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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
Drugs used for symptomatic treatment of milder forms of HF
Thiazide diuretics
26
Used in treatment of EDEMA associated with congestive heart failure, liver cirrhosis, CKD, nephrotic syndrome
Thiazide diuretics | Loop diureticsp
27
These drugs loose their efficacy at GFR <30-40 mL/min
Thiazide diuretics
28
Drugs that potentiate the effects of loop diuretics in severe HF
Thiazide diuretics
29
These drugs have high risk for HYPOKALEMIA & ARRHYTHMIA when combined with QT prolonging drugs
Thiazide diuretics | Loop diuretics
30
Thiazide type diuretics
Chlorothiazide | Hydrochlorothiazide
31
Thiazide like diuretics
Chlorthalidone Indapamide Metolazone
32
Used in symptomatic treatment of severe HF and acute decompensation
Loop diuretics
33
Loop diuretics drugs for HF
Bumetanide Furosemide Torasemide
34
Loop diuretics superior to furosemide in HF
Torasemide
35
Used in HF of Africans & Americans
ISDN/Hydralazine
36
``` This drug when used with B blockers will have adverse effects like headache nausea flushing hypotension palpitations tachycardia dizziness angina pectoris ```
ISDN/Hydralazine
37
Can cause lupus syndrome
ISDN/Hydralazine
38
Positive inotropes will low therapeutic index
Digoxin | Digotoxin
39
Exerts benefits in HF & Atrial fibrillation
``` Positive inotropes (Digoxin & Digotoxin) ```
40
Half life of digoxin
1.5 days
41
Half-life of digotoxin
7 days
42
Plasma concentration of digoxin
0.5-0.8 ng/mL
43
Plasma concentration of digotoxin
10-25 ng/mL
44
Drug used for HR reduction
Ivabradine
45
Exert effects in patients not tolerating B blockers or having HR >75 under B blockers
Ivabradine
46
Unwanted effects: bradycardia, QT prolongation, atrial fibrillation & phosphenes
Ivabradine
47
Drugs for acutely decompensated HF
Intravenous vasodilators | Intravenous positive inotropes
48
Intravenous vasodilator drugs
Nitroglycerin (sodium nitroprusside) | Nesiritide
49
Intravenous positive inotropes drugs
Dobutamine Dopamine Epinephrine Norepinephrine Enoximone Milrinone Levosimendan
50
Increase CO in acute congestion by increasing filling pressure and dilation
Nitroglycerin (Sodium nitroprusside)
51
How does nitroglycerin (Na nitroprusside) and neseritide increase CO in acute congestion?
By decreasing preload and afterload
52
NO releaser, stimulates soluble guanylyl cyclase
Nitroglycerin (Na nitroprusside)
53
This drug is avoided if systolic blood pressure is <110 mmHg
Nitroglycerin (Na nitroprusside)
54
Last option in patients with systolic BP <85 mmHg
Positive Inotropes Dobutamine Dopamine Epinephrine Norepinephrine
55
Increases cardiac energy consumption and risk of arrhythmia
Positive inotropes Dobutamine Dopamine Epinephrine Norepinephrine
56
Positive inotropes that causes less tachycardia than epinephrine
Dobutamine
57
Recombinant human BNP
Neseritide
58
Stimulates membrane bound guanylyl cyclase
Neseritide
59
Positive inotropes that causes less afterload increase thab norepinephrine
Dobutamine
60
PDE3/4 inhibitors and increases cellular cAMP
Enoximone | Milrinone
61
Increase CO and dilate blood vessels (inodilator)
Enoximone | Milrinone
62
Can be used in patients on B blockers and with high peripheral and pulmonary arterial resistance
Enoximone | Milrinone
63
Dose limiting of Enoximone & Milrinone
Blood pressure decrease
64
Increase CO and decrease vascular resistance (inodilator)
Levosimendan
65
Combined Ca2+ sensitizer (troponin C binding) and PDE3 inhibitor
Levosimendan
66
HF symptoms like fatigue, dizziness, muscle weakness and shortness of breath are caused by?
Low output (forward failure)
67
HF signs like congestion of the organs upstream of heart is caused by?
Increased filling pressure (backward failure)
68
Most common reason for systolic heart failure.
