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Advanced Pediatric Pharmacology Exam 1 > Cardiology 1 > Flashcards

Cardiology 1 Flashcards

1
Q

Preload

A

Ventricular filling pressure or left ventricular end-diastolic volume

(filling pressure and volume at the end of diastole)

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2
Q

Afterload

A

Left ventricular wall tension or stress during systole

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3
Q

Cardiac Output

A

Volume of blood ejected per unit of time

CO= HR x SV

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4
Q

Cardiorenal HF

A

Sodium/Water excess –> think diuretics as first line of treatment

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5
Q

Cardiocirculatory HF

A

inadequate contractility –> think positive inotropes for treatment

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6
Q

Neurohormonal HF

A

Initial insult activates sympathetic system; but progression is mediated by neurohormones –> modulate hormonal activation

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7
Q

Systolic Dysfunction (3)

A
  1. Decreased Ejection Fraction <40%
  2. Impaired wall motion
  3. Dilated ventricle
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8
Q

Diastolic Dysfunction (5)

A
  1. Preserved Ejection Fraction >40%
  2. Impaired ventricular relaxation and filling
  3. Normal wall motion
  4. Loss in elasticity of the cardiovascular system
  5. Usually caused by cardiomyopathies (restrictive, infiltrative, hypertrophic)
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9
Q

Signs and Symptoms of HF (6)

A
  1. Growth failure (INCREASED METABOLISM)
  2. Respiratory distress
  3. Exercise intolerance, difficulty feeding
  4. Edema
  5. Dyspnea
  6. Fatigue
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10
Q

PHFI +1 Classification for HF (5)

A
  1. Marked cardiomegaly by x-ray or physical exam
  2. Reported physical activity intolerance or prolonged feeding time
  3. Pulmonary edema by x-ray or auscultation
  4. Hepatomegaly less than 4cm below costal margin
  5. Mild to moderate tachypnea or dyspnea
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11
Q

PHFI +2 Classification for HF (8)

A
  1. Abnormal ventricular function by echo or gallop
  2. Dependent edema, pleural effusion, or ascites
  3. Failure to thrive or cachexia
  4. Poor perfusion by physical exam
  5. Resting sinus tachycardia
  6. Retractions
  7. Hepatomegaly over 4cm below costal margin
  8. Moderate to severe tachypnea or dyspnea
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12
Q

Medications for PHFI +1 (4)

A
  1. Digoxin
  2. Low to moderate dose diuretics
  3. ACE-Inhibitors, non-ACE inhibitor vasodilators or ARBs
  4. Beta Blockers
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13
Q

Medications for PHFI +2 (3)

A
  1. High dose diuretics or more than 1 diuretic
  2. Anticoagulants not related to prosthetic value
  3. Anti-arrhythmic agents or ICD
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14
Q

How to calculate PHFI

A

Total score derived by adding scores attributed to each individual criterion

0= no HF
30= severe HF
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15
Q

Vasoconstriction Compensatory Mechanisms of HF

A

Vasoconstriction increases BP and decreases CO to shunt blood to the brain and the heart; get a decrease in SV which further activates compensation of vasoconstriction

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16
Q

Pharmacologic Therapy Principles for Systolic HF (6)

A
  1. Block the compensatory neurohormonal activation caused by decreased cardiac output
  2. Prevent/minimize Na and water retention
  3. Eliminate/minimize symptoms of HF
  4. Slow progression of cardiac dysfunction
  5. Decrease mortality (prolong survival)
  6. Increase quality of life
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17
Q

Diuretics Mechanism of Action (3)

A
  1. Inhibits reabsorption of sodium and chloride in the renal tubules
  2. Increased Na excretion –> increased volume excretion –> decreased preload
  3. Rapid improvement in edema
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18
Q

Loop Diuretic Agents (3)

A
  1. Furosdemide (Lasix)
    * Main diuretic used with children; if patient is going from IV to oral, double the dose
  2. Torsemide
  3. Bumetanide (Bumex)
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19
Q

