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Pharm II > Lecture 3 (Conduction Disorder)-Exam 2 > Flashcards

Lecture 3 (Conduction Disorder)-Exam 2 Flashcards

1
Q

Sick Sinus Syndrome:
* What is it?
* What does not meet the physiologic needs of body?

A
  • Dysfunction of SA automaticity and impulse generation
  • Atrial rate does not meet physiologic needs of body
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2
Q

Sick Sinus Syndrome
* What is the MCC?
* What can be apart of sick sinus syndrome?

A

MCC – idiopathic SA node fibrosis
* Sinus bradycardia
* Sinus pause < 3 seconds
* Sinus arrest > 3 seconds
* Bradycardia-tachycardia syndrome

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3
Q

What are some pharm causes of SSS?

A
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4
Q

What do you need to diagnosis SSS?

A

Bradycardia ± tachycardia plus
Symptoms of end organ hypoperfusion
* Presyncope/syncope (CNS)-MC
* Lightheadedness
* Confusion
* Fatigue
* Palpitations

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5
Q

Who is hemodynamically unstable with SSS?(5)

A
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6
Q

What is the first line treatment of SSS?

A

atropine

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7
Q

SSS treatment algorithm:
* What dx tests and placements should you do?
* What is the first dose?
* What can be successful at first? BUT what should you be prepared for?

A
  • ECG: electrocardiogram; BP: blood pressure; IV: intravenous; PPM: permanent pacemaker; SSS: sick sinus syndrome.
  • The initial dose of atropine is 0.5 mg IV push. This dose may be repeated every three to five minutes to a total dose of 3 mg
  • While transcutaneous pacing may be initially successful in stabilizing the patient, it may not be consistently reliable and is frequently uncomfortable for the patient. Prepare for urgent transvenous pacing (if required) and obtain central venous access (preferably right internal jugular vein access).
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8
Q

SSS treatment algorithm:
* What should you look for once they are stable?

A

Reversible causes:
* Medications
* Electrolyte abnormalities
* Ischemia
* Automic dysfunction

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9
Q

When is a permanent pacemaker recommended?
* What are the pros (2) and one con?

A

PPM placement recommended for symptomatic patients with SSS and documented bradycardia
* Relieves symptoms
* Improves QOL
* Does not impact survival

LAST LINE

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10
Q

Bradycardia treatment algoritum
* What do you do first?
* How do you identify and treat underlying causes?
* What happens if there is persistent bradyarrhtythmia?
* What do you give?

A
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11
Q

What is the dosing of atropine, dopamine and epinephrine?

A
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12
Q

What is the MOA of atropine?

A

Blocks acetylcholine from binding to muscarinic receptors

Blocks the rest and digest effects of the parasympathetic nervous system on the heart
* Rapid firing of nodes
* Decrease conduction time of AV node
* Increases HR

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13
Q

Atropine:
* What are the cardiac indications? (2)

A
  • First-line therapy for symptomatic bradycardia
  • Structural disease of infra-nodal system of the heart or heart rate < 50 bpm
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14
Q

What are the SE of Atropine?(6)

A
  • Xerostomia
  • Blurred vision
  • Tachycardia
  • Flushing
  • Constipation
  • Urinary retention
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15
Q

What is the dose of atropine?

A

0.5 to 1mg IV push q3 to 5min; max 3mg

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16
Q
A
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17
Q

What are the causes and clinical signifiance of all 4 types of AV blocks?

A
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18
Q

Heart Block Causes:
* What is key?
* What can be some causes?

A
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19
Q

Heart block causes:
* What do you give for overdoses on CCB, BB, digoxin?

A
  • CCB - calcium
  • Beta blockers - glucagon / insulin
  • Digoxin - digibind
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20
Q

Heart Block causes:
* What do you do/give for hypothermia, hypothyroidsm and lyme’s disease?

A
  • Hypothermia - re-warm
  • Hypothyroidism - levothyroxine
  • Lyme’s Disease - ceftriaxone

  • past lecture: Ceftriaxone for advance, doxy for not advance and amox for preg
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21
Q

First degree Mobitz I treatment
* What is it?
* What is the txt for table, aymptomatic patients?
* What is the txt for unstable patients?

A

Prolonged conduction through AV node

Stable, asymptomatic patients (MC)
* Watch and wait
* Look for underlying cause

Unstable patients – drug therapy
* Atropine

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22
Q

First degree /Mobitz I treatment
* What is rarely indicated?
* What may patients with low BP or HF require?

