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CPR II Drugs test 1 > Drugs for HF > Flashcards

Drugs for HF Flashcards

1
Q

Main list of Drugs for Heart failure

A 
•
ACE inhibitors: captopril and other \_\_prils
•
angiotensin receptor blockers (ARBS): losartan and other \_\_sartans
–
valsartan/sacubitril(adds neprilysininhibitor)
•
carvedilol
•
spironolactone
•
diuretics: loop, thiazide, K+-sparing
•
direct vasodilators: nitroglycerin/isosorbide dinitrate, nitroprusside, hydralazine
•
digoxin
•
dobutamine, dopamine
•
milrinone
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2
Q

What are the two types of Left sided Heart failure?

A

systolic = HFrEF≡ Heart Failure reduced Ejection Fraction
–
failure of the pump function of the heart (ejection fraction < 45%, normal = 60 –70%) typically due to dysfunction or destruction of cardiac myocytes or their molecular components
–
usually has progressive chamber dilation with eccentric remodeling

diastolic = HFpEF≡vHeart Failure preserved Ejection Fraction
–
occurs when the ventricular capacitance is diminished and/or when the ventricle becomes “stiff“ and cannot fully relax during diastole
–
diagnosis is now fairly common, especially among older women
–
typically due to concentric ventricular hypertrophy (e.g.,from chronic hypertension) or connective tissue diseases (e.g., amyloidosis)

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3
Q

what are the changes in Pressure Volume loops for Systolic failure?

A

Decreased ESPVR slope

increased ESV and EDV

decrease SV and EF

Ventricular dilation

Loss of Inotropy

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4
Q

what are the changes in pressure volume loops for Diastolic Failure?

A

increased EDPVR Slope

decreased EDV

Increased EDP

decreased compliance

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5
Q

in diastolic HF what can worsen the prognostics?

A

increasing the MAP which can raise left atrial pressure leading to angina with wheezing, shortness of breath and cause a life threatening flash Pulmonary edema

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6
Q

what is poorly tolerated in DHF?

A

atrial fibrillation

tachycardia

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7
Q

what is the overall goal we are trying to prevent after an MI event?

A

Remodeling of the heart

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8
Q

what are the main Heart Failure Vicious cycles that lead to Cardiac Remodeling?

A

Renin System (angotensin I, II, aldosterone)

Increased sympathetic activity (vasoconstriction leading to increased cardiac filling pressures

Renal Na+ and H20 retention

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9
Q

How does ACE inhibitors and ARBs help in Heart failure?

A

Less Angiotensin II leads to:

decreased Vasoconstriction (decreased afterload)

Less aldosterone secretion and less sodium/water

Decreased cell proliferation and remodeling

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10
Q

MOA, Effects and Clinical Applications of Captopril

A

MOA: ACE inhibitor (competitive

Effects: lowers levels of angiotension II, increases plasma renin activity and decreases aldosterone secretion
-lowers BP

Applications:

  • Hypertension
  • acute hypertension
  • HFrEF (systolic)
  • Diabetic Nephropathy
  • off label aldosteronism
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11
Q

Pharmokinetics and toxicities of Captopril

A

Pharmokinetics: rapidly absorbed
ecreted in urine
-CYP2D6
half life is 1.7 hours

Toxicities:

  • BB = Fetal toxicity
  • angioedema
  • cough
  • hypotension
  • cholestatic jaundice
  • drowsiness
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12
Q

What is Enalapril?

A

another early ACEI that has a prodrug form and available for IV

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13
Q

what is benazepril?

A

now widely used ACE inhibitor that has a longer half life for 1x/day dosing

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14
Q

what is lisonopril

A

now widely used ACEI longer half life now permitting 1X day dosing

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15
Q

MOA, Effects and Clinical application of Losartan

A

Competitive nonpeptide angiotensin II receptor antagonist (AT1 more than AT2)

Effects:

  • blocks Vasoconstriction and aldosterone secreting effects
  • does not effect response to bradykinin
  • more complete inhibition of RAAS

Clinical:

  • diabetic nephropathy with increased SCr and proteinuria in DM and HT
  • HTN
  • CKD
  • HF if intolerant of ACE inhibitors
  • Off-label Marfan syndrome
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16
Q

Pharmacokinetics and TOxicities of Losartan

A

Pharmacokinetics: Extensive first pass metabolism to get to active metabolite
-half life 2 hours

Toxicities:
-adverse effects more in diabetic nephropathy
-hypotension
-fatigue
-anemia
BB = fetal toxicity
-hypoglycemia
-hypokalemia
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17
Q

What is Valsartan?