Ischemic Heart Disease
69
Ischemic heart diseases causes
1. Acute myocardial infarction 2. Chronic loss of viable heart muscle mass 3. Valvular disease 4. Viral infections
70
Other factors that causes ischemic heart disease
1. Excessive Alcohol 2. Cocaine 3. Amphetamines 4. Doxorubicin (cancer drugs) 5. Trastuzumab (cancer drugs)
71
The pathophysiology of heart failure involves
Heart Vasculature Kidney Neurohumoral regulatory circuits
72
The overload of myocardium means that
There is primary contractile defect of the myocardium caused by atrophy of the heart
73
The response of the heart to the overload is?
Hypertrophy (growing in size and assembling more sarcomeres that can increase contractile force)
74
Direct consequence of cardiac myocyte hypertrophy
Reduced capillary/myocyte ratio (less O2 and nutrient supply per myocyte)
75
Reduced capillary/myocyte ratio will lead to?
Energy deficit and metabolic reprogramming
76
1st step in Pathologic remodelling
Gene expression for ion channels, Ca2+ regulating proteins and contractile proteins will be energy-saving adaptations and can aggravate contractile failure and favors arrhythmias
77
2nd step in cardiac remodelling
Fibroblast proliferate and deposit increased amounts of EC matrix > fibrosis> arrhythmias> overload> cardiac myocyte death
78
Critical parameter of cardiac function
Stiffness of the vasculature
79
Stiffness of vasculature determines?
The resistance against which the heart has to expel the blood and increases with aging
80
Major reasons for premature stiffening of blood vessels which increases afterload
Arterial hypertension | Diabetes mellitus
81
In HF, endothelial dysfunction is?
Disturbed balance between vasodilating NO and proconstrictor ROS
82
ROS inactivates 2 critical enzymes
eNOS and sGC and converts NO in peroxynitrite, a strong ROS, favor vasoconstriction
83
Cardiovascular drugs that improve endothelial function
ACEi ARBs MRAs Statins
84
Inhibits cGMP degradation in smooth muscle cells and thereby promotes relaxation
PDE5 inhibitors
85
How does Ang II regulates filtration rate in the kidney?
Regulate the diameter of efferent glomerular arteriole
86
How does regulation of kidney perfusion is achieved?
Balance between Ang II @ AT1 receptors (constrictor) Vasopressin @ V1 receptors ( constrictor Prostaglandins (vasodilator)
87
How does kidney regulates Na and water excretion?
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
88
Immediate response of the body during decrease CO
Activation of SNS and RAAS system | To ensure perfusion to brain & heart
89
Deleterious effects of chronic activation of neurohumoral system?
Ang II, NE & ET (endothelin) accelerate pathological cardiac remodeling (hypertrophy, fibrosis and cell death) Aldosterone has profibrotic actions
90
Neurohumoral effects that increases afterload
Prolonged vasoconstriction via Ang II
91
Neurohumoral response that increases cardiac preload, dilation, and ventricular wall stress
Decreased kidney perfusion | Increased aldosterone production
92
Major determinant of cardiac O2 consumption
Cardiac preload Dilation Ventricular wall stress
93
What do you mean by INOTROPHIC EFFECTS?
Chang the force of the heart’s contraction
94
What do you mean by CHRONOTROPHIC EFFECTS?
Those drugs that causes Increase HR
95
In a failing, energy depleted heart, what is the effect of tachycardia and positive inotrophic drugs?
Aside from increasing CO which the first effect. | During prolonged stimulation, it will promote arrhythmias and increase O2 consumption
96
Drug that reduce deleterious effects of Ang II by blocking AT1 receptors
Valsartan
97
Drug that inhibits degradation of ANP & BNP
Sacubitril
98
Combination drug that appears superior to ACEi Enalapril in reducing the rates of hospitalization in patients with HReRF
Valsartan-sacubitril
99
BNP and ANP are normally in the atria and ventricles, when does these peptides be released into the bloodstream?
During INCREASED PRELOAD (stretch)
100
Heart failure in reduced ejection fraction (EF: < 30%)
Systolic heart failure
101
Patients with preserved ejection fraction have?
HF symptoms but normal or >50% or only mildly reduced EF.
