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Pharmacology > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

Cardiovascular infections

A

Rheumatic fever

Infective endocarditis

Pericarditis

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2
Q

Rheumatic fever

A

Autoimmune reaction to infection with group A strep

Group A strep URI progresses to ARF and potentially rheumatic heart disease

Kids 5-14

Molecular mimicry-immune response targets both bacteria and human tissue
-can lead to lysis of endothelial cells on heart valve

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3
Q

Heart and ARF

A

Valvular damage

Mitral valve almost always affected

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4
Q

Joint pain ARF

A

Knees, ankles, hips, elbows (asymmetric

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5
Q

Factors associated with increase risk of ARF

A

Multiple previous attacks of ARF

Short intervals between attacks of acute rheumatic fever

Increased risk of exposure to strep infections
-kids and adolescents, parents of young kids, teachers, physicians, nurses, day care workers, military recruits, individuals living in crowded situations

Young

High risk patient having poor adherence to secondary prophylaxis

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6
Q

Empiric treatment ARF

A

Penicillin G and gentamicin

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7
Q

Treat ARF if penicillin allergy or hypersensitive to beta lactams

A

Erythromycin, azithromycin, clarithromycin, clindamycin

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8
Q

Concern for recurrent acute rheumatic fever in a patient hypersensitive to beta lactams

A

Erythromycin, azithromycin, clarithromycin

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9
Q

Clindamycin

A

Not used for prophylaxis of recurrent acute rheumatic fever due to the chance of clindamycin eliciting the opportunistic infection of the GI tract C diff

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10
Q

How manage joint pain and fever with ARF

A

NSAIDS like asprin or naproxen

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11
Q

Macrolides

A

Erythromycin

Azithromycin

Clarithromycin

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12
Q

NSAIDS

A

Asprin (acetylsalicylic acid)

Naproxen

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13
Q

Aminoglycosides

A

Gentamicin

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14
Q

Infective endocarditis

A

Prototypic lesion=vegetation

Oral-viridans strep

Skin-staph

URI-HACEK

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15
Q

Empiric treatment for infective endocarditis

A

Vancomycin (IV) and ceftriaxone

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16
Q

Penicillin and strep viridans

A

Great

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17
Q

Ceftriaxone and strep viridans

A

Highly penicillin susceptible

Mid penicillin allergy

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18
Q

Strep viridans gentamicin and penicillin g

A

Shorter course, no renal disease

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19
Q

Gentamicin and ceftriaxone strep viridans

A

Shorter drug course no renal disease

Mid penicillin allergy

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20
Q

Vancomycin strep viridans

A

Severe penicillin allergy

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21
Q

Penicillin desensitization strep viridans

A

Severe penicillin allergy

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22
Q

Strep viridans

A

Highly penicillin G susceptible
-penicillin G or ceftriaxone

No preexisting renal disease, uncomplicated native valve infective endocarditis, shorter drug course
-gentamicin+ penicillin or ceftriaxone

Mid beta lactam sensitivity
-ceftriaxone

Severe beta lactam hypersensitivity (history of anaphylaxis)
-preferred: penicilllin G desensitization
Alternat_vancomycin

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23
Q

Penicillin desensitization

A

Small dose of drug that is gradually increased until the therapeutic dose is acheived
-1 unit of drug is given IV and the patient observed for 15-30 min

No reaction=dose gradually increased every 15-30 min
-tenfold or doubling
Cove 2 million units reached, the remainer of dose can be given

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24
Q

What kind of reaction is penicillin desensitization

A

IgE mediated allergic

Drug must be physically present to maintainability desensitization

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25
Q

S aureus methicillin susceptible

A

Nafcillin

Oxacillin

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26
Q

A aureus MRSA

A

Daptomycin (Alt)

Vancomycin

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27
Q

S aureus mild penicillin allergy

A

Cefazolin

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28
Q

S aureus severe penicillin allergy

A

Daptomycin

Vancomycin

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29
Q

S aureus brain abscess accompanying infective endocarditis

A

Nafcillin

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30
Q

Daptomycin

A

Similar spectrum of activity as vancomycin

-gram positive, including MRSA

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31
Q

MOA daptomycin

A

Not known

Binds to the cell membrane via calcium dependent insertion of its lipid tail leading to depolarization, K efflux, and rapid cell death

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32
Q

Treat S epidermis and other coagulates negative staphylococci

A

Vancomycin

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33
Q

HACEK treat

A

Ceftriaxone

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34
Q

Enterococci (E faecalis)

A

Penicillin G or ampicillin or vancomycin)+gentamicin

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35
Q

Aminoglycosides

A

Gentamicin

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36
Q

1st class cephalosporins

A

Cefazolin

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37
Q

Aminopenicillin

A

Ampicillin

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38
Q

3rd gen cephalosporin

A

Ceftriaxone

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39
Q

Glycopeptide

A

Vancomycin

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40
Q

Penicillinase resistant penicillins

A

Nafcillin

Oxacillin

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41
Q

Pericarditis

A

Inflammation of the pericardial sac

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42
Q

Treat pericarditis in immunocompetent patients

A

NSAIDS (asprin or naproxen)+colchicine
-important to order CRP to track treatment

Corticosteroids (prednisone) are used in severe or refractory cases
-risk prolong illness or to increase the chance of relapse

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43
Q

Colchicine pharmacodynamics

A

Anti-inflammatory action mediated by binding to tubulin

  • prevents tubulin polymerization into microtubules
  • leads to inhibiton of leukocyte migration and phagocytosis
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44
Q

AE colchicine

A

Diarrhea and occasional nausea, vomiting and abdominal pain

Hair los, bone marrow depression, peripheral neuritis, myopathy
-more likely seen with IV colchicine versus oral colchicine

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45
Q

A 42 yo has fever and unintentional weight loss. A diagnosis of IE is made and blood cultures are positive for s epidermidis

A

Ok

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46
Q

A 54 male fever, joint pain, night sweats. Past history of rheumatic fever at the age of 9 and for dental surgery 1 month ago. Symptoms started 2 weeks after dental procedure. PE shows mitral regurgitation. The blood cultures were ordered and an empiric therapy was started

A

Ok

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47
Q

32 females heroin addict was admitted with 2 day fever, shaking, chills, Rigors, and night sweats. Her vitals 100/60, pulse 120, respiration’s 24 , fever. 3 small vegetations tricuspid valve (echo). Three blood cultures drawn and empiric therapy was initiated

A

Ok

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48
Q

Fast action potential

A

Ventricular contractile cardiomyocytes

Atrial cardiomyocytes

Purkinje fibers

Deconvolution of cationic fluxes of the cardiac AP

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49
Q

Slow action potential

A

SA node

AV node

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50
Q

Pacemaker AP phase 4

A

Slow spontaneous depolarization

  • poorly selective ionic influx (NA K) known as pacemaker current (funny current If)-activated by hyperpolarization
  • slow Ca influx (T type (transient) Chanel’s)
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51
Q

Pacemaker AP phase 0

A

Upstroke of action potential

Ca influx through the relatively slow L type (long acting ) Ca channels

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52
Q

Pacemaker AP phase 3

A

Repolarization

Inactivation of calcium channels with increased K efflux

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53
Q

Factors that determine the rate of firing or automaticity of pacemaker AP

A

Rate of spontaneous depolarization in phase 4
-decreased slope-decreased rate (need more time to reach threshold potential)

Threshold potential
-the potential at which action potential is triggered

Resting potential
-if potential is less negative, less time is needed to reach the threshold-firing rate increases

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54
Q

Class 1 antiarrhythmic drugs

A

Na channel blocking drugs

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55
Q

Antiarrhythmic drugs 1A

A

Quinidine

Procainamide

Disopyramide

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56
Q

1B drugs

A

Lidocaine

Mexiletine

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57
Q

1C drugs

A

Flecainide

Propafenone

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58
Q

Class 2 antiarrhythmic

A

Beta beta blockers

  • esmolol
  • propranolol
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59
Q

