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Peds Cardiology > 11. Pharmacology > Flashcards

11. Pharmacology Flashcards

1
Q

What drug can be used in a patient with long QT who develops non-sustained polymorphic ventricular tachycardia?

A

Mg Sulfate

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2
Q

True or false: Mg Sulfate is unlikely to be effective fr non-sustained polymorphic ventricular tachycardia in patients with a normal QT interval?

A

True

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3
Q

What do procainamide, sotalol, quinidine and dofetilide do to the QT interval?

A

Prolong

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4
Q

Type of long QT in a patient with a mutation in Na channel gene SCN5A?

A

Type 3

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5
Q

What drugs can be considered for a patient with LQT3 and torsades de pointes?

A
  1. IV lidocaine

2. PO mexiletine

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6
Q

What constitutes low-risk thrombosis for prosthetic vavles?

A

Mechanical aortic valve and no risk factors (A-fib, previous thromboembolism, LV dysfunction, hypercoaguable conditions, older-generation thrombogenic valves, mechanical tricuspid valves, more than 1 mechanical valve)

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7
Q

What constitutes high-risk thrombosis for prosthetic valves?

A

Mechanical mitral valve or mechanical aortic valve + RF (A-fib, previous thromboembolism, LV dysfunction, hypercoaguable conditions, older-generation thrombogenic valves, mechanical tricuspid valves, more than 1 mechanical valve)

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8
Q

Operative anticoagulation plan for low-risk?

A

Stop warfarin 48-72 hours prior to procedure (goal INR <1.5) and re-start within 24 hours after procedure… no need to bridge

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9
Q

Operative anticoagulation plan for high risk?

A

Stop warfarin 48-72 hours prior to procedure (goal INR <1.5) and bridge with heparin once INR <2. Stop heparin 4-6 hours after surgery and resume heparin ASAP and continue until INR therapeutic with warfarin

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10
Q

INR goal after mitral valve replacement?

A

INR 2.5-3.5 (warfarin)

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11
Q

Anticoagulation needed after mechanical mitral valve?

A

Coumadin (INR 2.5-3.5) and ASA

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12
Q

What are risk factors in terms of anticoagulation needs?

A

A-fib, previous thromboembolism, LV dysfunction, hypercoaguable conditions, older-generation thrombogenic valves, mechanical tricuspid valves, more than 1 mechanical valve

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13
Q

When should ASA be used for artificial valves?

A

All mechanical valves, biological valves with risk factors

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14
Q

Anticoagulation for mechanical prosthetic valves in pregnancy?

A

Chronic warfarin: Can stop between 6-12 weeks gestation and use heparin v. continuing until 36 weeks gestation then transitioning to heparin and delivering in 2-3 weeks

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15
Q

What is lowest fetal risk for anticoagulation in Mom during pregnancy?

A

Continuous IV UFH

-But, maternal risk of prosthetic valve thrombosis, systemic embolization, infection, osteoporosis, and HIT are higher

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16
Q

Goal Xa if using LMWH in pregnancy?

A

BID dosing with anti-Xa 0.7-1.2 4 hours after dose

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17
Q

Goal PTT for UFH in pregnancy?

A

At least twice control

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18
Q

INR goal for warfarin in pregnancy?

A

2.5-3.5

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19
Q

When does warfarin HAVE to be switched to continuous IV UFH in pregnancy?

A

2-3 weeks prior to planned delivery

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20
Q

What is the cause of cough as a side effect of ACEi?

A

Increased bradykinin

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21
Q

What does ACE do?

A

Converts angiotensin I to angiotensin II

Inactivates bradykinin

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22
Q

What effect to ACEi have on angiotensin II and bradykinin?

A

Decrease angiotensin II

Increase bradykinin

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23
Q

What drug inhibits the Na-K ATPase?

A

Digoxin

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24
Q

What do CCB do?

A

Inhibit Ca entry into vascular smooth muscle

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25
Q

How to ARBs function?

A

Inhibit activation of angiotensin II receptors

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26
Q

Irregularly irregular wide complex tachycardia, electrical cardioversion didn’t work, what is arrhythmia and which drug most likely to work?

A

A-fib with preexcitation (conducting antegrade to ventricle via AV node and accessory pathway, some beats are likely fusion beats)

Amiodarone

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27
Q

If you have a-fib with prexcitation, what drugs do you need to avoid?