102
HF that are associated with arterial hypertension, ischemic heart disease, DM and obesity
HFpEF
103
Sign of chronically elevated end-diastolic pressures (HFpEF)
Not dilated Enlarged wall thickness (hypertrophy) Enlarged left atria
104
Molecular alterations in HFpEF
Increased myocardial fibrosis | Reduced phosphorylation of titin
105
Sarcomeric protein that spans Z to M band that had spring domains whose elastic modulus determines the passive tension of cardiomyocytes
Titin
106
Titin stiffness is determined by?
Its isoform | cGMP-dependent phosphorylation
107
Only intervention that increases maximal physical activity in HFpEF patients
Exercise training
108
According to NYHA, what class of HF where there is a left ventricular dysfunction but no symptoms?
Class I
109
According to NYHA, what class of HF, where symptoms are at low medium-to-high levels of physical exercise?
Class II
110
According to NYHA, what class of HF where symptoms are at low levels of physical exercise.
Class III
111
According to NYHA, what class of HF where symptoms are presence even at test or daily life physical activities like brushing teeth?
Class IV
112
According to recent guidelines of AHA and ACC, what is the stage of heart failure, where there are presence of risk factors?
Stage A
113
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?
Stage B
114
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?
Stage C
115
According to recent guidelines of AHA and ACC, what is the stage of heart failure, where refractory heart failure is present?
Stage D
116
Therapy goals for Stage A HF
Heart-healthy lifestyle Prevent vascular coronary disease Prevent LV structural abnormalities
117
Therapy goals for Stage B HF
Prevent HF symptoms | Prevent further cardiac remodelling
118
Therapy goals for Stage C HF
Control symptoms Prevent hospitalization Prevent mortality
119
Therapy goals for Stage D HF
Control symptoms Improve HRQOL Reduce hospital readmissions Establish end-of-life goals
120
Drugs used for Stage A HF
ACEi ARBs Statins
121
Drugs used for Stage B HF
``` ACEi ARB ICD (implantable cardioverter-defibrillator Revascularization Valvular surgery ```
122
Drugs used for Stage C HF with preserved EF
Diuretics | Treat comorbidites like hypertension, AF, CAD, DM
123
Drugs for ROUTINE use in patients with for Stage C HF with reduced EF
``` Diuretics ACEi or ARB ARNI B Blocker Aldosterone antagonist Ivabradine ```
124
Drug used in selected patients with reduced EF
Hydralazine/ISDN ACEi and ARB Cardiac glycoside In selected patients: CRT ICD Revascularization or valvular surgery
125
Drugs used for Stage D HF
``` Heart transplant Chronic inotropes Surgery Pallative care and hospiece ICD deactivation ```
126
Hydralazine, a vasodilator is mostly combined with?
Sympatholytic agents and diuretics
127
Hydralazine directly relaxes what smooth muscle?
Arteriolar smooth muscle
128
Main MOA of hydralazine
Reduced intracellular Ca2+ concentration
129
How does hydralazine reduced Ca2+ concentrations?
Inhibits inositol triphosphate-induced released of Ca2+ from intracellular storage sites Open Ca2+ activated K+ channels in SMC
130
Drug that is sensitive to NSAIDs, because it activates arachidonic acid, COX and prostacyclin pathway.
Hydralazine
131
This drug is combined in the pill containing isosorbide dinitrate (BiDil) in the HF treatment
Hydralazine
132
In congestive HF, hydralazine is combined with ______ for patients that cannot tolerate ACEi and AT1 Blockers
Nitrates
133
Hydralazine should be used in CAUTION in elderly patients and hypertensive with CAD because it can cause
Myocardial ischemia due to reflex tachycardia (increased O2 demand)
134
Maximum recommended dose of hydralazine to minimize the risk of drug-induced lupus syndrome.
200 mg/d
135
A vasodilator that has a hypotensive effect and can cause reflex tachycardia due to stimulation of baroreceptor reflex.
Hydralazine
136
Class of drugs that are beneficial in HF because they reduce afterload so that heart can expel blood against lower resistance.
Vasodilators
137
Orally available organic nitrate
ISDN (Isosorbide 2,5’-dinitrate)
138
Main effect of the vasodilator ISDN
Venous pooling | Reduction of diastolic filling pressure (preload) with little effect on systemic vascular resistance
139
Vasodilator that prevents nitrate tolerance by reducing ROS-mediated inactivation of NO
Hydralazine | Should be combined with ISDN
140
Dose combination of hydralazine & ISDN
37.5 mg hydralazine and 20 mg ISDN | Uptitrated to a target dose of 2 tablets, thrice daily
141
Vasodilators that reduce preload and afterload
Nitroglycerin and Nitroprusside
142
Nitroglycerin & Nitroprusside reduce preload by?