A

ARBs that has a half life of 6-10 hours that is not a prodrug

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18
Q

what is Candesartan?

A

half life is 5-9 hours and is noteworthy for its relatively irreversible binding

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19
Q

when should ARBs and ACEI not be used in heart failure?

A
  • Not tolerated (cough, angioedema, try ARB)
  • Pregnant
  • Hypotensive
  • Serium creatinine > 3mg/dL
  • Hyperkalemia
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20
Q

what are the affects of ANP/BNP?

A

causes natriuresis and diuresis

increase GFR
decrease renin secretion
decrease aldosterone
-decrease Na and H20 water reabsorption
-decreased ADH secretion and ADH effects in collecting duct
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21
Q

what can BNP and NT-proBNP be used for?

A

BNP made by the ventricles and can be used as a biomarker

NT-proBNP is inactive until it is cleaved off

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22
Q

what is the MOA, Effects, Clinical applications of Valsartan/sacubitril

A

MOA: Sacubitril is a prodrug that inhibits the Neprilysin (neutral endopeptidase)

  • Valsartan is an ARB
  • these drugs co crystalized

Effects:
-increase ANP and BNP

clinical applications:
-Heart failure

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23
Q

Pharmokinetics and Toxicities of Valsartan/sacubitril

A

Pharmokinetics:

  • twice daily dosing
  • half life of 9-11 hrs

Tocicites:

  • Hypotension
  • hyperkalemia
  • increased sCr
  • angioedema
  • cough
  • renal failure
  • decreased Hct, Hgb
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24
Q

what makes Carvedilol beneficial in HF

A

Inverse antagonist thus preventing the downstream signaling rather than being an antagonist

others that are beneficial that are not inverse:

  • metoprolol
  • bisoprolol
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25
Q

Carvedilol MOA, effects, Clinical application

A

MOA: racemic mixture of nonselective beta and alpha adrenergic blocker
-b more than a

Effects:
-in HT decreased cardiac output and increased levels of ANP

in CHF decreased pulmonary pressure
-increased stroke volume index

Clinical applications:
-if stable, used in recent or remote history of MI and in HFrEF prevent symptomatic HF

off label: rate control in afib, chronic stable angina, gastroesophageal varices

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26
Q

what are the pharmacokinetics and toxicities of Carvedilol

A

Pharmacokinetics:

  • rapid and extensive absorption
  • half life 7/10 hours
  • metabolized by liver
toxicities:
-allergy
-dizziness weight gain
swelling of legs
-SOB
-Bradycardia
-angina and heart attack if abruptly discontinued
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27
Q

What is use of Labetalol

A

another alpha/beta blocker used primarily for severe hypertension and hypertensive emergiencies

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28
Q

general use of Carvedilol

A

Prevent down regulation of the B1 adrenergic receptors in the Heart due to excessive sympathetic stimulation

Keeps heart responsive to sympathetic drive

  • protects against dysrhythmias
  • reduces renin secretion
  • reduces myocardial O2 consumption
  • limits heart remodeling

given at low doses initially and cautioned in a stable patient

given to patients with diastolic HF

and symptomatic of CHF and LVEF<40%

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29
Q

what is the big black box warning for Beta blockers

A

Beta blocker therapy should not be withdrawn abruptly (particularly in patients with CAD) but gradually tapered to void acute tachycardia, hypertension, and/or ischemia

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30
Q

MOA, effects and Clinical appication of Ivabradine?

