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CRNA Pharmacology > Positive Inotropic Agents > Flashcards

Positive Inotropic Agents Flashcards

1
Q

Digoxin MOA?

A
  • Selectively and reversibly binds to alpha subunit of Na+/K+ ATPase
  • ↓ in outward Na+ movement and ↑ in intracellular Na+
  • This ↓ outward movement of Ca2+ via Na+/Ca2+ exchanger.
  • ↑ in intracellular Ca2+ concentrations
  • Net effect is ↑ force of contractions
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2
Q

3 examples of cardiac glycoside drugs

A
  • Digoxin
  • Digitoxin
  • Quabain
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3
Q

Digoxin’s Cardiac effects

A
  • Positive inotrope
  • Negative chronotrope
  • Negative dromotrope
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4
Q

Digoxin’s indirect effect on the PSNS

A
  • Indirectly activates vagal nuclei and nodose ganglion which slows HR
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5
Q

Neurohormonal effects of Digoxin

A
  • Sensitizes baroreceptors which ↓ SNS and RAAS
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6
Q

Cardiovascular effects of Digoxin

A
  • ↑ SV and CO
  • ↓ Heart size
  • ↓ LV end diastolic pressure and ↓ wall pressure
  • ↓ O2 consumption
  • ↑ Renal function and diuresis
  • ↓ PAP and PWP
  • Ventricular function curve (Frank Starling curve) shifts left and up
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7
Q

Effect of positive Inotropes such as Digoxin and Dobutamine on the Frank Starling Curve

A

Shifts the curve up and to the left towards normal - meaning there is greater CO or SV for a given level of left ventricular filling

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8
Q

Digoxin EKG effects

A
  • Prolonged PR interval bco delayed conduction through AV node
  • ST segment depression
  • Short QT intervals
  • T wave diminished or inverted
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9
Q

When Digitalis is Dc’d, how long does it take for ECG changes to disappear?

A

Weeks - Long half life

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10
Q

Why is it important to assess PTs on Digitalis for AMI?

A

SGT and T wave changes are common in PTs on Digitalis but may also suggest myocardial ischemia.

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11
Q

Clinical uses for Digoxin

A
  • Rate control for SVTs

- Mgmt of chronic CHF

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12
Q

Digoxin Pharmokinetics

A
  • Absorption in small intestine
  • Bioavailability 70 to 100% depending on oral dosage form
  • Distributes more to heart and skeletal tissue
  • Onset 1.5 to 6 hrs (PO) and 5 to 30 mins (IV)
  • Does not distribute into adipose tissue or cross placenta
  • Low protein binding (20 to 30%)
  • Loading and maintenance doses based on LBW
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13
Q

Digoxin Metabolism

A
  • Small % metabolized by liver (not dependent on CYP450)
  • Primarily excreted by kidneys (2/3 of unchanged drug)
  • t 1/2 = 36hrs +/= 8 hrs (↑ with renal failure)
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14
Q

Explain why Digoxin is not removed by exchange transfusions and dialysis?

A

Most of the drug is bound to tissue and does not circulate in plasma.

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15
Q

Which diseases increase and decrease levels of Digoxin?

A
  • Reduced by CHF, hypothyroidism, renal dysfunction

- Increased by hyperthyrroidism (because of high CO)

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16
Q

Digoxin Therapeutic Ranges

A
  • Adults (0.5 to 2ng/mL)
  • Pediatric (2.5 to 3.5ng/mL)
  • CHF (0.5 to 0.9ng/mL)
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17
Q

When should you obtain Digoxin levels once the PT starts to take it?

A

6 to 8 hrs after a dose due to the long distribution phase

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18
Q

Take precaution when giving Digoxin to which PTs?

A
  • Hypokalemia, hypomagnesemia, and hypercalcemia
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19
Q

Digoxin contraindicated in which PTs?

A
  • Acute ↓ LV contractility
  • Cardioversion
  • Wolfe-Parkinson White Syndrome (causes VFIB)
  • Severe A-V block
  • Constrictive pericarditis
  • Idiopathic hypertrophic sub aortic stenosis
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20
Q

Which drugs ↑ serum levels of digoxin and which ones ↓ serum levels of digoxin?

A
  • ↑ digoxin levels by ↓ clearance (diltiazem, verapamil, quinidine, amiodorone, dronedarone, erythromycin)
  • ↓ digoxin levels by ↑ clearance (antacids, rifampin, phenobarbital, phenytoin, metoclopramide
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21
Q

Drug-drug interactions with Digoxin

A
  • ↑ Pharmacodynamic effect (Beta-adrenergic agonists and IV calcium)
  • ↓ Pharmacodynamic effect (Halothane)
  • Beta blockers ↑ risk of bradycardia and AV block
  • Thiazide and loop diuretics can cause hypokalemia and hypomagnesemia
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22
Q

Which drugs can protect against Digitalis-enhanced cardiac automaticity?

