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PAM Semester 3 > Pharm Cardiology Exam 1 > Flashcards

Pharm Cardiology Exam 1 Flashcards

1
Q

Most common first line Medication

A

Ace inhibitor

-Pril

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2
Q

Most common side effects for Ace

A

Cough

Angioedema

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3
Q

Types of diuretics

A

Loop
Osmotic
K+ Sparring
Thiazides

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4
Q

MOA of Loop Diuretics

A

Inhibit the Na / K / Cl transporter at the thick ascending loop of Henle

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5
Q

MOA of Osmotic diuretics

A

Promote osmotic diuresis

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6
Q

MOA of K+ Sparring Diuretics

A

Antagonize the actions of aldosterone to affect Na+/K+ exchange

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7
Q

MOA of Thiazide diuretics

A

Inhibit reabsorption by Na+/Cl transporter at distal tubule

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8
Q

Common Loop Diuretics

A

Bumetanide
Furosemide
Torsemide

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9
Q

Common osmotic diuretics

A

Mannitol

Glucose

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10
Q

Common K+ sparring Diuretics

A

Spironolactone

Eplerenone

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11
Q

Common Thiazide diuretics

A

HCTZ

Metolazone

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12
Q

Acetazolamide location of action

A

PCT

Pulls sodium bicarb out of tubule

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13
Q

Osmotic diuretic location of action

A

Pulls H2O out of

PCT
descending loop
Collecting duct

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14
Q

Location of action of loop diuretics

A

Thick ascending loop of henle

Pulls K+, CA2+, Mg2+, NA+
out of tubule

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15
Q

Thiazide location of action

A

Proximal tubule/ descending loop
DCT

Pulls NaCl out of tubule

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16
Q

Location of action of aldosterone antagonists

A

Collecting duct

Pulls NaCl out of Collecting duct

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17
Q

Beta Blocker
Non selective
B1 & B2

A

Nadolol
Propranolol
Timolol
Sotalol

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18
Q

Beta Blockers
Cardio selective
B1

A 
Atenolol
Metoprolol
Esmolol
Betaxolol
Bisprolol
Nebivolol
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19
Q

Beta Blockers
Mixed
A1 & B1 & B2

A

Carvedilol

Labetalol

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20
Q

Beta Blockers

Mortality benefit for HFrEF

A

Carvedilol
Metoprolol Succinate
Bisoprolol

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21
Q

Beta Blockers

With ISA

A

Acebutolol
Pindolol

(Associated with less resting bradycardia)

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22
Q

Contraindications for beta blockers

A

Asthma

Liver disease

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23
Q

Calcium channel blockers

2 types

A

Dihydropyridine
-dipines

Non dihydropyridine

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24
Q

Calcium Channel Blockers
Dihydropyridines
-dipines

A 
Amlodipine
Felodipine
Nicardipine
Nifedipine
Nimodipine
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25
Q

Calcium Channel Blockers

Non Dihydropyridines

A

Di-Ver

Diltiazem
Verapamil

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26
Q

Common side effects of Calcium Channel Blockers

A 
Dizzy
HA
Edema (pedal edema)
Constipation
Facial redness
Gingival overgrowth
Altered HR
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27
Q

Digoxin

A

+ Ionotrope (increased contraction)

  • Chronotrope (slows heart rate)
  • dromotrope (decreased AV node conduction)

For SVT , afib/aflut, cardiogenic shock and HF

Cardiac glycoside

Antidote is digibind

Therapeutic range is 0.5-2

monitor for toxicity
S/S of tox = N/V, dysrhythmias, vision changes (yellow/green hue & halos)

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28
Q

Vasodilators

A

Nitroglycerine

Sodium nitroprusside

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29
Q

Unstable angina tx

A

Always treat as if having an MI

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30
Q

Stable angina Tx

A

Manage dyslipidemia
Stain (improves mortality)

Antiplatelet
ASA

Beta blocker
Slow the heart, allow for increased ventricular filling and reduce oxygen demand

Calcium channel blocker
Reduce afterload and contractility and dilate coronary arteries (not nifedipine due to reflex tachycardia)

