what must happen next?
They must be put on a continuous infusion of the medication (amiodarone or lidocaine) that brought them back.
61
Magnesium is mainly reserved for a __________ __ ___________.
Torsades de Pointes
62
What is ECPR?
This is extracorporeal pulmonary resuscitation that is only used in those with shockable rhythms that have been witnessed. It basically is ECMO but for ACLS.
63
ECPR has been shown to work well in those with _________ rhythms and the event was witnessed.
Shockable
64
For non-shockable rhythms including asystole and pulseless electrical activity, what needs to be initiated ASAP?
CPR and Epinephrine (1mg bolus)
65
T or F: Shocks need to given in cases of asystole or pulseless electrical activity.
False. No shocks here. Just CPR and epinephrine
66
T or F: Besides epinephrine, there are no other medications used in non-shockable rhythms unless treating the underlying cause.
True!
67
Even though calcium chloride is not guideline recommended in ACLS situations, why is it sometimes given?
Calcium is a direct myocardial agonist causing heart to contract harder. Rapid and frequent administration has no improvement in mortality. Can be given in hyperkalemic patients.
68
Even though sodium bicarbonate is not guideline recommended in ACLS situations, why is it sometimes given?
Considered if patient in arrest for more than 15-20 minutes due to increased lactic acid causing decreased pH. Does not show improved outcomes.
69
Atropine sulfate is reserved for patients with symptomatic ___________ with a pulse.
Bradycardia
70
If a fibrinolytic were to be given during a code (ie: causes of ACLS due to thrombosis), what needs to happen afterwards?
High quality CPR (10 minutes) needs to be initiated or continued so the fibrinolytic can reach the site of action.
71
If IV access it unable to obtained, what is the next access port used in situations of ACLS?
Intraosseous
Could also be endotracheal but not ideal due to dose increases and lung flooding.
72
What things need to be done immediately after a patient experiences return of spontaneous circulation (ROSC)?
1. Obtain 12-lead EKG to rule out a STEMI
2. Give airway and oxygen
3. Prevent hypotension (SBP greater than 90, MAP greater than 65)
4. Gets labs rechecked
5. Consider targeted temperature management (maintain BT between 32-36 degrees 24 hours after ROSC in comatose patients)
73
How is the initiation of targeted temperature management decided in post-ROSC?
TTP is initiated if the patient does not respond to commands (comatose), then TTP is initiated. This means the patient is kept between 32-36C for 24 hours following their ROSC.
74
The _______ node is the internal pacemaker of the heart.
SA node
75
The right side of the heart has ______ fascicle of purkinje fibers while the left side of the heart has 2 fascicles.
One
76
What do cardiac muscle cells look like?
They are branched cells with a striated (striped) pattern under a microscope, containing a single, centrally located nucleus, and are connected to each other by specialized junctions called intercalated discs; this structure allows for coordinated contractions of the heart muscle.
77
What do the intercalated discs between cardiac myocytes do?
They facilitate the pinpoint action potentials going through the cardiac myocytes.
78
What is automaticity?
This is the ability of certain cardiac cells to depolarize spontaneously. This is mainly seen in the pacemaker cells within the SA node.
79
What is an action potential?
This is the event in which an electrical membrane potential of a cell rapidly increases and decreases with CONSISTENT pattern.
80
What is depolarization?
This is a shift in membrane potential from negative to positive. Activates the action potential.
81
What is repolarization?
This is a shift in membrane potential from a positive to negative charge. Inhibiting the action potential.
82
What is the effective refractory period?
This is the period of time in which new cardiac action potentials/action potentials in general cannot be generated.
83
What is conduction velocity?
This is the rate at which the action potential impulse propagates.
84
What are the two types of cardiac myocytes?
Pacemaker and non-pacemaker cells
85
Pacemaker cells located in the SA, AV, and ventricular conducting systems of the heart possess ____________, or the ability to depolarize above the threshold voltage in rhythmic fashion.
Automaticity
86
Non-pacemaker cells are found in the atrial and ventricular myocytes that are responsible for cardiac __________ and they respond to ________.
Contraction
Depolarization
87
Cardiac action potentials are created via the transport of what 3 ions?
K+, Na+, and Ca2+
88
Is potassium mainly stored intra or extracellularly?
Intracellular
89
Is sodium mainly stored intra or extracellulary?
Extracellularly
90
Is calcium mainly stored intra or extracellulary?
Extracellularly
91
Understand the steps of an acton potential within a pacemaker cell of the heart.
1. Na+ leaks into cell allowing it to become slightly depolarized
2. At -40mV, action potential is triggered and Ca2+ channels open and they flood the cell causing full depolarization
3. K+ channels then open and leave the cell repolarizing it
92
Understand the steps of an action potential within a non-pacemaker cell of the heart.
1. Upon stimulation, Na+ channels open and flood into the cell rapidly depolarizing it
2. At 123 mV, K+ channels open briefly and K+ leaves the cell while Ca2+ channels open up and enter to cell causing a flat life
3. Ca2+ channels close and K+ channels open again and leave the cell allowing for repolarization
93
What is occurring during the P-wave on an EKG?
Depolarization of the atria in response to the SA node triggering
94
What is occurring during the PR interval on an EKG?
Delay of AV node to allow filling of ventricles
95
What is occurring during the QRS complex on an EKG?
Depolarization of the ventricles which triggers the main pumping contraction. Massive amount of energy needed here.
96
What is occurring during the ST segment on an EKG?
This is the beginning of ventricle repolarization and it should always be flat.
97
What is occurring during the T wave on an EKG?
Ventricular repolarization
98
The depolarization of the pacemakers cells correlates to the ________ wave on an EKG
P-wave
99
The repolarization of the pacemaker cells correlates to the ________ interval and __________ on an EKG.
PR interval and Q-wave
100
The depolarization of non-pacemaker cells correlates to the _____ and _____ waves on an EKG.
R and S waves
101
The slightly flat portion at the top of non-pacemaker cells almost getting repolarized correlates to the ________ segment.
ST segment
102
Full repolarization in non-pacemaker cells is correlated to the _______ wave on an EKG.
T wave
103
When is treatment required for cardiac arrhythmias?
1. Cannot correct by removing the precipitating cause
2. Hemodynamic compromise
3. Active disturbance may lead to more serious arrhythmia
104
______ ________ are the most likely mechanism of an arrhythmia during anesthesia.
Re-entry circuits
105
Arrhythmias are most common in the _______________ phase after cardiac surgery.
Peri-operative phase
106
T or F: Many anti-arrhythmic drugs can potentiate arrhythmias.
True. Drugs are actually bad and too much of a good thing can lead to bad outcomes.
107
What is the main goal of anti-arrhythmic medications?
To modify impulse generation and conduction through blockage of ions
108
Class 1A anti-arrhythmics employ _________ binding and receptor affinity for _______ AND __________ ion channels.
MODERATE
SODIUM and POTASSIUM
109
Class 1A anti-arrhythmics reduce the phase ______ slope and ______ ____________ peak.
Phase 0 slope
Action potential peak
110
What are the 4 big things that class 1A anti-arrhythmics do to the heart?
1. DECREASE phase 0 slope and action potential peak
2. INCREASE effective refractory period
3. PROLONGs overall conduction velocity
4. MODERATE binding/affinity for SODIUM AND POTASSIUM ion channels
111
What is a major negative aspect about class 1A anti-arrhythmics?
They are proarrhythmic in around 8-12% of people who take them.
112
What are the 3 class 1A anti-arrhythmics we need to know?
Quinidine
Procainamide
Disopyramide
113
What are the 3 major adverse effects associated with Quinidine?
Torsades de Pointes (TdP)
Hepatoxicity
Myelosuppression
114
What are the 5 major adverse effects associated with Procainamide?
