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Pharmacology > Heart Failure Drugs > Flashcards

Heart Failure Drugs Flashcards

1
Q

First choice of drugs in treating heart failure

A

ACE Inhibitors

Beta Blockers

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2
Q

Examples of ACE Inhibitors for Heart Failure

A 
Benazepril
Captopril
Enalapril
Lisinopril
Quinapril
Ramipril

Fosinopril
Trandolapril
Perindopril

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3
Q

Short acting ACEi used only for initiation of therapy

A

Captopril

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4
Q

ACEi that requires daily dosing

A

Enalapril

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5
Q

Major side effects of ACEi

A

Cough

5-10% of patients

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6
Q

Adverse effects of ACEi

A 
Cough
Angioedema
Hypotension 
Hyperkalemia
Skin Rash
Neutropenia
Anemia
Fetopathic syndrome
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7
Q

ACEi are contraindicated in patients with?

A

Renal artery stenosis

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8
Q

ACEi are caution in patients with?

A

Impaired renal function

Hypovolemia

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9
Q

ACEi drugs that are cautious in patients with renal or hepatic impairment (TFP)

A

Trandolapril
Fosinopril
Perindopril

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10
Q

Drugs that are used for HF only in cases of intolerance to ACEi

A

Angiotensin Receptor Blockers (ARBs)

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11
Q

Examples of ARBs for HF

A 
Candesartan
Eprosartan
Irbesartan
Losartan
Olmesartan
Telmisartan
Valsartan
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12
Q

Drugs that have same effects with ACEi but no COUGH or ANGIOEDEMA

A

ARBs

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13
Q

Drugs that is not used in combination with ACEi because it causes more harm than benefit

A

ARBs

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14
Q

First choice of drugs for HF with a low start and slow go

A

Beta Blockers

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15
Q

B Blockers for HF

A

Bisoprolol
Carvedilol
Nebivolol
Metoprolol

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16
Q 
This drugs have adverse effects like
bradycardia
AV block
Bronchospasm
Peripheral vasoconstriction
Worsening of ACUTE HF
Worsening of psoriasis 
Depression
A

B Blockers

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17
Q

B Blocker that has a polymorphic CYP2D6 metabolism

A

Metoprolol

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18
Q

First drug of choice in SYMPTOMATIC HF

A

Mineralocorticoid Receptor Antagonists

Eplerenone & Spironolactone

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19
Q

Most serious effects of mineralocorticoid receptor antagonists (eplerenone & spironolactone)

A

Hyperkalemia

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20
Q

Mineralocorticoid receptor antagonist that causes painful breast swelling, dysmenorrhea in women and impotence in men

A

Spironolactone

Due to nonselective binding to sex hormone receptors

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21
Q

Neprilysin Inhibitor used as first drug of choice in HF

A

Sacubatril/ Valsartan

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22
Q

Neprilysin inhibitor superior to the ACEi enalapril

A

Sacubatril/Valsartan

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23
Q

Action of sacubatril/valsartan

A

Decrease degradation of natriuretic peptides

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24
Q

Adverse effects of sacubatril/valsartan

A

Hypotension

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25
Q

Drugs used for symptomatic treatment of milder forms of HF

A

Thiazide diuretics

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26
Q

Used in treatment of EDEMA associated with congestive heart failure, liver cirrhosis, CKD, nephrotic syndrome

A

Thiazide diuretics

Loop diureticsp

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27
Q

These drugs loose their efficacy at GFR <30-40 mL/min

A

Thiazide diuretics

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28
Q

Drugs that potentiate the effects of loop diuretics in severe HF

A

Thiazide diuretics

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29
Q

These drugs have high risk for HYPOKALEMIA & ARRHYTHMIA when combined with QT prolonging drugs

A

Thiazide diuretics

Loop diuretics

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30
Q

Thiazide type diuretics

A

Chlorothiazide

Hydrochlorothiazide

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31
Q

Thiazide like diuretics

A

Chlorthalidone
Indapamide
Metolazone

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32
Q

Used in symptomatic treatment of severe HF and acute decompensation

A

Loop diuretics

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33
Q

Loop diuretics drugs for HF

A

Bumetanide
Furosemide
Torasemide

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34
Q

Loop diuretics superior to furosemide in HF

A

Torasemide

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35
Q

Used in HF of Africans & Americans

A

ISDN/Hydralazine

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36
Q 
This drug when used with B blockers will have adverse effects like 
headache 
nausea
flushing
hypotension 
palpitations 
tachycardia 
dizziness
angina pectoris
A