A

AV nodal blocking agents - Unopposed ventricular activation via accessory pathway can lead to V-fib

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28
Q

Name some AV nodal blocking agents

A
  1. Adenosine
  2. Dig
  3. Diltiazem
  4. B-blocker
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29
Q

What class is amiodarone?

A

III (slows cardiac conduction)

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30
Q

What is treatment of choice for a-fib with pre-excitation and RVR?

A

DC cardioversion

-Can use amiodarone if needed (will restore a-fib to sinus rhythm and decrease accessory pathway conduction)

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31
Q

What drug can commonly cause GI upset (nausea/vomiting)?

A

Digoxin

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32
Q

What can e seen on tele as a side effect of digoxin?

A

High grade AV block with activation of ectopic pacemakers

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33
Q

What is first line treatment in a patient with cateocholaminergic polymorphic v-tach with a VT/VF storm?

A

IV beta-blocker

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34
Q

Last resort for a patient with CPVT in VT/VF storm if IV beta-blockade isn’t working?

A

General anesthesia

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35
Q

Who benefits from palivizumab?

A

< 24 months with hemodynamically significant cyanotic and acyanotic CHD (meds for HF, mod-severe PH)

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36
Q

What is primary benefit of immunoprophylaxis with palivizumab?

A

Decrease rate of RSV-associated hospitalization

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37
Q

True or false: Studies haven’t shown a significant decrease in rate of mortality attributable to RSV in infants who receive prophylaxis?

A

True

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38
Q

How does lasix work?

A

Inhibits Na-2CL-K cotransporter in the loop of Henle

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39
Q

How do thiazide diuretics work?

A

Inhibits Na-Cl cotransporter

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40
Q

How does digoxin work?

A

Inhibits Na-K ATPase

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41
Q

What is the treatment for idiopathic viral pericarditis?

A

Ibuprofen and ASA

-Help to relieve pain, don’t alter natural history of disease

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42
Q

Dosing of ASA for pericarditis?

A

Higher dosing- 800mg q6h-q8h for 7-10 days followed by gradual tapering of dose

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43
Q

True or false: Acute pericarditis usually responds dramatically to corticosteroids?

A

True

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44
Q

What is the use of corticosteroids in acute pericarditis associated with?

A

Risk of relapsing pericarditis

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45
Q

If NSAID therapy hasn’t worked in acute pericarditis, what other drug can be used?

A

Colchicine (4-6 weeks)

*Especially if NSAIDS haven’t had benefit after 1 week

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46
Q

What can NIRS be a good surrogate for?

A

Mixed venous saturation (tissue level saturation/oxygenation)

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47
Q

What is the difference between SaO2 and MVO2 a surrogate for?

A

CO

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48
Q

Qp:Qs equation?

A

Ao sat – MV sat / Pulm vein sat- PA sat

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49
Q

How would norepinephrine affect Qp:Qs?

A

Potent vasoconstrictor, will increase SVR and increase Qp:Qs

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50
Q

When are steroids indicated for Kawasaki?

A

Fever relapse after 2 doses IVIG

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51
Q

Initial therapy for Kawasaki?

A

IVIG + high dose ASA

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52
Q

What form of steroids are used if needed in Kawasaki?

A

IV methylprednisolone (PO not appropriate)

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53
Q

Therapy for mild-moderate carditis due to RF?

A

High dose ASA (80-100mg/kg/day divided q6h)

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54
Q

Therapy for severe carditis (HF, severe valve regurgitation, significant pericarditis/myocarditis) due to RF?

A

PO prednisone

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55
Q

Should you use PO steroids + ASA for acute RF?

A

No- no recommendation to combine these

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56
Q

How does sirolimus work?

A

Blocks gene transcription

-Acts at a distal site in lymphocyte activation cascade and blocks transcription of activation genes

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57
Q

What are tacrolimus and cyclosporine?

A

Calcineurin inhibitors

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58
Q

Which drug, cyclosporine or tacrolimus, offers survival advantage in heart transplant patients?

A

Neither- no survival advantage with one versus other

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59
Q

What is a potential advantage of sirolumis

A

Less nephrotoxicity

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60
Q

Abx recommendations for RF with carditis and residual heart disease (persistent valvular disease)?

A

Treatment for 10 years or until 40 years of age (whichever is longer, sometimes lifelong) after last attack of RF

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61
Q

Abx recommendations for RF with carditis, but no residual heart disease (no valvular disease)

A

Treatment for duration of 10 years or until 21 years of age (whichever is longer) after the last attack of RF

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62
Q

Abx recommendations for RF patients without carditis

A

Treatment for a duration of 5 years or until 21 years of age (whichever is longer) after the last attack of RF

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63
Q

IE Prophylaxis?