Nitroglycerine
Decrease preload, dilate cornary arteries (Acute or chronic use)

PCI/CABG

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31
Q

Most common adverse reaction to statin is

A

Increased LFT’s

Check AST/ALT and AP at baseline

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32
Q

High intensity statins

A

Atorvastatin
Rosuvastatin

LDL Goal is <70

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33
Q

Preferred Med for initial treatment and prevention of anginal symptoms

A

Beta Blockers

Calcium channel blockers and long acting nitrates are alternatives if Beta Blockers are contraindicated

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34
Q

Angina Treatments

A 
Lifestyle mods
Sublingual Nitro
Long acting Nitrates (isosorbide mononitrate)
Beta Blockers
ACE (for unstable and s/s of HF)
CCB (considered alternative to BB)
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35
Q

Angina treatment
with Beta blockers effects
HR / BP / MOA

A

Decrease in HR
Decrease in BP

Decreased Pump function

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36
Q

Angina treatment
with Calcium Channel Blockers
HR / BP / MOA

A

Decrease in HR
Decrease in BP

Decreased Pump function + vasodilation

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37
Q

Angina treatment
with Nitrates
HR / BP / MOA

A

Increased HR
Decreased BP

Vasodilation

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38
Q

Angina treatment
with Ranolazine (ranexa)
HR / BP / MOA

A

No change in HR
No change in BP

Reduces Cardiac Stiffness

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39
Q

Ranolazine

A

Ranexa
Chronic stable angina
can be used with BB, nitrates, CCB, ACE, ARB, Anti platelet and lipid lowering therapies.

Contra:
Liver cirrhosis

Warnings:
Not for acute angina or Diabetes

Adverse:
Prolonged QT, Dizziness, headache, constipation, nausea

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40
Q

Ranolazine (Ranexa)

MOA

A

Inhibits the late inward sodium current

Prevents diastolic stiffness and thereby preserves myocardial blood flow.

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41
Q

Vasospastic angina (Prinzmetal)

A

Calcium channel blocker
Start with diltiazem

Sublingual nitro
in an attempt to decrease the frequency of myocardial infarction and life threatening arrhythmia

Nonselective beta blockers
such as propranolol should be avoided

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42
Q

ACS encompasses

A

STEMI, NSTEMI, Unstable angina

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43
Q

Unstable angina treatment

A

Reduce progression to Acute MI

Antiplatelet - ASA
Beta blockers
ACE
Statin

Revascularization

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44
Q

Absolute contraindications to thrombolytics

A 
Known intracranial neoplasm
Active internal bleeding
Suspected aortic dissection
Recent head trauma
History of Hemorrhagic CVA
Major surgery or trauma <2 weeks

C B D T S S

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45
Q

Cocaine related ACS

A

Benzos
Lorazepam 2-4 mg IV q 15 mins
as needed to relive symptoms

DO NOT GIVE BB

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46
Q

Nitroglycerine

A

Acute relief of angina
Acute prophylaxis of angina

Dose: 0.4mg tab
1 tab sublingual at onset, q 5mins x 3
(max=3 tabs in 15mins)

Contraindications:
Severe anemia, Increased ICP, TBI, Cerebral hemorrhage, Acute circulatory failure or shock. PDE-5 use.

Interactions:
PDE-5

Adverse reactions:
HA, dizzy, paresthesia, vertigo, weakness, palpitations, postural hypotension, syncope

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47
Q

Beta blockers

A

Improves symptoms by decreasing HR and contractility

Decrease myocardial oxygen consumption
Increase ventricular diastolic filling
Decrease cardiac output gradient

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48
Q

Metoprolol Tartate

A

Lopressor (immediate release)
Cardioselective Beta blockers

For use in stabilized patients after MI to reduce mortality

Contra:
All Heart blocks, BP under 100, HR under 45
Moderate/Severe cardiac failure

Warning:
Avoid abrupt discontinuation in ischemic heart disease

Adverse reactions:
Fatigue, dizzy, depression, hypotension (discontinue), bronchospasm, heart block