ISDN/Hydralazine

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37
Q

Can cause lupus syndrome

A

ISDN/Hydralazine

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38
Q

Positive inotropes will low therapeutic index

A

Digoxin

Digotoxin

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39
Q

Exerts benefits in HF & Atrial fibrillation

A 
Positive inotropes
(Digoxin &amp; Digotoxin)
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40
Q

Half life of digoxin

A

1.5 days

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41
Q

Half-life of digotoxin

A

7 days

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42
Q

Plasma concentration of digoxin

A

0.5-0.8 ng/mL

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43
Q

Plasma concentration of digotoxin

A

10-25 ng/mL

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44
Q

Drug used for HR reduction

A

Ivabradine

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45
Q

Exert effects in patients not tolerating B blockers or having HR >75 under B blockers

A

Ivabradine

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46
Q

Unwanted effects: bradycardia, QT prolongation, atrial fibrillation & phosphenes

A

Ivabradine

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47
Q

Drugs for acutely decompensated HF

A

Intravenous vasodilators

Intravenous positive inotropes

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48
Q

Intravenous vasodilator drugs

A

Nitroglycerin (sodium nitroprusside)

Nesiritide

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49
Q

Intravenous positive inotropes drugs

A

Dobutamine
Dopamine
Epinephrine
Norepinephrine

Enoximone
Milrinone

Levosimendan

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50
Q

Increase CO in acute congestion by increasing filling pressure and dilation

A

Nitroglycerin (Sodium nitroprusside)

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51
Q

How does nitroglycerin (Na nitroprusside) and neseritide increase CO in acute congestion?

A

By decreasing preload and afterload

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52
Q

NO releaser, stimulates soluble guanylyl cyclase

A

Nitroglycerin (Na nitroprusside)

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53
Q

This drug is avoided if systolic blood pressure is <110 mmHg

A

Nitroglycerin (Na nitroprusside)

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54
Q

Last option in patients with systolic BP <85 mmHg

A

Positive Inotropes

Dobutamine
Dopamine
Epinephrine
Norepinephrine

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55
Q

Increases cardiac energy consumption and risk of arrhythmia

A

Positive inotropes

Dobutamine
Dopamine
Epinephrine
Norepinephrine

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56
Q

Positive inotropes that causes less tachycardia than epinephrine

A

Dobutamine

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57
Q

Recombinant human BNP

A

Neseritide

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58
Q

Stimulates membrane bound guanylyl cyclase

A

Neseritide

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59
Q

Positive inotropes that causes less afterload increase thab norepinephrine

A

Dobutamine

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60
Q

PDE3/4 inhibitors and increases cellular cAMP

A

Enoximone

Milrinone

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61
Q

Increase CO and dilate blood vessels (inodilator)

A

Enoximone

Milrinone

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62
Q

Can be used in patients on B blockers and with high peripheral and pulmonary arterial resistance

A

Enoximone

Milrinone

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63
Q

Dose limiting of Enoximone & Milrinone

A

Blood pressure decrease

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64
Q

Increase CO and decrease vascular resistance (inodilator)

A

Levosimendan

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65
Q

Combined Ca2+ sensitizer (troponin C binding) and PDE3 inhibitor

A

Levosimendan

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66
Q

HF symptoms like fatigue, dizziness, muscle weakness and shortness of breath are caused by?

A

Low output (forward failure)

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67
Q

HF signs like congestion of the organs upstream of heart is caused by?

A

Increased filling pressure (backward failure)

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68
Q

Most common reason for systolic heart failure.