A

Dental procedures that involve manipulation of either gingival tissue or the periapical region of teeth or perforation of oral mucosa:

  • Prosthetic cardiac valves or prosthetic material used for cardiac valve repair
  • Previous IE
  • Unrepaired cyanotic CHD (including palliative shunts/conduits)
  • Completely repaired, 6mo following procedure if prosthetic material used
  • Residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device
  • Cardiac transplant recipients with valve regurgitation due to a structural abnormal valve
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64
Q

What dental procedures don’t require SBE prophylaxis?

A
  • Routine anesthetic injections through noninfected tissues
  • Dental radiographs,
  • Placement/removal of orthodontics/ prosthodontic appliances
  • Shedding of deciduous teeth
  • Bleeding from trauma to lips/oral mucosa
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65
Q

What drug is recommended as first line for children meeting criteria to start lipid-lowering drug therapy?

A

Statin

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66
Q

When to consider drug therapy in children for hyperlipiemia?

A
  1. > 10 (usually after menarche in girls) and after 6-12 month trial of fat/cholesterol restricted diet
  2. If LDL remains >190 or >160 + FHx premature cardiovascular disease or >/= 2 other risk factors after vigorous attempts to control
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67
Q

What are risk factors and high risk conditions for hyperlipiemida in kids?

A
  • Male
  • Family history of premature cardiovascular disease or events
  • Presence of associated low HDL
  • High triglycerides
  • Obesity and aspects of the metabolic syndrome
  • Diabetes
  • HIV infection
  • SLE
  • Organ transplantation
  • Survivors of childhood cancer
  • Presence of HTN
  • Smoking
  • Elevated lipoprotein (a), homocysteine and CRP
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68
Q

Why are bile acid-binding resins unlikely to achieve target LDL cholesterol levels in children?

A
  • Poor compliance: GI issues, tastes bad

- Limited effectiveness

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69
Q

When are fibric acid derivatives used in kids?

A

Severe elevations in triglyceride levels + risk for pancreatitis

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70
Q

True or false: Niacin isn’t routinely recommended for kids with hypercholesterolemia?

A

True

-Poor tolerance, potential for serious adverse events and limited data

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71
Q

What is the traditional medication for HCM?

A

B-blocker

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72
Q

If a CCB is used in HCM, which is preferred?

A

Diltiazem or verapamil

*Dihydropyridine CCB like nifedipine would cause peripheral vasodilation and reflex tachycardia

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73
Q

Why isn’t lasix used in HCM?

A

Decreases preload and LV filling which can worsen the degree of obstruction

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74
Q

What medication inhibits smooth muscle proliferation and may have the advantage of inhibiting coronary vasculopathy?

A

Sirolimus

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75
Q

True or False: Sirolimus is a calcineurin inhibitor

A

False

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76
Q

What type of drug is sirolimus often used in combination with?

A

Calcineurin inhibitor (cyclosporine or tacrolimus)

*Sometimes sirolimus can be used instead of calcineurin inhibitors (may be less nephrotoxic over time)

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77
Q

Following cardiopulmonary bypass for a Norwood, what medication can increase systemic perfusion?

A

Phenoxybenzamine

*Anesthesia can’t eliminate stress response with hypothermia and increased SVR

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78
Q

How does phenoxybenzamine work?

A

Long-acting irreversible alpha-adrenergic blocker… decreases SVR, but can cause hypotension/hypoperfusion

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79
Q

Immediately following a Norwood, what causes an unfavorable Qp/Qs ratio with reduced systemic blood flow and low CO?

A

Increased SVR

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80
Q

List some post-operative drugs which can help reduce SVR

A
  1. Phenoxybenzamine
  2. Milrinone
  3. Nitroprusside
  4. Dobutamine
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81
Q

True or False: Norepinephrine causes systemic vasoconstriction and elevates SVR

A

True

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82
Q

What is the most common side effect of rabbit antithymocyte globulin (ATG?

A

Fever (60%)

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83
Q

List side effects of rabbit antithymocyte globulin (ATG)

A
  1. Fever (60%)
  2. Rash (<25%)
  3. Hyperkalemia (25-30%)
  4. Abdominal pain (45-40%)
  5. Myalgia (40%)
  6. Shivering (55-60%)
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84
Q

What are 2 drugs used in pediatric cardiology that may exacerbate bronchospasm? u

A
  1. Adenosine

2. B-blocker

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85
Q

Which last longer… the EP effect of adenosine or the bronchospasm effect?