Class 3 antiarrhythmic

A

K channel blocking

  • amiodarone
  • sotalol
  • dofetilide
  • ibutilide
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60
Q

Class 4 antiarrhythmic

A

Cardioactive CCB

  • verampamil
  • dilitazem
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61
Q

Miscellaneous antiarrhythmic

A

Adenosine

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62
Q

Class 1 function of the sodium channel

A

When sodium channel is activated, Na current occurs down electric and concentration gradients

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63
Q

Resting state

A

The channel is closed but ready to generated AP

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64
Q

Activated state

A

Depolarization to threshold opens m gates greatly increasing Na permeability

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65
Q

Inactivated state

A

H gates are closed, inward Na flux is inhibited , the channel is not available for reactivation-this state is responsible for the refractory period

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66
Q

State dependent block

A

Drugs have different affinities toward the ion channel protein while it shutttles through different states of the cycle
-most therapeutically useful drugs block activated or inactivated Na channels, with very little affinity towards channels in a resting state

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67
Q

The role of the ___ form of class 1 drugs in binding to a channel

A

Cationic

Lidocaine! Bind pka 7.8

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68
Q

Kinetics and dissociation na channel blockers

A

Determines how quickly drugs dissociate fromt he channel

-fast, intermediate or slow kinetics

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69
Q

Class 1A effects

A

Block Na channels, slow impulse conduction, reduce automatism of latent (ectopic) pacemakers

State dependent block-preferential bind to open sodium chennsle
-ectopic pacemaker cells with faster rhythms will be preferentially targeted

Dissociated from channel with intermediate kinetics

Block K channels

Prolong action potential duration

Prolong QRS and QT intervals of the ECG

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70
Q

Class 1B

A

Block Na channels

State dependent block-bind to inactivated Na channels
-preferentially bind to depolarize cells

Dissociate from channel with fast kinetics-no effect on conduction in normal tissue

May shorten AP

More specific action on Na channels-do not block K channels, do not prolong AP or QT duration on ECG

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71
Q

Class 1C

A

Block Na channels, slow impulse conduction

State dependent block-preferentially bind to open (activated Na channels

Dissociate from channel with slow kinetics

Block certain K channels

Do not prolong AP duration and QT interval duration of the ecg

Prolong QRS interval duration

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72
Q

Class 2 drugs

A

Beta blockers

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73
Q

Sympathetic effect on SA nodal cells

A

Role of cAMP

Effect on the funny current-If

Effect on Ca channels-lower the threshold

Increased slope due to effects of If and T type Ca channels

Reduce threshold due to effect on L type ca channels

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74
Q

What drugs class 2

A

Propranolol

Esmolol

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75
Q

How b blockers work

A

SA node
Decreased HR

AV node
Decreased AV conductance (increase PR interval)

Decreased slope due to effects on If and T type Ca channels

Increased threshold due to effect on L type Ca channels

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76
Q

Type 3

A

K channel blockers

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77
Q

Types of K channels

A

Calcium activated

Inwardly rectifying

Tandem pore domain

Voltage gated

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78
Q

K channel blockers regulation of resting potential

A

Inward (electric) gradient is in equilibrium with the outward (concentration) gradient in the resting cell

Inwardly rectifying k channels are open int he resting state

No current occurs in these channels in a steady state bc of this equilibrium

If extracellular K concentration changes, membrane potential will have to readjust to reach a new equilibrium

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79
Q

K channel blockers regulation of action potential

A

Voltage gated K channels contribute to the regulation of AP

Repolarization of cell membrane during AP

Limit the frequency of AP (regulate the duration of refractory period)

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80
Q

Class 3 drugs MOA

A

Block K channels

Prolong AP duration

Prolong QT interval on ECG

Prolong refractory period

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81
Q

Class 4 drugs

A

Block both activated and inactivated L type calcium channels

Active in slow response cells

  • decrease the slope of phase 0 depolarization
  • increase L type Ca channel threshold potential
  • prolong refractory period in AV node

Decrease the slope of phase 0, increase the threshold of potential at SA node

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82
Q

Name class 4 drugs

A

Verampamil, dilitazem

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83
Q

MOA class 4

A

Slow SA node depolarization, cause bradycardia

Prolong AP and conduction in AV duration and conduction time in AV node

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84
Q

Adenosine

A

Activates K current and inhibtiors Ca and funny currents, causing marked hyperpolarization and suppression of AP in slow cells

Inhibits AV conduction and increases nodal refractory period

Turns on AC increase cAMO and activated protein kinase to open If and ca into cell

K out

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85
Q

Clinical use adenosine

A

Conversion to sinus rhythm in paroxysmal SVT

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86
Q

AE adenosine

A 
SOB
Bronchoconstriction (both a1 and a2b adenosine receptors cause bronchoconstriction)

Chest burning

AV block

Hypotension

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87
Q

Phase 0 fast action potential in cardiac muscle

A

Voltage dependent fast Na channels open as a result of depolarization; Na enters the cells down its electrochemical gradient

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88
Q

Phase 1 fast action potential in cardiac muscle

A

K exits cells down its gradient, while fast Na channels close, resulting in some repolarization

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89
Q

Phase 2 fast action potential inc radial muscle

A

Plateau phase results from K exiting cells offset by and Ca entering through slow voltage dependent Ca channels

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90
Q

Phase 3 fast action potential in cardiac muscle

A

Ca channels close and K begins to exit more rapidly resulting in repolarization

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91
Q

Phase 4 fast action potential inc radial muscle

A

Resting membrane potential is gradually restored by Na/K atpase and Na/Ca exchanger

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92
Q

Deconvolutoin of cationic fluxes of the cardiac action potential

A

Inward Na

Inward Ca

Outward K

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93
Q

Phase 4

A

Slow spontaneous depolarization

  • poorly selective ionic influx (na K) known as pacemaker current (funny current If)-activated by hyperpolarization
  • slow Ca influx (via t type (transient ) channels)
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94
Q

Phase ) upstroke of action potential

A

Ca influx through the relatively slow L type (long acting) Ca channels

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95
Q

Phase 3 repolarization pacemaker action potential

A

Inactivation of Ca channels with increased K efflux

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96
Q

Factors tha determine the firing rate of pacemaker AP

A

Rate of spontaneous depolarization in phase 4
(Slope): decreased slope-decreased rate (need more time to reach threshold potential)

Threshold potential-the potential at which AP is triggered

Resting potential -if potential is less negative, less time is needed to reach the threshold-firing rate increases

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97
Q

Procainamide

A

Class 1a

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98
Q

What is procainamide used to treat

A

Sustained ventricular tachycardia, may be used in arrhythmias associated with myocardial

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99
Q

MOA procainamide

A

Directly depresses the activities of SA and AV nodes

Possesses antimuscarinic activity

Has ganglion blocking properties, reduces peripheral vascular resistance-may cause hypotension

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100
Q

Pharmacokinetics procainamide

A

Active metabolite N acetylprocainamide has class 3 activity, has longer half life, accumulates in renal dysfunction-measurements of both parent drug and metabolite are necessary in pharmacokinetics studies

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101
Q

AE procainamide

A

Cardiac

  • QT interval prolongation
  • induction of torsades de pointes arrhythmias and syncope
  • excessive inhibition of conduction

Extracardiac

  • lupus erythematosus syndrome with arthritis, pleuritis, pulmonary disease , hepatitis fever
  • nausea, diarrhea
  • agranulocytosis
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102
Q

Quinidine

A

Natural alkaloid from cinchona bark

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103
Q

Pharmacodynamics and clinical use

A

Used occasionally for restoring rhythm in atrial flutter/fibrillation patients with normal (but arrhymic) hearts

Sustained ventricular arrhythmia

In clinical trials patients on quinidine twice as likely have normal sinus rhythm, but the risk of death is increased two to three fold