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49
Q

Fibrinolytics

Thrombolytics

A 
Alteplase
Reteplase
Tenecteplase
Streptokinase
Anistreplase
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50
Q

Alteplase

A

Treatment of acute myocardial infarction to reduce mortality and the incidence of heart failure

Interactions:
Increased risk of bleeding with anti-coags, anti platelets. Angioedema risk with ACE

Adverse:
Bleeding (fatal)

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51
Q

Antiplatelet drugs

A

Cox inhibitors
ASA

ADP inhibitor
Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor

GP IIB/IIIA inhibitor
Abciximab
Eptifibatide
Tirofiban

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52
Q

Anti coagulants

A

Vitamin K antagonists
Warfarin

Thrombin inhibitors (direct)
Dabigatran
Argatroban
Hirudin
Bivalidurin
Thrombin Inhibitors (indirect)
Heparin
Enoxaparin
Dalteparin
Tinzeparin
-Xabans
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53
Q

GP IIB / IIIA antagonists

A

Abciximab (irreversible)
Eptifibatide (reversible)
Tirofiban (reversible)

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54
Q

HFrEF

A

The goals of management is to reduce morbidity

(including reducing symptoms, improving health-related quality of life and functional status, and decreasing the risk of hospitalization),

and to reduce mortality.

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55
Q

ACE MOA (Chart)

A

Stops angiotensin I from converting to angiotensin II

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56
Q

Renin inhibitors (Chart)

A

Stops renin from converting to angiotensin I

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57
Q

Spironolactone MOA (Chart)

A

Helps stop cardiac remodeling

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58
Q

Beta Blocker MOA (Chart)

A

Helps stop cardiac remodeling

Suppress renin secretion

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59
Q

Digoxin MOA (Chart)

A

Increases cardiac output

improves CO and decreases HF (ionotropics)

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60
Q

Diuretics MOA (Chart)

A

Decrease NA+ and H2O retention

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61
Q

Vasodilators MOA (Chart)

A

Decreases vasoconstriction

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62
Q

AT1 receptor antagonists (ARB) (MOA) (Chart)

A

Decrease cardiac remodeling
Inhibits angiotensin from converting to aldosterone
Decreases vasoconstriction

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63
Q

MOA of ACE Inhibitors (-prils)

A

inhibit the activity of angiotensin-converting enzyme

Stops angiotensin I from becoming angiotensin II

There by decreasing the formation of angiotensin II, a vasoconstrictor, and increase the level of bradykinin, a peptide vasodilator

Causes relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart

64
Q

MOA of ARB (-sartans)

A

Drugs that bind to and inhibit the angiotensin II receptor type 1 (AT1)

and thereby

block the arteriolar contraction and sodium retention effects of renin–angiotensin system

65
Q

Angiotensin receptor neprilysin inhibitor

ARNI

A

Sacubitril / valsartan
Entresto

Inhibit BNP breakdown

66
Q

What medications raise levels of kinins which may have beneficial hemodynamic effects but also increase the risk of angioedema and dry cough.

A

ACE inhibitor and ARNI (but not single agent ARB)

Angiotensin receptor neprilysin inhibitor

67
Q

ACE and ARB MOA in HF

A

Vasodilation
Reduce cardiac preload and afterload which improves systolic function and CO

Facilitate salt and water excretion by complex effects on the kidneys (attenuation of aldosterone effect)

ACE inhibitors and ARBS reduce LVH, Myocardial fibrosis and stiffness

68
Q

Lisinopril

A

Reduce symptoms of systolic HF

Contraindications
History of ACE associated or other angioedema

Warning:
Fetal Toxicity

Adverse reactions
HA, cough, angioedema, dizzy, hypotension, chest pain, hyperkalemia, renal impairment

69
Q

Valsartan

A 
HF (NYHA class II-IV)
Reduce cardiovascular mortality in stable post MI patients with LV failure or dysfunction

Contra:
Concomitant aliskiren in patients with diabetes

Warning:
Fetal toxicity

Adverse:
Dizzy, hypotension, diarrhea, arthralgia, back pain, fatigue, hyperkalemia