A
  • Pacing is rarely indicated
  • Patients with low BP or HF may required pressors / transvenous pacing
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23
Q

Second degree Mobitz II treatment
* What is it?
* What do you do for stable patients?

A
  • Conduction disease below AV node (Bundle of His)
  • Stable patients: Transcutaneous pacer pads in place
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24
Q

Second degree Mobitz II treatment
* What is the treatment for unstable (4)
* What should you do once stabilized?
* What if nothing is found?

A

Unstable
1. Atropine
2. Transcutaneous pacing
3. Dopamine (low BP) or dobutamine (HF)
4. Transvenous pacing

Once stabilized evaluate for reversible causes

Permanent pacemaker if no underlying cause found / does not respond to treatment

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25
Complete heart block: * What is it? * What do you do for stable patients?
* Conduction disease below AV node (Bundle of His) * Stable patients: Transcutaneous pacer pads in place
26
Complete heart block treatment * What is the treatment for unstable * What should you do once stabilized? * What if nothing is found?
Unstable 1. Atropine 2. Transcutaneous pacing 3. Dopamine or dobutamine 4. Transvenous pacing Once stabilized evaluate for reversible causes Permanent pacemaker if no underlying cause found / does not respond to treatment
27
Which of the following is definitive treatment for symptomatic bradyarrhythmias due to sick sinus syndrome (SSS)? * Cardioversion * Radiofrequency ablation * Atropine * Permanent pacemaker * Digoxin
* Permanent pacemaker
28
A 66 year-old female with a history of coronary artery disease presents with a new onset of dizziness and fatigue for two weeks. She recalls nearly passing out on one occasion. Examination is unremarkable except for bradycardia. Electrocardiogram (ECG) reveals a heart rate of 50 with a normal PR interval followed by a normal QRS. There are several non-conducting P waves and no lengthening of the PR interval. Which of the following interventions is the therapy of choice? * Atropine * Automatic implantable cardioverter defibrillator * Maze procedure * Permanent pacemaker * Radiofrequency ablation
* Permanent pacemaker
29
Antiarrhythmic medications * What are the Medications that suppress the rate through AV node (rate control)?
* Beta blockers * Calcium channel blockers * Adenosine * Digoxin | ABCD
30
Medications that shut down re-entrant circuits (rhythm control): * Blocks what? * More specific to what? * What are the examples (3)
Block triggered cells, reentrant circuits, abnormal myocytes from firing More specific to cells with fast action potentials (cardiac myocytes) * Sodium channel blockers * Potassium channel blockers * ± beta-blockers
31
Class I – Sodium channel blockers * Impacts what? * Wht does it decrease? * What can it prolong and alter? * What does it increase? * What does slow down?
Impact the cardiac myocytes * Decrease the slope of phase 0 * ± prolong effective refractory period * ± alter action potential duration * Increase the time between heart beats * Slow heart rate
32
What rhythm does class 1 treat?
SVT
33
Class II – beta blockers * Impact what? * Blocks what? * What does it decrease (5)? * Prolongs what?
Impact cardiac pacemaker cells * Block beta receptors in the SA and AV nodes * Decrease the effects of the SNS * Decrease the slope of phase 4 * Prolong the time to threshold * Decrease SA node firing * Decrease AV conduction * Decrease the HR
34
What does class 2 treat?
SVTs, VT
35
Class III – Potassium channel blockers * What does it impact? * Prolongs what? * Increases what? (2) * Decreases what? * Elongation of what? What does this increase the risk of?
Impact cardiac myocytes * Prolong repolarization * Increase Effective refractory period * Increase action potential duration * Decrease the heart rate * Elongation of phase 3 = long QT interval * Long QT interval increases risk of Torsades de Pointes-> Vfib
36
Class III – Potassium channel blockers * What does it treat?
SVTs, VT
37
Class IV – Calcium channel blockers * What does it impact? * What are the examples? * What does it decrease (4)? * What does it prolong?
Impact cardiac pacemaker cells Non dihydropyridines – DiVers * Decrease the slope of phase 0 * Prolong time to depolarization * Decrease SA node firing * Decrease AV conduction * Decrease the HR
38
What does Class IV treat?
SVT
39
What are the two primary cardiac effects of digoxin?
* Slows cardiac conduction – pacemaker cells * Increases cardiac contractility – cardiac myocytes