Reducing wall stress and O2 consumption
143
Vasodilators nitroglycerin and nitroprusside are avoided in patients with systolic BP ______
<110 mmHg
144
Organic nitrate with low molecular mass and are volatile, oily liquids and is explosive
GTN (glycerin trinitrate) or nitroglycerin
145
Second choice in ALL stages of Heart failure (if patients cannot tolerate AcEI)
ARBs
146
Peak plasma levels of Candesartan
3-4 hours after oral administration
147
Plasma half-life of Candesartan
9 hrs
148
Plasma clearance of Candesartan
``` Renal elimination (33%) Biliary excretion ( ```
149
Physiological effects of ACEi
1. Vasodilation 2. Reduce aldosterone levels 3. Direct antiremodelling effects of the heart 4. Produce sympatholytic effects
150
Why does ACEIs are contraindicated in bilateral renal stenosis?
Because when renal perfusion is compromised, inhibition of RAAS by ACEIs will cause sudden and marked decrease in GFR
151
Heart failure patients have low renal perfusion, and aggressive treatment of this drug will induce renal heart failure.
ACEIs
152
What are being monitored in patients on ACEIs?
Blood pressure Blood creatinine K+ levels
153
Long term effects of ACEIs
Chronic lowering of glomerular pressures protects glomerulus from FIBROTIC REGENERATION
154
What is the effect of reduce aldosterone levels by ACEIs?
It will reduced expression of ENaC in the distal tubule (Thus less absorption of Na and less excretion of K+)> HYPERKALEMIA
155
Why does ACEIs friendly with HF patients?
Because HF patients are hypokalemic and ACEIs favors hyperkalemia by reducing K+ excretion
156
Drugs that reduced the production of prostaglandins, antagonized the effects of ACEIs and should be avoided in patients with HF
NSAIDS
157
Increases bradykinin and substance P levels
ACEIs
158
ARBs shows competitive antagonism to ________ receptors
AT1 receptors
159
Positive clinotrophy means
Quicken the rate of force development
160
Positive lusitropic effect means
Accelerate cardiac muscle relaxation
161
Poisitive dromotrophic effect means
accelerate atrial-ventricular conduction rate
162
Positive bathmotropic effect
Enhance cardiac myocyte automaticity and lower threshold for arrhythmias
163
Acute effects of B adrenergic antagonist are mediated by _______ receptors
B1 receptors (smaller extent B2 receptor)
164
Reduce B receptor-mediated actions of catecholamines (NE & EPI)
B blockers
165
Drugs given under stable condition and at very low doses
B blockers
166
Dose escalation time of B blockers must be
Doubling every 4 weeks
167
What is the importance of start low, and go slow B blocker therapy?
Heart had time to adapt to decreasing stimulation by catecholamines and find new equilibrium at a lower adrenergic drive
168
Effects of competitive antagonism of B blockers
B blockers do not fully block the receptors, instead they shift the concentration response curve of the catecholamines to the right
169
Protects the heart from the adverse long term consequences of adrenergic overstimulation
B blockers
170
Improve perfusion of the myocardium by prolonging diastole, thereby reducing ischemia
B blockers
171
Non-selective B blocker and an a1 Receptor antagonist
Carvedilol
172
Plasma half-life of metoprolol
3-5 hrs
173
Disadvantage of metoprolol
Dependency on polymorphic CYP2D6 for its metabolism
174
Long plasma half-life of bisoprolol
10-12 hrs (daily dosing)
175
Plasma half-life of carvedilol
6-12 hrs (requires twice-daily dosing)
176
Plasma half-life of Nebivolol
10 hrs
177
B blockers for HF that is not metabolized by CYP2D6
Bisoprolol
178
Patients that must be treated with B blockers
With symptomatic HF (Stage C, class II-IV) With ventricular dysfunction (Stage B, Class I)
179
The improvement of left ventricular dysfunction under the treatment of B blockers is ______ months
3-6 months
180
Should not be administered in new-onset of acutely decompensated heart failure
B blockers
181
If patients are hospitalized with acute decompensation under current therapy with B blockers, what will should be done?