A

Ischemic Heart Disease

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69
Q

Ischemic heart diseases causes

A
  1. Acute myocardial infarction
  2. Chronic loss of viable heart muscle mass
  3. Valvular disease
  4. Viral infections
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70
Q

Other factors that causes ischemic heart disease

A
  1. Excessive Alcohol
  2. Cocaine
  3. Amphetamines
  4. Doxorubicin (cancer drugs)
  5. Trastuzumab (cancer drugs)
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71
Q

The pathophysiology of heart failure involves

A

Heart
Vasculature
Kidney
Neurohumoral regulatory circuits

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72
Q

The overload of myocardium means that

A

There is primary contractile defect of the myocardium caused by atrophy of the heart

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73
Q

The response of the heart to the overload is?

A

Hypertrophy (growing in size and assembling more sarcomeres that can increase contractile force)

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74
Q

Direct consequence of cardiac myocyte hypertrophy

A

Reduced capillary/myocyte ratio (less O2 and nutrient supply per myocyte)

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75
Q

Reduced capillary/myocyte ratio will lead to?

A

Energy deficit and metabolic reprogramming

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76
Q

1st step in Pathologic remodelling

A

Gene expression for ion channels, Ca2+ regulating proteins and contractile proteins will be energy-saving adaptations and can aggravate contractile failure and favors arrhythmias

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77
Q

2nd step in cardiac remodelling

A

Fibroblast proliferate and deposit increased amounts of EC matrix > fibrosis> arrhythmias> overload> cardiac myocyte death

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78
Q

Critical parameter of cardiac function

A

Stiffness of the vasculature

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79
Q

Stiffness of vasculature determines?

A

The resistance against which the heart has to expel the blood and increases with aging

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80
Q

Major reasons for premature stiffening of blood vessels which increases afterload

A

Arterial hypertension

Diabetes mellitus

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81
Q

In HF, endothelial dysfunction is?

A

Disturbed balance between vasodilating NO and proconstrictor ROS

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82
Q

ROS inactivates 2 critical enzymes

A

eNOS and sGC and converts NO in peroxynitrite, a strong ROS, favor vasoconstriction

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83
Q

Cardiovascular drugs that improve endothelial function

A

ACEi
ARBs
MRAs
Statins

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84
Q

Inhibits cGMP degradation in smooth muscle cells and thereby promotes relaxation

A

PDE5 inhibitors

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85
Q

How does Ang II regulates filtration rate in the kidney?

A

Regulate the diameter of efferent glomerular arteriole

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86
Q

How does regulation of kidney perfusion is achieved?

A

Balance between
Ang II @ AT1 receptors (constrictor)
Vasopressin @ V1 receptors ( constrictor
Prostaglandins (vasodilator)

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87
Q

How does kidney regulates Na and water excretion?

A
  1. Ang II
  2. Balance between constrictors and vasodilators
  3. Aldosterone (mediates Na reabsorption in distal tubule)
  4. AVP-regulated water transport in the collecting ducts @V2 receptors
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88
Q

Immediate response of the body during decrease CO

A

Activation of SNS and RAAS system

To ensure perfusion to brain & heart

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89
Q

Deleterious effects of chronic activation of neurohumoral system?

A

Ang II, NE & ET (endothelin) accelerate pathological cardiac remodeling (hypertrophy, fibrosis and cell death)
Aldosterone has profibrotic actions

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90
Q

Neurohumoral effects that increases afterload

A

Prolonged vasoconstriction via Ang II

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91
Q

Neurohumoral response that increases cardiac preload, dilation, and ventricular wall stress

A

Decreased kidney perfusion

Increased aldosterone production

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92
Q

Major determinant of cardiac O2 consumption

A

Cardiac preload
Dilation
Ventricular wall stress

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93
Q

What do you mean by INOTROPHIC EFFECTS?

A

Chang the force of the heart’s contraction

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94
Q

What do you mean by CHRONOTROPHIC EFFECTS?

A

Those drugs that causes Increase HR

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95
Q

In a failing, energy depleted heart, what is the effect of tachycardia and positive inotrophic drugs?

A

Aside from increasing CO which the first effect.

During prolonged stimulation, it will promote arrhythmias and increase O2 consumption

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96
Q

Drug that reduce deleterious effects of Ang II by blocking AT1 receptors

A

Valsartan

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97
Q

Drug that inhibits degradation of ANP & BNP

A

Sacubitril

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98
Q

Combination drug that appears superior to ACEi Enalapril in reducing the rates of hospitalization in patients with HReRF

A

Valsartan-sacubitril

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99
Q

BNP and ANP are normally in the atria and ventricles, when does these peptides be released into the bloodstream?