A
  • Fentanyl
  • Enflurane
  • Isoflurane
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23
Q

Diagnosis of Digoxin Toxicity

A
  • < 0.5ng/mL rules out toxicity
  • 0.5 to 2ng/mL considered therapeutic but can be toxic in PTs with certain conditions or on certain meds
  • > 3ng/mL is toxic
  • Infants and children toxicity is above 3.5ng/mL
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24
Q

How can Anesthesia and Hypoxemia affect Digoxin toxicity?

A
  • Hyperventilation during anesthesia can ↓ serum K+ causing hypokalemia
  • Arterial Hypoxemia ↑ sympathetic activity which can ↑ digoxin toxicity
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25
Q

Why do the elderly have an ↑ risk of developing Digoxin toxicity?

A
  • ↓ Renal function
  • ↓ muscle mass
  • Drug/drug interaction (they take more meds)
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26
Q

Digoxin effects on certain serum Electrolytes

A
  • K+ : Digitalis competes for K+ binding sites at the Na+/K+, so hypokalemia ↑ digoxin effects while hyperkalemia ↓ digoxin effects
  • Mg+ : Hypomagnesemia ↑ digoxin’s effect
  • Ca2+ : Hypercalcemia ↑ digoxin’s effect
27
Q

SxS of Digoxin toxicity

A
  • N and V (most common)
  • Visual disturbances
  • CNS symptoms (confusion, drowsiness, fatigue, weakness, dizziness, headache, neuralgia)
28
Q

Cardiovascular SxS of Digoxin Toxicity

A
  • PAT with AV block (most common)
  • Vtac, Vfib, (most likely to cause death)
  • Sinus bradycardia
  • PVCs
  • AV block
29
Q

Treatment of Digoxin Toxicity

A
  • Digibind or Digifab
  • Correct underlying issue (i.e. hypokalemia)
  • Maintain serum K in normal levels (4 to 5.5mmol/L)
  • Lidocaine IV or Phenytoin may be used for digoxin induced ventricular arrhythmias
  • Activated charcoal for overdose
  • Atropine or pacemaker for bradycardia
30
Q

Which treatment options should be avoided for digoxin toxicity?

A
  • Sympathomimetics - will wisen arryhthmias
  • Quinidine and Amiodarone - will ↑ digoxin levels
  • Cardioversion is CONTRAINDICATED
31
Q

Digoxin Immune Fab (Digifab) MOA

A
  • Digiband is an antigen binding agent from antibodies produced in sheep
  • Fab molecule bind digoxin making them unavailable to bind recepters
  • Digband/digoxin binded molecule is then excreted by kidneys
32
Q

Selective Phosphodiesterase PDE Type III inhibitors MOA?

A
  • Aka cAMP PDEIII inhibitors
  • Non-catecholamine, nonglycosie compound that exert competitive inhibition of the isoenzyme PDEIII
  • Inhibition of PDE III ↑ cAMP in in cardiac muscle
  • ↑ cAMP ↑ Ca+ which ↑ inotropic effects
33
Q

Why are PDE III Inhibitors referred to as Inodilators?

A

They have inotropic effects as well as decreasing preload and afterload at the same time.

34
Q

Effect of using catecholamines with Selective PDE III Inhibitors

A
  • Catecholamines also ↑ cAMP but via Beta receptors, so they can used together to get a synergistic effect without getting toxicity
35
Q

Selective PDE III Inhibitors clinical uses

A
  • Acute left ventricular dysfunction
36
Q

Selective PDE III Inhibitors current products

A
  • Milranone (primacor)

- Inamrinone (inacor) - replaced with milranone because of its tendency to cause thrombocytopenia

37
Q

Milranone shouldn’t be used in which PTs?