Lethal ventricular arrhythmias
Torsades de Pointes (TdP)
+ antinuclear antibodies
Lupus-like syndrome
Agranulocytosis
115
Out of the 3 class 1A anti-arrhythmics, which one is most 'pro-arrhythmic'?
Procainamide
116
What are the 2 adverse effects associated with disopyramide?
Anticholingeric effects and pro arrhythmic
117
T or F: Class 1A anti-arrhythmic are broad therapeutic index drugs.
False. These are narrow therapeutic index drugs.
118
Which of the following class 1A anti-arrhythmics can result in agranulocytosis?
Procainamide
119
In what two ways do class 1A anti-arrhythmics alter an EKG?
1. Widened QRS wave
2. Prolonged QT interval
120
What is the main risk associated with persistent QTc prolongation?
Ventricular tachycardia (torsades de pointes)
121
In a situation of Torsades de Pointes (type of ventricular tachycardia), what medication should be pushed right away?
Magnesium
122
Class 1B anti-arrhythmics employ ______ binding and affinity for only _________ channels.
WEAK
SODIUM CHANNELS
123
What are the 4 big things that class 1B anti-arrhythmics do?
1. Reduces phase 0 slope and action potential peak
2. Biggest decrease in overall conduction velocity here
3. Decreases effective refractory period
4. Weakly binds and inhibits sodium ion channels
124
T or F: Class 1B anti-arrhythmics are efficacious in the treatment of atrial arrhythmias.
False. They are only effective in ventricular arrhythmias like V.tach and V.fib
125
What are the two class 1B anti-arrhythmics we need to know?
Lidocaine and Mexilitene
126
What are the 3 adverse effects associated with the class 1B anti-arrhythmics, lidocaine?
Seizures, paresthesias, and methemoglobinemia
127
What is the big main adverse effect associated with the class 1B anti-arrhythmic, Mexilitene?
GI intolerance. Very rough on the gut.
128
Which anti-epileptic medication also serves as a class 1B antiarrhymthic?
Phenytoin
129
Which class has the biggest overall decrease in conduction velocity?
Class 1B
130
Mexilitene is the oral ___________ version of lidocaine.
Prodrug
131
What is the desirable serum range for lidocaine?
1.5-5 mcg/mL
132
Which class 1A anti-arrhythmic medications has the shortest half life?
Procainamide (2.5-4.5 hours)
133
What is the major metabolite of procainamide?
NAPA (N-acetylprocainamide)
134
In patients with asthma, lidocaine monitoring is important. Especially because at concentrations greater than ______ mcg/mL, it can lead to status asthmaticus.
10 mcg/mL
Concentration 10 or higher can also lead to a heart block, seizures, and bradycardia
135
What is the half-life of lidocaine?
1.5 hours
136
What are the EKG changes seen with class 1B anti-arrhythmics?
Narrowed QRS complex and shortened QT interval.
137
Which class of anti-arrhythmic has the most pronounced reduction in phase 0 slope and action potential peak?
Class 1C anti-arrhythmics
138
Class 1C anti-arrhythmics employ _________ binding and affinity for only _________ ion channels.
STRONG
SODIUM
139
T or F: Class 1C anti-arrhythmics have moderate effects on reducing conduction velcocity and the effective refractory period.
False. Class 1C anti-arrhythmics have no effect on conduction velocity and effective refractory period. They only have the most pronounced effect on decreasing the phase 0 slope and action potential peak.
140
What are the 2 main things that class 1C anti-arrhythmics do?
1. Most pronounced decrease in phase 0 slope and action potential peak
2. Strong binding for sodium ion channels
141
What are the two class 1C anti-arrhythmics we need to know?
Flecainide and Propafenone
142
What is unique about the two class 1C anti-arrhythmics?
Besides being strong sodium channel blockers, Flecainide also weakly inhibits potassium channels while propafenone moderately inhibits beta receptors.
143
Flecainide, a class 1C anti-arrhythmic, also has ______ _________ blockade activity.
Weak potassium (in addition to strong sodium ion channel inhibition)
144
Propafenone, a class 1C anti-arrhythmic, also has ________ _______ blockade activity.
Moderate Beta
145
T or F: Flecainide can be used in those with heart failure.
False. Never use flecainide with any level of severity heart failure.
146
What are the two adverse events associated with flecainide?
QRS prolongation and sudden cardiac death of post-MI
147
What is the main adverse effect associated with propafenone?
SA/AV/bundle branch block
148
What are the EKG effects seen with class 1C anti-arrhythmics?
Widened QRS complex
149
Class II anti-arrhythmics are all _____ ______ drugs.
Beta-blocker
150
What are the 4 big things that class II anti-arrhythmics do?
1. Prolongs AV node depolarization and repolarization
2. Prolongs conduction velocity
3. Decreases automaticity regulation
4. Increases effective refractory period
151
What does it mean that class II anti-arrhythmics decrease automaticity regulation?
This means that this class of medications decreases the spontaneous depolarization of pacemaker cells.
152
How do class II anti-arrhythmics alter an EKG?
Increased PR interval
153
What is the initial dose of the class II anti-arrhythmic, Atenolol?
25-50mg PO QD
154
What is the maintenance dosing for the class II anti-arrhythmic Atenolol?
50-200 mg PO QD
155
What adrenergic receptors does atenolol work at?
Beta 1
156
Is atenolol long or short acting?
Long-acting.
157
Can atenolol be given IV?
No, it only comes in oral formulations.
158
What is the brand name for atenolol?
Tenormin
159
Which metoprolol is approved for use in heart failure?
Metoprolol succinate (Toprol XL)
160
What adrenergic receptors do both metoprolol work at ?
Beta 1
161
Can metoprolol only be given orally?
No. Metoprolol is available IV and oral
162
What is the initial dosing for metoprolol succinate (Toprol XL)?
25-50mg PO QD
163
What is the maintenance dosing for metoprolol succinate (Toprol XL)?
25-200 mg PO QD
164
What is the brand name for metoprolol succiante?
Toprol XL
165
What is the brand name for metoprolol tartrate?
Lopressor
166
What is the initial dosing for metoprolol tartrate (Lopressor)?
50-100 mg PO in divided doses
167
What is the maintenance dosing for metoprolol tartrate (Lopressor)?
50-450 mg PO in divided doses
168
What receptor dos metoprolol tartrate act on?
Beta 1
169
What is the brand name for the class II anti-arrhythmic, Nebivolol?
Bystolic
170
What receptors does the class II anti-arrhythmic drug Nebivolol act on?
Beta 1 and Nitric Oxide
171
Out of all the class II beta blockers discussed, which two are renally cleared and may require renal dose adjustments?
Atenolol and Nebivolol
172
What is the initial dosing for Nebivolol (Bystolic)?
5 mg PO daily
173
What is the maintenance dosing for Nebivolol (Bystolic)?
5-40 mg PO QD
174
T or F: Carvedilol (Coreg) is approved in the treatment of heart failure.
True
175
Why three beta-blockers are approved for use in heart failure?
Bisoprolol (Zebeta)
Carvedilol (Coreg)
Metoprolol Succinate (Toprol XL)
176
What is the brand name for Carvedilol?
Coreg
177
What is the initial dosing for Carvedilol (Coreg)?
12.5 mg PO BID
for continuous release coreg: 20 mg PO QD
178
What is the maintenance dosing for Carvedilol (Coreg)?
12.5-25 mg PO BID
for continuous release coreg: 20-80 mg PO QD
179
Can carvedilol be given IV?
No. It is only available orally
180
What is the brand name for Bisoprolol?
Zebeta
181
What is the brand name for Esmolol?
Brevibloc
182
What is the brand name for Labetalol?
Normodyne
183
What receptors does the class II antiarrhythmic Bisoprolol work at?
Beta 1
184
What receptors does the class II antiarrhythmic Esmolol work at?
Beta 1
185
What receptors does the class II antiarrhythmic Labetalol work at?
Beta 1 and alpha
186
What receptors does the class II antiarrhythmic propranolol work at?