A

During INCREASED PRELOAD (stretch)

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100
Q

Heart failure in reduced ejection fraction (EF: < 30%)

A

Systolic heart failure

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101
Q

Patients with preserved ejection fraction have?

A

HF symptoms but normal or >50% or only mildly reduced EF.

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102
Q

HF that are associated with arterial hypertension, ischemic heart disease, DM and obesity

A

HFpEF

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103
Q

Sign of chronically elevated end-diastolic pressures (HFpEF)

A

Not dilated
Enlarged wall thickness (hypertrophy)
Enlarged left atria

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104
Q

Molecular alterations in HFpEF

A

Increased myocardial fibrosis

Reduced phosphorylation of titin

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105
Q

Sarcomeric protein that spans Z to M band that had spring domains whose elastic modulus determines the passive tension of cardiomyocytes

A

Titin

106
Q

Titin stiffness is determined by?

A

Its isoform

cGMP-dependent phosphorylation

107
Q

Only intervention that increases maximal physical activity in HFpEF patients

A

Exercise training

108
Q

According to NYHA, what class of HF where there is a left ventricular dysfunction but no symptoms?

A

Class I

109
Q

According to NYHA, what class of HF, where symptoms are at low medium-to-high levels of physical exercise?

A

Class II

110
Q

According to NYHA, what class of HF where symptoms are at low levels of physical exercise.

A

Class III

111
Q

According to NYHA, what class of HF where symptoms are presence even at test or daily life physical activities like brushing teeth?

A

Class IV

112
Q

According to recent guidelines of AHA and ACC, what is the stage of heart failure, where there are presence of risk factors?

A

Stage A

113
Q

According to recent guidelines of AHA and ACC, what is the stage of heart failure, where there is a structural heart disease but without signs & symptoms of HF?

A

Stage B

114
Q

According to recent guidelines of AHA and ACC, what is the stage of heart failure, where there is a presence of structural heart disease with prior or current symptoms of HF?

A

Stage C

115
Q

According to recent guidelines of AHA and ACC, what is the stage of heart failure, where refractory heart failure is present?

A

Stage D

116
Q

Therapy goals for Stage A HF

A

Heart-healthy lifestyle
Prevent vascular coronary disease
Prevent LV structural abnormalities

117
Q

Therapy goals for Stage B HF

A

Prevent HF symptoms

Prevent further cardiac remodelling

118
Q

Therapy goals for Stage C HF

A

Control symptoms
Prevent hospitalization
Prevent mortality

119
Q

Therapy goals for Stage D HF

A

Control symptoms
Improve HRQOL
Reduce hospital readmissions
Establish end-of-life goals

120
Q

Drugs used for Stage A HF

A

ACEi
ARBs
Statins

121
Q

Drugs used for Stage B HF

A 
ACEi
ARB
ICD (implantable cardioverter-defibrillator
Revascularization
Valvular  surgery
122
Q

Drugs used for Stage C HF with preserved EF

A

Diuretics

Treat comorbidites like hypertension, AF, CAD, DM

123
Q

Drugs for ROUTINE use in patients with for Stage C HF with reduced EF

A 
Diuretics
ACEi or ARB
ARNI
B Blocker
Aldosterone antagonist 
Ivabradine
124
Q

Drug used in selected patients with reduced EF

A

Hydralazine/ISDN
ACEi and ARB
Cardiac glycoside

In selected patients:
CRT
ICD
Revascularization or valvular surgery

125
Q

Drugs used for Stage D HF

A 
Heart transplant 
Chronic inotropes
Surgery
Pallative care and hospiece
ICD deactivation
126
Q

Hydralazine, a vasodilator is mostly combined with?

A

Sympatholytic agents and diuretics

127
Q

Hydralazine directly relaxes what smooth muscle?

A

Arteriolar smooth muscle

128
Q

Main MOA of hydralazine

A

Reduced intracellular Ca2+ concentration

129
Q

How does hydralazine reduced Ca2+ concentrations?