A
  • Pt’s with severe obstructive aortic or pulmonary valvular disease
  • Severe CHF bco ↑ morbidity and mortality with chronic use
38
Q

Milranone in PTs with Acidosis

A

Inotropic effects are ↓ bco ↓ cAMP formation in acidotic muscle

39
Q

Milranone Characteristics

A
  • Loading dose (50μg/kg/ IV over 10 mins, followed by CI of 0.375 to 0.75 μg/kg/min)
  • Elimination t1/2 is 2.3 hrs
  • Elimination is via kidneys (80% of drug excreted is unchanged)
40
Q

Milranone Adverse Effects

A
  • Hypotension
  • Headache
  • Thrombocytopenia
  • Angina
  • Ventricular arrhythmias
41
Q

Theophyline

A
  • Similar in structure to methylxanthine and caffeine
  • Bronchodilator with anti-inflammatory, immunomodulatory, and stimulatory properties
  • Available IV and PO
  • ↑ contraction of diagram
  • Is a CNS stimulant
  • Stimulates release of endogenous catecholamines
42
Q

Theophyline Clinical Uses

A
  • Airflow obstruction associated with asthma and lung disease
  • Bronchospasm due to asthma
  • Primary apnea of prematurity
43
Q

Theophyline MOA

A

Competitive antagonist of A1 and A2 adenosine receptors, resulting in bronchodilation

44
Q

Theophyline Pharmokinetics

A
  • Metabolized in liver by CYP450 system
  • Active metabolites include caffeine
  • 40% protein bound
  • t1/2 is 8 hrs but 4 hrs in smokers
  • Narrow therapeutic index
45
Q

Aminophylline

A
  • An ethylenediamine salt form of Theophyline
  • 79% Theophyline
  • Given IV
  • Both theophylline and Aminophyline pass freely across placenta
46
Q

Theophyline Therapeutic Range

A

5 to 15 mg/L

47
Q

Clinical situations in which Theophyline clearance might be reduced?

A
  • Elderly
  • Cirrhosis
  • CHF
  • Fever
48
Q

What would be the effect of reduced clearance of Theophyline?

A

Active metabolites such as caffeine would build up in body

49
Q

Drugs that increase theophylline clearance

A
  • Rifampin
  • Phenytoin
  • Phenobarbital
  • Carbamazepine
  • Cigarrette smoking (most significant)
50
Q

Drugs that decrease Theophyline clearance

A
  • Erythromycin and Clarythromycin
  • Cimetidine and Cipro
  • Diltiazem, amioderone, and propanolol
51
Q

Theophyline Adverse effects

A
  • Serum level of 15 to 25mg/L = headache, n and v (most common), tachycardia and palpitations
  • Serum levels > 25mg/L = severe n and v, tachyarrhythmias, PVCs, Vtach, seizures, and death
  • Theophyline relaxes the LES causing GERD and aspiration risks
52
Q

Theophyline and Ketamine

A

Ketamine lowers Theophyline seizure threshold and increase risk for seizures in PTs

53
Q

Theophyline and Benzos

A

Theophyline decreases the effectiveness of benzos

54
Q

Theophyline and neuromuscular blocking agents

A

Theophyline decreases the effects of neuromuscular blocking agents

55
Q

Pentoxifylline

A
  • A methylxanthine derivative
  • A hemrrheologic agent that ↑ flexibility erythrocytes and ↓ blood viscosity
  • Improves blood flow to peripheral limbs
56
Q

IV Calcium

A
  • Used for positive inotropic effects –> ↑ SV
  • Inotropic effects are enhanced in PTs with hypocalcemia and hyperkalemia
  • Duration 10 to 20 mins
  • Risk of arrhythmias if given to PTs taking digoxin especially if they have hypokalemia
57
Q

IV Calcium dosing

A
  • 5 to 10 mg/kg IV for Calcium Chloride
  • Ca chloride or Ca gluconte IV can be given
  • Ca Chloride contains 3x more Ca than Ca gluconate
58
Q

IV Calcium Adverse Reactions

A
  • Rapid injection cause hypotension, tingling, and oppression (sense of heat wave)
  • Local burning sensation
  • Irritating to veins
59
Q

Glucagon

A
  • Polypeptide hormone from Alpha cells in pancreas
  • Produced by recombinant DNA technology
  • Antihypoglycemic agent with positive inotropic and chronotropic effects
  • May be given IM, IV, or SC
60
Q

Glucagon MOA

A
  • Binds to Glucagon receptors that are G-proteins coupled receptors and stimulates adenyl cyclase to ↑ cAMP
  • ↑ cAMP promotes Ca influx
  • Does NOT activate or bind to Beta adrenergic receptors
  • Does not inhibit PDE
  • Can evoke release of catecholamines
61
Q

Glucagon clinical use

A
  • Used to reverse beta blockers
  • Reverse spasms in sphincter of oddi
  • Tx of hyperglycemia
  • Used to inhibit movement of GI tract during radiological procedures
62
Q

Glucagon Side Effects

A
  • N and V that is dose-dependent
  • Tachycardia and HTN
  • Hyperglycemia and Hypokalemia
63
Q

Glucagon Effects in Pts with Afib

A

Abrupt increases in HR

CRNA Pharmacology (8 decks)

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