Loop Diuretic Site of Action, Mechanism of Action, and Adverse Effects (3)

A
  1. Site of Action: Ascending loop of henle
  2. Mechanism of Action: inhibits chloride, sodium, and potassium reabsorption
  3. Adverse Effects: increased potassium and sodium loss
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20
Q

Thiazide Diuretics Available Agents (2)

A
  1. Hydrochlorothiazide

2. Chlorothiazide (Diuril)

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21
Q

Thiazide Diuretics Site of Action, Mechanism of Action, and Adverse Effects (3)

A
  1. Site of Action: Early distal tubule
  2. Mechanism of Action: Inhibits chloride reabsorption = inhibit sodium reabsorption
  3. Adverse Effects: Increased potassium, sodium, and chloride loss
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22
Q

Aldosterone Antagonist (K sparing) Diuretic Agents (3)

A
  1. Spironolactone
    * Also commonly used with children
  2. Eplerenone
  3. Amiloride
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23
Q

Aldosterone Antagonist (K sparing) Diuretic Site of Action, Mechanism of Action, and Adverse Effects (3)

A
  1. Site of Action: Late distal tubule, early collecting ducts
  2. Mechanism of Action: inhibits na/k antiports, so it inhibits sodium and increases potassium secretion
  3. Adverse Effects: increased potassium
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24
Q

Osmotic Diuretic Agent, Site of Action, Mechanism of Action, Adverse Effects (4)

A
  1. Agent: Mannitol
  2. Site of Action: proximal tubule, thin descending lim, distal tubule, and collecting ducts
  3. Mechanism of Action: prevents water reabsorption; indirectly inhibits sodium reabsorption
  4. Adverse Effects: increased electrolyte imbalance, hyperglycemia
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25
Q

Carbonic Anyhydrase Inhibitors Diuretic Agent, Site of Action, Mechanism of Action, Adverse Effects (4)

A
  1. Agent: Acetazolamide
  2. Site of Action: Proximal Tubule
  3. Mechanism of Action: Inhibits HCO3, H, Sodium reabsorption
  4. Adverse Effects: HCO3 loss –> acidosis
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26
Q

Diuretics Resistance (2)

A
  1. Decreased absorption due to edema at GI tract and hypoperfusion
  2. Increased exposure leads to changes in renal tubules altering ion transport
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27
Q

How to overcome diuretic resistance (4)

A
  1. Administer as continuous infusion
  2. Add positive inotropic agent
  3. Increase dose or frequency of diuretic*
  4. Add additional diuretic for synergy
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28
Q

General Adverse Effects of Diuretics (4)

A
  1. Electrolyte depletion
    - Decrease Na, K, Mg, Ca, Cl
  2. Hypotension
  3. Dizziness
  4. Dehydration/azotemia
    * Azotemia=increased nitrogen-containing compounds
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29
Q

Loop Diuretic ADEs (4)

A
  1. Nephrotoxic
  2. Caution with sulfa allergy (all contain sulfur moiety)
  3. hyperglycemia
  4. Hearing loss (reversible)
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30
Q

Spironolactone ADEs (2)

A
  1. Hyperkalemia –> used in pediatrics mainly for this affect
  2. Gynecomastia
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31
Q

What to monitor with Diuretics (6)

A
  1. All electrolytes
  2. SCr (serum creatinine for renal function)
  3. Vitals (BP)
  4. Body weight - trend weight increases/decreases with urine output
  5. HF symptoms
  6. ADEs
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32
Q

Diuretic Clinical Pearls (5)

A
  1. Loops are recommended as first line therapy
  2. Do not over-diurese; maintain euvolemic state
  3. Monitor and replace K and Mg as needed, especially with loops
  4. Dose in morning! unless multiple daily dose are required
  5. May combine classes of diuretics for synergy
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33
Q

