Lesson 4 Flashcards
1
Q
have a resting membrane potential of - 90 mV
A
fast response fibers
2
Q
impulse conduction of slow response fibers
A
0.1 - 1 m per sec
3
Q
impulse conduction of fast response fibers
A
0.3 - 3 m per sec
4
Q
resting membrane potential of slow response fibers
A
negative 60 mV
5
Q
produce rapid upstroke (phase 0) of action potential when depolarized
A
fast response fibers
6
Q
produce slower upstroke of action potential
A
slow response fibers
7
Q
The more negative the RMP, results to?
A
greater the rise of phase 0 and faster is the rate of impulse
8
Q
sequence of voltage changes occurring as a result of changes in ionic conductances across cell membrane
A
action potential
9
Q
fast channels are activated in what mV
A
negative 70 to negative 50 mV
10
Q
fast channels during phase 0 or depolarization is inactivated for how many milliseconds
A
0.5 milliseconds
11
Q
reactivation of voltage-dependent sodium channels occur in what phase
A
phase 3
12
Q
slow component of depolarization is mediated by inward movement of
A
calcium
13
Q
phase caused by calcium influx and partially potassium efflux
A
limited repolarization or phase 1
14
Q
plateau is caused by the inward movement of this important ion
A
calcium
15
Q
it is due to algebraic sum of the inward calcium and outward potassium current
A
phase 2 or plateau
16
Q
due to time dependent outward current of potassium and sodium channels are reactivated
A
phase 3 or repolarization
17
Q
the restored intracellular potassium concentration caused by sodium potassium ATPase pump
A
phase 4 or diastole
18
Q
frequency of discharge of action potential is determined by
A
- distance between the maximal diastolic potential and threshold potential; 2. slope of diastolic depolarization
19
Q
inability of an excitable tissue to respond to elicit action potential
A
refractory period
20
Q
absolute refractory period mV
A
0 to -60 mV
21
Q
relative refractory period mV
A
negative 60 to negative 90 mV
22
Q
refractory period which refers to a minimal interval between two propagating impulses
A
effective refractory period
23
Q
refractory period in which premature stimuli will elicit action potentials with slow response characteristics
A
relative refractory period
24
Q
a refractory period wherein premature stimuli will not elicit action potential
A
absolute refractory period
25
drugs used for treatment of CHF
cardiac glycoside or digitalis glycosides
26
active glycosides of digitalis purpuria
Digitoxin, gitoxin, and gitalin
27
active glycosides of lanata
Digitoxin, digoxin, and gitoxin
28
active glycosides of strophantus kombe
strophantin
29
active glycosides of gratis
ouabain
30
contain cardioactive poisons similar to cardiac glycosides
skin glands of toads
31
a positive inotropic effect of glycosides
direct action
32
direct action is not dependent upon adrenergic stimulation but rather of
consequence of inhibition of the sodium pump
33
increased inward calcium current occurs at this phase of myocardial action potential
phase 2 or plateau
34
made through the parasympathetic autonomic nervous system that influence EXCITABILITY and AUTOMATICITY of cardiac tissues
indirect action
35
magnitude of an electric impulse required in producing an action potential
excitability
36
reduced RMP results to?
decreased amplitude of action potential or rate of rise of action potential, and reduced conduction velocity
37
behavior by which cardiac tissues spontaneously generate action potential
automaticity
38
the EXTRACELLULAR concentration of this ion influences the action of cardiac glycosides on automaticity
potassium
39
low concentration of potassium influence glycosides to?
enhance automaticity
40
cause the appearance of after-depolarization, or depolarization appearing immediately following repolarization
administration of glycosides with normal or high potassium concentration
41
appears as subthreshold depolarization early during phase 4
after-depolarization
42
the beat outside of normal cardiac rhythm
ectopic beat
43
Give one cause of ectopic beat
after-depolarization
44
normal or high concentration of potassium effect on automaticity of the heart
leads to after-depolarization
45
clinically important effects of a digitalis glycoside on the rate of formation of impulses by the SA and AV nodes are due to its
indirect VAGAL action
46
common effect of digitalis glycosides on the electrical activity of the SA and AV nodes
increase in the REFRACTORY period; decrease in the CONDUCTION velocity
47
digitalis glycosidesalso influence on atria and ventricles also leads to
decreased contractility
48
overshadows the indirect negative inotropic effects on atria and the ventricles
direct positive inotopic effect
49
commonly used as indicator of adequate blood levels o digitalis in patients
gut disturbances
50
glycosides effect on kidney when edema is present
diuresis, due to failing heart and not direct action to kidney
51
these glycosides are commonly administered orally in clinical setting
digoxin an digitoxin
52
on set of action of ouabain and peak action
3-10 mins and 0.5-2 hours, respectively
53
(blank) is more readily absorbed from the gut than (blank)
digitoxin, digoxin
54
onset of action and peak action of digoxin tablets
15-30 mins an 6-8 hrs, respectively
55
peak action of alcohol or elixir digoxin
1-2 hours
56
digitoxin is bound to plasma protein to about 5 times greater than digoxin in these species
dogs
57
human elimination of digoxin is through
direct renal excretion
58
human elimination of digitoxin
hepatic metabolism
59
in dogs, digitoxin are eliminated through
renal excretion and hepatic metabolism
60
an important part of therapy of CHF or DILATED CARDIOMYOPATHY (DCM)
cardiac glycoside or digitalis glycosides
61
Why are glycosides a drug of choice for cardiac arrhythmias
because it BLOCKS OR REDUCES IMPULSES conducted in AV node, causing less number of impulses reaching the ventricles than are produced in atria
62
Digitalis is beneficial in the treatment of ventricular associated with congestive heart failure by improving?