Beta 1 and beta 2
187
What are the 3 big things that class III anti-arrhythmic medications do?
1. Block potassium channels resulting in delayed repolarization (phase 3)
2. Prolongs conduction velocity
3. Increases effective refractory period
188
What are the 4 class III anti-arrhythmics we need to know?
Amiodarone
Sotalol
Dofetilide
Ibutilide
189
What is unique about the class III anti-arrhythmic, Amiodarone?
Amiodarone also blocks sodium, calcium, alpha, and beta channels and receptors. This additionally delays depolarization (phase 0) and AV node repolarization.
190
T or F: Drugs that alter potassium channels increase the risk of torsades de pointes as an adverse effect.
True! This is why many class III antiarrhythmics have this as a side effect for most of those drugs.
191
What is the main adverse effect seen with the following class III antiarrhythmics; sotalol, dofetilide, and ibutilide?
Torsades de pointes
192
What are the side effects associated with amiodarone?
Pulmonary fibrosis, altered thyroid function, hepatotoxicity, skin discoloration, and corneal deposits.
193
What makes amiodarone unique in terms of its PK properties?
40-55 day half life and very high volume of distribution. This means this drug goes into every tissue and stays in the body for almost 2 months.
194
After Ibutilide administration, a patient needs to be closely monitored for the next ______ hours.
8 hours
195
Which two class III antiarrhythmics are renally eliminated?
Sotalol and Dofetilide
196
What is the brand name for sotalol?
Betapace
197
What is the brand name for Dofetilide?
Tikosyn
198
What is the brand name for Ibutilide?
Corvert
199
What is the brand name for amiodarone?
Cordarone or Pacerone
200
When using class III antiarrhythmics, there is a potential to increase __________ interval. This in turn increases the risk for _________ ___ ________.
QTc interval
Torsades de Pointes
201
Before administering any class III antiarrhythmics in an inpatient setting, ___________ levels should be checked.
Magnesium
202
T or F: There must be a washout period when initiating patients on dofetilide.
True.
203
T or F: There must be a washout period when initiating patients on amiodarone. That washout period is 3 weeks.
False. The washout period for amiodarone is 3 months, not 3 weeks.
204
T or F: Sotalol (class III antiarrhythmics) and other beta blockers seen in class II can be used together.
True!
205
What is the black box warning associated with Amiodarone?
BBW for appropriate use, pulmonary and hepatic toxicities and proarrhythmic potential
206
The primary metabolite of amiodarone is ________________________.
N-desethylamiodarone
207
N-desethylamiodarone, the metabolite of amiodarone, initiates rapid __________ blockade with an IV push.
Beta
208
How does the action potential change when amiodarone is added?
- delays depolarization (phase 0) and AV repolarization
- prolongs conduction velocity
- increases effective refractory period
209
What 3 EKG changes are seen with the class III antiarrhythmic, amiodarone?
- Widened QRS complex
- Prolonged PR interval
- Prolonged QT interval
210
What changes are seen in an EKG with class III antiarrhythmics (not amiodarone)?
Prolonged QT interval
211
The class IV antiarrhythmics include _____ ___________ ________ blockers.
Non-DHP calcium channel blockers like diltiazem and verapamil
212
What is the MOA of the class IV antiarrhythmics which are non-DHP calcium channel blockers like diltiazem and verapamil?
Non-DHP CCBs block L and T-type voltage gated calcium channels with specificity to myocardium. It is mainly concentrated in the SA and AV nodes.
213
What are the 3 big things that class IV antiarrhythmics do?
1. Slow phase 0 calcium influx
2. Prolong AV node repolarization
3. Block L and T-type voltage gated calcium channels with specificity to myocardium concentrated in the SA and AV nodes
214
Which non-DHP CCB has a greater effect on calcium channels?
Verapamil
This medication also moderately blocks alpha receptors.
215
What is a big contraindication for the use of non-DHP CCBs like Verapamil and Diltiazem?
Do not use in patients with heart failure or post-MI patients.
216
What EKG changes are seen with class IV antiarrhythmics?
Prolonged PR interval
217
What is the indication for the use of digoxin?
Digoxin is used for control of ventricular response rate in atrial flutter and fibrillation
218
What is the MOA of digoxin?
Digoxin inhibits sodium-potassium ATPase therefore increasing intracellular sodium concentrations leading to increased intracellular calcium concentration. This improves cardiac contractility and increases cardiac vagal tone which decreases cardiac sympathetic activity.
219
What are the two brand names for digoxin?
Lanoxin or Digitek
220
Through digoxin's MOA, it improves cardiac ____________ and decreases cardiac __________ activity.
Contractility
Sympathetic
221
Digoxin does what two main things besides its actual MOA?
1. Prolongs effective refractory period and conduction velocity of the SA node
2. Shortens refractory period in atrial and ventricular myocardial cells
222
Digoxin increases inotropy (contractility) by inhibiting ________________ which increases intracellular __________ concentrations. This ion then binds to troponin C to increase contractility.
Na+/K+ ATPase
Calcium
223
T or F: Digoxin is hepatically cleared.
False. Digoxin is renally cleared therefore proceed with caution in those with renal dysfunction.
224
Digoxin loading dose is typically ________ mg in 24 hours.
1 mg in 24 hours
225
Digoxin maintenance dosing is ______-_______ mgIV/PO daily.
0.125- 0.25 mg daily
226
What is the reversal agent of digoxin?
Digoxin immune Fab
227
T or F: After giving Digoxin Immune Fab for digoxin overdose, do not check digoxin levels for the next 1-3 days.
False. After giving reversal agent, do not check digoxin levels for 5-7 days.
228
In heart failure, the ideal serum range for digoxin is _______-_____ ng/mL.
0.5-1 ng/mL
229
In atrial fibrillation, the ideal serum range for digoxin is ______-______ ng/mL.
0.8-1.5 ng/mL
230
What are the main 7 adverse effects associated with digoxin?
Arrhythmia (slowing of AV conduction), Anorexia, N/V, headache, fatigue, confusion, blurred vision (halos/ color perception changes)
231
What factors increase the risk for experiencing adverse effects associated with digoxin?
1. Electrolyte disturbances (hypokalemia, hypomagnesemia, and hypercalcemia)
2. Drug interactions (Quinidine, verapamil, amiodarone)
3. Disease states (hypothyroidism, hypoxia, renal failure, myocarditis
232
________________ can precipitate serious arrhythmias.
Hypokalemia
233
What is the brand name for Adenosine?
Adenocard
234
What is the MOA for adenosine (Adenocard)?
Adenosine inhibits cAMP-induced Ca2+ influx therefore suppressing Ca2+ dependent action potentials (ie pacemaker cells). It inhibits SA node, AV node, and atrial conduction.
235
What is the indication for use of adenosine?
1. Narrow complex paroxysmal supraventricular tachycardia (PSVT)
2. Wolff-Parkinson-White syndrome (WPW)
DO NOT USE IN A.FIB, A.FLUTTER, and V.TACH
236
What is the dosing for adenosine?
6 mg rapid IV push
(if rhythm is unchanged, can add two more 12mg doses pushed over 1 minute)
6-12-12
237
T or F: All adenosine IV pushes must be followed by a 20mL saline flush.
True.
238
T or F: Adenosine is best used in situations of atrial fibrillation, atrial flutter, and ventricular tachycardia.
False. Adenosine will not fix these rhythms. It will only fix PSVT and WPW.
239
The half life of adenosine is ___________ _____ (units).
10 seconds
240
What is one very unique side effect associated with adenosine?
Asystole. Pulse may bottom out for about 10 sounds and then go back to normal.
241
What are the adverse effects associated with adenosine?
Feeling of impending doom, asystole, flushing, chest discomfort, bronchoconstriction, transient new arrhythmia of short duration
242
The ________ _________ anti arrhythmic table is a tool attempting to classify anti arrhythmic medications based on receptor kinetics, affinity, and specificity.