Furosemide Pearls and Dosing (4)

A
  1. Dosing: 1-2 mg/kg
  2. Available as tablet and solution
  3. Most common diuretic used in children
  4. Generally well tolerated but can see rare and serious side effects
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34
Q

Acetazolamide Dosing and Pearls (2)

A
  1. Dosing: 5mg/kg up to 3x/day

2. Used in inpatient setting to help secrete bicarb (for alkalosis)

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35
Q

Spironolactone Dosing and Pearls (2)

A
  1. Dosing: 1mg/kg q8-q24

2. Used primarily for potassium sparing effects to avoid KCl supplementation

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36
Q

KCl supplementation dosing and Pealrs (2)

A
  1. Dosing: 1-4mEq/kg q8-24

2. Available as liquid and delayed release tablets

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37
Q

ACE Inhibitor Mechanism of Action (7)

A
  1. Blocks production of angiotensin II
  2. Decreased sympathetic stimulation
  3. Decreased production of aldosterone and vasopressin
  4. Decreased vasoconstriction (afterload)
  5. Increased bradykinins
  6. Increased vasodilatory prostaglandins
  7. May affect cardio remodeling
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38
Q

ACE Inhibitor ADEs (6)

A
  1. Non-productive cough
  2. Increased potassium
  3. Angioedema
  4. Renal insufficiency
  5. Hypotension
  6. Neutropenia
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39
Q

ACE Inhibitor Monitoring (4)

A
  1. BMP; mainly SCr and K
  2. BP
  3. CBC
  4. HF symptoms
40
Q

ACE Inhibitor and ARB Contraindications (3)

A
  1. Potassium over 5.5
  2. History of angioedema
  3. Pregnancy
41
Q

ACE Inhibitor and ARB Cautions (3)

A
  1. Potassium over 4.5 or taking other medications that increase potassium
  2. SCr over 3mg/dL (monitor SCr in children)
  3. Bilateral renal artery stenosis
42
Q

Enalapril Dose interval, available dosage forms, clinical pears (3)

A

Enalapril is the prodrug!

  1. Dose interval: once daily dosing (can dose q12)
  2. Available dosage forms: oral tablet, compound suspension, 1mg/ml manufacturer suspension
  3. Clinical pearls: because of significant risk of Hypotension, test dose is 0.05mg/kg and max dose is 0.4mg/kg/dose BID
43
Q

Captopril Dose interval, available dosage forms, clinical pears (3)

A
  1. Dose interval: Usually given 3 times per day (shortest half-life)
  2. Available dosage forms: tablet, compound suspension, transdermal patch IV
  3. Clinical pearls: Shortest 1/2 lift so easier to titrate the dose initially, but for compliance not used as much
44
Q

Lisinopril Dose interval, available dosage forms, clinical pears (3)

A
  1. Dose interval: Once daily dosing
  2. Available dosage forms: oral tablet, manufracturer suspension
  3. Clinical pearls: All equally effective
45
Q

Enalapril test dose and max dose

A

Because of significant risk of Hypotension, test dose is 0.05mg/kg and max dose is 0.4mg/kg/dose BID

Ex: starting a patient on Enalapril and he weighs 8kg, what would the dose be?
0.05*8=0.4mg

46
Q

ACE Inhibitor Clinical Pearls (1C, 2A)

A
  1. May see more pronounced 1st dose response
    1A. Decreased Serum Na, volume depletion, concurrent
    diuretics
    1B. CHF exacerbations
    1C. Hemodynamic instability
  2. African American (AA) Patients are more likely to have low renin activity
    2A. 2-4 fold incidence in angioedema and cough
47
Q

ARB Mechanism of Action

A

Selectively blocks binding of angiotensin II to the AT1 receptor found in tissues

  • Decreased production of aldosterone and vasopressin
  • Decreased vasoconstriction (afterload)
  • Does not inhibit metabolism of bradykinin
48
Q