A

MOA: specific inhibition of the hyperpolarization-activated cyclic nucleotide gated (HCN) channels (If cannels) within the SA node

-prolongs diastole and slows HR

Clinical applications:

  • treatment of resting HR greater than 70 in stable and chronic HF with EF<35% who are sinus rhythm with:
  • maximally tolerated doses of beta blockers
  • contraindications to beta blocker use

off label: stable angina

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31
Q

Pharmokinetics and toxicites of and recomendations for ivabradine?

A

Given PO due to intestinal and hepatic metabolism
-half life 6hrs

TOxicities:

  • bradycardia
  • hypertension
  • increased risk of atrial fib
  • heart block

Contraindicted in:

  • acute decompensated HF
  • Hypotension
  • bradycardia
  • pacemaker dependance
  • hepatic impairment
  • strong CYP3A4 inhibitors

beneficial to reduce HF hospitilizations with stable chronic HFrEF (<35%)

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32
Q

MOA, effects and CLinical applications of Spoironolactone

A

MOA: competitive antagonist of aldosterone receptors

effects: K+sparing diuretic by preventing Na K+ exchange in collecting ducts

Clinical app:

  • counteracts K+ loss induced by other diuretics in treatment of HF
  • treat hyperaldosteronism
  • ascites in cirrhosis

reduced fibrosis in HFrEF and post MI heart failure

treatment of androgenic alopecia in females

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33
Q

Pharmacokinetics and toxicities of Spironolactone

A

drug has active metabolites
-steroid effects are slow on and slow off so single dose

Toxicities:

  • Hyperkalemia
  • amenorrhea, hirsutism, gynecomastia, impotence
  • tumorigen
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34
Q

what is eplerenone

A

more selective aldosterone antagonist, approved for use in Post MI heart failure and alone or in combination for treatment of hypertension

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35
Q

what are the general benefits from the use of Spironolactone

A

block Aldosterone

  • prevent Na+ and water retention
  • prevent K+ loss
  • prevent Mg++ loss
  • increase the baroreceptor reflex
  • prevent cardiac fibrosis
  • prevent ischemia
  • decrease sympathetic activation
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36
Q

what is the common clinical reasons for administering a diuretic?

A

Essential hypertension

Edema associated with:

  • congestive heart failure
  • liver failure
  • kidney failure
37
Q

what are the K+ sparing diuretics?

A

–
triamterene, amiloride… Na+ channel blockers
–
spironolactone… aldosterone antagonist

38
Q

what are the K+ losing diuretics?

A

–
thiazides… Na+Cl- co transporter blockers
–
loop diuretics… Na+K+2Cl-cotransporter blockers
–
carbonic anhydrase inhibitors (seldom used)
–
osmotic diuretics… non reabsorb able solutes

39
Q

what are the locations of K+ losing diuretics?

A

PCT
THick segment ascending limb of heneles loop
Early distal Convoluted tubule

40
Q

what are the locations of the K+ sparing diuretics

A

Late convoluted tubule and collecting duct

41
Q

Hyperkalemic effects on the heart

A 
•
tall T waves
•
prolonged PR interval
•
widened QRS interval
•
flattened P waves
•
arrhythmias including bradycardia, ventricular tachycardia or fibrillation
•
sinus arrest or nodal rhythm with possible asystole

much easier to fire AP since the resting membrane is depolarized

42
Q

what are the effects of Hypokalemia on the heart

A 
•
flattened T waves
•
ST segment depression
•
prolonged QT interval
•
tall U waves
•
atrial arrhythmias
•
ventricular tachycardia or ventricular fibrillation

harder to get AP because membrane is hyperpolarized

43
Q

what diuretic causes the highest ceiling of diuresis

A

Furosemide

  • works on the thick ascending limb of henle
  • considered a loop diuretic
44
Q

MOA, Effects, and clinical applications of furosemide

A

inhibits Na+ K+ 2Cl- cotransporter at the TAL preventing sodium and chloride reabsorption
-indirectly inhibits reabsorption of Ca and Mg due to loss of K+

effects: massive fluid removal and excretion of Na K+ Cl, Mg, Ca and H20

Clinical application:
-management of edema associate with HF, hepatic disease, and renal disease

acute pulmonary edema
-decreases preload and decreases EDV, rapid dyspnea relief

treatment of HTN and works in patients with a low GFR

45
Q

Pharm kinetics and Toxicities of Furosemide

A

half life .5-2hrs
eliminated primarily as unchanged drug in urine

Ototoxicity

Sulfonamide (hypersensitivity)

  • Hypokalemia
  • Hyponatremia
  • Hypocalcemia (decreased kidney stone risk)
  • Hypomagnesemia
  • Hypochloremic metabolic alkalosis
  • Hyperglycemia
  • Hyperurcemia
  • increased cholesterol and tryglycerides
46
Q

what is torsemide?