Vaughan Williams
243
What is cerebral blood flow (CBF)?
This is the volume of blood that passes through a specific quantity of the brain tissue during a period of time.
50mL/100 g of brain tissue/minute
244
What is intracranial pressure (ICP)?
This pressure within the craniospinal compartment (normally 5-10 mmHg)
245
What is cerebral profusion pressure?
This is the net pressure gradient that drives oxygen delivery to cerebral tissue. Normally 60-80 mmHg.
246
What is the Monroe-Kelli Doctrine?
The Monroe-Kellie Doctrine states that the sum of the volumes of the brain, cerebrospinal fluid (CSF), and blood in the skull is constant. This means that if the volume of one of these components increases, the volume of one or both of the others must decrease.
247
What is an EEG?
This is a recording of summed electrical activity within the brain via the placement of electrodes.
248
What is a CT scan?
This is a fast series of x-rays put together to create images of an area.
249
What is an MRI?
This is when a strong magnetic field takes pictures of the inside of the body.
250
What is pupillometry?
These tests evaluate brain stem reflexes and optic/oculomotor nerves.
251
What is transcranial Dopplers (TCD's)?
This is an ultrasound that monitors cerebral blood flow velocity.
252
What are intraparenchymal bolts?
This is when a sterile catheter is advanced through the skull into the dura right into the right frontal region of the brain. It only measures intracranial pressure.
253
Intraparenchymal bolts only measure _______________ pressure.
Intracranial
254
What is an external ventricular drain (EVD)?
This is when a sterile catheter is advanced through the skull, dura, and brain parenchyma into the ventricles. It drains CSF and/or infection/blood as well as measures intracranial pressure
255
What are the two functions of an external ventricular drain (EVD)?
1. Drains CSF (or blood/infection)
2. Measure intracranial pressure
256
What guidelines are used for stroke decision making in pharmacy?
AHA/ASA guidelines
257
What are the two types of strokes?
A. Acute ischemic stroke (AIS)
B. Acute spontaneous intracranial hemorrhage (ICH)
258
What is the difference between a transient ischemic attack (TIA) and an acute ischemic stroke?
A TIA is a temporary blockage of blood flow to the brain but symptoms only last around 5 minutes as the clot dissolves on its own.
259
_____________ score estimates risk of stroke after a suspected TIA.
ABCD2
260
Are more strokes ischemic or hemmorrhagic?
Ischemic (87%)
261
What are the 8 different possible causes for a stroke?
- Atherosclerosis
- Vascular Malformation
- Arrhythmia
- Hyper coagulable state
- Small vessel disease
- Congenital heart disease
- genetic disorder
- Unknown
SHAAV CUG
262
What is the mnemonic the remember the presentation of a stroke?
BEFAST
Balance (unbalanced)
Eyes (blurred)
Face (drooping)
Arms (unable to lift)
Speech (slurred)
TIME (CALL 911)
263
What is the scale used to determine the severity of a stroke?
NIHSS scale (not sure if we actually need to memorize how to score or just the numbers)
264
What scale is used to determine the severity of an acute ischemic stroke?
ASPECTS
265
What is the time window in which thrombolytics can be given in cases with acute ischemic stroke?
Within 3-4.5 hours of the symptoms
266
What is the function of T-Pa?
T-Pa activates plasminogen to plasmin which goes into and breaks down fibrin to degrade a clot.
267
What is the dosing for Tenecteplase in cases is acute ischemic stroke?
0.25 mg/kg
268
What is maximum dose of Tenecteplase in the case of acute ischemic stroke?
25 mg
269
What is the dosing for Alteplase in cases of acute ischemic stroke?
0.9 mg/kg
270
What is the maximum dose of alteplase in the case of acute ischemic stroke?
90 mg
271
Does Tenecteplase or Alteplase have a longer half life?
Tenecteplase with a half life of 90-130 minutes. Alteplase is 5 minutes.
272
Tenecteplase is incompatible with _________ bolus over 5-10 seconds.
Dextrose
273
When giving alteplase, the first ______% must be given as a bolus while the rest is given as a continuous infusion over _________ hours.
10%
2 hours
274
How often must patients be monitored after receiving a fibrinolytic?
- Every 15 minutes for the first 2 hours
- Every 30 minutes for the next 6 hours
- Every hour until the 24 hour mark since given is hit
275
What are the ABSOLUTE contraindications for fibrinolytic use?
Intracranial hemorrhage
Cerebral vascular malformation
**Acute ischemic stroke within the last 3 months
Head injury in last 3 months**
Aortic dissection
Active bleeding
**Recent intracranial or spinal surgery**
On anticoagulants (INR >1.7 on warfarin)
Active endocarditis
Bolded are the ones I can't remember
276
What are the relative contraindications for fibrinolytic use?
Poorly managed HTN
Prolonged CPR
Major surgery within the last 3 weeks
**History of acute ischemic stroke**
Dementia
Internal bleeding within the last 2-4 weeks
Pregnancy
Peptic ulcer
**Recent lumbar puncture**
NIHSS > 25
**Coagulopathy**
(Bolded are the ones I keep forgetting)
277
Those who are candidates for thrombolytics with acute ischemic stroke must arrive to the hospital within _______-________ hours of their stroke.
3-4.5 hours
278
What are the 3 things patients must have in order to be a fibrinolytic candidate?
-last known 'well' was within 3-4.5 hours from arrival
- no contraindications
- BP less than 180/110
279
If a patient is a candidate for fibrinolytics but their BP is above 180/110, what 3 medications can be used to reduce BP before giving the fibrinolytic?
Nicardipine
Clevidipine
Labetalol
280
What is the IV dosing for Nicardipine?
1-15 mg /hr
281
What is the IV dosing for Clevidipine?
1-21 mg/hr
282
Between Nicardipine, Clevidipine, and Labetalol, which one has the fastest onset?
Nicardipine (1-2 minutes)
283
Between Nicardipine, Clevidipine, and Labetalol, which one has the fastest half-life?
Clevidipine (1 minute)
284
What is the dosing for labetalol?
10-20 mg over 1-2 minutes
285
The blood pressure goal for those presenting with acute ischemic stroke is less than ______/______.
180/110 mmHg
286
What is an endovascular thrombectomy?
This is a minimally invasive procedure that removes blood clots (thrombi) from blood vessels using a catheter
287
In order to be a candidate for a thrombectomy, what 3 criteria within the brain must be met?
1. Infarct volume less than 70 mL
2. Ratio of ischemic tissue to initials infarct volume of 1.8 or more
3. penumbra greater than 15 mL
288
In order to be a candidate for a thrombectomy, what 2 criteria within the patient must be met?
1. Within 24 hours of last known 'well'
2. Large vessel occlusion in either middle cerebral artery, internal carotid artery, or basilar artery
289
What is an infarct core?
This is the brain tissue that has already died and cannot be reversed due to the stroke.
290
What is the penumbra?
This area surrounds the infarct core and is at high risk of dying but damage is reversible here.
291
What is the oligemi?
This is areas of hypoperfusion surrounding the infarct core and penumbra. This area will recover without treatment.
292
T or F: It is fairly normal for patients with acute ischemic stroke to receive both fibrinolytic and a thrombectomy.
True.
293
In order for a patient to be a candidate for a thrombectomy, what 3 vessels could be blocked?
Middle cerebral artery
Internal Carotid artery
Basilar artery
294
If the thrombolytic is not working well in the treatment for an acute ishcemic stroke, ________________ can be added on.
Antiplatelets including GpIIb/IIIa inhibitors like Tirofiban and Eptifibatide or P2Y12 inhibitor like Cangrelor.
295
What is a decompressive hemicraniectomy?
This is when a large flap of skull is removed and the dura remains open in order to relieve pressure on the brain.