Affords antimuscarinic effect ont he heart-may enhance AV conductance-consequences for AF treatment

Exhibits beta-blocking activity (effect on PR interval is variable)

May cause hypotension->tachycardia

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104
Q

AE quinidine

A

Cardiac: QT interval prolongation

  • Induction of torsades de pointes arrhymia and syncope
  • Excessive slowing of conduction throughout the heart

Extracardiac

  • GI side effects (diarrhea, nausea, vomiting)
  • HA, dizziness, tinnitus (cinchoism)
  • thrombocytopenia, hepatitis, fever
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105
Q

Disopyramide use

A

Recurrent ventricular arrhythmias

Affords potent antimuscarinic effect on the heart

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106
Q

AE disopyramide

A

Cardiac-QT interval prolongation, induction of torsades de pointes arrhythmia and syncope, negative inotropy effect-may precipitate heart failure, excessive depression of cardiac conduction

Extracardiac
-atropine like symptoms-urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma

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107
Q

Lidocaine MOA

A

Blocks inactivated sodium channels

Selectively blocks conduction in depolarized tissue, making damaged tissue electrically silent

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108
Q

AE cardiac lidocaine

A

Rapid kinetics results in recovery form block between AP, with no effect on cardiac conductivity in normal tissue

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109
Q

Use lidocaine

A

Mono and polymorphic ventricular tachycardia

-very efficient in arrhythmias associated with acute MI

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110
Q

Pharmacokinetics lidocaine

A

Extensive first pass metabolism-used only by the intravenous route

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111
Q

AE lidocaine

A

The least toxic of all class 1 drugs

Cardio-may cause hypotension in patients with heart failure by inhibiting cardiac contractility, proarrhythmic effects are uncommon

Neurological effects: paresthesia, tremor, slurred speech, convulsions

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112
Q

Mexiletine

A

Orally active drug

Electrophysiological and antiarrhythmic effects are similar to lidocaine

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113
Q

Clinical use mexiletine

A

Ventricular arrhythmias

To relieve chronic pain, espicially pain due to diabetic neuropathy and nerve injury

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114
Q

AE mexiletine

A

Tremor, blurred vision, nausea, lethargy

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115
Q

Flecainide

A

1C
Blocks sodium and potassium channels

Has no antimuscarinic effects

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116
Q

Clinical use flecainide

A

In patients with normal hearts

Treating supraventricular arrhythmias including AF, paroxysmal SVT (AVNRT, AVRT)

Life threatening ventricular arrhythmias, such as sustained ventricular tachycardia

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117
Q

AE flecainide

A

May be effective in suppressing premature ventricular arrhythmias when administered to

  • patients with preexisting ventricular tachyarrhythmias
  • patientswith a previous myocardial infarction
  • patients with ventricular ectopic rhythms
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118
Q

Propafenone

A

Class 1C possesses weak b blocking activity

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119
Q

Use propafenone

A

Prevent paroxysmal AF and SVT in patients with structural disease

In sustained ventricular arrhythmias

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120
Q

AE propafenone

A

Exacerbation of ventricular arrhythmias

A metabolic tase
Constipation

Do not combine with the CYP2D6 and CYP3A4 inhibtiors as the risk of proarrhythmia may be increased

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121
Q

Clinical indications for the propranolol use in cardiac arrhythmias (class 2 drugs)

A

Arrhythmias associated with stress

Re-entrant arrhythmias that involve AV node

  • AV nodal recent rant tachycardia (AVNRT)
  • AV recent rant tachycardia (AVRT)

A fib and flutter

Arrhythmias associated with MI
-decreased mortality in patients with acute MI

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122
Q

Asmolol

A

Short acting selective beta 1 blocker

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123
Q

HL esmolol

A

10 min bc of hydrolysis by blood esterases

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124
Q

How is esmolol given

A

Uses as continuous iv infusion, with rapid onset and termination of its actions

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125
Q

Clinical use esmolol

A

Supraventricular arrhythmias

Arrhythmias associated with thyrotoxicosis

Myocardial ischemia or acute myocardial infarction with arrhythmias

As an adjunct drug in general anesthesia to control arrhythmias in perioperative period

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126
Q

AE beta blockers (class 2)

A

Reduced cardiac output

Bronchoconstriction

Impaired liver glucose mobilization

Produce an unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)

Sedation, depression

Withdrawal syndrome associated with sympathetic hyperresponsiveness

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127
Q

Contraindications beta blockers

A

Asthma

Peripheral vascular disease

Raynaud syndrome

Type 1 diabetics on insulin

Brady arrhythmias and AV conduction abnormalities

Severe depression of cardiac function

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128
Q

Amiodarone

A

Class 3 blocks K channels

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129
Q

MOA amiodarone

A

Prolongs QT interval and APD uniformly over a wide range of heart rates

Blocks inactivated sodium channels

Possesses adrenoleukodystrophy activity

Has calcium channel blocking activities

Causes bradycardia and slows AV conduction
Causes peripheral vasodilation (effect may be related to the action of the vehicle)

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130
Q

Clinical use amiodarone

A

Treatment of ventricular arrhythmias

A fib

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131
Q

Pharmacokinetics amiodarone

A

CYP3A4-its half life is affected by drugs that inhibit CYP3A4 (cimetidine), or induce it (rifampin)

Major metabolite is active, with very long elimination half life (weeks-months)

Effects are maintained 1 to 3 months after discontinuation, and metabolites are found in the tissues 1 year after discontinuation

Inhibits many CYP enzymes-may affect the metabolism the metabolism of many other drugs

All medications should be carefully reviewed in patients on amiodarone-dose adjustments may be necessary

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132
Q

AE amiodarone

A

Cardiac

  • AV block and bradycardia
  • incidence of torsades de pointes is low as compared to other class 3 drugs

Extracardiac

  • fatal pulmonary fibrosis
  • hepatitis
  • photodermatitis, deposits in the skin, give blue grey skin discoloration in sub exposed areas
  • deposits of drug in cornea and other eye tissues, optical neuritis
  • blocks the peripheral conversion of thyroxine to tiiodothyronine, also a source of inorganic iodine in the body-may cause hypo or hyperthyroidism
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133
Q

Sotalol

A

Class 2 (non selective beta blocker) and class 3 agent (prolongs APD)

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134
Q

Clinical use sotalol

A

Treatment of life threatening ventricular arrhythmias

Maintenance of sinus rhythm in patients with a fib

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135
Q

AE sotalol

A

Depression of cardiac function

Provokes torsades de pointes

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136
Q

Dofetilide

A

Class 3

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137
Q

MOA dofetilide

A

Specifically blocks rapid component of the delayed rectifier potassium current-effect is more pronounced at lower heart rates

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138
Q

Pharmacokinetics dofetilide

A

Eliminated by kidneys, has very narrow therapeutic window-dose has to be adjusted based on creatinine clearance

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139
Q

Use dofetilide

A

Convert AF to the sinus rhythm and maintain the sinus rhythm after cardioversion

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140
Q

AE dofetilide

A

QT interval prolongation and increased risk of ventricular arrhythmias

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141
Q

Ibutilide

A

Similar to dofetilide, slows cardiac repolarization by blockade of the rapid component of the delayed rectified potassium current

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142
Q

How give ibutilide

A

IV and rapidly cleared by hepatic metabolism

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143
Q

Use ibutilide

A

Convert a flutter and a fib to sinus rhythm

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144
Q

AE ibutilide

A

QT interval prolongation and increased risk of ventricular arrhythmias

Patients require continuous ECG monitoring until QT returns to baseline

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145
Q

Clinical use verampamil, dilitiazem

A

Prevention of paroxysmal SVT

Rate control in AF and a flutter

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146
Q

AE verampamil, dilitazem

A

Cardiac

  • negative inotropy
  • AV block
  • SA node arrest
  • bradyarrhythmias
  • hypotension

Extracardiac
-constipation (verampamil)