40
How does dignoxin slows cardiac conduction – pacemaker cells?
* Stimulates increased acetylcholine release from the Vagus nerve * Slows conduction through the AV node
41
How does digoxin Increases cardiac contractility – cardiac myocytes?
* Inhibits sodium/potassium ATPase pumps * Increases intracellular Na * Na leaves cell via Na / Ca exchanger * Ca accumulates inside the cell * Increases myocardial contractility
42
What are the SE of digoxin?
43
Digoxin * What are the therapeutic levels? What are the toxic levels? * What are the risk factors for toxicity?
44
New onset afib * What orders do you need to do? (4)
* ECG – confirm diagnosis, ST elevations, LVH * CXR – COPD, PNA, CHF, cardiomegaly, DCM * Labs – CBC, electrolytes, thyroid function, blood ETOH, UDS * Transthoracic ECHO – atrial thrombus, mitral valve issues, LVEF, LVH
45
New onset of afib: * What do you need to evaluate for?
* Cardioversion * Rate control * Anticoagulation * Rhythm control
46
New onset AFIB General approach * What do you do for unstable? * What do you do for stable?
Unstable = cardioversion = immediate restoration of sinus rhythm Stable patients 1. Rate control 2. Determine need for anticoagulation 3. Rhythm control
47
Afib-> acute rate control for stable patients * No need for what? * Focus on what? * Responsible for what? * medications should do what?
48
What are the goals for acute rate control of afib?
49
What are the first line agents for afib rate control?
50
Afib: acute rate control * What do you avoid if patient is LVEF less than 40%? * What can you still use with caution?
Second-line agents (MC in patients with LVEF < 40%) * ­Avoid CCB – negative inotropic effects * ­Use beta blockers with caution (if decompensated HF)
51
Afib: acute rate control * What do you use if patient is in decompensated HF or other medications are contrainated? What are their issues?
Digoxin * Longer time to rate control * Increased risk mortality * No rate control with sympathetic stimulation Amiodarone * Caution: may also convert patient into SR – risk of stroke
52
53
Afib-Chronic rate control * What are the two medications used?
BB and CCB
54
Afib-Chronic rate control: BB * Decrease what? * Specific agent absed on what? * Preferred with patients with what?
* ­ Decrease resting HR/blunt exercise response * ­ Most beta blockers have similar efficacy * ­ Specific agent based on side effect profile and concomitant disease states * ­ Preferred for patients with HRrEF In * ­ Use beta blockers with proven benefit for HRrEF
55
Afib-Chronic rate control: CCB * What are the examples (2) * Caution? Not indicated in who?
* Verapamil * Diltiazem * Caution – negative inotropic effects * Not indicated for patients with HFrEF
56
## Footnote * A-M = beta-1 selective * N-Z = beta-1 and beta-2
57
Pindolol and acebutolol * What activity? * Stimulate and mildly block what? * Decrease what? * Less what?
Pindolol and acebutolol – intrinsic sympathomimetic activity * Stimulate and mildly block beta1 and 2 * Decreased effect on HR and CO * Less bradycardia
58
Metoprolol: tartrate vs succinate * Both what? * used for what? * What do they both reduce? * Different what?
* Both beta blockers * ­ Used for different indications * ­ Both reduce BP and angina symptoms * ­ Different dosage forms and pharmacokinetics
59
Metoprolol: tartrate vs succinate * When is tartrate and succinate given? * What forms is tartrate in? * What is Succinate not used for?
* Tartrate reduces risk of death or subsequent MI when given immediately after a heart attack * Succinate used in heart failure * Tartrate only available as IV or IR formulations only * Succinate not used for ACS
60
Contraindications to beta blockade following an acute myocardial infarction include which of the following? * Hypertension * Afib with RVR * Third degree AV block * Sinus tachycardia * HFrEF
* Third degree AV block
61
Anticogulation: * What patients should get this? * What does conversion to sinus rhythm do (2)?
62
When is anticoagulation Recommended prior to conversion to sinus rhythm in all patients with A. fib? Why?
63
What is the CHAD2S2VASc score?
64
What is the low, moderate and high risk of CHAD2S2VASc?
65
AF anticoagulation * When do you give, maybe give and not give anticogulation before Cardioversion?
66
AF anticoagulation: Afib >48 hours or unknown duration? * What do you need to do with the patient?
67
If you do not want to anticoagulation before cardioversion, what is another option?
68
Anticoag: DOACs * Recommended when? * What are the examples?