296
In order to be eligible for a decompressive hemicraniectomy, patients must be between the ages of _______-_______ years and have at least ________ of territory infarcted.
18-60 years
2/3rds
297
What are massive complications associated with acute ischemic strokes?
Possible hemorrhagic conversion, brain edema, UTIs, VTEs, and pneumonia
298
In order to prevent hemorrhagic conversion following an acute ischemic stroke, blood pressure should be kept below ______/_____ if the patient had ____________ therapy.
180-105
Reperfusion
299
What 2 things increase the risk for hemorrhagic conversion following an acute ischemic stroke?
Bigger strokes (NIHSS >20) and reperfusion therapy
300
Why is pneumonia a major complication following an acute ischemic stroke?
Stroke patients often have dysphagia after a stroke and aspirate things into the lungs leading to pneumonia.
301
What is the 3rd leading cause of death following a stroke?
Pneumonia
302
__________ ________ accounts for 10% of deaths following a stroke.
Pulmonary embolism
303
How are VTEs (DVT/PE) prevented during stroke treatment?
Think prophylaxis anticoagulation here:
-5000 Units unfractionated heparin TID
-Enoxaparin 40 mg SubQ daily
**
24 hours post clean CT in hemorrhagic stroke
24 hours post thrombolytic in ischemic stroke**
304
What is the key thing to prevent VTEs following a stroke?
Early mobilization
305
What is the black box warning for prasugrel?
Fatal bleeding in those with history of TIA or stroke
306
What are the things that need to be checking in a patient after getting care for a stroke?
- Lipid level check for atherosclerosis
- PFO check (hole in heart)
- Intracranial atherosclerotic disease (ICAD) check
- EKG check for possible arrhythmia
- Glucose + HbA1c for diabetes
- BP for hypertension check
- smoking habits
- Hypercoagulablility testing
307
T or F: Clopidogrel is not a prodrug.
False. Clopidogrel is a prodrug
308
What is the dosing for the irreversible P2Y12 inhibitor anti platelet, clopidogrel?
Loading dose: 300-600 mg
Then 75 mg daily
309
What is the dosing for Ticagrelor?
Loading dose: 180 mg
Then 90 mg BID
310
What are the 3 antiplatelets typically used following a stroke?
Clopidogrel, ticagrelor, and/or aspirin
311
A ___________ _____ scan is needed to exclude intracranial hemorrhagic stroke before giving IV TPA.
Noncontrast CT
312
For those with intracranial atherosclerotic disease following a stroke, AHA guidelines state that _________ at doses of ________ mg per day is the superior antiplatelet for this population.
Aspirin
325 mg/day
313
___________ mg of ___________ decreased overall incidence of stroke and cardiovascular events.
80 mg of atorvastatin
314
T or F: Most stroke patients should be on a high intensity statin like atorvastatin 80mg or rosuvastatin 40 mg.
True.
315
Ticagrelor efficacy is reduced when used in combination with aspirin doses greater than __________ mg.
100 mg
316
If a person who had a acute ischemic stroke and also has a atrial fibrillation/flutter, what 3 anticoagulants could be used?
Warfarin, apixaban, or rivaroxaban
317
Before initiating/ reinitating any anticoagulants after an acute ischemic stroke, a time period of _____-______ days must be waited.
4-14 days all dependent on stroke size
318
What is the dosing for apixaban for atrial fibrillation following an acute ischemic stroke?
5 mg PO BID
319
What is the dosing for rivaroxaban for atrial fibrillation following an acute ischemic stroke?
20 mg daily
320
After giving thrombolytics or endovascular therapy, the systolic blood pressure goal is between _________-_________ mmHg.
130-180 mmHg
321
If a person receives no treatment following their acute ischemic stroke (ie; they got to the hospital too late), what is their blood pressure goal?
Less than 220/110 mmHg for 48-72 hours. This is letting the body naturally regulate
322
For any form of treatment or no treatment, what is the blood pressure goal for everyone that was treated for an acute ischemic stroke after 72 hours?
140/90 mmHg
If higher, initiate blood pressure lowering agents
323
T or F: Secondary prevention is key for preventing future strokes.
True
324
What is a hemorrhagic stroke?
This is bleeding into the brain tissue or parenchyma (functional brain tissue)
325
What are some things about the brain that increase the risk for a hemorrhagic stroke?
Aneurysms, AV malformations, tumors, angiopathy, coagulopathy, trauma, on anticoagulants
326
Hemorrhagic strokes make up ____-_____% of all strokes.
10-15%
327
What are the two hemorrhagic type strokes discussed in class?
Intracerebral/ Parenchymal hemorrhage
Subarachnoid hemorrhage
328
What are typical causes of intracranial hemorrhages?
Trauma or spontaneous
329
What are modifiable risk factors that increase the likelihood of getting an intracranial hemorrhage?
Hypertension
Coagulopathy (impaired clot formation)
Current smoker
Excessive alcohol (alcohol is blood thinner)
Diabetes
Sympathomimetic and illicit drug use
330
What are nonmodifiable risk factors that increase the risk for intracranial hemorrhage?
Prior intracranial hemorrhage
Advanced age
Male sex
Non-white ethnicity
Cerebral amyloid angiopathy
CKD
Congenital coagulopathy
Tumor
Vascular abnormalities
331
Do ischemic and hemorrhagic strokes have similar symptoms?
Yes! Both types will present with BEFAST
332
What tool is used to evaluate the severity of an intracranial hemorrhage?
ICH Score
333
What is desmopressin?
Medication that increases Von Willebrand factor receptors so that platelet aggregation can be increased.
334
A patient presents with an intracranial hemorrhage and is on anticoagulants. What is the first thing to be done once this information is uncovered?
Discontinue to anticoagulant. Based on the anticoagulant type, may need to administer the antidote to stop bleeding.
335
A patient presents with an intracranial hemorrhage and is on warfarin. What should be done next?
1. STOP THE WARFARIN
2. MEASURE INR
A. INR 1.3-1.9: give 4F PCC 10-20 IU/kg
B. INR >2: give 4F PCC 25-50 IU/kg
3. GIVE VITAMIN K
336
A person on warfarin presents with ICH. At what INR range would they receive 10-20 IU/kg of 4-factor PCC (and vitamin K of course)?
1.3-1.9 INR
337
A person on warfarin presents with ICH. At what INR range would they receive 25-50 IU/kg of 4-factor PCC (and vitamin K of course)?
INR of 2 or greater
338
A patient presents with an intracranial hemorrhage and is on dabigatran. What should be done next?
1. Figure out when dose was last taken
2. If taken within the last 2 hours: GIVE ACTIVATED CHARCOAL
3. Longer than 2 hours: Give Idarucixumab
339
A patient presents with an intracranial hemorrhage and is on an Xa-inhibitor like rivaroxaban or apixaban. What should be done next?
1. Figure out when dose was last taken
2. If taken within the last 2 hours: GIVE ACTIVATED CHARCOAL
3. Longer than 2 hours: Give andexanet alfa (if not available can use 4F PCC)
340
A patient presents with an intracranial hemorrhage and is on unfractionated heparin. What should be done next?
1. STOP HEPARIN
2. Give protamine
341
A patient presents with an intracranial hemorrhage and is on LMWH like dalteparin or enoxaparin. What should be done next?
1. STOP THE LMWH
2. Give protamine
342
A patient presents with an intracranial hemorrhage and is on an antiplatelet like clopidogrel or aspirin. What should be done next?
There is no specific reversal agent for anti-platelet agents unfortunately. If the patient HAS to undergo rapid intervention, can initiate platelet transfusion.
343
T or F: Desmopressin is proven to be an adequate agent for antiplatelet reversal.
False. It is unknown if desmopressin with platelet transfusions decreases hematoma size.
344
If the patient is not on anticoagulants or antiplatelets and just had the most random ICH, what is the last treatment option?
Tranexamic acid (TXA)
345
What is the MOA of tranexamic acid?