A

Bronchospasm (can last a long time)

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86
Q

How does adenosine dosing need to be adjusted in heart transplant recipients?

A

Give 1/4 to 1/2 usual dose

  • Sensitive to adenosine
  • Long periods of AV block can be noted at higher doses
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87
Q

What is the half life of adenosine?

A

<2 seconds

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88
Q

How should adenosine be given?

A
  • Fast as possible with flush following
  • Large bore IV
  • Close to heart as possible
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89
Q

What are 2 common side effects of adenosine?

A
  1. Flushing

2. Hypotension

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90
Q

Why do you need an AED if giving adenosine?

A

The bradycardia it causes can precipitate other arrhythmias (A-fib or V-tach)

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91
Q

Typical dosing for adenosine in kids?

A

0.1-0.5mg/kg

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92
Q

MOA Ambrisentan?

A

Selective endothelin A receptor antagonist

*Doesn’t induce or inhibit cytochrome P450 enzymes

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93
Q

Why is ambrisentan much less hepatotoxic than bosentan?

A

Metabolized through glucuronidation

94
Q

MOA Epoprostenol?

A

Postacyclin (PGI2) analogue

95
Q

MOA Sildenafil?

A

Phosphodiesterase 5 inhibitor, works through NO-cyclic GMP cascade

96
Q

MOA Milrinone?

A

Phosphodiesterase 3 inhibitor

97
Q

True or False: ECG changes for Brugada can be dynamic and missed on a single ECG

A

True

98
Q

What type of testing can help with diagnosis of Brugada?

A

Drug challenge with Na channel blockers like procainamide

*This can exacerbate Na channel dysfunction

99
Q

What are some Na channel blockers that be used for a drug challenge?

A

Ajmaline, flecainide, procainamide, pilsicainide, disopyramide, propafenone

100
Q

When is an epinephrine challenge helpful?

A

To diagnosed concealed LQTS

101
Q

What imaging should be done in the workup of suspected arrhythmogenic RV?

A

MRI

102
Q

What drug is commonly used in the EP lab to induce arrhythmia?

A

Isoproterenol

103
Q

What type of testing is helpful in diagnosis and management of CPVT?

A

Exercise stress testing

104
Q

Name 3 class IB antiarrythmics

A
  1. Phenytoin
  2. Lidocaine
  3. Mexiletine
105
Q

What do the class IB antiarrhythmics do?

A

Na channel blocking with rapid recovery of blocked Na channel

106
Q

What do class IB antiarrhythmics do the QT?

A

Slightly shorten it

107
Q

Can you use phenytoin in LQTS patietns?

A

Yes- Class IB Na Channel blocker

108
Q

Name 3 class III antiarrhythmics

A
  1. Amiodarone
  2. Sotalol
  3. Ibutilide
109
Q

How do the class III anti-arrhythmic work?

A

Block K channels

110
Q

What do the class III anti-arrhythmic do the the QTc?

A

Prolong it

111
Q

Best option for symptomatic, but hemodynamically stable atrial flutter?

A

IV Diltiazem (will slow RVR and give relief of symptoms)

  • Could also use B-blocker or sotalol
  • Cardioversion not 1st line for a stable patient
112
Q

What effect can flecainide have in atrial flutter?

A

Slow atrial conduction within flutter circuit and slow flutter rate (can convert fast flutter with AV block to slow flutter with 1:1 AV conduction)

113
Q

What effect can disopyramide have in atrial flutter?

A

May enhance AV node conduction (worsen situation if used alone)

*Class I with anticholinergic activity

114
Q

For atrial flutter, flecainide and disopyramide are best used in conjunction with what?

A

An AV nodal blocking agent

115
Q

What drug is a Ca-sensitizing agent that binds to troponin C and improves contractile efficiency and reduces afterload?

A

Lecosimendan

116
Q

What drug is a “L”-type CCB and reduces intacellular Ca by reducing Ca-induced Ca release?

A

Verapamil

117
Q

What drug is a Na-K ATPase inhibitor and indirectly increases intracellular Ca?

A

Digoxin

118
Q

MOA milrinone?

A

Phosphodiesterase 3 inhibitor

119
Q

What drug is a synthetic BNP used to treat decompensated HF patients?

A

Nesiritide

120
Q

What drug is useful in complete AV block?

A

Isoproterenol

*Can result in stable junctional/ventricular escape rhythm

121
Q

How does isoproterenol work?