Adverse Effects of ARBs

A
  1. Increased K
  2. Angioedema
  3. Renal Insufficiency
  4. Hypotension
  5. Neutropenia
49
Q

Monitoring for ARBs

A
  1. BMP (SCr and K)
  2. CBC
  3. BP
  4. HF symptoms
50
Q

ARB Clinical Pearls (3)

A
  1. Indicated in patients intolerant to ACE inhibitors due to cough or angioedema (although angioedema is a caution with ARBs)
  2. Same cautions and contraindications as ACE inhibitors
  3. Mainly used in pediatrics - Marfans syndrome
51
Q

Beta Blocker Mechanism of Action (6)

A
  1. Blocks effect of sympathetic neurotransmitters (norepinephrine) on the heart and vasculature. Beta receptor stimulation normally leads to increase in HR, myocardial contractility, BP and myocardial O2 demand.
  2. Decreased ventricular arrhythmias
  3. Decreased cardiac hypertrophy and myocardial cell death
  4. Decreased vasoconstriction and HR
  5. Beta 1 = heart
  6. Beta 2 = lungs
52
Q

Timolol

A

Non-selective Beta blocker topically used for intraocular pressure

53
Q

Nadolol (4)

A
  1. Non-selective Beta blocker with longer half life
    * Needs dosage adjustment if patient has renal impairment
  2. 100% urine elimination
  3. Nonselective so works on splancneic
  4. Used commonly in patients with HTN or liver disease to decrease risk of esophageal varices
54
Q

Propranolol (5)

A

Non-selective BB that is also used for:

  1. Tet spells
  2. HTN
  3. Anxiety
  4. Migrane ppx
  5. Hemangioma
55
Q

Sotalol

A

Non-selective BB primary used for arrhythmias

56
Q

Atenolol (4)

A
  1. Beta-1 selective (heart)
  2. Requires renal adjustment (40% excreted as unchanged drug)
  3. Once or twice daily administration
  4. Only available as tablet so requires compounding for suspension
57
Q

Esmolol (4)

A
  1. Beta-1 selective (heart)
  2. Used primarily for treatment of supraventricular tachycardia (SVT), atrial fib/flutter, and hypertensive emergency.
  3. IV formulation only, very fast acting with short half life (3 to 6 min in children, 9 min in adults)
  4. Causes dramatic drop in BP
58
Q

Metoprolol (4)

A
  1. Hepatic metabolism (no renal interactions)
    * good for patients with renal impairment
  2. IV dosing is much lower
  3. ER and IR oral formulations; recipe for suspension available (ER and IR would have different dosing)
  4. Beta-1 selective (heart)
59
Q

Carvedilol (3)

A
  1. Beta-1 selective (heart)
  2. B1 and alpha-1blockade –> decreased afterload
  3. Greater reduction in BP compared to metoprolol
60
Q

Labetalol

A

beta 1 selective and alpha1 blockade

61
Q

Beta Blocker ADEs (6)

A
  1. Hypotension
  2. Decreased HR
  3. Fluid retention
  4. Depression
  5. Fatigue/weakness
  6. Sexual dysfunction
62
Q

How to manage BB hypotension

A

Decreased vasodilator therapy –> if hypotension persists then decrease beta blocker dose

63
Q

How to manage BB fluid retention

A

Increase diuretic dose –> if fluid retention persists then decrease BB dose

64
Q

How to manage BB bradycardia

A

Decrease beta blocker dose! –> if bradycardia persists then d/c BB

65
Q

Beta blocker cautions (4)

A
  1. Severe bronchospastic disease (asthma)
  2. Bradycardia
  3. Symptomatic hypotension
  4. 2nd or 3rd degree heart block
66
Q

Beta blocker monitoring (4)

A
  1. Body weight
  2. Vitals (BP, HR)
  3. HF symptoms
  4. ADEs
67
Q

Beta blocker clinical pearls (5)