70
Q

Beta blockers that improve mortality in HFrEF

A 
Carvedilol (coreg)
Metoprolol Succinate (Toprol XL)
Bisoprolol fumerate (Zebeta)
71
Q

Carvedilol

A

Non-cardioselective BB / Alpha 1 blocker (Coreg)

Mild to severe heart failure, increase survivability and reduce hospitalization risk.
Reduce post MI mortality with left ventricular EF <40%

Contraindications
Cardiogenic shock, decompensated HF,
Asthma with bronchospasms, 2nd/3rd degree AV blocks, sick sinus syndrome, severe bradycardia (unless paced)

Adverse:
dizzy, edema, hypotension, syncope, bradycardia, AV block

72
Q

Aldosterone antagonists

A

Spironolactone
Eplerenone

(K+ sparring)

73
Q

Aldosterone antagonist MOA

mineralocorticoids

A

Has diuretic and blood pressure lowering effects, raises serum potassium concentration via reduced urinary potassium loss

Side effects:
spironolactone has anti-androgen effects such as erectile dysfunction and gynecomastia in men
(use eplerenone in men)

74
Q

Spironolactone

A

K+ sparring diuretic

NYHA class III–IV HF and reduced ejection fraction to increase survival, manage edema, and reduce the need for hospitalization for HF, when used in addition to standard therapy.

Contra:
Hyperkalemia, Addison’s disease, concomitant eplerenone

Warnings:
Hyperkalemia in renal patients

Interactions:
Severe hyperkalemia with K+ supplements

Adverse:
Gynecomastia, GI upset, Hyperkalemia

75
Q

Sacubitril / Valsartan (entresto)

A

Neprilysin inhibitor + angiotensin II receptor blocker
Dose: 49mg/51mg BID (initial)

To reduce risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II–IV) and reduced ejection fraction; usually given with other therapies, in place of an ACEI or other ARB. To treat symptomatic heart failure with systemic left ventricular systolic dysfunction in children aged ≥1 year.

Contra:
History of angioedema, Concomitant ACE or aliskiren use.

Warning
Fetal toxicity

Adverse
Hypotension, hyperkalemia, cough, angioedema, renal failure

76
Q

Vasodilators Doses

Hydralazine

A

Hydralazine
(25-50mg TID-QID)
(Target=300mg QD)

77
Q 
Vasodilators Doses
Isosorbide dinitrate (ISDN)
A

Isosorbide dinitrate
(20-30mg TID-QID)
(target=120mg QD)

78
Q

Isosorbide dinitrate and hydralazine

Indications

A

Bidil
The combined use ofhydralazineand nitrates reduces cardiac afterload and preload, and may also enhance nitric oxide bioavailability.

Indicated when
ACE and ARBS are contraindicated (i.e. renal failure)

Systolic dysfunction

Acute episodes of CHF (via preload and afterload reduction)

Indicated for black patients

79
Q

Digoxin side effects

A 
Dizzy
HA
Blurred vision
Yellow or green vision
AV / SA block
PR prolongation
ST Depression
Diarrhea
80
Q

Digoxin MOA

A

Inhibits the NA+ K+ ATPase pump

81
Q

Digoxin indications

A

Severe systolic dysfunction

Used as an inotrope (does not reduce mortality but does reduce hospitalizations)

Positive pressure ventilation

82
Q

Digoxin

A

Cardiac Glycoside

Mild-to-moderate heart failure (with a diuretic and an ACE inhibitor when possible). Increase myocardial contractility in pediatrics with heart failure

Contra
V-Fib

83
Q

Dilated cardiomyopathy

A

Most common type 95%
Common cause = ETOH

Diagnostics
Chest X ray for cardiomegaly
Echo for LV dilation and dysfunction
(high diastolic pressures with low CO)

Treatment:
Treat underlying cause or offending agent

84
Q

Hypertrophic cardiomyopathy

A

Massive septum hypertrophy
small left ventricle
diastolic dysfunction

Usually autosomal dominant, genetic or chronic hypertension

Diagnostics
Echo
LVH, asymmetrical septal hypertrophy, small LV, diastolic dysfunction