Tranexamic acid is a synthetic derivative of lysine that exerts antifibrinolytic effects by blocking lysine binding sites on plasminogen molecules, inhibiting the interaction of plasminogen with formed plasmin and fibrin.
346
Managing _______ _________ for an ICH patient is crucial to their recovery.
Blood pressure
347
Blood pressure treatment for those presenting with ICH needs to be initiated with ______ hours of hospital arrival.
2 hours
348
What is the systolic blood pressure goal for those with ICH?
Systolic between 130-150
349
T or F: Even though the goal for systolic blood pressure in ICH patients is 130-150, going below 130 mmHg improves outcomes.
False. Reducing systolic BP below 130 may be harmful as the brain is not getting perfused.
350
What are the two main agents used to control blood pressure in ICH patients?
Typically use Nicardipine or Clevidipine as there is not too much variability in blood pressure with these DHP CCBs.
351
What is the dosing for Nicardipine in terms of blood pressure regulation?
0-15 mg/hour
352
What is the half-life of nicardipine?
3 minutes
353
What is the dosing for Clevidpine?
0-21 mg/hour
354
What is the half-life for clevidpine?
1 minute
355
If a patient presents with an ICH and is on any type of anticoagulant, rapid reversal (assuming applicable), need to be initiated within ________ hour of arrive.
1 hour
356
If a DOAC or dabigatran was taken within the last _______ hours of arrival, give activated charcoal.
2 hours
357
T or F: Platelet transfusion are only indicated if a patient needs emergency surgery.
True. Giving platelets if a patient is on an antiplatelet but does not need surgery is not indicated in the guidelines.
358
For warfarin reversal, 4F PCC is given. What is this medication?
4F PCC is also called KCENTRA. It replaces factors II, VII, IX, and X, as well as protein C and S.
359
Warfarin reversal includes giving 4F PCC and _________________ via IV push.
Vitamin K
360
What is the reversal agent for DOACs like rivaroxaban and apixaban?
Andexanet alfa
361
What is the reversal agent for dabigatran?
Idarucizumab (Praxbind)
362
What is the MOA of andexanet alfa?
This is the reversal agent for DOACs. It works by being a factor Xa decoy molecule that sequesters the DOACs and prevents them from inhibiting the real factor Xa.
363
What is the MOA for idarucizumab (Praxbind)?
It is a monoclonal antibody that binds and inhibits dabigatran itself.
364
What is the MOA of protamine?
Protamine reverses heparins. Protamine is a highly alkaline protein molecule with a + charge that binds heparin which is - charged.
365
Why is the maximum dose for protamine 50 mg?
At doses higher than 50 mg, protamine turns into an anticoagulant.
366
What are the 4 things that go into secondary prevention following an intracranial hemorrhagic stroke?
1. Finding underlying cause
2. Glucose control
3. Seizure management
4. Surgical management (external ventricular drain)
367
What is the surgical management for a spontaneous ICH with obstructive hydrocephalus?
External ventricular drain placement
368
What is the surgical management for a spontaneous ICH with less than 30mL of blood collected and a GCS greater than 3?
External ventricular drain with possible small amount of thrombolytic placed into the stroke site within the brain.
369
What is the surgical management for a spontaneous ICH with less than 30 mL of blood collected?
Possible neuroendoscopy with an external ventricular drain placed and a small amount of thrombolytic placed at the brain site of injury.
370
What are the 5 common complications associated with ICH?
Expansion of hemorrhage
Seizures (no seizure prophylaxis tho)
cerebral edema
Hydrocephalus
VTE
371
When would we restart an ICH patient on their anticoagulants for VTE prophylaxis?
24 hours following the last stable CT scan
372
Having a subarachnoid hemorrhage is actually really bad because of what anatomical freature?
This section of the protective layers of the brain actually houses most of the cerebral arteries.
372
T or F: Most subarachnoid hemorrhages are nonspontaneous.
False. Most are spontaneous
373
What are risk factors that increase the risk of developing an aneurysm?
Family history
Connective tissue disorders
polycystic kidney disease
Injury
374
What is an aneurysm?
It is a weak or thin spot on an artery in the brain that bulges out and fills with blood. Majority of these forms in major arteries along the base of the skull. They can range from 1/8 inch to a full inch.
374
What are the risk factors that increase the risk for a ruptured aneurysm?
Hypertension
smoking
alcohol abuse
Race
sympathomimetic drugs
Aneurysm greater than 7 mm
375
What scoring tool estimates the survivability based on symptoms for a subarachnoid hemorrhage?
Hunt and Hess Scoring tool
375
What is the hallmark presentation of a subarachnoid hemorrhage?
Worst headache of entire life
376
T or F: An aneurysm leads to a hemorrhage.
True
377
What is the most common cardiac arrhythmia?
Atrial Fibrillation
378
What scoring tool evaluates the risk for vasospasm after a subarachnoid hemorrhage?
Modified Fischer Scale
379
What are the different ways to diagnose a subarachnoid hemorrhage?
Noncontrast head CT or a lumbar puncture
380
What is the blood pressure goal for someone with an unsecured aneurysm?
SBP less than 160, but 130-140 is the real goal!!!
381
What is the systolic blood pressure goal for someone with a secured aneurysm?
SBP 130-160
382
If a patient with a subarachnoid hemorrhage is on anticoagulants, what is the first thing to do?
STOP THE ANTICOAGULANT AND GIVE REVERSAL AGENT PER ICH GUIDELINES
383
Is it reasonable to consider antifibrinolytic therapy (TXA) for acute management in subarachnoid hemorrhage?
Yes. Note that the results when using TXA in a subarachnoid hemorrhage is not that beneficial.
384
What are the two ways in which an aneurysm can be secured?
Clip or coil
385
What are the complications associated with subarachnoid hemorrhage?
Vasospasm which lead to delayed cerebral ischemia
Rebleeding
Seizures ( prophylaxis here)
Hydrocephalus
Medical issues like pneumonia
386
___________ __________ is a type of ultrasound that can see vasospasm.
Transcranial dopplers
387
What scoring tool is used to evaluate the risk for vasospasms?
Modified Fischer scale
388
How are vasospasm managed in patients following a subarachnoid hemorrhage?
Nimodipine 60 mg Q4H for 21 days
389
What is the MOA of Nimodipine?
It is a calcium channel blockers that improves delayed ischemic neurological deficit but not the actual vasospasm.
390
What is a side effect associated with Nimodipine?
Hypotension
391
Atrial fibrillation is higher in ________ and ________ people.
Women
White
391
T or F: 80% of patients with permanent atrial fibrillation have an identifiable underlying casue.
True
391
T or F: 1 in 6 strokes occurs in patients with atrial fibrillation.
True
391
T or F: For both ischemic and hemorrhagic strokes, VTE prophylaxis should be resumed as soon as possible.
True
(24 hours after a clean CT scan for ICH)
(24 hours post-thrombolytic for AIS)
391
It is important to maintain ______________ for a patient while they are on Nimodipine.
Euvolemia
391
If delayed cerebral ischemia is suspected, what can be done?
Pressors can be given to increase blood pressure to open up those shut vessels and increase perfusion.
392
What is the pathophysiology surrounding atrial fibrillation?
Supraventricular impulses penetrate the AV conduction system in variable degrees resulting in an irregular activation of the ventricles and an irregularly, irregular pulse. The AV junction will not conduct most of the supraventicular impulses causing ventricular response to be considerably closer.
The pathophysiology of atrial fibrillation (AF) revolves around chaotic electrical activity in the atria, leading to an uncoordinated and ineffective contraction of the upper chambers of the heart. Here’s a breakdown of what happens:
1. Electrical Dysfunction
Normally, the sinoatrial (SA) node in the right atrium is the heart’s natural pacemaker, sending out regular electrical impulses that coordinate heartbeats.
In AF, ectopic electrical signals (abnormal impulses) originate mostly in the pulmonary veins of the left atrium.