A
  1. Utilized in clinically stable patients on ACE-I and diuretics
  2. Should be fluid stable before starting therapy
  3. May become more symptomatic for first few weeks when starting therapy
  4. ‘Start low, titrate slow’
  5. If therapy is held for over 72 hours, consider restarting beta blocker at 50% of previous dose
68
Q

Aldosterone Antagonist Mechanism of Action (5)

A
  1. Blocks effects of aldosterone in the kidneys, heart and vasculature
  2. Decreased potassium and magnesium loss - decreased ventricular arrhythmias
  3. Decreased sodium retention - decreased fluid retention
  4. Decreased catecholamine potentiation - decreased BP
  5. Blocks direct fibrotic actions on myocardium
69
Q

Types of Aldosterone Antagonists (2)

A
  1. Spironolactone

2. Eplerenone

70
Q

ADEs of Aldosterone Antagonists (3)

A
  1. Increased K
  2. Gynecomastia or breast pain
  3. Sexual dysfunction
71
Q

Clinical Pearls of Aldosterone Antagonists (3)

A
  1. Spironolactone is used in pediatric cardiology primarily for potassium sparing effect
  2. Only tablets are available so it requires compounding pharmacy to prepare suspension
  3. Avoid used in combination with both an ACE-I and ARB due to risk of increased potassium
72
Q

Benefits of Digoxin (4)

A
  1. Improved symptoms
  2. Improved exercise tolerance
  3. Decreased hospitalizations
  4. No effect on mortality
73
Q

Digoxin Mechanism of Action

A
  1. Inhibits Na-K ATPase
  2. Decreased central sympathetic outflow
  3. Decreased renal reabsorption of Na
  4. Increased minimal in cardiac contractility due to inhibition of Na-K ATPase
74
Q

Digoxin ADEs (4)

A
  1. Dig toxicity
  2. Cardiac toxicity - ventricular arrhythmias, heart blocks, bradycardia
  3. GI disturbances
  4. CNS toxicities - confusion, vision changes
75
Q

Digoxin Risk Factors for ADEs (6)

A
  1. Increased Ca
  2. Decreased K
  3. Decreased Mg
  4. Hypothyroidism
  5. Interacting medications
  6. Renal insufficiency
76
Q

Digoxin Contraindications

A

2nd or 3rd degree heart blocks

77
Q

Digoxin Cautions while on…. (5)

A
  1. Amiodarone
  2. Diuretics (ex: Furosemide)
  3. Cholestyramine
  4. Spironolactone
  5. Verapamil
78
Q

Digoxin Monitoring (5)

A
  1. BMP (K and SCr)
  2. Serum digoxin levels
    - Therapeutic: 0.8-1.2
  3. Vitals (HR)
  4. HF symptoms
  5. Signs/Symptoms of digoxin toxicity
79
Q

Increased Digoxin Monitoring is required if…(4)

A
  1. Changes in renal function
  2. Changes in EKG
  3. Signs/Symptoms of digoxin toxicity
  4. Initiation or d/c of interacting medications
80
Q

Digoxin Clinical Pearls (4)

A
  1. NOT indicated for acute exacerbations
  2. Loading dose not needed in HF
  3. Decreased starting dose in patients with conduction abnormalities, decreased renal function, low lean body mass
  4. Decreased dose by 50% for concomitant amiodarone therapy
81
Q

Hydralazine Mechanism of Action (2)

A
  1. Vasodilator

2. Enhances effects of nitrates

82
Q

Nitrates Mechanism of Action (2)

A
  1. Stimulates nitric acid signaling in endothelium

2. Decreases preload

83
Q

Nitrates ADEs (5)

A
  1. Headache
  2. Hypotension
  3. Dizziness
  4. Flushing
  5. Flu-like symptoms
84
Q

Hydralazine ADEs (5)

A
  1. Headache
  2. Hypotension
  3. Dizziness
  4. Leucopenia/thrombocytopenia
  5. Lupus-like symptoms
85
Q