A

sulfonamide similar to furosemide with a longer T1/2 and better oral absorption and some evidence it works better in HF

47
Q

what is bumetanide

A

similar to furosemide but more predictable oral absorption

48
Q

what is ethacrynic acid

A

Non-sulfaonamide loop diuretic reserved for those with a sulfa allergy

49
Q

what are some major drug interactions of Loop diuretics

A

–
digoxin: frequent since both drugs are often used to treat heart failure and the risk of digoxin toxicity is increased by low potassium due to the diuretic
–
ototoxic drugs: increased chance of hearing loss if combined with drugs having similar toxicity (e.g., gentamicin)
–
potassium-sparing diuretics can counter balance potassium-wasting effects
–
can also increase lithium toxicity, potentiate effects of other antihypertensive agents and have diuretic effects antagonized by NSAIDs

50
Q

what are the benefits from diuretics in the aspect of congestion?

A

Relieve congestion

get rid of excess volume to allow for the return of ventricular fiber length for more optical range

51
Q

MOA, effects, and clinical applications of Hydrochlorothiazide

A

MOA: inhibits sodium reabsorption in the Distal tubules via blockade of Na+ Cl- cotransporter

effects: increase excretion of Na and H20
- K+ losing as well

Clinical applications:

  • management of HTN alone or in combination with other drug
  • not effective in patients with low GFR
  • treat edema
  • off label calcium nephrolithiasis
52
Q

Pharmokinetics and toxicities of HCTZ

A

well absorbed
half life 6-15 hours
excreted in urine

Toxicities:

  • Hypotension
  • hypokalemia
  • hypomagnesemia
  • hyponatremia
  • hypochloremic metabolic alkalosis

sulfonamide drug

53
Q

what are the characteristics of chlorothiazide, and chlorthalidone

A

Chlorothiazide: poor oral absorption

Chlorthalidone: much longer half life

54
Q

what is the characteristics of Metolazone

A

Another long acting thiazide diuretic that is favorite of cardiologists for use as adjunct in the treatment of congestive HF

55
Q

what can cause Diuretic Failure during HF treatment

A

Decreased renal perfusion and glomerular filtration rate

  • via excessive volume depletion
  • decline in CO

NSAIDS

Renal pathology

Reduced or impaired diuretic absorption

56
Q

Benefits of Isosorbide dinitrate

A

Beneficial in African Americans

dilate veins and decrease preload and is given with hydralazine that dilates arteries and decreases afterload

57
Q

MOA, effects, and CLinical applications of nitroglycerin

A

MOA: forms NO that activates guanate cyclase to produce more cGMP that will dephosphorylate myosin light chains and cause relaxation

effects:
- Vasodilation more in veins
- decrease preload
- moderately decrease afterload
- dilates coronary bloodflow and collateral flow

Clinical applications:

  • treat angina
  • acute decompensated HF especially in MI
  • preoperative hypertension
  • induce hypotension
  • help with anal fissure
58
Q

Pharmacokinetics and toxicities of Nitroglycerin

A

half life 1-4 min
but can be given anyway for how fast and long want to work

TOxicities:

  • reflex tachycardia
  • headache
  • paresthesia
  • dyspnea
  • diaphoresis
59
Q

what is isosorbide dinitrate?

A

similar drug with slower onset of action that is administered orally for prevention of angina and for HF with reduced ejection fraction

60
Q

MOA, Effects, and clinical applications of Hydralazine?