A

Inhibits inositol triphosphate-induced released of Ca2+ from intracellular storage sites

Open Ca2+ activated K+ channels in SMC

130
Q

Drug that is sensitive to NSAIDs, because it activates arachidonic acid, COX and prostacyclin pathway.

A

Hydralazine

131
Q

This drug is combined in the pill containing isosorbide dinitrate (BiDil) in the HF treatment

A

Hydralazine

132
Q

In congestive HF, hydralazine is combined with ______ for patients that cannot tolerate ACEi and AT1 Blockers

A

Nitrates

133
Q

Hydralazine should be used in CAUTION in elderly patients and hypertensive with CAD because it can cause

A

Myocardial ischemia due to reflex tachycardia (increased O2 demand)

134
Q

Maximum recommended dose of hydralazine to minimize the risk of drug-induced lupus syndrome.

A

200 mg/d

135
Q

A vasodilator that has a hypotensive effect and can cause reflex tachycardia due to stimulation of baroreceptor reflex.

A

Hydralazine

136
Q

Class of drugs that are beneficial in HF because they reduce afterload so that heart can expel blood against lower resistance.

A

Vasodilators

137
Q

Orally available organic nitrate

A

ISDN (Isosorbide 2,5’-dinitrate)

138
Q

Main effect of the vasodilator ISDN

A

Venous pooling

Reduction of diastolic filling pressure (preload) with little effect on systemic vascular resistance

139
Q

Vasodilator that prevents nitrate tolerance by reducing ROS-mediated inactivation of NO

A

Hydralazine

Should be combined with ISDN

140
Q

Dose combination of hydralazine & ISDN

A

37.5 mg hydralazine and 20 mg ISDN

Uptitrated to a target dose of 2 tablets, thrice daily

141
Q

Vasodilators that reduce preload and afterload

A

Nitroglycerin and Nitroprusside

142
Q

Nitroglycerin & Nitroprusside reduce preload by?

A

Reducing wall stress and O2 consumption

143
Q

Vasodilators nitroglycerin and nitroprusside are avoided in patients with systolic BP ______

A

<110 mmHg

144
Q

Organic nitrate with low molecular mass and are volatile, oily liquids and is explosive

A

GTN (glycerin trinitrate) or nitroglycerin

145
Q

Second choice in ALL stages of Heart failure (if patients cannot tolerate AcEI)

A

ARBs

146
Q

Peak plasma levels of Candesartan

A

3-4 hours after oral administration

147
Q

Plasma half-life of Candesartan

A

9 hrs

148
Q

Plasma clearance of Candesartan

A 
Renal elimination (33%)
Biliary excretion (
149
Q

Physiological effects of ACEi

A
  1. Vasodilation
  2. Reduce aldosterone levels
  3. Direct antiremodelling effects of the heart
  4. Produce sympatholytic effects
150
Q

Why does ACEIs are contraindicated in bilateral renal stenosis?

A

Because when renal perfusion is compromised, inhibition of RAAS by ACEIs will cause sudden and marked decrease in GFR

151
Q

Heart failure patients have low renal perfusion, and aggressive treatment of this drug will induce renal heart failure.

A

ACEIs

152
Q

What are being monitored in patients on ACEIs?

A

Blood pressure
Blood creatinine
K+ levels

153
Q

Long term effects of ACEIs

A

Chronic lowering of glomerular pressures protects glomerulus from FIBROTIC REGENERATION

154
Q

What is the effect of reduce aldosterone levels by ACEIs?

A

It will reduced expression of ENaC in the distal tubule

(Thus less absorption of Na and less excretion of K+)> HYPERKALEMIA

155
Q

Why does ACEIs friendly with HF patients?