A

Stimulates myocardial B1 receptors…increased chronotropy and inotropy

122
Q

How does atropine work in AV block?

A

Only works in reversing AV block due to excessive vagal effect…anticholinergic/vagolytic agent

123
Q

Patient in low CO state with pulmonary edema due to severe MR… what drug is helpful to increase CO?

A

Nitroprusside

  • Large % of LV SV going back to LA causing elevated LA pressure and pulmonary edema
  • Needs systemic vasodilator to increase forward SV
124
Q

How can anemia cause drop in SpO2 in a Tet?

A
  • Get systemic vasodilation with anemia… more R-L shunting

- Increased tissue oxygen extraction… lower mixed venous saturation

125
Q

Side effects of PGE1?

A
  1. Apnea
  2. Fever/hyperthermia
  3. Hypotension
  4. Seizures
  5. Cutaneous vasodilation
  6. Edema
126
Q

What is a long-term side effect of PGE?

A

Cortical hyperostosis

127
Q

What drug used in Marfan blocks TGF-B signaling?

A

Losartan

128
Q

MOA Losartan?

A

Angiotensin receptor 1 antagonist (this antagonizes TGF-B signaling)

*Exact mechanism uncertain: Activation of angiotensin type 1 receptors increases expression of TGF-B ligands and receptors and induces activation of thrombospondin (powerful TGF-B activator)

129
Q

What is Eplerenone?

A

Mineralocorticoid receptor (aldosterone receptor) antagonist

*Similar effects of spironolactone (hyperkalemia)

130
Q

List 3 drugs that amiodarone increases levels of

A
  1. Cyclosporine
  2. Digoxin
  3. Warfarin

*Inhibits activity of cytochrome P450

131
Q

What needs considered when putting a patient taking B-blocker on amiodarone?

A

Potential for heart block… due to AV nodal blocking effect of amiodarone

132
Q

What is the primary effect of amiodarone?

A

Class III antiarrhythmic- primarily K channel blocker

*Prolongs repolarization and QTc interval

133
Q

What are additional effects of amiodarone besides K channel blocking?

A
  1. Some degree CCB
  2. Blocks cardiac Na channels
  3. Produces B-blockade (causes reduced AV nodal conduction)

*NOT a vagolytic agent

134
Q

What can exacerbate the pro-arrhythmic potential of amiodarone and can precipitate torsades de pointes?

A

Hypokalemia

135
Q

Patients taking which medication, tacrolimus or cyclosporine have a higher instance of post-transplant diabetes?

A

Tacrolimus

Tacrolimus (8%)
Cyclosporine (2%)

136
Q

Name 3 things that predispose to post-transplant diabetes

A
  1. Higher tacrolimus levels
  2. HLA-DR mismatch
  3. Older age at transplantation
137
Q

Which post-transplant medication is associated with bone marrow suppression?

A

Sirolimus

*Especially when used with tacrolimus

138
Q

True or False: Lipid abnormalities are common even in younger children who are heart transplant recipients and lipid-lowering therapy is often instituted in this subgroup

A

True

139
Q

What 2 types of medication are typically used for managing HTN in pediatric heart transplant recipients?

A

CCB

ACEi

140
Q

Which is less nephrotoxic… sirolimus, cyclosporine, tacrolimus?

A

Sirolimus

141
Q

List drugs which lower PVR

A
  • Tolazoline: Non-selective competitive alpha-adrenergic receptor antagonist
  • Nitric oxide: NOT nitrous oxide
  • Dobutamine
  • Milrinone
  • Prostaglandins
  • Prostacyclins
  • Sodium nitroprusside
  • Sildenafil

*Ketamine may increase PVR

142
Q

What might cause an acute drop in platelets in a post-op patient on heparin?

A

HIIT- Heparin induced thrombocytopenia with thrombosis

143
Q

What is the pathophysiology of HIIT?

A
  • Heparin combines with platelet factor 4 complex and makes it immunogenic
  • Resulting antibodies to this complex may result in formation of platelet aggregates which can cause vaso-occlusion and cause immune-mediated platelet destruction resulting in thrombocytopenia (> 50% drop in plt count)
144
Q

How is HIIT diagnosed?

A
  • Specific antibody assay

* Once a thrombotic complication has occurred however, need urgent therapy even w/o diagnosis

145
Q

How do you manage HIIT?

A
  • Stop heparin

- Other form of anticoagulation

146
Q

True or False: You often need a platelet transfusion with HIIT?