A

MOA: endothelium dependant

  • hypepolarizes
  • requires activation of COX
  • mediated by prostacyclun (PGI2) receptor

effects: direct vasodilation of arterioles

Clinical applications:
-management of hypertension (not for initial treatment)

off label:

  • HF with reduced ejection fraction if not tolerable for ACEI or ARB
  • HF (african american)
  • Hypertensive emergency in pregnancy
61
Q

Pharmokinetics and toxicities of Hydralazing?

A

Pharmokinetics: oral or IV

  • eliminated in urine
  • half life 2-8 hrs

Toxicities: ots!

  • angina, flushing
  • peripheral edema
  • tachycardia
  • pruritus
  • drug induced lupus like syndrome
62
Q

what order is Digitalis (dioxin) used

A

second line agent

63
Q

MOA, Effects and Clinical applications of digoxin

A

MOA: inhibition of the Na+-K+ ATPase
-leads to more Ca stuck in the cell

Effects:

  • leads to increased contractility
  • suppression of the AV node conduction

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

Clinical applications:

  • Control of ventricular response rate for patients with atrial fibrillation
  • treatment of patients with increase myocardial contractility
64
Q

What are the Pharmacokinetics and toxicities of Digoxin

A

Pharm: administered orally, IV and IM

  • half life is 36-48 hours so needs a loading dose
  • can cross the placenta but is safe in pregnant women with supraventricular tachycardia

Toxicites

  • accelerated rhythm
  • diziness mental disturbances
  • rash
  • nausea
  • weakness
  • blurred or yellow vision
  • laryngeal edema
65
Q

what happens if there is low potassium with a patient taking digoxin?

A

it competes with K+ for binding to the Na+/K+ ATPase

need normal K+ levels if there is too little then there is too much block

66
Q

what are the Hemodynamic benefits and electrical effects of digoxin?

A

Hemodynamic benefits:
-increased cardiac output that causes decreased sympathetic tone, increased urine production, and decreased renin release

Electrical effects:

  • Increases the firing rate of vagal fibers
  • increases the responsiveness of the SA node to acetylcholine
67
Q

effects of Digoxin on the electrocardiogram

A

typical changes:
-depression of the ST segment and longer PR interval

Toxic effects on AV conduction: AV dissociation
-lack of relationship between the P and QRS complexes

Toxic effect of digitalis on purkinje automaticity and ventricular refractory period
-ectopic ventricular beats canned bigeminy (ectopic beat alternating with normal beat

68
Q

how does digotoxin affect the AV node

A

increase duration of refractory period

decrease the conduction velocity

69
Q

how does digitalis effect the purkinje fibers

A

increased the automaticity

70
Q

how does digitalis effect the ventricular myocardium

A

decrease the duration of refractory period

71
Q

what are noncardiac adverse effects of digoxin?

A 
–
anorexia, nausea, vomiting, salivation
–
excessive urination
–
fatigue, visual disturbances (blurred vision, halos, yellowish or greenish tinge to objects)
72
Q

what are the drug interactions of digoxin?

A

–
diuretics… the “biggie”; diuretics cause hypokalemia, which leads to increased digoxin binding, which leads to increased digoxin toxicity
–
ACE inhibitors and ARBs –can increase plasma K+levels, decreasing digoxin effects
–
sympathomimetics–beneficial interaction on contractility, detrimental effects on arrhythmias
–
quinidine, spironolactone, verapamil, propafenoneand alprazolam are among a range of drugs that interfere with clearance of digoxin
–
cholesterol-binding resins block digoxin absorption from GI tract

73
Q

what is the treatment of too much digoxin?

A

KCl

lidocaine to block Na+ channels

Phenytoin to block Na channels

Anti-digitalis antibodies

74
Q

what are the guidelines for treatment for HFrEF?

A

ACEI, ARB, and ARNI

all in conjunction with beta blockers and aldosterone antagonist

75
Q

What are the drug of choice treatments for HFpEF

A

direct therapy at symptoms
-hypertension, lung disease, coronary artery disease, atrial fibrillation, obesity anemia, diabetes mellitus, kidney disease, sleep disordered breathing

exercise is beneficial/recommended, but avoid: tachycardia, abrupt ↑blood pressure, ischemia, atrial fibrillation

loop diuretics against edema

Aldosterone receptor antagonists

if justified by symptoms:
-β-blockers, ACEI/ARBs, CCB

76
Q

what drugs have shown to have no evidence of benefit against HFpEF

A

no evidence of benefit: nitrates, PDE5 inhibitors, digoxin

77
Q

what to give to a patient who has Acute decompensated Heart failure?