85
Q

Positive iontropes

A 
Dopamine
dobutamine
epi/norepi
Digoxin
PDE inhibitors (milrinone)
Glucagon
Insulin
Amiodarone
86
Q

Negative iontropes

A

Beta Blockers
Calcium channel blockers
Class 1A antiarrhythmics (Quinidine, procainamide)
Class 1C antiarrhythmics (flecainide)

87
Q

If the patient has contraindications to a beta blocker (eg, reactive airway disease) in Hypertrophic cardiomyopathy

A

Monotherapy with a nondihydropyridine calcium channel blocker can be considered
or,
in the appropriate patient, proceeding directly to combination therapy with an atrioventricular nodal blocking agent anddisopyramide.

88
Q

Beta blocker treatment for patients with left ventricular dysfunction

A

Start at very low doses and gradually increase if lower doses are well tolerated

Start as soon as LV dysfunction is diagnosed

89
Q

Calcium channel blocker drugs

A 
Dihydropyridines
-dipines 
Amlodipine
Felodipine
Nicardipine
Nifedipine
Nimodipine

Non dihydropyridines
“di-ver”
Di - Diltiazem
Ver - Verapamil

90
Q

Calcium channel blocker drugs

Dihydropyridines

A 
-dipines 
Amlodipine
Felodipine
Nicardipine
Nifedipine
Nimodipine
91
Q

Calcium channel blocker drugs

Non dihydropyridines

A

“di-ver”
Di - Diltiazem
Ver - Verapamil

92
Q

Calcium channel blocker drugs

Non dihydropyridines

A

“di-ver”
Di - Diltiazem
Ver - Verapamil

93
Q

Verapamil

A

CCB
Non dihydropyridine

Contraindications

Severe left ventricular (LV) dysfunction or LV dysfunction treated with β-blockers.

Moderate to severe heart failure. 
Hypotension. 
Cardiogenic shock. 
Sick sinus syndrome, 
2nd- or3rd-degree AV block,
94
Q

Diltiazem

A

Cardizem
CCB
Non dihydropyridine

Vasospastic or chronic unstable angina

Contra
sick sinus syndrome, 2nd- or3rd-degree AV block (unless paced), hypotension

Adverse
Edema, HA, fatigue, dizzy, asthenia, 1st degree AV block, bradycardia

95
Q

disopyramide indications

A

use in combination with BB or CCB
Negative inotrope (for CHF and CM)
Anti-arrhythmic

96
Q

disopyramide contraindications

A

Cardiogenic shock.
2nd- or 3rd- degree AV block, unless paced.
QT prolongation

97
Q

Hypertrophic cardiomyopathy treatment

A

Avoid strenuous exercise, sports, dehydration

Do not give diuretics, ACE, Vasodilators or positive inotropes

Screen 1st degree relative with EKG and Echo

98
Q

Stress induced cardiomyopathy

A

transient regional left ventricular dysfunction in the absence of significant coronary artery disease

Causes may include
catecholamine excess, microvascular dysfunction, and multi-vessel coronary artery spasm

Generally a transient disorder managed with supportive therapy. Conservative treatment and resolution of physical or emotional stress usually results in rapid resolution of symptoms

99
Q

Restrictive cardiomyopathy

A

Secondary / infiltrative causes include
Amyloidosis
Sarcoidosis

Treatment
Relieve congestive symptoms with loop diuretics

100
Q

Antiarrhythmics Class 1a

Medications

A

Intermediate dissociation

Procainamide
Disopyramide
Quinidine

P D Q

101
Q

Antiarrhythmics Class 1b

Medications

A

Rapid dissociation

Lidocaine
mexilitine

102
Q

Antiarrhythmics Class 1c

Medications

A

slow dissociation

Propafenone
Flecainide

103
Q

Antiarrhythmics Class IIa
Medications
(non selective)