A

False: Platelet drop usually isn’t enough to cause clinically significant bleeding

147
Q

What other form of anticoagulation isn’t used in HIIT?

A

LMWH (enoxaparin)

-May not provoke HIIT, but could cross-react with heparin antibodies and isn’t used in HIIT patients

148
Q

Teratogenic effects of warfarin?

A
  • Defects in calcification of epiphyses (chondrodysplasia puctata)
  • Retarded intrauterine growth
  • Psychomotor deficit
  • Hypotonia
  • Convulsions
  • Nasal hypoplasia
  • Ocular and CNS abnormalities
149
Q

When is the risk of teratogenicity highest with warfarin use?

A
  • 1st trimester (10%)- Critical period is between 6-9 weeks gestation
  • Risk is estimated 3-5% during 2nd/3rd trimester
150
Q

Teratogenic effect of Lithium?

A

Ebstein

151
Q

Teratogenic effect of Amiodarone?

A

Thyroid issues (hypo or hyper)

152
Q

Teratogenic effect of ACEi?

A
  • Renal damage
  • Cranial ossification defects
  • Oligohydramnios
  • Delayed intrauterine growth
153
Q

Which trimesters is it especially important to avoid ACEi?

A

2nd/3rd

*But contraindicated during all of pregnancy

154
Q

What is protective against neural tube defects?

A

High dose folic acid therapy

155
Q

Symptoms of digoxin toxicity?

A

Dizzy, mild hypotension, high-grade AV block, significant ventricular ectopy including non-sustained VT

156
Q

What should be done for high-degree symptomatic AV block due to digoxin toxicity?

A
  • IV atropine

- Temporary pacing

157
Q

What should be given for patients with serious signs of digoxin toxicity?

A

Digoxin antibody Fab

158
Q

Besides digoxin antibody Fab, what else can be given to help with digoxin toxicity?

A
  • Activated charcoal
  • Cholestyramine

*Bind digoxin in the gut and help with GI elimination and increased systemic clearance

159
Q

How is digoxin eliminated in the body?

A

50-70% via kidneys

*No significant hepatic contribution

160
Q

What clinical history should you consider with digoxin toxicity?

A

-Any renal dysfunction, chronic or acute due to illness, dehydration, etc.

161
Q

What electrolyte abnormality exacerbates digoxin toxicity?

A

Hyperkalemia

*Treating hyperkalemia is helpful as well

162
Q

What can be given if a patient develops symptomatic ventricular arrhythmias due to digoxin toxicity and no digoxin antibody is available?

A

IV Lidocaine

163
Q

What are 3 options for persistent post-operative HTN?

A
  1. Beta-blockers: Use with caution in asthma
  2. Nitroprusside: Use with caution in renal/hepatic dysfunction due to build up of cyanide
  3. Nicardipine (CCB): No adverse effects on the myocardium
164
Q

What kind of drug is Precedex?

A

Selective alpha-2 receptor agonist

165
Q

What sedative can cause a dose-dependent decrease in BP/HR from alpha 2 agonist effect on sympathetic ganglia with resultant sympatholytic effects?

A

Precedex

166
Q

What can happen after relief of a distal fixed pulmonary valve obstruction?

A

Suicidal RV: Persistent dynamic infundibular/subpulmonary obstruction

*Severe subvalvular obstruction in absence of a distal fixed obstruction can cause complete or near complete RVOTO and lead to acute RV failure with poor RV filling and R-L shunt through PFO

167
Q

What can be given to help with a suicidal RV?

A

IV beta-blocker

168
Q

What are 2 drugs which may worsen a suicidal RV?

A
  1. Milrinone: Inotrope

2. IV Diuretics: Reduce RV preload

169
Q

List potential side effects of statins

A
  • Rhabdomyolysis (rare): Muscle pain, liver damage, kidney failure, death
  • Diarrhea
  • Liver damage
  • GI problems (diarrhea or nausea)
  • Rash/flushing
  • Neurological side effects
170
Q

What is the most common symptom associated with rhabdomyolysis due to stain use?

A

Muscle pain

171
Q

What lab can help diagnose rhabdomyolysis due to statin use?

A

Creatine kinase (CK)

172
Q

What are 2 induction agents for anesthesia which would cause a drop in SVR and be problematic for someone with complete mixing physiology?

A
  1. Inhaled anesthetic

2. Midazolam

173
Q

What effects do inhaled anesthetic agents have on BP?

A
  • Decrease BP due to vasodilation

* Variable impact on the CP system, but pose risk for hemodynamic compromise in a child with limited reserve

174
Q

Which of the following has the least impact on BP: Halothane, isoflurane, sevoflurane?