A

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

place in seated position

  • pulse ox
  • asses blood pressure
  • place 2 IV lines
  • Monitor urine output
78
Q

how can patients present with acute decompensated heart failure and how are they treated

A

Hypertensive: treat with loop diuretic and vasodilator

Normotensive: treat with loop diuretic and vasodilator

Hypotensive: typically treat with loop diuretic

79
Q

what is the difference between Nitroprusside and Nitroglycerin?

A

Nitroprusside will target both arterial and venous sides

Nitroglycerin will preferentially dilate the venous side
decrease preload

80
Q

when to give inotropic agents?

A

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

dobutamine
dopamine
milrinone

81
Q

when giving an inotropic agent what must you make sure of?

A

make sure you discontinued carvedilol
-beta blocker

only time keep giving is if the patient is mild decompensation without hypotension or evidence of hypoperfusion

82
Q

MOA, effects and clinical applications of dobutamine

A

MOA: stimulates both beta1 and Beta 2 adrenergic receptors
-some alpha 1 agonism as well

Effects:

  • increased contractility and HR
  • lowers central venous pressure and wedge pressure
  • no effect on pulmonary vascular resistance

Clinical applications:

  • management of patients with cardiac decompensation
  • bridge therapy
  • pallative therapy
  • severe systolic dysfunction
83
Q

what are the pharmacokinetics and toxicities of dobutamie?

A

Pharm: administer IV
half life 2 min
metabolized by tissues and liver

toxicities:
-tachycardia
angina
-fever
-headache
-hypertension
-local pain
84
Q

what are the MOA, effects, clinical applications of dopamine

A

MOA: Catecholamine that activates B1 adrenergic receptors at low doses and stimulates a adrenergic receptors at higher doses

effects: increases HR and contractillity

low does: dilate renal vessels but does no selectively preserve renal function

Clinical applications:

  • adjunct in the treatment of shock that persists after adequate fluid volume replacement in cases of:
  • MI
  • Open heart surgery
  • renal failure
  • cardiac decompensation
85
Q

Pharmacokinetics and TOxicities of dopamine

A

Pharm:

  • given IV
  • half life 2 min
  • COMT (MAO) breakdown
  • excreted in urine

Toxicities:
•angina pectoris, atrial fibrillation, bradycardia, ectopic beats, hypertension, hypotension, palpitations, tachycardia, vasoconstriction, ventricular arrhythmia, widened QRS complex on ECG
•anxiety, headache
•local tissue necrosis, gangrene (high dose), piloerection
•nausea, vomiting
•increased intraocular pressure, mydriasis
•dyspnea

86
Q

MOA, effects, and clinical application of milrinone?

A

MOA: selective phosphodiesterase type 3 inhibitor

Effects: Inhibitor in cardiac and vascular tissue resulting in vasodilation and inotropic effects

Clinical applications:
-Inotropic therapy for patients unresponsive to other acute heart failure

87
Q

Pharmacokinetics and toxicities of milrinone

A

administered IV

  • half life 2.5 hrs
  • excreted in urine

Toxicities

  • ventricular arrhythmia
  • supraventricular arrhythmia, hypotension angina
  • headache
88
Q

what is the use of inamrinone

A

a similar drug to milrinone but is less safe and has been removed from the market in 2011

89
Q

Drugs to avoid in Acute decompensated heart failure

A

•
class I antiarrhythmics… some are negative inotropesand all can cause arrhythmias in heart failure patients
–
consider amiodarone…
•
calcium channel blockers… directly suppress myocardial contractility, especially non-dihydropyridines
•
nonsteroidalanti-inflammatory drugs…impair renal salt and water excretion which can exacerbate heart failure

CPR II Drugs test 1 (8 decks)

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