69
Anticoag: Warfarin * Recommended in who? * What should the INR levels be? Heparin and LMWH * When should this be used?
70
Warfarin * What is the moa?
* Factors II, VII, IX and X dependent on vitamin K for synthesis * Warfarin inhibits vitamin K recycling and synthesis * Not available for factor production
71
Warfarin * What are the indications? (2)
* DVT, atrial fibrillation, prosthetics valves * **Only oral anticoagulant indicated for patients with mechanical heart valves**
72
Warfarin-Pharmacokinetics: * What is half life? What is onset? * Requires what? * How is metabolized?
* Generally long half-life; prolonged onset * Requires bridging therapy with heparin or LMWH-> if INR therapeutic for two days then then you can stop * Metabolized by CYP2C9 – many drug interactions
73
CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?
74
Monitoring Warfarin * What levels do you need to look at? * Adjuct dose to what? * _ algorithms * initial dose for most patients? * What do you need to check daily intil therapeutic?
PT/**INR** – goal 2 to 3 in most cases * Adjust dose to INR * Evidence-based algorithms * Initial dose for most patients: 5mg PO daily * INR daily until therapeutic (then decrease interval of checking)
75
What are the diet issues with warfarin?
Vit K needs to be stabilized with txt * for example: winter vs summer months
76
Warfarin * What are the SE? (3) * What is CI (1)?
77
Warfarin overdose: * Txt based on what?
Treatment depends on INR level and if patient is bleeding
78
Warfarin overdose: * What do you with a patient who is not bleeding? (3)
* Hold warfarin * Give vitamin K (1 to 5 mg PO) * Resume warfarin at lower dose once INR is 2 to 3
79
Warfarin overdose: * What do you with a patient who is bleeding? (2)
* 4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k OR * Fresh frozen plasma (FFP)
80
Direct inhibitors * What are the two types and their MOA?
Factor Xa inhibitors * Directly bind factor Xa * Prevent conversion of prothrombin to thrombin Thrombin inhibitors * Bind to and inhibit thrombin
81
Direct oral anticoagulants (DOACS) * First oral agent since what? * What is dadigratran? * What are the types of oral factor Xa inhibitors (4)
82
Direct oral anticoagulants (DOACS) * What are the benefits over warfarin?
* Faster onset of action * **No direct monitoring required** * Minimal drug-food interactions * Comparable bleeding rate * Less drug-drug interactions * **Fixed dose per indication** – varies by indication, age, renal and hepatic function * ± parenteral anticoagulation bridging
83
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85
A 68 year-old male with a history of atrial fibrillation treated with warfarin (Coumadin) presents to the emergency department after vomiting large amounts of bright red blood. INR is 3. Which of the following is most appropriate to rapidly lower the patient's INR? * Protamine * Packed RBCs * Fresh frozen plasma * Discontinue warfarin * Idarucizumab (Praxbind)
* Fresh frozen plasma
86
AFIB rhythm Control * Not recommended in who? Why?
87
AFIB rhythm Control * Rhythm control may be reserved for patients with what? (5)
88
What are the different cardioversion for afib into sinus? (3)
89
Cardioversion of AF: Antiarrhtymics (general principals) * Less effective than what? * Most effective when? * What are some issues? Why?
* Less effective than direct current cardioversion * Most effective if started with 7 days of Afib onset * Many drug / drug interactions and adverse effects * Most started inpatient due to potential for significant adverse effects
90
What are the SE of medication cardioversion of AF?
* Arrythmias * Bradycardia * QT prolongation * Heart failure * Stroke * Greatest risk in first 24 hours
91
cardioversion of AF: Antiarrhythmics (Class Ic) * What are the examples? * When is it first line?
Class Ic * ­ Flecainide or propafenone * ­ First-line if no structural heart disease (SHD) * ­ LV hypertrophy, CAD, valve disease, LV dysfunction ## Footnote Most evidence for Class Ic and Class III agents
92
Cardioversion of AF: antiarrhythmics (Class 3) * What are the are the examples? What is the issue with one of them? * What is best for maintence therapy?
Pure potassium channel blockers – ibutilide, dofetilide Amiodarone * High efficacy * High adverse effects Sotalol best for maintenance therapy ## Footnote Most evidence for Class Ic and Class III agents
93
What are the two drugs that are safe for medication cardioversion of AF in severe congestive heart failure?
* Dofetilide (Tikosyn) * Amiodarone
94