A

Because HF patients are hypokalemic and ACEIs favors hyperkalemia by reducing K+ excretion

156
Q

Drugs that reduced the production of prostaglandins, antagonized the effects of ACEIs and should be avoided in patients with HF

A

NSAIDS

157
Q

Increases bradykinin and substance P levels

A

ACEIs

158
Q

ARBs shows competitive antagonism to ________ receptors

A

AT1 receptors

159
Q

Positive clinotrophy means

A

Quicken the rate of force development

160
Q

Positive lusitropic effect means

A

Accelerate cardiac muscle relaxation

161
Q

Poisitive dromotrophic effect means

A

accelerate atrial-ventricular conduction rate

162
Q

Positive bathmotropic effect

A

Enhance cardiac myocyte automaticity and lower threshold for arrhythmias

163
Q

Acute effects of B adrenergic antagonist are mediated by _______ receptors

A

B1 receptors (smaller extent B2 receptor)

164
Q

Reduce B receptor-mediated actions of catecholamines (NE & EPI)

A

B blockers

165
Q

Drugs given under stable condition and at very low doses

A

B blockers

166
Q

Dose escalation time of B blockers must be

A

Doubling every 4 weeks

167
Q

What is the importance of start low, and go slow B blocker therapy?

A

Heart had time to adapt to decreasing stimulation by catecholamines and find new equilibrium at a lower adrenergic drive

168
Q

Effects of competitive antagonism of B blockers

A

B blockers do not fully block the receptors, instead they shift the concentration response curve of the catecholamines to the right

169
Q

Protects the heart from the adverse long term consequences of adrenergic overstimulation

A

B blockers

170
Q

Improve perfusion of the myocardium by prolonging diastole, thereby reducing ischemia

A

B blockers

171
Q

Non-selective B blocker and an a1 Receptor antagonist

A

Carvedilol

172
Q

Plasma half-life of metoprolol

A

3-5 hrs

173
Q

Disadvantage of metoprolol

A

Dependency on polymorphic CYP2D6 for its metabolism

174
Q

Long plasma half-life of bisoprolol

A

10-12 hrs (daily dosing)

175
Q

Plasma half-life of carvedilol

A

6-12 hrs (requires twice-daily dosing)

176
Q

Plasma half-life of Nebivolol

A

10 hrs

177
Q

B blockers for HF that is not metabolized by CYP2D6

A

Bisoprolol

178
Q

Patients that must be treated with B blockers

A

With symptomatic HF (Stage C, class II-IV)

With ventricular dysfunction (Stage B, Class I)

179
Q

The improvement of left ventricular dysfunction under the treatment of B blockers is ______ months

A

3-6 months

180
Q

Should not be administered in new-onset of acutely decompensated heart failure

A

B blockers

181
Q

If patients are hospitalized with acute decompensation under current therapy with B blockers, what will should be done?

A

Doses with B blockers should be reduced or drug must be discontinued

182
Q

If doses of B blockers are increases rapidly, what are the circumstances that doses must be reduced?

A

When there is a fall in blood pressure, fluid retention and dizziness

183
Q

Major cardiovascular responses to B blockers

A

Lowers HR
Bronchiconstriction
AV Block
Peripheral vasoconstriction

184
Q

Drugs that has life-prolonging effects in patients with HF

A

Mineralocorticoid receptor antagonists (MRAs)

185
Q

Most appropriate drug symptomatic Stage C HFrEF patients

A

MRAs

186
Q

Effects of aldosterone that has adverse effects in HF setting

A 
Na and fluid retention 
Sympathetic activation 
Parasympathetic inhibition 
Myocardial and vascular fibrosis
Baroreceptor dysfunction
Vascular damage
187
Q

Inhibits all effects of aldosterone

A

MRAs

188
Q

Most important adverse effects of MRAs

A

Hyperkalemia

189
Q

MRA that is selective for the mineralocorticoid receptor and does not cause gynecomastia

A

Eplerenone

190
Q

Guidelines for the use of MRAs

A
  1. administration no more than 50 mg/d
  2. DO NOT administer if GFR is <30 mL/min
  3. Careful in elderly patients
  4. Careful in diabetic patients (increase risk of hyperkalemia
  5. Do not combine with NSAIDS
  6. Do not combine with K+ sparing diuretics
191
Q

A peptidase mediating the enzymatic degradation and inactivation of natriuretic peptides (ANP, BNP, CNP), bradykinin and substance P

A

Neprilysin

192
Q

Prodrug that after deesterization, inhibits neprilysin

A

Valsartan/Sacubatril

193
Q

Beneficial effects of ARNI (Valsartan/Sacubitril (promotion)