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147
Q

Clinical use adenosine

A

Conversion to sinus rhythm in paroxysmal SVT

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148
Q

AE adenosin

A

SOB

Bronchoconstriction (both a1 and a2b adenosine receptors cause bronchoconstriction)

Chest burning

AV block

Hypotension

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149
Q

MOA adenosin

A

Activates K current and inhibits Ca and funny currents, causing marked hyperpolarization and suppression of action potentials in slow cells

Inhibits AV conduction and increases nodal refractory period

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150
Q

Proarrhythmia

A

Drug induced significant new arrhythmia or worsening of an existing arrhythmia

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151
Q

Torsades de pointes (TdP, twisting the pointe)

A

Rapid form of polymorphic VT associated with the evidence of prolonged ventricular repolarization (long QT syndrome)

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152
Q

What is long qt and torsades de pointes associated with

A

Often associated with the impaired function of K channels leading to a prolonged period of repolarization

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153
Q

What exacerbates long qt and torsades de pointes

A

Factors that prolong action potential duration

  • slow heart rates
  • electrolyte abnormalities (hypokalemia, hypomagnesemia)
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154
Q

Drugs causing long qt syndrome and torsades de pointes arrhythmias

A

Antiarrhymic drugs-groups 1A and 3 (amiodarone very rarely induces TdP)

Antipsychotics

Antihistamines

Antibiotics

Antidepressants

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155
Q

Long qt syndrome and torsades de pointes

156
Q

Mechanism of TdP arrhythmias:

A

A type of a triggered activity resulting from early afterdepolarizations

157
Q

Triggered activity

A

Depolarizing oscillations in the membrane potential induced by the preceding AP

158
Q

Early afterdepolarizations

A

Often associated with the impaired function of K channels leading to a prolonged period of repolarization

Abnormal depolarizations that occur during phase 2 or phase 3 of AP are due to the opening of Ca or Na channels, respectively

159
Q

To prevent TdP, monitoring what is necessary

A

QTc (QT corrected for heart rate)

160
Q

Do not give TdP inducing drugs if QTis

161
Q

What drugs cause long QT

A

Many

FDA ordered cardiotoxicity studies

  • a number of long QT inducing drugs have been removed from the market
  • requirement to test the effect of new drugs on QT interval before they are approved
162
Q

Termination of TdPs if drug induced

A

Discontinuation of the potentially causative agent

163
Q

Termination of TdPs if hemodynamically unstable

A

Immediate synchronized direct current cardioversoin

Correction of electrolyte abnormalities, such as hypokalemia and hypomagnesemia

Magnesium sulfate iv irrespective of whether the patient is hypomagnesemia or not

Transvenous temporary pacemaker for overdrive pacing or isoproterenol iv

164
Q

Flecainide and other 1C drugs

A

Cause ventricular arrhythmias, such as PVCs, sustained VT and VF

165
Q

Flecainide

A

Was included in cardiac arrhythmia suppression trial (CAST), a. Long term multi center, randomized double blind study in patients with asymptomatic non life threatening ventricular arrhythmias who had a MI

An excessive mortality or non fatal cardiac arrest rate was seen in patients treated with flecainide compared with that seen in a carefully matched placebo treated group

166
Q

Why was CAST terminated prematurely

A

Bc flecainide and other class 1C drugs increased the mortality by 2.5 fold

167
Q

MOA of digoxin induced arrhythmias

A

Tachyarrhymias and ectopic rhythms

  • a type of a triggered activity resulting from delayed afterdepolarization
  • occur during phase 4 as a result of increased cytosolic Ca due to Ca overload
  • spontaneous Ca release from SR activated 3 Na/Ca exchange leading to a net depolarizing current
168
Q

Bradyarrhythmias and AV blocks digoxin

A

Central parasympathetic activity accentuation of vagal effects on the heart

169
Q

Treatment of digoxin induced arrhythmias

A

Cancel digoxin

Anti-digoxin antibodies

K supplementation to upper normal levels

170
Q

A fibrillation

A

Ventricular Rate Control (see the scheme on the next slide)

  • ca channel blockers
  • beta blockers
  • digoxin
  • amiodarone
171
Q

What do with paroxysmal or persistent AF

A

Assess LV function
-no HF, LVEF >40%->CCB or B block->CCB and digoxin or b blocker and dogoxin->amiodarone

HF with LVEF<40%->B blocker->B blocker and digoxin->amiodarone

Decision algorithm for long term ventricular rate control therapy. Goal less than 100 bpm or 20% reduction rate reduction with symptom relief. If goal is not met, move to the next step in algorithm

172
Q

Stroke prevention in patients with a fib

A

Most patients require therapy with oral anticoagulants

In patients with no risk factors for stroke, anticoagulation may not be necessary

173
Q

CHADS score

A 
CHF 1 point
HTN 1 point
Age greater than or equal to 75 1 point 
Diabetes 1 point 
Stroke TIA history 2 points
174
Q

CHADs score 0

A

Low degree of risk for a fib

Antithrombotic therapy is not recommended. For patients who choose antithrombin therapy: asprin 75-325 mg daily

175
Q

CHADs >1

A

Moderate high risk for a fib

Give oral anticoagulation with warfarin or DOAC

176
Q

A fib treat

A

Rhythm control (conversion to sinus rhythm)

Maintence of sinus rhythm after conversion to sinus rhythm

177
Q

Rhythm control

A

Cardioversion using direct current cardioversion

Pharmacological (chemical) cardioversion

  • amiodarone
  • flecainide
  • dofetilide
  • ibutilide
  • propafenone
178
Q

Maintenance of sinus rhythm after the conversion to sinus rhythm

A 
Dronedarone
Flecainide
Propafenone
Sotalol
Amiodarone
Dofetilide
Catheter ablation
179
Q

AF-> consider DCC-> if DCC is unreadable to undesirable or unsuccessful, consider what

A
  • no HF, LVEF>40%->amiodarone, dofetilide, flecainide, ibutilide, propafenone
  • HF with LVEF <40->amiodarone, dofetilide ibutilide

Decision algorithm for conversion of hemodynamically stable AF to sinus rhythm

180
Q

Termination paroxysmal supraventricular tachycardia

A

Adenosine

Verampamil or dilitazem

Beta blockers

Digoxin

Amiodarone

181
Q

Prevention paroxysmal supraventricular tachycardia

A

Verapamil
Digoxin
Catheter ablation

182
Q

PSVT_>vagal maneuvers->adenosine

A
  • LVEF>40% or no history of HF->dilitazem or verampamil->b blocker->digoxin
  • LVEF<40% or history of HF->digoxin->amiodarone->dilitazem
183
Q

Treat AV block

A

Rarely necessary; patients should be monitored

184
Q

Acute high grade AV block that is symptomatic

A

Atropine

If ineffective, dopamine or epinephrine
-transvernous cardiac pacing can be initiated

185
Q

Long standing AV second or third degree block

A

If patients take medications that may cause AV block, the drugs should be discontinued
-if AV block persists, or discontinuation of drugs causing AV block is undesirable, implantation of a permanent pacemaker is indicated

186
Q

Drugs for heart failure

A

ACE inhibitors

ARBC

Carvedilol

Spironolactone

Diuretics

Direct vasodilators

Digoxin

Dobutamine, dopamine, milrinone

187
Q

Name ACE inhibitors

188
Q

Name ARDS

A

Losartan
Vallarta’s
Sacubitril

189
Q

Name diuretics

A

Loop, thiazide, k sparing

190
Q

Name direct vasodilators

A

Nitroglycerin/isosorbide, dinitrate, nitroprusside, hydralazine

191
Q

What is Cor pulmonale

A

Right sided heart failrue due to increased pressure transferred back through lungs bc of left side HF

Causes include COPD, interstitial lung disease, pulmonary HTN, thromboembolic disease, obstructive sleep apnea