Nitrates and Hydralazine Monitoring (5)

A
  1. CBC - WBC and Platelets
  2. Vitals - BP
  3. ANA profile - only if lupus symptoms appear
  4. HF symptoms
  5. ADEs
86
Q

Calcium Channel Blocker Benefits (3)

A
  1. No mortality benefit
  2. May be beneficial in treatment of hypertension in patients at target doses of ACE-I, beta blockers, and ARBs
  3. No observed decompensated HF when using amlodipine or felodipine
87
Q

Anti-Arryhtmics (2)

A
  1. ONLY 2 anti-arrhythmics have been proven safe in treating arrhythmias in HF
    – Amiodarone
    – Dofetilide
  2. Therapy indicated for sustained or hemodynamically unstable ventricular tachycardia, ventricular fibrillation, recurrent/sustained atrial arrhythmias
88
Q

Red Flag Medications in HF (12)

A
  1. All class I agents of anti-arrhytmics (ex: Stalol)
    - Instead, use amiodarone or dofetilide
  2. Ditiazem
  3. Verapamil
  4. Metformin (oral hypoglyemic)
  5. Rosiglitazone (oral hypoglyemic)
  6. Pioglitazone (oral hypoglyemic)
  7. Systemic glucocorticoids
    - prednisone, methylprednisolone, hydrocortisone, dexamethasone
  8. HRT therapies (estrogens and androgens)
  9. NSAIDs - Ibuprofen and Naproxen
  10. Doxorubicin
  11. Daunorubicin
  12. Cilostazol
89
Q

Aspirin (5)

A
  1. Used post Norwood and other procedures that require the least amount of anticoagulation
  2. Used for IVIG resistant Kawasaki Disease for anti-inflammatory effects as well as protection from aneurysm clotting
  3. Dosing: 5-10mg/kg, 1/4, 1/2, and 1 tablet dosing
  4. Unstable in liquid, therefore tablet must be crushed and diluted with small amount of water just before administration
  5. Caution with Reye’s syndrome
90
Q

Warfarin Mechanism of Action (3)

A
  1. Competitively inhibits VKORC1 depleting functional Vitamin K reserves
  2. Limits the amount of vitamin K dependent coagulation factors needed for clotting
  3. Factors affected: Factors II, VII, IX, X, Protein C & S (natural anticoagulants)
    * blocks body’s natural coagulants and increases clearance to form a clot; hyperthrombotic patient on heparin/lovenox to prevent hyperthrombotic state
91
Q

Warfarin Place in Pediatric Medicine (2)

A
  1. Post-Fontan procedures

2. Extracardiac devices (usually INR is higher)

92
Q

Warfarin Dosing (3)

A
  1. 0.2mg/kg starting dose
  2. Usually given at night for AM lab draws
  3. May require a bridge anticoagulation for first 3-4 days or until therapeutic INR due to earlier depletion of protein C and S
93
Q

Warfarin Monitoring (2)

A
  1. Nutrition
  2. INR goal (2-3)
    * Especially watch INR in patients on antibiotics
  3. Drug/Food Interactions
    - Many!
    - Watch Vitamin K intake because Warfarin is a Vitamin K antagonist; if they eat increased Vitamin K they may need higher dose of Coumadin
94
Q

Enoxaparin (4)

A

Lovenox

  1. DVT prophylaxis; inhibits factor Xa to prevent clots
  2. Tx of any thrombosis (ex: pulmonary embolism, catheter associated clot)
  3. Dosing is based on therapeutic anti-Xa
  4. Monitoring is based on the peak level drawn 4-6 hours after the dose
  5. Protamine is only minimally useful in reversing anticoagulation
95
Q

Enoxaparain Dosing in children

A

1-2 mg/kg/dose q12 hours

*only available in SC injection

Advanced Pediatric Pharmacology Exam 1 (8 decks)

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