A

Sevoflurane

175
Q

What does ketamine do to SVR?

A

Increases

176
Q

What can be given in combination with an inhaled anesthetic or midazolam to offset the vasodilatory effects?

A

Ketamine

177
Q

Under what circumstance would it take a long time for an inhaled anesthetic like isoflurane to induce sedation?

A
  • Someone with an shunt (PDA, BTT, etc.) and complete mixing physiology
  • Isoflurane decreases BP due to vasodilation
  • Decreased SVR increases R-L shunting
  • A bigger R-L shunt reduces uptake of isoflurane from lungs, so longer time to achieve sedation
178
Q

True or False: Isoflurane is a powerful bronchodilator and can even be used to break bronchospasm in life-threatening status asthmaticus

A

True

179
Q

True or False: Bronchospasm doesn’t typically reduce uptake of inhalational anesthetic

A

True

180
Q

Symptoms of B-blocker toxicity?

A
  1. Bradycardia
  2. Hypotension
  3. Hypoglycemia
181
Q

What should be given for significant bradycardia due to beta-blocker toxicity?

A

Atropine (anticholinergic)

182
Q

What should be given for hypotension due to beta-blocker toxicity?

A
  • Atropine if bradycardic (increasing HR can help hypotension)
  • IVFs
  • Vasoactives
183
Q

What should be given for hypoglycemia due to beta-blocker toxicity?

A

Glucagon

184
Q

What things can increase warfarin effect (higher INR levels) and result in need to decrease warfarin dose?

A
  • Amiodarone
  • Levothyroxine
  • Propranolol
  • Sertraline
185
Q

What supplement has been shown to decrease the efficacy of warfarin resulting in need for a higher dose?

A

St. John’s Wort

*Herbal supplement that can improve mood and treat depression

186
Q

Do all babies with reflux need treated?

A

No… Babies that feed well despite regurgitation episodes, maintain weight gain and hydration and don’t experience significant irritability won’t require treatment

*All infants reflux

187
Q

True or False: Research shows that acid suppression isn’t effective for alleviating reflux-related symptoms or regurgitation and irritability in infants

A

True

188
Q

What can PPI and HR antagonists increase the susceptibility for?

A

Enteric infection

PNA

189
Q

What are symptoms of withdrawal?

A

Anxiety, insomnia, restlessness, yawning, stomach cramps, rhinorrhea, diaphoresis, mydriasis, vomiting, diarrhea, fever, muscle spasms, tremor, tachycardia, hypertension, seizures

190
Q

True or False: Delirium common in critically ill patients and can occur after even short periods of sedation

A

True

*In adults, benzodiazepines increase risk for delirium

191
Q

What medication can reduce narcotic and benzodiazepine requirements and shorten the duration of mechanical ventilatino?

A

Precedex (dexmedetomidine)

*Also helps with anxiety and withdrawal symptoms during weaning

192
Q

How does precedex work?

A

Centrally acting alpha-2 agonist

193
Q

What effects does precedex have?

A

Anxiolytic, sedative, analgesic

*Doesn’t interfere with respiratory drive

194
Q

What are potential side effects of precedex?

A

Hypotension/Hypertension
Bradycardia
A-fib

*Generally well tolerated

195
Q

What medication can be given acutely in a pulmonary hypertensive crisis if the patient is intubated?

A

Paralytic- Vecuronium

  • Paralytic + 100% O2 can help to reduce PVR
  • Vec/Roc take effect within 120 seconds of administration
  • Sedation is important, but doesn’t have immediate onset
196
Q

At high doses, what does Epinephrine do to PVR?

A

Increases it

197
Q

What can be given prior to suctioning or intubation to prevent laryngospasm?

A

Lidocaine

198
Q

What effects does ketamine have?

A

Analgesia and sedation

*Doesn’t interfere with respiratory drive

199
Q

What are 2 drugs used for sedation that can cause respiratory depression and increase risk for respiratory compromise?

A

Fentanyl and propofol

200
Q

What are the effects of fentanyl?

A

Good analgesia

Inadequate sedation

201
Q

What are 2 risks with ketamine?

A

Laryngospasm

Bronchorrhea

202
Q

What are 2 things you should have available if using ketamine for sedation?

A 
Muscle relaxant (laryngospasm)
Glycopyrrolate or atropine (bronchorrhea)
203
Q

What are symptoms of cyanide toxicity?