192
Q

High output heart failure

A

Body’s need for cardiac output is abnormally elevated to a point beyond the hearts capabilityy

Causes include hyperthyroidism, preg, anemia, arteriovenous fistula, wet beri

193
Q

Major causes of HF

A

Coronary artery disease/MI

Chronic HTN

Diabetes

194
Q

Systolic failure

A

Decrease ESPVR slope
Increase ESV and EDV

Decrease SV and EF

195
Q

Diasolic failure

A

Increase EDPVR
Decrease EDV
Increase end diastolic pressure

196
Q

Systolic HF characteristics

A

Reduced LVEF
-usually 60-70%
With SHF, LVEF<50%=HFrEF

Progressice chamber dilation ith eccentric remodeling

197
Q

Characteristics of DHF

A

Prevelance now estimated at 40-69% of HF; espicially common finding in elderly women

Preserved HFpEF

198
Q

What does CHF cause

A

Poor tolerance of a fib since loss of atrial contraction-> decreased ventricular filling

-poor tolerance of tachycardia since shorter duration of diastole limited time for relaxation and filling

Worsened by increase MAP, espicially if abrupt or severe

Worsening of DHF by ischemia raises left atrial pressure->angina pain with wheezing, SOB, flash pulmonary edema

199
Q

Digitalis

A

Decreased hospitalization

Did not prolong life

People felt better right up until the moment they would have otherwise dies and then died typically due to a fatal arrhythmia

200
Q

Consequences of vascular remodeling

A

High pressure in the ventricle during systole and diastole heightens myocardial oxygen consumption, a situation that promotes further hypertrophy and activates neurohormonal systems

  • reduction in ejection fraction
  • reduced ventricular erformance
  • morbid and mortality

And incrase in CO is transient and never enough so cycle repeats continuously with diminishing returns

201
Q

Adaptive mechanisms in HF from a drop in CO

A

Increase renin
Increase aldosterone
Increase sympathetic discharge
Increase in preload and afterload of the heart
Increase in release of Natiuretic peptides (effects are overwhelmed
Increase INR emodeling of the heart..deleterious, leads to cycle of worsening heart function

202
Q

MI remodeling

A

Fibrous scar tissue , spherical ventricular dilation with hypertrophy of adjacent myocytes surround by increased levels of collagen

203
Q

What are the thee patterns of remodeling after an MI

A

Concentric
Eccentric hypertrophy
Concentric hypertrophy

204
Q

Heart failure treatment objectives

A

Remove the precipitating cause

Correct the underlying cause

Prevent deterioration of cardiac function
-ACI/ARB/BB/spironolactone/eplerenone

Control the CHF state
-diet, diuretics, vasodilators to Reduce cardiac work, dogixin to increase contractility

205
Q

RAAS inhibtors

A

Aliskiren

ACEI

ARB

Spironolactone

206
Q

Aliskiren

A

Block angiotensinogen to angiotensin I

Renin inhibitor

207
Q

ACE_

A

Block angiotensin I to II

Kinase I

208
Q

ARB

A

Block angiotensin II action on kidney and adrenal gland (which reduced aldosterone)

AT1 receptos

209
Q

Spironolactone

A

Stops aldosterone action on the kidney to reabsorbed NaCl and water

210
Q

How do ACE and ARB work-major drugs for heart failure! Have been shown to increase survival in heart failure patients (high doses required)

A

Prils and Spartans

Less angiotensin II leads to

  • less vasoconstriction (decreased afterload
  • less aldosterone secretion and less Na/water retention (decrease preload)
  • decrease cell proliferationa and remodeling
211
Q

MOA captopril (ACE)

A

Competitive inhibitor of angiotensin converting enzyme ACE

212
Q

Effects captopril

A

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and nitrogen for cardiovascular remodeling

Lowers levels of angiotensin II-> increase plasma renin activity and decrease aldosterone secretion

Lowers BP

213
Q

Clinical captopril

A

HTN, add thiazide or loop diuretic if additional lowering is needed at max recommended dose

Acute HTN

HF with reduced ejection fraction (HFrEF)

LV dysfunction following MI

Diabetic nephropathy

O

214
Q

Pharmacokinetics captopril

A

Rapidly absorbed

CYP2D6

Excreted primarily in uring 40-50% as unchanged drug

HL 1.7 hours

215
Q

AE captopril

A

Cough

Hypotension

Angioedema

216
Q

Enalapril

A

Another early ACEI, a prodrug with active form

217
Q

Benazepril

A

Now widely used ACE inhibitor, longer HL permitting 1 day dosing

218
Q

Lisonopril

A

Now widely used ACE inhibtors, longer HL permitting once day dosing

219
Q

Losartan MOA

A

Competitive nonpeptide angiotensin II receptor antagonist with 1000x greater selectivity for AT1 than AT2 receptor

220
Q

Effects losartan

A

Blocks vasoconstrictor and aldosterone secreting effects of angiotensin II

Induces a more complete inhibition of the renin angiotensin system than ACE inhibtiors

Dose not affect the response to bradykinin

221
Q

Clinical losartan

A

Heart failure if intolerant to ACEI

Off label Marian

HT

222
Q

Pharmacokinetics losartan

A

CYP2C9 and 3A4

1/2 is 6-9 hours

223
Q

AE losartan

A

With diabetic nephropathy

Fatigue, dizzy, fever

Hypoglycemia, hyperkalemia,

Cough

Anemia, weaknesss

224
Q

Vallarta’s

A

6-10 hours

Not a prodrug requiring activation

225
Q

Candesartan

A

5-9 hours

Irreversible binding

226
Q

Valsartan/sacubitril MOA

A

Prodrug that inhibits neprilysin through the active metabolites LBQ657

Valsartan ARB

Drugs are co-crystallized

227
Q

Effects valsartan/sacubitril

A

Block leads to increased levels of peptides, including netriuretic peptides

Valsartan antagonizes AT1 receptors

228
Q

Clinical valsartan/sacubitril

A

HF to reduce risk of cardiovascular death and hospitalization

229
Q

Pharmacokinetics valsartan/sacubitril

A

Twice daily dosing

LBQ657 11 hours

Valsartan 9 hours

230
Q

AE valsartan/sacubitril

A

Common
Hypotension

Hyperkalemia

Increased serum creatinine

231
Q

When secrete natriuretic peptide

A

Atrial distention

Sympathetic stimulation

Angiotensin II
Endothelin1

232
Q

Blocks neurologic endopeptidase by valsartan/sacubitril

A

Blocks degradation of ANP

233
Q

Effects of ANP

A

Increase GFR, decrease renin, decrease aldosterone, decrease Na and water reabsorption in collecting duct

Decrease ADH secretion and ADH effects in collecting duct

234
Q

ACE or ARB better

235
Q

Who gets ACE ARB

A 
All patients with LV systolic failure or LV dysfunction without heart failure unless:
Not tolerated
-pregnant
-hypotensive
-serum creatinine >3 
-hyperkalemia
236
Q

HF increases sympathetic activity

A

Increase HR, myocardial contractility, vascular resistance

237
Q

What beta blockers use in HF

A

Metoprolol

Bisoprolol

Carvedilol* best

Not all beneficial!