A

Natriuresis
Diuresis
Vasodilation of arteries and veins

194
Q

Beneficial effects of ARNI (Valsartan/Sacubitril (inhibition)

A 
Inhibits: 
Thrombosis
Fibrosis
Cardiac myocyte hypertrophy 
Renin release
195
Q

Treatment II for preload reduction

A

Loop Diuretics
Thiazide Diuretics
K+ sparing Diuretics

196
Q

Oral bioavailability of furosemide

A

40%-70%

197
Q

Loop diuretics required for initiation of diuresis in patients with worsening symptoms

A

Furosemide

198
Q

Loop diuretics for patients with impaired GI absorption, hypervolemic patients witn CHF-induced GI edema

A

Furosemide

199
Q

Oral bioavailability of bumetanide and torasemide (loop diuretics)

A

Greater than 80%

200
Q

Half life of bumetanide

A

1-1.5 hours

201
Q

Half life of furosemide

A

1

202
Q

Half life of Torasemide

A

3-4 hours

203
Q

Causes of diuretic resistance in HF

A

Noncompliance with medical regimen
Excess Na intake
Decreased renal perfusion and glomerular filtration rate
NSAIDS
Primary Renal Pathology
Reduced/Impaired diuretic absorption to gut wall edema and reduced splanchnic blood flow

204
Q

Thiazide diuretics is used in combination with loop diuretics and has an effective refractory caused by?

A

Upregulation of Na+Cl cotransporter in the distal convoluted tubule

205
Q

Diuretics that has a greater degree of K+ wasting

A

Thiazide diuretics

206
Q

K+ sparing diuretics that is largely dispensable in the therapy of heart failure

A

Amiloride & Triamterene

207
Q

Treatment III for afterload reduction

A

Vasodilators (ISDN)

208
Q

Organic nitrate that dilate large blood vessels

A

Hydralazine (ISDN)

209
Q

direct vasodilator prevents nitrate tolerance by reducing ROS-mediated inactivation of NO

A

Hydralazine

210
Q

Fixed-combination formulation

A

37.5 mg hydralazine

20 mg ISDN

211
Q

Patients who Hydralazine and ISDN, generally also takes

A

B blocker

212
Q

Dose of hydralazine that is associated with SLE

A

> 200 mg

213
Q

Dose-limiting adverse effects of ISDN & Hydralazine

A

Hypotension

214
Q

Frequent adverse effects of hydralazine & ISDN

A

Dizziness & headaches

215
Q

Treatment principle IV: increasing cardiac contractility

A

Cardiac glycosides

216
Q

Ca2+ sensitizer used in acute heart failure that has additional selective and potent inhibitory effects on PDE III

A

Levosimendan

217
Q

MOA of calcium sensitizers

A

Increase the affinity of the myofilaments for Ca2+

218
Q

increases myofilament Ca2+ sensitivity due to increased myosin light phosphorylation

A

Agonist of Gq-coupled receptors

(a1, AT1, ET1)

219
Q

Serum digoxin concentration that should be avoided

A

> 0.8 ng/mL

220
Q

drugs that inhibit the cardiac Na+/K+ ATPase

A

Cardiac glycosides (Digoxin)

221
Q

CGs shorten action potentials by?

A

accelerating inactivation of L-type Ca channels due to higher Ca2+

222
Q

Why does CGs promote atrial fibrillation?

A

Because CGs shorten action potentials =refractory method

223
Q

Plasma concentrations of CG associated with beneficial effects

A

0.5 and 0.8 ng/mL

224
Q

Plasma concentrations of CG associated with increased mortality

A

1.2 ng/mL and greater

225
Q

Most frequent and serious adverse effects of CGs?