A

Metabolic acidosis
AMS
Bradycardia
Convulsions

204
Q

What drug can cause cyanide toxicity in a post-op patient?

A

Sodium nitroprusside

*Especially with renal insufficiency

205
Q

How often should cyanide levels be monitored in post-operative patients on sodium nitroprusside?

A

Every 72 hours (with prolonged use)

206
Q

Treatment for cyanide toxicity due to sodium nitroprusside?

A
  • Support airway, breathing, circulation
  • Hydroxocobalamin
  • Sodium thiosulfate
207
Q

What conditions increase risk for cyanide toxicity when using sodium nitroprusside?

A

Hepatic impairment
Cardiopulmonary bypass
Therapeutic hypotermia

208
Q

What can be given with nitroprusside to prevent cyanide toxicity?

A

Sodium thiosulfate

209
Q

What type of anti-arrhythmic is flecainide?

A

IC

210
Q

How does flecainide work?

A

Primarily a Na channel blocker- Prolongs phase 0 of action potential in the atrial myocardium, His-Purkinje system and ventricular myocardium

211
Q

What are 2 changes that can be seen with Flecainide initiation?

A
  • Increased QRS duration
  • Lengthened PR interval

*Generally very little effect on QT interval, ST segments or T-waves unless toxic levels reached

212
Q

What class antiarrhythmic is Procainamide?

A

IA

213
Q

How does procainamide work?

A

Primarily blocks Na channels and K channels

214
Q

What is the cardiac effect of procainamide?

A
  • Slower conduction though atrial myocardium, His-Purkinje system, ventricular myocardium
  • Little to no effect on sinus and AV node
215
Q

What effect could procainamide have on atrial flutter with 2:1 conduction?

A
  • Conduction through atrial muscle can slow this slows the atrial rate
  • Slower atrial rate can change AV nodal conduction from 2:1 to 1:1
  • This may increase ventricular rate and effect clinical status
216
Q

What is diltiazem often used for?

A
  • CCB

- Slows AV conduction during macroreentrant atrial arrhythmias

217
Q

Name 2 class IB antiarrhythmics?

A

Lidocaine

Mexilitine

218
Q

What is the effect of esmolol?

A

-Slowed conduction through AV node (BB)

219
Q

What are 2 drugs which may be used in adults with IART and complex CHD with ventricular dysfunction who fail ablation and have no treatable precipitating factors?

A
  • Amiodarone (use with caution if hepatic disease)

- Dofetilide

220
Q

How is dofetilide excreted?

A
  • Kidneys

* Need to dose adjust with renal disease

221
Q

Which populations do you need to avoid flecainide in?

A
  • Depressed ventricular function
  • Complex CHD + Ventricular dysfunction

*Increased mortality

222
Q

When is dronaderone not recommended?

A
  • Heart failure
  • Mod-severe systolic ventricular dysfunction
  • Mod-complex CHD

*May worsen HF and increase mortality

223
Q

What medication can be used for rate control in IART, but won’t maintain long-term sinus rhythm?

A

Metoprolol

224
Q

What class is dofetilide?

A

III

225
Q

How does dofetilide work?

A

Selectively inhibits the rapid component of the delayed rectifier K current

226
Q

What do patients need to be monitored for when starting dofetilide?

A

QT prolongation and arrhythmia

*Risk of torsades

227
Q

How is dofetilide excreted?

A

Kidneys

  • Dose must be adjusted for impaired creatine clearance
  • No effect on thyroid function
228
Q

What are contraindications to Dofetilide?

A
  • Creatine clearance <20
  • Hypokalemia
  • QTc >440 or >500 with ventricular conduction delay
229
Q

What are the most common side effects of amiodarone?

A
  • Hypothyroidism
  • Hyperthyroidism
  • Hepatitis (>2x normal AST/ALT- can progress to hepatic failure)
  • Pulmonary toxicity (cough, fever, dyspnea, opacities on CXR, decreased DLCO on pulmonary function tests)
  • Derm photosensitivity to UV light
  • Blue-gray skin discoloration
  • Corneal microdeposits (benign)
  • Optic neuropathy
230
Q

What medications do you need to be careful using in asthmatics?

A
  • Non-selective BB (bronchospasm)

* Selective BB (like esmolol) should only act on beta 1 receptors, but still need to be cautious

231
Q

What are 3 options for IV BP medications in a post-op patients with moderately controlled asthma?

A
  • Nicardipine
  • Clevidipine
  • Hydralazine

Peds Cardiology (20 decks)

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