238
Q

Carvedilol MOA

A

A racemic mixture is a nonselective beta and alpha adrenergic blocker with no intrinsic sympathomimetic activity

239
Q

Effects carvedilol

A

In HT, reduction of cardiac output, exercise or beta agonist induced tachycardia, reflec orthostatic tachycardia

Increased ANP

In CHF, decreased pulmonary capillary wedge pressure, pulmonary artery pressure, heart rate, systemic vascular resistance, right atrial pressure
-increased stroke volume index

240
Q

Linical carvedilol

A

If clinically stable,

Recent or remote history of MI or ACS and reduced ejection fraction (rEF;<40)
REF to prevent symptomatic HF

Reduced morbidity and mortality

241
Q

Pharmacokinetics carvedilol

A

Rapid and extensive absorption

CYP2D6, 2C9, 2D6, 3A4, 2C10, 1A2, 2E1

242
Q

AE carvedilol

A

Hypotension, bradycardia, syncope, edema, angina, AV block

Impotence

Blurred vision

Cough, anemia

243
Q

Labetalol

A

Another alpha/beta blocker used primarily for severe HTN, treatment of hypertensive emergencies

244
Q

Carvedilol

A

Prevent down regulation of B1 adrenergic receptors in the heart as a result of excessive sympathetic stimulation

245
Q

What does carvedilol do

A

Keeps heart responsive to sympathetic drive

Protects against dysrhthmias

Reduce renin secretion

Reduces myocardial oxygen consumption

Limits heart msucle remodeling and reduces necrosis and apoptosis of myocardial cells

246
Q

How give carvedilol

A

Low dose initially with caution in patients that is stable

ONLY GIVE TO CLINCIALLY STABLE

247
Q

Who give carvedilol

A

Patients with diastolic heart failure will benefit from a lower heart rate

B blockers should be given to all patients with symptomatic CHF and LVEF<40% unless contraindication

  • bronchospasm is disease
  • symptomatic bradycardia or heart block

With ACE I to all patients with left ventricular systolic dysfunction caused by myocardial infarction to reduce mortality

248
Q

AE carvedilol

A

Allergy
Chest pain, discomfort, tightness, or heaviness
Dizziness, lightheaded ness, or fainting
Generalized swelling or swelling of the feet, ankles or lower legs
Pain
SOB
Bradycardia
Weight gain
Angina/heart attack if abruptly iscontinued

249
Q

Ivabradine MOA

A

Selective and specific inhibition of the hyperpolarization

-activated cyclic nucleotide gated (HCN) channels (f channels) within the SA node of cardiac tissue

250
Q

Effects ivabradine

A

Disrupts If (funny current) to prolong diastole and slow HR

251
Q

Clinical ivabradine

A

Treatment of resting HR >70 bpm in patients with stable , symptomatic chronic heart failure <45% who are in sinus rhythm with

  • max tolerated dose of beta blockers
  • contraindication to use beta blocker use
252
Q

Pharmacokinetics ivabradine

A

PO 40% bioavailability due to intestinal and hepatic CYP3A4

6 hours

253
Q

AR ivabradine

A

Bradycardia, HTN, increase risk of a fib , heart block, SA arrest

254
Q

Spironolactone MOA

A

Competitive antagonist of aldosterone receptors, decreases aldosterone stimulated gene expression

Side effects due in part to it being a partial agonist at androgen receptors

255
Q

Effects spironolactone

A

K sparing diuretic, blunts ability of aldosterone to promote NaK exchange in collecting duct

256
Q

Clinical spironolactone

A

Counteracts K loss induced by other diuretics in the treatment of HTN, heart failure, ascitestreatment of primar hyperaldosteronism

Reduce fibrosis post MI

257
Q

Pharmacokinetics spironolactone

A

Drug has active metabolites including canrenone with 20 hour 1.2
Steroid effects are slow on and slow off….single dose give effects 2-3 days

258
Q

AE spironlactone

A

Hyperkalemia

Amenorrhea hirstiutism

Gynecomastia

Impotence

Tumorigen inchronic animal toxicity studies

259
Q

Eplerenone

A

More selective aldosterone antagonist, approved for use in post MI heart failure and alone or in combo for treatment of HTN

260
Q

Spironolactone and ep

A

Competitive inhibtiors of the mineralocorticoid, aldosterone

-increases plasma K, decreases plasma Na and volume by opposing the effects of aldosterone on kidney

261
Q

Beneficial heart effects of spironolactone after MI

A

Decrease myocardial fibrosis

Reduces early morning rise in heart rate

Reduces mortality and morbidity in patients with severe HF

Prevent Na and water retention, k loss, mg los, reduced baroreceptor reflex, cardiac fibrosis, ischemia, sympathetic activation

262
Q

After damaged heart vasculature synthesizes aldosterone after MI…

A

Locally produced aldosterone contributes to cardiac fibrosis

263
Q

Clinical use spironolactone

A

Cardioprotective, antifibrotic and antiarrhythmic effects have been proven in animal experiments

Effects on morbidity and mortality have been demonstrated in RCT

Approved for treatment of symptomatic HF with reduced systolic function but…
-most underutilized of all classes of medications for HF< primarily bc of feat of hyperkalemia

264
Q

Sarcomere length vs strength

A

Cardiac has longer length than skeletal but similar tension?

265
Q

Furosemide MOA

A

Directly inhibits reabsorption of Na and Cl in the thick ascending limb of the TAL by blocking Na K 2Cl

Indirectly inhibits paracellular reabsorption of Ca and Mg by the TAL due to loss of K backleak responsible for lumen +transepithelial potential

266
Q

Effects furosemide

A

Causes increased excretion of water, Na, K, Cl, mg and Ca

267
Q

Clinical furosemide

A

Edema
-HF, hepatic, renal

Acute pulmonary edema by decreasing preload

  • decreases EC col
  • rapid dyspnea

Treatment of HTN

Works if low GFR

268
Q

Pharmacokinetics furosemide

A

IV-5 min onset
PO-30-60 min
IM-30 min

269
Q

AE furosemide

A

Hypok, na, ca, mg,
Hypochloremic met alkalosis

Hyperglycemia

Hyperuricemia

Ototoxicity

Sulfonamides, so risk hypersensitivity

270
Q

Torsemide

A

Sulfonamide similar to furosemide with longer t1/2 better oral absorption and some evidence that is works better in heart failure

271
Q

Bumetanide

A

Sulfonamide similar to furosemide, but more predictable oral absorption

272
Q

Ethacrynic acid

A

Non sulfonamide loop diuretic reserved for those with sulfa

273
Q

Hydrochlorothiazide MOA

A

Inhibits Na reabsorption in the distal tubules cia blockade of Na Cl cotransporter

274
Q

Effects hydrochlorothiazide

A

Increases urinary excretion of Na and H2O

Also increases urinary excretion of K and Mg

K losing

275
Q

Clinical hydrochlorothiazide

A

HTN
Not ok if GFR low

Edema

Calcium nephropathy Asia

276
Q

AE hydrochlorothiazide

A

Sulfonamide-hypersensitivity
Hypok, mg, na,

Hypochloremic metabolic alkalosis

277
Q

Chlorothiazide

A

Similar to HCTZ but poor oral absorption

278
Q

Chlorthalidone

A

Similar to HCTZ but half life of 40-60 hrs…prolonged stable response with proven benefits is reason it is preferred

279
Q

Metolazone

A

Another long acting thiazide diuretic , favorite of cardiologists for use as an adjunct diuretic int he treatment of CHF

280
Q

What do diuretics help with in HF

A

Relieve congestion

-must get rid of excess volume to relieve the congestion and return ventricular fiber length to more optimal range

281
Q

Which diuretics try first

A
  1. Loop

Add K sparing if needed

If still need more diuresis give thiazide

282
Q

Causes of diuretic failure during heart failure treatment

A

Noncompliance
Excess dietary Na
Decreased renal perfusion and GFR from
-excessive volume depletion and hypotension due to aggressive diuretic or vasodilator therapy
-decline in CO due to worsening HF, arrhythmias or other primary cardiac causes
-selective reduction in glomerular perfusion pressure following initiation or dose increase of ACEI therapy

NSAID

Renal

Reduced or impaired diuretic absorption due to gut wall edema and reduced splanchnic blood flow

283
Q

Vasodilators for chronic HF

A

Isosorbide dinitrate (to dilate veins, decrease preload) plus hydralazine (dilate arteries, decrease afterload)

  • packaged as BiDil
  • espicially in african Americans
  • new frontier of personalized medicine, the first drug even intended for one racial group
  • the reason why whites fail to respond is unknown