A

Beta blockers

non selective

Carvedilol
propranolol
nadolol

104
Q

Antiarrhythmics Class III

Medications

A

K+ channel blockers and openers

105
Q

Antiarrhythmics Class IIIa

Medications

A

Voltage dependent K+ channel blockers

Amiodarone
dronedarone
dofetilide
ibutilide
sotalol
106
Q

Antiarrhythmics Class IV

Medications

A

Ca2+ handling modulators

107
Q

Antiarrhythmics Class IIa
Medications
(selective)

A

Beta Blockers

selective

atenolol
bisoprolol
betaxolol
celiprolol
esmolol
metoprolol
108
Q

Antiarrhythmics Class IVa

Medications

A

Surface membrane Ca2+ channel blockers

Diltiazem
verapamil

109
Q

Antiarrhythmic drug class mneumonic

A 
PDQ = Police department questions
LM = Liquored man
FP = For peeing
BB = Behind building
ADSID = After drinking scotch in dark
DV = Dirty vehicle
Ia = procainamide, disopyramide, quinidine
Ib = lidocaine, mexilitine
Ic = Flecainide, propafenone
II = Beta blockers
III = Amiodarone, dronedarone, sotalol, ibutilide, dofetilide
IV = Diltiazem, verapamil
110
Q

Atropine

Mechanism of Action

A

inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves, and on smooth muscles, which respond to endogenous acetylcholine but are not so innervated

111
Q

Atropine ACLS

A

Bradycardia

0.5mg IV q3-5min PRN

112
Q

Heart block poem

1st degree

A

If the R is far from P,

then you have a first degree

113
Q

Heart block poem

2nd degree type 1

A

Longer longer longer drop,

then you have a Wenkebach

114
Q

Heart block poem

2nd degree type 2

A

If some P’s don’t get through,
then you have a Mobitz 2.
Pacemaker for you

115
Q

Heart block poem

3rd degree

A

If the p’s and Q’s don’t agree,

then you have a 3rd degree

116
Q

2 types of broad afib

A

Newly diagnosed Afib
decisions regarding anti-coag treatment, and rate and rhythm control strategies

Previously diagnosed and managed afib
Periodic assessments of the adequacy of treatment

TEE to check for clot in left atrial appendage
Don’t cardiovert if clot present (could dislodge)
Start on lovenox if clot present (reevaluate in 1 month)

117
Q

New onset afib

A

prevention of systemic embolization

The choice between rhythm and rate control strategy, both of which may improve symptoms

118
Q

Anti-coag therapy for nonvalvular afib patients

A 
Warfarin
dabigatran
rivaroxaban
apixaban
edoxaban

Reduce the risk by almost 70% (embolization)

119
Q

INR

A

International normalized ratio

therapeutic range usually between 2 and 3

120
Q

Most patients who present with afib will require

A

slowing of ventricular rate to improve symptoms

(afib with RVR is really just uncontrolled afib)

Treatment then focuses on
normalizing ventricular rate (60-99bpm)
to decrease symptoms and restoring NSR

121
Q

TEE

A

Treatment guided by the presence or absence of left atrial thrombus on TEE and the presence of HF

122
Q

Patients with thrombus or at high risk of thrombus formation including history of a fib >48hrs should be treated with

A 
Anticoagulants
Heparin or lovenox
and
warfarin or dabigatran
and
rate control for 3-4 weeks before attempting cardiovert
123
Q

Patients with afib and with no thrombus and at low risk for thrombus formation can be treated with

A

cardioversion once anticoagulation with heparin is established

124
Q

Rate control of afib

A

In presence of HF
digoxin or amiodarone

In absence of HF
IV beta blockers (metoprolol, propranolol, or esmolol)
or
dihydropyridine Calcium channel blockers

125
Q

Chronic rate control strategy in patients with afib

A

Generally use drugs that slow conduction across the AV node such as
Beta blockers
non-dihydropyridine calcium channel blockers or digoxin

126
Q

Cardioversion of unstable patients with afib

A

For a patient who is hemodynamically unstable due to afib and is at low risk for thrombus and aspiration,
Urgent cardioversion is recommended

127
Q

Cardioversion of stable patients with afib

A

Most patients with afib do not need emergent cardioversion.

rate slowing will often improve symptoms

Best to defer cardioversion until anti-coag treatment with heparin is initiated.