These abnormal, rapid impulses (300-500 per minute) override the SA node, causing the atria to quiver (fibrillate) instead of contracting properly.
2. Loss of Atrial Contraction
Because the atria are not pumping effectively, blood does not flow smoothly into the ventricles.
This can cause blood stasis (pooling) in the atria, increasing the risk of clot formation, which can travel to the brain and cause a stroke.
3. Irregular Ventricular Response
The atrioventricular (AV) node, which acts as a gatekeeper for electrical signals to the ventricles, gets bombarded with irregular impulses from the fibrillating atria.
The AV node filters out some impulses, but the ones that get through cause an irregularly irregular heartbeat with a ventricular rate of 120-180 bpm.
This irregular and rapid heart rate reduces the heart’s ability to pump blood effectively, leading to symptoms like fatigue, dizziness, shortness of breath, and palpitation
393
Which anti-arrhythmic agents prolongs the QT interval?
Class 1A drugs (Quinidine, procainamide, disopyramide), class III drugs + amiodarone
394
Which anti arrhythmic class does sotalol belong to?
Class III
395
What is the mechanism of action of digoxin?
Inhibits Na+/K+ ATPase increaasing Na+ and Ca2+ concentrations inside the cell. This improves cardiac contractility and increases cardiac vagal tone which decrease cardiac sympathetic activity.
396
Atrial fibrillation is characterized by by extremely rapid ________ rate of ______-______ bpm and disorganized atrial activation.
Atrial
300-500
397
Atrial fibrillation has an __________, _______ pulse.
Irregularly, irregular
398
What is considered recurrent atrial fibrillation?
2 or more episodes
399
What is considered paroxysmal atrial fibrillation?
Terminates spontaneously or with intervention within 7 days of onset.
400
What is considered persistent atrial fibrillation?
Sustained beyond 7 days
401
What is considered longstanding persistent atrial fibrillation?
Continuous atrial fibrillation with 12 months or longer of duration
402
What is considered permanent atrial fibrillation?
Term used to describe joint decision between care team and patient to cease further attempts to restore or maintain sinus rhythm.
403
What is nonvalvular atrial fibrillation?
Atrial fibrillation in the presence of rheumatic mitral stenosis, a heart valve, or mitral valve repair.
404
What are modifiable risk factors for atrial fibrillation?
Obesity
lack of fitness
HTN
Sleep apnea
alcohol
diabetes
smoking
heart failure
Coronary artery disease
thyroid disease
405
What are non-modifiable risk factors for atrial fibrillation?
Genetics
Male sex
Age
406
What are the 4 factors that decrease the chances of success in treating atrial fibrillation?
Presence of coronary artery disease
Heart failure
Age greater than 75
Prior stroke/TiA
407
What are the clinical consequences of atrial fibrillation?
Decreased cardiac output leading to heart failure, prolonged rapid ventricular response which may lead to cardiomyopathies, and stroke
408
What is the biggest consequence of atrial fibrillation?
Stroke
409
What are the signs and symptoms of atrial fibrillation?
Rapid heart rate, palpitations, shortness of breath, fatigue, syncope, peripheral edema, chest pain, and anxiety
410
What are the objective signs for atrial fibrillation?
EKG changes: dropped P wave, irregular irregular rhythm with fast ventricular rate (120+)
411
What are the two ways in which symptoms for atrial fibrillation are treated?
Rhythm control and rate control
412
T or F: All patients with **atrial fibrillation** should be evaluated for risk of stroke with the CHAD2DS2VASC score.
True!! always need to do this. If the patient does not have atrial fibrillation, this score would not be calculated.
413
Using the CHAD2DS2VASC score evaluates if a patient with atrial fibrillation needs to be on _________________ to prevent a stroke.
anticoagulation
414
Patients with atrial fibrillation should be evaluated for _________ risk with the HAs-BLEED scoring tool.
Bleed
415
What does CHADs2-VASc stand for?
CHF, HR
HTN
Age greater than 75
Diabetes
Stroke
Vascular disease (CAD, MI, PAD)
Age: 65-74
Sex: Female
416
For anticoagulation in atrial fibrillation ____________ is preferred over warfarin.
DOACs
417
T or F: Aspirin alone or with combination with clopidogrel is not recommended to reduce stroke risk in atrial fibrillation.
True
418
Should patients with a CHAD2DS2VASC score of 0 in men and 1 in women be anticoagulated?
No
419
Should patients with a CHAD2DS2VASC score of 1 in men and 2 in women be anticoagulated?
DOAC or warfarin is reasonable with patient and care team. DOAC is preferred.
420
Should patients with a CHAD2DS2VASC score of 2 in men and 3 in women be anticoagulated?
DOAC or warfarin needed. DOAC is preferred
421
_________________ estimates bleeding risk.
HAS-BLEED
422
T or F: HAS-BLEED score allows you to exclude patients for anticoagulation.
No. It is only used to identify high risk patients. We do not exclude patients for anticoagulation based on their HAS-BLEED score.
423
What does it mean for a medication to be a rate control agent?
Allows the arrhythmia to continue but control ventricular rate using mainly class II and IV antiarrythmics
424
What does it mean for a medication to be a rhythm control agent?
Stops the arrhythmia using class I and III antiarrythmics
425
T or F: Both rate control and rhythm control agents have comparable clinical outcomes.
True
426
What are the first line rate control agents for atrial fibrillation?
Beta blockers and Non-DHP CCBs
427
Rate control agents like beta-blockers and Non-DHP CCBs work by slowing ________ node conduction.
AV node
428
T or F: Digoxin can be added to other agents to further benefit rate control and it just as effective as a stand along agent.
False. Digoxin is commonly added with other rate control agents but it less effective as a stand alone medication.
429
T or F: Rate control agents for atrial fibrillation are typically given daily.
True
430
What is the IV dosing for metoprolol tartrate?
2.5-5 mg IV bolus over 2 minutes. Can give up to 3 doses
431
What is the IV dosing for metoprolol succiante?
Only available as oral formulation. Oral dosing is 50-400 mg daily.
432
What is the IV dosing for diltiazem?
0.25 mg/kg IV bolus over 2 minutes. then 5-15 mg/hour following
433
Acute rate control for atrial fibrillation generally requires ________ agents.
IV (first line are beta-blockers and nonDHP CCBs)
434
T or F: It is not possible to convert IV dosing of antiarrythmics to PO dosing.
False. It is possible to do this and there are equations for it. We do not need to know the equations or how to use them for the exam.
435
What are the first line classes of medications for long-term oral rate control in atrial fibrillation?
Beta blocker or nonDHP CCBs are recommended first.
435
________________ _______ are not recommended with heart failure with left ventricular ejection fraction less than 40% in long-term oral rate control for atrial fibrilaltion.
NonDHP CCBs
436
What is the serum digoxin target level in long-term oral rate control for atrial fibrillation?
Less than 1.2 ng/mL
437
Those with heart failure that are being treated with rate controls agents for atrial fibrillation have a heart rate goal of less than __________ bpm.
80 bpm
438
Those with atrial fibrillation on rate controls agents that are asymptomatic and/or have preserved LV systolic function have a heart rate goal of less than ___________ bpm.
110 bpm
439
T or F: Anyone with heart failure being treated for atrial fibrillation has a heart rate goal of less than 80 bpm.
True
440
T or F: The choice of rhythm control agents for atrial fibrillation is dependent upon underlying heart disease and comorbidities.
True
441
What are the first indicated rhythm control agents for those with atrial fibrillation but have normal LV function, no prior MI, or significant heart disease?
Dofetilide
Dronedarone
Flecainide
Propafenone
442
____________ rhythm control medication for atrial fibrillation should be avoided in heart failure.
Dronedarone
(Dronedarone is avoided in heart failure because clinical studies have shown that it can significantly increase the risk of mortality in patients with severe heart failure, particularly those with recently decompensated symptoms, leading to worsening of their condition and increased likelihood of death)
443
What is the second indicated rhythm control agents for those with atrial fibrillation but have normal LV function, no prior MI, or significant heart disease?