Rhythm Control of AF: Antiarrhythmics * Most evidence for what classes? * WHich class increases mortality?
* Most evidence for class Ia, Ic and III * Significant increase in mortality with class Ia agents
95
96
Fill in for class one
97
What are the class 3 drugs?
98
Amiodarone: * MC used what? * What is the MOA? * What are the uses?
* MC used class III antiarrhythmic * Actions of all antiarrhythmic classes Active against most types of arrythmias * Control life-threatening ventricular tachycardias * Atrial fibrillation (not 1st line) * Atrial flutter
99
Amiodarone: What are the SE?
100
Amiodarone:
101
Amiodarone:
102
Sotalol (class 3) * What is the MOA? * How does affect HR and contracility? * What are the inications (3)
103
Sotalol (class 3) * What are the SE?
104
Dofetilide (Tikosyn) * What is the MOA? * Route? * What is it for? * What are the SE? (2)
Dofetilide * Selective potassium blocker * Oral * Long term prevention of A. fib (esp in HF patients) Adverse effects * QT prolongation * Torsades de Pointes
105
Dofetilide (Tikosyn) * What is it based on? * Dose modified how?
* Based on CrCl * Dose modified based on QTc 2 to 3 hours after first dose * QTc > 15% increase or > 500msec * Dose reduced by 50% * If QTc still > 500msec; discontinuation is recommended
106
A 74 year-old patient presents with signs and symptoms of heart failure. EKG shows the patient to be in atrial fibrillation at a rate of 80 bpm. Blood pressure is 120/76. The patient denies palpitations, chest pain, or syncope. Which of the following is the most important long-term therapy in this patient? * Atenolol * Dofetilide * Apixaban * Verapamil * Furosemide
Apixaban
107
What is SVT?
108
Paroxysmal SVT * What it is?
Paroxysmal SVT – subset of SVT; regular and rapid tachycardia of abrupt onset and termination
109
AVRT * What type of pathoway? * What are the two electrical windows? * What is AVNRT
110
# KNOW What is the definitive treatment of paroxysmal SVT?
Definitive treatment is radiofrequency ablation of abnormal conduction pathway
111
Wolff-Parkinson-White (WPW) Syndrome * What is the PR interval * QRS? * What wave is seen? * What are the pts vulnerable to?
* PR interval < 0.12 seconds * Wide QRS complexes * Delta wave seen in some leads * Patients with WPW are vulnerable to PSVT
112
Adult tachycardia with pulse * How do you treat underlying cause?
Dehydration (give fluids) / fever (anti-pyro)
113
Adult tachycardia with pulse: Not sinus rhythm and narrow complex * What do you do for stable and unstable?
114
115
Adult tachycardia with pulse: Not sinus rhythm / wide complex * What do you give if regulat and monomorphic? * What are the Antiarrhythmic infusions for stable wide complex?
Not sinus rhythm / wide complex * Adenosine if regular and monomorphic Antiarrhythmic infusions for stable wide complex * Procainamide * Amiodarone * Sotalol
116
Adenosine: * What is the MOA? * What is the overall effect?
117
Adenosine * What are the pharmacokinetics?
* T ½ = 10 seconds * Requires rapid push with rapid flush * ± three-way stop cock
118
Adenosine: What are the SE?
119
SVT - Chronic Treatment * What is first line?
* Radiofrequency ablation 95% cure * Diagnostic and curative * Avoids drug therapy
120
SVT: Chronic Treatment * What is second-line? What do they do? * When do you not use this?
Flecainide or propafenone Beta blockers or CCBs * Prevent recurrent episodes * Best for occasional or rare bouts of minimal or mildly symptomatic palpitations (orthodromic or antidromic AVRT) * Do not use if also has Afib or flutter
121
Which of the following antiarrhythmic drugs can be associated with hyper- or hypothyroidism following long-term use? * Flecainide * Amiodarone * Mexiletine * Dofetilide * Lidocaine
Amiodarone
122
Which of the following is the mechanism of action of Class III antiarrhythmic drugs? * Na channel blocker * Potassium channel blocker * Beta blocker * Calcium channel blocker * Na/K ATPase inhibitor
Potassium channel blocker
123
A 25 year-old male with history of syncope presents for evaluation. The patient admits to intermittent episodes of rapid heart beating that resolve spontaneously. 12 Lead EKG shows delta waves and a short PR interval. Which of the following is the treatment of choice in this patient? * Cardioversion * Metoprolol * Digoxin * Percutaneous coronary intervention * Radiofrequency ablation
* Radiofrequency ablation
124
Which of the following medications used in the treatment of supraventricular tachycardia is able to cause sinus arrest and asystole for a few seconds while it breaks the paroxysmal supraventricular tachycardia? * Amiodarone * Metoprolol * Verapamil * Adenosine * Digoxin