Doses with B blockers should be reduced or drug must be discontinued
182
If doses of B blockers are increases rapidly, what are the circumstances that doses must be reduced?
When there is a fall in blood pressure, fluid retention and dizziness
183
Major cardiovascular responses to B blockers
Lowers HR Bronchiconstriction AV Block Peripheral vasoconstriction
184
Drugs that has life-prolonging effects in patients with HF
Mineralocorticoid receptor antagonists (MRAs)
185
Most appropriate drug symptomatic Stage C HFrEF patients
MRAs
186
Effects of aldosterone that has adverse effects in HF setting
``` Na and fluid retention Sympathetic activation Parasympathetic inhibition Myocardial and vascular fibrosis Baroreceptor dysfunction Vascular damage ```
187
Inhibits all effects of aldosterone
MRAs
188
Most important adverse effects of MRAs
Hyperkalemia
189
MRA that is selective for the mineralocorticoid receptor and does not cause gynecomastia
Eplerenone
190
Guidelines for the use of MRAs
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
A peptidase mediating the enzymatic degradation and inactivation of natriuretic peptides (ANP, BNP, CNP), bradykinin and substance P
Neprilysin
192
Prodrug that after deesterization, inhibits neprilysin
Valsartan/Sacubatril
193
Beneficial effects of ARNI (Valsartan/Sacubitril (promotion)
Natriuresis Diuresis Vasodilation of arteries and veins
194
Beneficial effects of ARNI (Valsartan/Sacubitril (inhibition)
``` Inhibits: Thrombosis Fibrosis Cardiac myocyte hypertrophy Renin release ```
195
Treatment II for preload reduction
Loop Diuretics Thiazide Diuretics K+ sparing Diuretics
196
Oral bioavailability of furosemide
40%-70%
197
Loop diuretics required for initiation of diuresis in patients with worsening symptoms
Furosemide
198
Loop diuretics for patients with impaired GI absorption, hypervolemic patients witn CHF-induced GI edema
Furosemide
199
Oral bioavailability of bumetanide and torasemide (loop diuretics)
Greater than 80%
200
Half life of bumetanide
1-1.5 hours
201
Half life of furosemide
1
202
Half life of Torasemide
3-4 hours
203
Causes of diuretic resistance in HF
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
Thiazide diuretics is used in combination with loop diuretics and has an effective refractory caused by?
Upregulation of Na+Cl cotransporter in the distal convoluted tubule
205
Diuretics that has a greater degree of K+ wasting
Thiazide diuretics
206
K+ sparing diuretics that is largely dispensable in the therapy of heart failure
Amiloride & Triamterene
207
Treatment III for afterload reduction
Vasodilators (ISDN)
208
Organic nitrate that dilate large blood vessels
Hydralazine (ISDN)
209
direct vasodilator prevents nitrate tolerance by reducing ROS-mediated inactivation of NO
Hydralazine
210
Fixed-combination formulation
37.5 mg hydralazine | 20 mg ISDN
211
Patients who Hydralazine and ISDN, generally also takes
B blocker
212
Dose of hydralazine that is associated with SLE
>200 mg
213
Dose-limiting adverse effects of ISDN & Hydralazine
Hypotension
214
Frequent adverse effects of hydralazine & ISDN
Dizziness & headaches
215
Treatment principle IV: increasing cardiac contractility
Cardiac glycosides
216
Ca2+ sensitizer used in acute heart failure that has additional selective and potent inhibitory effects on PDE III
Levosimendan
217
MOA of calcium sensitizers
Increase the affinity of the myofilaments for Ca2+
218
increases myofilament Ca2+ sensitivity due to increased myosin light phosphorylation
Agonist of Gq-coupled receptors | (a1, AT1, ET1)
219
Serum digoxin concentration that should be avoided
> 0.8 ng/mL
220
drugs that inhibit the cardiac Na+/K+ ATPase
Cardiac glycosides (Digoxin)
221
CGs shorten action potentials by?
accelerating inactivation of L-type Ca channels due to higher Ca2+
222
Why does CGs promote atrial fibrillation?
Because CGs shorten action potentials =refractory method
223
Plasma concentrations of CG associated with beneficial effects
0.5 and 0.8 ng/mL
224
Plasma concentrations of CG associated with increased mortality
1.2 ng/mL and greater
225
Most frequent and serious adverse effects of CGs?