Can consider in patients who cant tolerate ACE I

284
Q

Nitroglycerin MOA

A

Forms free radical NO, which in SM activates soluble granulated cyclase to increase cGMP->dephosphorylation of myosin light chains and smooth muscle relaxation

285
Q

Effects ntiroglycerin

A

Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects ont he veins

Primarily reduces cardiac oxygen demand by decreasing preload

May modestly reduce afterload

Dilated coronary arteries/improves collateral flow

286
Q

Clinical nitroglycerin

A

Treatment or prevention of angina pectoris

Acute decompensated HF (specially when associated with acute MI)

Perioperative HTN

287
Q

AE nitroglycerin

A

Reflex tachycardia
Flushing
Hypotension

288
Q

Isosorbide dinitrate

A

Slower onset of action, administered orally for prevention of angina and for HF with reduced ejection fraction

289
Q

Hydralazine MOA

A

Not understood

Endothelium dependent
Hyperpolarized

Requires COX

Mediated by PGI2

290
Q

Effects hydralazine

A

Direct vasodilation of arterioles_>decreased systemic resistance

291
Q

Clinical hydralazine

A

HTN(not Initial)

HF with reduced ejection fraction if intolerance to ACE or ARB

HF with reduced ejection fraction NYHA class III IV (self identified african American)

Hypertensive emergency in pregnancy

Post op htn

292
Q

pharmacokinetics hydralazine

A

Ordeal or IV

Hepatically acetylated with extensive first pass effect

293
Q

AE hydralazine

A

Angina pectoris flushing peripheral edema, tachycardia

Drug induced lupus like syndrome

Pruritis

294
Q

Digoxin MOA

A

Inhibits Na K ATPase pump in myocardial cels

295
Q

Effects digoxin

A

Increased contractility

Direct suppression of AV node conduction

Positive inotropic effect, enhanced vagal tone and decreased ventricular rate to fast atrial arrhythmias

296
Q

Clinical digoxin

A

Control of ventricular response rate in adults with chronic a fib …

Treatment of mild to moderate Herat failure in adults and pediatric patients to increase myocardial contractility

297
Q

Pharmacokinetics digoxin

A

Administered orally

1/2 is 36-48 hours
-needs a loading dose

Crosses the placenta but long history of safe in preg with supraventricular tachycardia

298
Q

AE dogixin

A

Accelerated junctional rhythm, asystole, a tachycardia with or without block , AV dissociation, first second or third block, PVC(bigeminy or tri), ST depression, ventricular fib,

Mental disturbances, rash, laryngeal edema

299
Q

Digitalis

A

Naturally occurring

Increases myocardial contractility
-increase cardiac output, decrease sympathetic tone, increase vagal tone

300
Q

AE digitalis

A

Severe dysrhythmias

301
Q

MOA digitalis

A

Blocks Na K atpase

302
Q

Why get digitalis toxicity

A

Myocytes become overloaded with Ca and spontaneous oscillatory uptake and release from the SR causes delayed afterdepolarizations and aftercontractions contributing to arrhythmias…excess free radicals

303
Q

Cardiac effects digoxin

A

Positive inotropic action on the heart

Increases the force of ventricular contraction

304
Q

How tell if too little or too much dogixin

305
Q

Hemodynamically benefits dogoxin

A

Increased CO
-decreased sympathetic tone
Increased urine production
Decreased renin release

306
Q

Electrical effects digoxin

A

Increases the firing rate of vagal fibers

Alters the electrical properties of the heart
-increases the responsiveness of the SA node to acetylcholine

307
Q

Automaticity digoxin

A

Increase or decrease SA

Increase purkinje

308
Q

Duration of refractory period digitalis

A

Increase AV node

Decrease ventricular myocardium

Incrase purkinje fibers

309
Q

Excitability digoxin

A

Increase atrial myocardium

Increase purkinje fibers

Increase ventricular myocardium

310
Q

Conduction velocity digoxin

A

Increase atrial myocytes

Decrease AV node

Increase ventricular myocardium

311
Q

Overall digoxin

A

Uncouple atria from ventricles while making regular cardiomyocytes more twitchy/prone to arrhythmias

312
Q

Effects of digoxin ecg

A

Depression of ST and longer PR

Toxic effect of digitalis on AV conduction involves AV dissociation
-lack of relationship between P and QRS

Toxic effect of digitalis on purkinje automaticity and ventricular refractory perior results one ctopic ventricular beats
-arrow shows example of bigeminy (ectopi beat alternating with normal beat)

313
Q

What must be normal before giving digoxin

314
Q

Non cardiac effects digoxin

A

Anorexia, nausea, vomiting, salivation

Excessive urination

Fatigue, visual disturbances (blurred vision, halos, yellowish or greening tinge to objects)

315
Q

Digoxin treatment for too much

A

KCI

Lidocaine

Phenytoin

Antidigitalis antibodies

316
Q

Drug interactions digoxin

A

Diuretics cause hypokalemia, which leads to increased digoxin binding, which leads to increased digoxin toxicity

ACE and ARB cau increase K levels decreasing digoxin effect

Sympathomimetics

Quinidine ,spironolactone, verampamil, propafenone and alprazolam are among a range of drugs that interfere with clearance of digozin

317
Q

Clinical digoxin

A

Used in patiets with left ventricular systolic heart failure in combinations ith diuretics, b blockers and ACE inhibits

Espicially useful in patients with a fib…benefit comes from prolongation of the effective refractory period at the AV node

318
Q

Pharmacokinetics digoxin

A

Readily absorbed but affected by disease states , other drugs, bioavailability can be inconsistent dissolution of oral formations

Cross placenta

Eliminated by renal

HL 1.5 days…loading dose is required to get beneficial effects immediately

319
Q

Loading dose digoxin

A

For when u need that therapeutic concentration now

320
Q

ACC/AHA A HF

A

At high risk HF but without structural heart disease or symptoms of HF

321
Q

ACC/AH B HF

A

Asymptomatic

322
Q

ACC/AHA structural heart disease with prior or current symptoms of HF

A

Symptomatic with moderate exertion

Symptomatic with minimal exertion

323
Q

ACC/AHA D HF

A

Advanced structural heart disease with marked symptoms of HF at rest despite maximal medical therapy. Specialized interventions required

Symptomatic at rest

324
Q

Drug to reduce fluid volume

A

Thiazide and loop diuretics

325
Q

Drug to reduce synthesis of angiotensin II to prevents remodeling

326
Q

Drug to reduce effect of angiotensin II at receptor preventing remodeling

A

Angiotensin II receptor blockers

327
Q

Inhibits effects of aldosterone

A

Spironolactone

328
Q

Direct cardiotonic effect

329
Q

Reduce sympathetic effect

Prevent remodeling

Prevent arrhythmia

A

B blockers

330
Q

Reduce afterload and preload

A

Vasodilators

331
Q

Drug choice overview for HFpEF (diastolic failrue)

A

Neutral results from clinical trials so must direct therapy at symptoms and associated conditions Cush as
-HTN, lung disease, CAD, a fib, obesity anemia, DM, kidney disease, sleep disordered breathing

Exercise is beneficial and need but avoid: tachycardia, abruptin increase in bp, ischemia, a fib

Use judicially: loop diuretics to treat edema….but decrease preload too much, decrease CO, hypotension, death

Spironolactone…mixed benefit

If justified symptoms-bb, ACEI.ARB, CCB

No evidence of benefit-nitrates, digoxin, PDE5 inhibtiors

332
Q

Adherence causes of acute decompensated HF

A

Dietary

Nonadherance to meds

Iatrogenic volume overload

Significant drug interactions/side effects associated with new drug addition

333
Q

Cardiac causes of ADHF

A

Myocardial infarction and myocardial ischemia

Valvular disease
A fib

Progression of underlying cardiac dysfunction

Stress

Toxic agents

334
Q

Non cardiac cause of ADHF

A

HTN
Renal fail
Pulmonary emboli

335
Q

Symptoms of ADHF

A

Acute dyspnea, orthopnea, tachypnea, tachycardia, and HTN

Hypotension reflects severe disease and arrest may be imminent; assess for inadequate peripheral or end organ perfusion