Adenosine
125
Which electrolyte abnormality is associated with an increase in the risk for digoxin toxicity? * Hyponatremia * Hypermagnesemia * Hypercalcemia * Hypokalemia * Hyperphosphatemia
* Hypokalemia
126
VENTRICULAR TACHYCARDIAS * What are the most common causes? * Chronic VT MC associated with what?
127
128
monomorphic: * What do you need to workup for monomorphic with and without structural abnormality?
129
monomorphic: * What do you need to tx for monomorphic with and without structural abnormality?
130
131
maintenance therapy of v.tach * Covert to what? What is the example? * What does it decrease? What no what/ * What medication do most patients have an indication for? What is the benefit?
132
Maintenace therapy v.tach: * What can be placed in most patients? * What is for specific patients?
133
134
What are the doses of epinephrine, amiodarone and lidocane?
135
Polymorphic VT * What is the MCC? * What is it always associated with? * What is the QTc longation in males and females? * May do what?
136
What are the causes of polymorphic VT? (4)
* Inherited disease – congenital prolonged QT, Brugada, etc * Electrolyte related – hypokalemia, hypocalcemia, * hypomagnesemia * Medications
137
TdP treatment: * Wat do you do for unstable? * What do you for stable patients (general)
Hemodynamically unstable - prompt cardioversion/defibrillation Hemodynamically stable patient: * Stop causative medications * Replace abnormal electrolytes
138
Tdp Treatment * What is first line? * What is the gial? * Benefit seen with what?
* Magnesium sulfate 2 grams IV over 15 minutes; followed by continuous infusion magnesium * Goal = magnesium level > 2 mmol/L * Benefit seen with normal magnesium levels
139
TdP treatment: * What do you give for TdP resistant to mag?
Isoproterenol for TdP resistant to magnesium * Increases HR and shorten QT interval
140
Patent ductus arteriosus * What is the fetal circualtion? * How does blood move around fetuses body?
Fetal circulation: * Blood from placenta travels to right atrium of heart via IVC Moves to: * LA via foramen ovale->LV->aorta->back to placenta via umbilical artery * RV via tricuspid->pulmonary trunk-> mostly through ductus arteriosus to aorta->back to placenta via umbilical artery
141
Patent ductus arteriosus (PDA) * What happens normally when closing thr ducus?
* Postnatal increase in left sided cardiac oxygenated blood and decrease in circulating prostaglandin E2 and prostacyclin * 02 sensing mechanism of ductal smooth muscle cause ductal constriction * Platelets – thrombotic closure of constricted ductus
142
Patent ductus arteriosus (PDA) * Preterm infant ductus is less sensitive to what?
is less sensitive to oxygen – spontaneous closure rates reduced
143
PDA closure – preterm infants (moderately conservative approach) * When do you need to medical txt? * What are the drugs (3)? What do they do?
Medical treatment if PDA not closed 1-week after birth * Indomethacin, ibuprofen, or acetaminophen (70 to 85% effective) * Promote PDA closure via prostaglandin inhibition * ECHO should be checked 24 to 48 hours after treatment each course * May repeat treatment course x 1 if no closure
144
PDA closure – preterm infants * What do you do if treatment is unsuccessful?
Percutaneous transcatheter occlusion or surgical ligation if medical treatment unsuccessful
145
PDA treatment: Nsaids * What are the SE?(6)
* Decreased cerebral, GI, and renal blood flow * Bleeding * Renal impairment * Necrotizing enterocolitis * Intraventricular hemorrhage * Intestinal hemorrhage
146
147
PDA closure – Term infants * Not all need what? * When is closure recommended? (3)
148
PDA closure – Term infants * What is the txt?
* Medical therapy NOT recommended * Percutaneous transcatheter occlusion or surgical ligation
149
Ductal dependent congenital heart disease * What are the different ones?
150
Ductal dependent congenital heart disease * Rely on what? * What can PDA closure result in?
151
Prostaglandin E1 (PGE1) Therapy * What is it indication?
Infants with or high clinical suspicion of a ductal- dependent congenital heart defect
152
Prostaglandin E1 (PGE1) Therapy * What is the dose for large PDA, Restrictive ductus or unknown status and the max dose?
153
Prostaglandin E1 (PGE1) Therapy * What is the MOA?
154
Prostaglandin E1 (PGE1) Therapy * What is the efficacy/initiation?
155
Prostaglandin E1 (PGE1) Therapy * What are the SE?(5)

Pharm II (14 decks)

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