Arrhythmias
226
In CG overdosing, patients exhibit
``` Arrhythmias (90%) GI symptoms (55%) Neurotoxic syndromes (12%) ```
227
Cardiac toxicity of CGs in healthy persons
Extreme bradycardia Atrial Fibrillation AV block
228
In patients with structural heart disease, frequent signs of CG toxicity are
Ventricular extrasystoles Bigeminy Ventricular tachycardia Fibrillation
229
Extreme sinus bradycardia, SA block, AV block grade II or III (CG toxicity)
Atropine 0.5-1 mg IV
230
Tachycardic ventricular arrhythmias and hypokalemia caused by CG toxicity can be treated with
K+ infusion (40-60 mmol/d)
231
An effective antidote for digoxin toxicity
Antidigoxin immunotherapy (Purified Fab fragments from ovine antidigoxin antisera- Digibind
232
Partial agonists at B receptor that increase nocturnal heart rate and associated with excess mortality in patient with HF
Xamoterol
233
Selective inhibitor of cardiac pacemaker channels (HCNs)
Ivabradine
234
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)
Ivabradine
235
Drug treatment for decompensated heart failure
1. Diuretics 2. Vasodilators 3. Positive inotropic agents 4. Dobutamine 5. Epinephrine 6. Norepinephrine 7. Dopamine 8. Phosdiesterase Inhibitors 9. Myofilament calcium sensitizers
236
Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with
40-80 mg IV Furosemide
237
Excessive doses of furosemide can cause
hypotension reduction in GFR electrolyte disturbance neurohumoral activation
238
Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure
Nesiritide
239
Positive inotropes should be restricted to patients with
Low CO and perfusion of vital organs
240
All inotrophic effects are
Increase cardiac energy expenditure (greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death
241
B adrenergic agonist for acute HF with systolic dysfunction
Dobutamine
242
The principal hemodynamic effect of Dobutamine
Increased in stroke volume with small decrease in systemic vascular resistance
243
2nd choice inotrope in acutely decompensated HF
Epinephrine
244
Drug treatment for decompensated heart failure
1. Diuretics 2. Vasodilators 3. Positive inotropic agents 4. Dobutamine 5. Epinephrine 6. Norepinephrine 7. Dopamine 8. Phosdiesterase Inhibitors 9. Myofilament calcium sensitizers
245
Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with
40-80 mg IV Furosemide
246
Excessive doses of furosemide can cause
hypotension reduction in GFR electrolyte disturbance neurohumoral activation
247
Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure
Nesiritide
248
Positive inotropes should be restricted to patients with
Low CO and perfusion of vital organs
249
All inotrophic effects are
Increase cardiac energy expenditure (greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death
250
B adrenergic agonist for acute HF with systolic dysfunction
Dobutamine
251
The principal hemodynamic effect of Dobutamine
Increased in stroke volume with small decrease in systemic vascular resistance
252
2nd choice inotrope in acutely decompensated HF
Epinephrine
253
Drug treatment for decompensated heart failure
1. Diuretics 2. Vasodilators 3. Positive inotropic agents 4. Dobutamine 5. Epinephrine 6. Norepinephrine 7. Dopamine 8. Phosdiesterase Inhibitors 9. Myofilament calcium sensitizers
254
Patients with acute decompensated HF wit dyspnea, signs with fluid overload/congestion will be treated with
40-80 mg IV Furosemide
255
Excessive doses of furosemide can cause
hypotension reduction in GFR electrolyte disturbance neurohumoral activation
256
Vasodilator that decreases preload and afterload and reduces pulmonary capillary wedge pressure
Nesiritide
257
Positive inotropes should be restricted to patients with
Low CO and perfusion of vital organs
258
All inotrophic effects are
Increase cardiac energy expenditure (greater and faster force development ➡️ more ATP consumption ➡️ greater O2 demand ➡️ risk of diffuse cardiac myocyte death
259
B adrenergic agonist for acute HF with systolic dysfunction
Dobutamine
260
The principal hemodynamic effect of Dobutamine
Increased in stroke volume with small decrease in systemic vascular resistance
261
2nd choice inotrope in acutely decompensated HF
Epinephrine

Pharmacology (4 decks)

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