For select stable patients, the restoration of sinus rhythm with either electrical or pharmacological cardioversion is necessary or reasonable

128
Q

Most patients with whom cardioversion is chosen will need

A

the ventricular rate controlled and the need for anti-coag assessment prior to cardioversion

For patients with no structural heart disease
(including no evidence of CAD)
Flecainide or propafenone is the recommended pharmacological choice

129
Q

Rhythm therapy in afib patients

A

Beta blockers are modestly effective in maintaining NSR and can be tried first in select patients.
(those without structural heart disease or who are concerned about proarrhythmic)

Compared to placebo
amiodarone, sotalol, dofetilide, dronedarone, fecainide, and propafenone are effective for the maintenance of sinus rhythm.
(maintenance rates at one year are significantly less than 75 %)

Amiodarone is consistently more effective than the other antiarrhythmic drugs

130
Q

Rhythm therapy

in patients with no structural heart disease and no apparent risk for drug induced brady/tachycardia

A

flecainide or propafenone is recommended as the preferred antiarrhythmic

Amiodarone, dofetilide, dronedarone or sotalol may be used

For patients with HF Amiodarone is recommended.

131
Q

Side effects of Amiodarone

A

T =
Thyroid = hyper or hypo (iodine in amiodarone)

2P =
Photosensitive (gray/blue skin discoloration when sun exposed)
Peripheral neuropathy = (shoulder, pelvic girdle)

2L =
Lung = Fibrosis (progressive and fatal) (most serious)
Liver = Liver damage

2C =
Cardiac depression = Decreased HR , decreased BP (usually due to IV)
Corneal micro deposits = (usually reversible or self correcting after drug is stopped)

132
Q

Amiodarone

A

Class IIIa antiarrhythmic

Life threatening recurrent v fib
or hemodynamically unstable v tac

Contra:
Cardiogenic shock sick sinus syndrome, 2nd or 3rd degree block, bradycardia with syncope unless paced

Adverse:
Pulmonary fibrosis, thyroid, heart block, sinus bradycardia, corneal deposits, optic neuritis, photosensitivity, skin pigment, peripheral neuropathy

133
Q

Base line test for amiodarone

A

All are done at base line and then……

LFT = q 6mo
TSH = q 6mo
Cr/electrolytes = PRN
Chest x ray = annually
Ophthalmic = PRN for symptoms
PFT = Symptoms
EKG = annually
134
Q

A flutter treatment options

A

Control of the ventricular rate
beta blocker, calcium channel blocker

Reversion to normal sinus rhythm
Radiofrequency catheter ablation (preferred treatment)

135
Q

SVT treatment options

A

If vagal maneuvers are ineffective
pharmacological therapy with an AV node blocking agent should be instituted.
(adenosine, verapamil, BB)

IV adenosine over IV verapamil initially due to its high efficacy and short half life.

If Adenosine is ineffective, use verapamil.

If AVRT persists, use IV procainamide and BB (propranolol, metoprolol, esmolol)
Consider amiodarone

136
Q

Adenosine

A

Contra
2nd/3rd block, sinus node disease unless paced, bronchoconstriction, asthma

Interactions
Adenosine may be potentiated by:
BB, cardiac glycosides (dig), CCB; use with caution

Adverse
Flushing, chest discomfort, dyspnea, head, neck, throat discomfort, gi discomfort, lightheadedness, dizziness, cardiac arrest, v tac, MI, bronchoconstriction, hypo or hyper tension, CVA, seizure, a fib

137
Q

Adenosine dosage

A

6mg IV once
Then 12mg IV after 1-2 mins
repeat dose again once after 1-2 mins

138
Q

Acute termination of orthodromic AVRT

unstable patients

A

Synchronized cardioversion

139
Q 
Acute termination of orthodromic AVRT
stable patients (WPW)
A 
1st line = Vagal
2nd = IV adenosine
3rd = IV verapamil or diltiazem
Other = IV procainamide or IV BB
Cardiovert if other therapies are ineffective or unfeasible.
140
Q