Accessory msucles used to breathe

Diffusion pulmonary crackles are common ; wheezing (cardiac asthma0 may be present

S3 is specific sign but may not be audible; elevated jugular venous pressure and/or peripheral edema may be present

336
Q

ECG ADHF

A

Looks for evidence of ischemia, infarction, arrhythmia, and left ventricular hypertrophy

337
Q

Obtain portable chest radiograph ADHF

A

Look for signs of pulmonary edema, cardiomegaly, alternative diagnosis; normal radiograph does not rule out ADHF

338
Q

Blood ADHF

A

CBC, troponin, electrolytes, BUN and cr, arterial blood gas, liver functions ests, BNP or NT proBNP if diagnosis is uncertain

339
Q

Echo ADHF

A

If cardiac or valvular function is not known

340
Q

ADHF now hat

A

Place in seated position

All need continuous pulse oximetry and supplemental oxygen and assisted ventilation to ensure adequate ventilation and oxygenation

Assess blood pressure noting if HTN or hypotensive set up for continuous cardiac monitoring

Monitor urine output

Give 2 IV lines

341
Q

All patients with ADHF ate volume overloaded

A

Must get rid of excess volume to relieve the congestion and return ventricular fiber length to more optimal range
-differs from cardiogenic shock, where volume needs to be checked first

Initiate diuretic therapy

342
Q

Purpose of diureticsin ADHF

A

Use loop fits

Add k if needed

If need more add thiazide

343
Q

Vasodilators for ADHF

A

Nitroprusside:dilates both arterial and venous

Nitroglycerin: dilates venous..decrease preload

344
Q

HTN ADHF

A

Diuretic and vasodilator (nitroglycerin, nitroprusside)

345
Q

Normotensive ADHF

A

Diuretic and vasodilator (nitroglycerin)

346
Q

Hypotensive ADHF

347
Q

Nitroprusside MOA

A

Forms free radical NO which in MS activeate cGMP and dephosphorylates myosin light chains…SM relax

348
Q

Effects nitroprusside

A

Peripheral vasodilation by direct action on venous and arteriolar smooth muscle

Reduces peripheral resistance

Will increase cardiac output by decreasing afterload

Reduces aorta and left ventricular impedance

349
Q

Clinical nitroprusside

A

HTN crises

ADHF

Controlled hypotension to reduce bleeding during surgery

Acute ischemic stroke

350
Q

Pharmacokinetics nitroprusside

A

IV 1/2 is 2 min

Metabolism generates cyanide

Eliminated in urine as thiocyanate

351
Q

AE nitroprusside

A

Tachycardia, ecg changes, flushing, hypotension, palpitation, substernal distress, increased intracranial pressure

Metabolic acidosis from cylinder toxicity

Tinnitus(thiocyanate toxicity)

352
Q

Nesiritide MOA

A

Synthetic B natiuretic peptide

Binds to guanylate cyclase receptor on vascular smooth muscle and endothelial cells surface to increase intracellular cGMP

353
Q

Effects nesiritide

A

Increases intracellular cGMP resulting in smooth muscle cell relaxation

Produces dose dependent reductions in pulmonary capillary wedge pressure and systemic arterial pressure

354
Q

Clinical nesiritide

A

Treatment of acutely decompensated HF with dyspnea at rest or with minimal activity

355
Q

Pharmacokinetics nesiritide

A

Proteolytic cleavage by vascular endopeptidase

Proteolysis following binding to the membrane bound natiuretic peptide ND CELLULAR INTERNALIZATION

1/2 IS EIGHT MINUTES

356
Q

AE NESIRITIDE

A

HYPOTENSION

Increased serum creatinine

Vent tachycardia

Ventricular extrasystoles, angina, tachycardia, a fib, AV node conduction abnormalities, pruritis, rash,

Amblyopia
Apnea, cough increased, hemoptysis

357
Q

What do catecholamines do

A

B-AR increase cAMP and PKA and msucle contraction

358
Q

Discontinue carvedilol

A

Kind of hard to stimulate adrenergic receptors when they’re blocked

359
Q

Inotropic agents

A

Short term rescue therapy in ED/ICU

Indicated if symptomatic hypotension with end organ dysfunction despite adequate filling pressure

360
Q

Sympathomimetics

A

Dobutamine

Dopamine

361
Q

Dobutamine

A

Synthetic catecholamines

Selectively activates B1 adrenergic receptors, preferred

362
Q

Dopamine

A

A catecholamines, activates B1 adrenergic receptors in the heart to increase HR and contractility

Also stimulates a adrenergic receptors at higher doses

363
Q

Phosphodiesterase inhibitors

A

Block the degradation of cAMP in heart and blood vessels

Prototype: milrinone

Restyling increases in cAMP lead to increased contractility in heart, vasodilation

Must be given IV , so genereally not suitable for outpatient use..can be combined with sympathomimetics

Have been shown to decrease survival in some studies

But may help if patient is not responding

364
Q

Dobutamine MOA

A

B1 and b2 adrenergic receptors

365
Q

Effects dobutamine

A

Increased contractility and heart rate

Lowers central venous pressure and wedge pressure, little effect pulmonary vascular resistance

366
Q

Clinical dobutamine

A

Short term management of patients with cardiac decompensation

367
Q

Pharmacokinetics dobutamine

A

IV

Metabolized by liver

368
Q

AE dobutamine

A

Tachycardia, ventricular premature contractions, angina, palpitations, HTN

Headache, paresthesia

Local pain

Dyspnea

Fever

369
Q

Dopamine MOA

A

Activates B1 adrenergic receptors at low doses and stimulates a adrenergic receptors at high doses

370
Q

Effects dopamine

A

Increases HR and contractility

Does not selectively presence renal function

371
Q

Clinical dopamine

A

Adjunct int he treatment of shock

MI
Open heart surgery

Renal failure

Cardiac decompensation

372
Q

Pharmacokinetics dopamine

A

IV 2 min half life

COMT and MAO

373
Q

AE dopamine

A

Angina, a fib, bradycardia, ectopic beats, HTN, hypotension, palpitations, tachy, wide QRS
Increase IOP

374
Q

Milrinone MOA

A

Selective phosphodiesterase 3 inhibitor

375
Q

Effects milrinone

A

Inhibitors in cardiac and vascular tissue, resulting in vasodilation and inotropic effects with little chronotropy activity

376
Q

Clinical milrinone

A

Inotropic therapy for patients unresponsive to other acute heart failure therapies

Outpatient for heart transplant candidates

Palliation of symptoms in end stage heart failure patients who cant otherwise be discharged form the hospital and are not transplant candidates

Perioperative inotropic support for heart transplant recipients

377
Q

Pharmacokinetics milrinone

A

IV

2.5 hours half life

378
Q

AE milrinone

A

> 10% incidence of ventricular arrhythmia

Also causes supraventricular arrhythmia, hypotension, angina/chest pain

HA

379
Q

Inamrinonr

A

Similar drug albeit less safe, withdrawn from market in 2011 but still shows up in drug lists

380
Q

Dobutamine

A

Direct cardiotonic

381
Q

Dopamine

A

Direct cardiotonic

382
Q

PDE III inhibitors

A

Reduce preload and afterload direct cardiotonic effect

383
Q

Nesiritide

A

Reduces preload and afterload

384
Q

Nitroglycerin nitroprusside

A

Reduce preload and afterload

385
Q

Drugs to avoid

A

Class I Antiarrhythmics …some are negative inotropes all can cause arrhythmias in heart failure patients
-consider amiodarone

CCB…directly suppress myocardial contractility

NSAIDS..impair renal salt and water excretion which can exacerbate HF

Pharmacology (52 decks)

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