Amiodarone
444
What are the first indicated rhythm controls agents for those with atrial fibrillation but have had a prior MI, or they have heart disease (including HFrEF LVEF < 40%)?
Amiodarone or dofetilide
445
What is the second indicated rhythm controls agents for those with atrial fibrillation but have had a prior MI, or they have heart disease (including HFrEF LVEF < 40%)?
Sotalol
446
What two medications for rhythm control in atrial fibrillation should absolutely be avoided in those post-MI as they increase the risk for arrhythmias?
Flecainide and Propafenone
447
What are the two non-drug/surgical treatments for atrial fibrillation?
Cardioversion or ablation
448
What are the two types of cardioversion?
Direct-current cardioversion (shocking) and pharmacologic cardioversion
449
Anticoagulation is recommended for at least ________ weeks prior to and ______ weeks after the cardioversion for patients with unknown atrial fibrillation duration.
3 weeks prior
4 weeks after
450
T or F: After around 48 hours in atrial fibrillation, the risk for clots increases.
True
451
T or F: Cardioversion without anticoagulation can be considered if the A.fib has lasted less than 48 hours and the patient is at low risk for stroke.
True.
452
For physical ablation, anticoagulation therapy should not be discontinued if that patient is already on them. If the patient is not on them, the anticoagulants should be continued for at least _________ months following the ablation.
3 months
453
Which of the following are shockable arrests?
A. Ventricular Fibrillation
B. Pulseless Ventricular tachycardia
C. Pulseless electrical activity
D. Asystole
A and B
V.Fib and Pulseless V.tachy
454
Which shockable pulseless arrest never has a pulse?
A. Ventricular fibrillation
B. Ventricular tachycardia
A. V.fib
(pulseless V.tach never has a pulse though)
455
Which of the following are reversible causes of pulseless electrical activity?
A. Tamponade
B. Toxins
C. Trauma
D. Thrombosis
E. Hyper metabolic state
F. Hyperkalemia
G. Hypovolemia
Tamponade, toxins, thrombosis, hyperkalemia, and hypovolemia (Hs and Ts)
456
Which of the following are components of the management of pulseless arrests?
A. Initiate chest compressions as soon as possible to restore blood flow to the heart and brain
B. Push hard/fast 1 inch, not allowing for a full recoil of the chest
C. Establish and airway
D. If an advanced airway or bag mask is placed, do not stop compression to provide a breath
E. Wait until EMS arrives to utilize defibrillation as it could lead to harm
F. Early defibrillation is key. CPR for 2 minutes and then shock with a defibrillator if it is a shockable arrest
A, C, D, and F
457
How often should epinephrine be administered in a code situation?
A. Every minute
B. Every 1-2 minutes
C. Every 3-5 minutes
D. Every 5-10 muntes
C. Every 3-5 minutes
458
Which of the following is the correct dose for amiodarone in a code?
A. 150 mg IV push, followed by 300 mg
B. 300 mg IV push, followed by 150 mg
C. 450 mg IV push
D. 250mg IV push, followed by 200 mg
B. 300 mg IV push followed by 150 mg (450 mg maximum)
459
What is the major adverse effect associated with the dilutent of amiodarone?
Vasodilation and hypotension (not due to the drug but due to the diluent)
460
What is the drug of choice for symptomatic bradycardia?
Atropine
461
Which node in the heart has the highest rate of spontaneous impulse generation?
SA node
462
During which phase of the cardiac action potential dose repolarization occur due to potassium efflux?
Phase 3
463
What are the non-modifiable risk factors for an acute ischemic stroke?
Age, sex, low birth weight, race/ethnicity, and family history of a acute ischemic stroke/TIA
464
What are the modifiable risk factors for an acute ischemic stroke?
Smoking, HTN, diabetes, high cholesterol, low HDL, a.Fib, asymptomatic carotid stenosis, postmenopausal hormone therapy, oral contraceptive use, poor diet, lack of exercise, obesity, coronary heart disease, peripheral arterial disease, and sickle cell disease
465
Which phase of the cardiac action potential involves a rapid influx of sodium ions?
A. Phase 0
B. Phase 1
C. Phase 2
D. Phase 3
Phase 0
466
Which class of antiarrhythmics prolongs the effective refractory period by blocking potassium channels?
A. Class I
B. Class II
C. Class III
D. Class IV
C. Class III
467
Which medication is a Class III antiarrhythmic known for its extensive hepatic metabolism and prolonged half-life?
A. Amiodarone
B. Diltiazem
C. Flecainide
D. Propafenone
A. Amiodarone
468
How often should you monitor liver function in a patient taking amiodarone?
A. Before TX and every week
B. Before TX, 6 months after starting TX, and then annually
C. Only before treatment
D. Only during treatment
B. Before TX, 6 months after starting TX, and then annually
Amiodarone is potent class III antiarrhythmic that has huge risk for hepatoxicity.
469
Class 1A antiarrhythmics are used in which arrhythmias scenarios?
Class 1As can be used in both atrial and ventricular arrhythmias.
470
Class 1B antiarrhythmics are used in which arrhythmias scenarios?
Class 1Bs are only effective in ventricular arrhythmias like ventriulcar fibrillation and ventricular tachycardia.
471
Class 1C antiarrhythmic, flecainide, is used in which arrhythmias scenarios?
Felcainide can be used in atrial or ventricular arrhythmias.
Remeber to not use Flecainide in any severity of heart failure.
472
Class 1C antiarrhythmic, propafenone, is used in which arrhythmias scenarios?
Propafenone is only used in cases of atrial fibrillation.
473
Class IV antiarrhythmics are used in which arrhythmias scenarios?
Class IV antiarrhythmics, diltiazem and verapamil, are used in situations of both atrial and ventricular arrhythmias.
474
Class III antiarrhythmics, amiodarone and sotalol, are used in which arrhythmias scenarios?
Amiodarone and Sotalol can be used in situations of both atrial and ventricular arrrhythmias.
475
Class III antiarrhythmics, dofetilide and ibutifilde, are used in which arrhythmias scenarios?
These are only used in cases of atrial fibrillation.
476
Besides being a class 1A antiarrhythmic, what other blockades does quinidine exert?
Moderate Acetylcholine and alpha block
477
Besides being a class 1A antiarrhythmic, what other blockades does disopyramide exert?
Moderate acetylcholine block
478
Besides being a class 1A antiarrhythmic, what other blockades does procainamide exert?
No other actions. Only moderate blocking of sodium and potassium channels
479
Besides being a class III antiarrhythmic, what other blockades does ibutifilde exert?
It actually also agonizes sodium channels increasing influx of sodium into the cell.
480
What is unique about verapamil in terms of its target?
Besides being a strong blocker of calcium channels, verapamil is also a moderate blocker of alpha receptors.
481
What is the IV dosing for verapamil in cases of arrhythmias?
5-10 mg IV bolus followed by 5 mcg/kg/min
482
What is the PO dosing for verapamil in cases of arrhythmias?
80-490 mg daily
483
What is the IV dosing for diltiazem in cases of arrhythmias?
0.25 mg/kg IV bolus, followed by 5-15 mg/hr
484
What is the PO dosing for diltiazem in cases of arrhythmias?
90-240 mg daily
485
In cases of acute ischemic stroke, how soon should aspirin be given?
If they were treated with a fibrinolytic, wait 24 hours after the infusion. In general, it is recommended 24-48 hours from the onset of the stroke.
486
In cases of patients presenting with a minor noncardioembolic ischemic stroke (TIA) who did not receive fibrinolytic, what two medications should be given within 24 hours?
Aspirin and clopidogrel
Continue this regimen for at least 21 days and up to 90 days.