Reversible causes of v tac
5 H’s
5 T’s

A 
Hypovolemia
Hypothermia
Hypoxia
Hydrogen ions (acidosis)
Hypo/Hyperkalemia
Tension pneumo
Tamponade
Toxins
Thrombus pulmonary
Thrombus cardiac
141
Q

Reversible causes of v tac

5 H’s

A 
Hypovolemia
Hypothermia
Hypoxia
Hydrogen ions (acidosis)
Hypo/Hyperkalemia
142
Q

Reversible causes of v tac

5 T’s

A 
Tension pneumo
Tamponade
Toxins
Thrombus pulmonary
Thrombus cardiac
143
Q

ACLS cardiac arrest meds

A

Epi IV/IO
1 mg q 3-5 min

Amiodarone IV/IO
1st dose = 300mg bolus
2nd dose - 150mg bolus

or

Lidocaine IV/IO
1st dose = 1.0 - 1.5 mg/kg
2nd dose = 0.5 - 0.75 mg/kg

144
Q

Torsade’s (polymorphic v tac) treatment

A

IV Mag sulfate
1 to 2 grams IV over 15 mins
(can be followed by an infusion)

145
Q

Polymorphic v tac other than torsade’s

A

Beta blockers if BP allows
metoprolol 5mg IV q 5mins, max of 15mg

IV amiodarone may prevent a recurrent episode

146
Q

V fib Treatment

A

Amiodarone is the most commonly studied antiarrhythmic for prevention of SCD

147
Q

Valvular diseases (aortic)

A

Surgery

148
Q

Aortic regurgitation

A

For treatment of hypertension (SBP >140) in patients with chronic Aortic regurg,

vasodilators such as ACE inhibitors, ARBs, or dihydropyridine calcium channel blockers (eg,amlodipine) are favored

since they may reduce systolic blood pressure in this setting.

149
Q

Tricuspid regurg

A

In symptomatic patients with severe Tricuspid regurg,

Diuretics are indicated

to treat volume overload and congestion

150
Q

Tricuspid regurg and Right sided HF

A

Loop diuretics are typically used.

Aldosterone antagonists may provide additional benefit, particularly in those with hepatic congestion with secondary hyperaldosteronism.

151
Q

Tricuspid regurg and Left sided HF

A

If heart failure due to left ventricular systolic dysfunction is present,

standard therapy, including beta-blockers and agents that inhibit the rennin-angiotensin-aldosterone system, are recommended.

152
Q

Tricuspid stenosis

TX

A

In patients with severe Tricuspid stenosis

symptoms of systemic venous hypertension, including lower extremity edema and hepatic congestion,

are treated with loop diuretics.

153
Q

Mitral regurgitation

A

Symptomatic patients with chronic primary MR (stage D) and left ventricular ejection fraction (LVEF) <60 percent who are awaiting valve surgery or who are not candidates for valve surgery

are treated with standard guideline-based medical therapy for heart failure with reduced ejection fraction (including angiotensin converting enzyme [ACE] inhibitor [or angiotensin II receptor blocker or angiotensin receptor-neprilysin inhibitor], beta blocker, diuretics, and possibly also mineralocorticoid receptor antagonist).

154
Q

Mitral Stenosis

A

Long-term oral anticoagulation (with vitamin K antagonist; target International Normalized Ratio 2.5, range 2.0 to 3.0) (Warfarin)

in patients with mitral stenosis who have a prior embolic event, left atrial thrombus, or paroxysmal, persistent, or permanent atrial fibrillation (AF).

155
Q

Mitral valve prolapse

A

Magnesium supplementation may benefit a subset of patients with symptoms and magnesium deficiency.

Beta blockers (i.e. propranolol) may be helpful in patients who present with hyperadrenergic symptoms such as tachycardia, palpitations, nervousness, and an exaggerated heart rate response to exercise.

156
Q

Secondary prophylaxis for rheumatic heart disease

A

Pen G IM 1.2 million units q 21-28 days

Pen V oral 250mg BID

PAM Semester 3 (8 decks)

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