A

Arrhythmias

226
Q

In CG overdosing, patients exhibit

A 
Arrhythmias (90%)
GI symptoms (55%)
Neurotoxic syndromes (12%)
227
Q

Cardiac toxicity of CGs in healthy persons

A

Extreme bradycardia
Atrial Fibrillation
AV block

228
Q

In patients with structural heart disease, frequent signs of CG toxicity are

A

Ventricular extrasystoles
Bigeminy
Ventricular tachycardia
Fibrillation

229
Q

Extreme sinus bradycardia, SA block, AV block grade II or III (CG toxicity)

A

Atropine 0.5-1 mg IV

230
Q

Tachycardic ventricular arrhythmias and hypokalemia caused by CG toxicity can be treated with

A

K+ infusion (40-60 mmol/d)

231
Q

An effective antidote for digoxin toxicity

A

Antidigoxin immunotherapy

(Purified Fab fragments from ovine antidigoxin antisera- Digibind

232
Q

Partial agonists at B receptor that increase nocturnal heart rate and associated with excess mortality in patient with HF

A

Xamoterol

233
Q

Selective inhibitor of cardiac pacemaker channels (HCNs)

A

Ivabradine

234
Q

Treatment of heart failure and stable angina pectoris in patients not tolerating B blockers or in whom B blockers did not sufficiently lower heart rate (<75/min)

A

Ivabradine

235
Q

Drug treatment for decompensated heart failure

A
  1. Diuretics
  2. Vasodilators
  3. Positive inotropic agents
  4. Dobutamine
  5. Epinephrine
  6. Norepinephrine
  7. Dopamine
  8. Phosdiesterase Inhibitors
  9. Myofilament calcium sensitizers
236
Q

Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with

A

40-80 mg IV Furosemide

237
Q

Excessive doses of furosemide can cause

A

hypotension
reduction in GFR
electrolyte disturbance
neurohumoral activation

238
Q

Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure

A

Nesiritide

239
Q

Positive inotropes should be restricted to patients with

A

Low CO and perfusion of vital organs

240
Q

All inotrophic effects are

A

Increase cardiac energy expenditure
(greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death

241
Q

B adrenergic agonist for acute HF with systolic dysfunction

A

Dobutamine

242
Q

The principal hemodynamic effect of Dobutamine

A

Increased in stroke volume with small decrease in systemic vascular resistance

243
Q

2nd choice inotrope in acutely decompensated HF

A

Epinephrine

244
Q

Drug treatment for decompensated heart failure

A
  1. Diuretics
  2. Vasodilators
  3. Positive inotropic agents
  4. Dobutamine
  5. Epinephrine
  6. Norepinephrine
  7. Dopamine
  8. Phosdiesterase Inhibitors
  9. Myofilament calcium sensitizers
245
Q

Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with

A

40-80 mg IV Furosemide

246
Q

Excessive doses of furosemide can cause

A

hypotension
reduction in GFR
electrolyte disturbance
neurohumoral activation

247
Q

Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure

A

Nesiritide

248
Q

Positive inotropes should be restricted to patients with

A

Low CO and perfusion of vital organs

249
Q

All inotrophic effects are

A

Increase cardiac energy expenditure
(greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death

250
Q

B adrenergic agonist for acute HF with systolic dysfunction

A

Dobutamine

251
Q

The principal hemodynamic effect of Dobutamine

A

Increased in stroke volume with small decrease in systemic vascular resistance

252
Q

2nd choice inotrope in acutely decompensated HF

A

Epinephrine

253
Q

Drug treatment for decompensated heart failure

A
  1. Diuretics
  2. Vasodilators
  3. Positive inotropic agents
  4. Dobutamine
  5. Epinephrine
  6. Norepinephrine
  7. Dopamine
  8. Phosdiesterase Inhibitors
  9. Myofilament calcium sensitizers
254
Q

Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with

A

40-80 mg IV Furosemide

255
Q

Excessive doses of furosemide can cause

A

hypotension
reduction in GFR
electrolyte disturbance
neurohumoral activation

256
Q

Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure

A

Nesiritide

257
Q

Positive inotropes should be restricted to patients with

A

Low CO and perfusion of vital organs

258
Q

All inotrophic effects are

A

Increase cardiac energy expenditure
(greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death

259
Q

B adrenergic agonist for acute HF with systolic dysfunction

A

Dobutamine

260
Q

The principal hemodynamic effect of Dobutamine

A

Increased in stroke volume with small decrease in systemic vascular resistance

261
Q

2nd choice inotrope in acutely decompensated HF

A

Epinephrine

Pharmacology (4 decks)

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