coronary artery perfusion and oxygenation
63
dose for digitalization is about (blank) of the lethal dose
40 percent
64
most severe toxic effect of glycosides
cardiac arrhythmias, especially fibrillation
65
a common side effect of digitalis
hypokalemia
66
Digitalization is usually accomplished in
7-14 days
67
dose of digitalis glycosides may be based on
body surface area in meters
68
loading dose of digoxin for dogs
0.66 mg per meter
69
maintenance dose of digoxin in dogs
0.22 mg
70
first ACE inhibitor to be developed
captopril
71
most commonly ACE inhibitor usesd in animals
enalapril
72
ACE which are not prodrugs and are therefore directly acting
captopril and lisinopril
73
ACE inhibitor now available
lisinopril, ramipril, perindropril, trandolapril
74
prodrug that is converted which competes with Angiotensin I for ACE
enalapril
75
onset of action of enalapril as well as duration time
4-6 hours (onset), 12-14 hrs (duration)
76
enalapril is used for treatment of HEART FAILURE and HYPERTENSION in
dogs, not to be given to cats
77
deviation from the normal heart rate and rhythm
arrhythmia
78
general classification of arrhythmias
supraventricular, ventricular
79
listening to body sounds with stethoscope
auscultation
80
most specific way to diagnose cardiac arrhythmias
electrocardiography
81
in screening for arrhythmia, a jugular pulse indicates
abnormality
82
a heart beat should have this pulse
femoral
83
feature common to all cardiac conduction and related to the slow inward movement of calcium ions
automaticity
84
characterized by enhanced responsiveness to catecholamines, which then increase calcium conductance during diastole
enhancd normal automaticity
85
altered automaticity wherein after-depolarization reaching threshold potential which result in repetitive firing of the cell
triggered activity
86
an altered automaticity wherein vagal activity increase potassium conductance which repolarizes the cell
sick-sinus syndrome
87
progression movement of an action potential from on area of myocardium to another
conduction
88
Class of membrane stabilization drugs
Class I
89
give the subclass IA drugs which reduces the inward current of sodium
quinidine, procainamide, disopyramide
90
give the members of subclass IB which increase the outward current of potassium
lidocaine, phenytoin, tocainide, mexiletin, aprindin
91
antiarrhythmic effect of this group results from a selection beta adrenergic blocking action
Class II
92
give examples of class which can decrease velocity, block automaticity, increase effectivity refractory period
propranolol, timolol, alprenolol, pindolol, metotrolol
93
Membrane of this class have action and effects as those in subclasses IA and IB but with very little effect on refractoriness and on action potential duration
Subclass 1C
94
Their major effect is to lengthen action potential duration and refractory period primarily in the Purkinje fibers and ventricular myocardium
Class III
95
Give examples of Class III
bretylium, amiodarone, sotalol
96
give examples of Subclass 1C
encainide, lorcainide, flecainide, propafenone
97
Class of antiarryhthmitic drugs which block the calcium entry
Class IV
98
members of Class IV
verapamil, nifedipine, diltiazem
99
it has little antiarrhythmic affect and is also used as antifungal agent in humans
diltiazem
100
A dextro-stereoisomer o quinine, an antimalarial drug
quinidine sulfate
101
half life of quindine in dogs
6 hours
102
half life of quindine in cats
19 hrs
103
half life of quindine in pony
4 hrs
104
quinidine is rapidly absorbed in how many minutes
60 to 90 mins
105
Clinical use of quinidine sulfate
atrial fibrillation in dogs and horses, and ventricular premature beats
106
has direct action similar to quindine but controlling ventricular arrhythmias
procainamide
107
clinically used for ventricular ectopic beats or ventricular tachyarrhythmias
procainamide
108
drug of choice for digitalis-induced ventricular arrhythmias
phenytoin (diphenyldantoin)
109
clinical uses of propanolol
1. for severe atrial fibrillation unresponsive to digitalis
2. sinus tachycardia associated with anesthesia
3. ventricular arrhythmias
4. hypertrophic cardiomyopathy
110
has direct antiarrhythmic action due to adrenergic blocking effect (decreased spontaneous firing in SA node)
A. Phenytoin
B. Propranolol
C. Lidocaine
D. both a and c
E. Quindine sulfate
B. Propranolol
111
What are the antiarrhythmic drugs proven useful in veterinary medicine?
1. QUINDINE SULFATE
2. PROCAINAMIDE
3. LIDOCAINE (without epinephrine)
4. PHENYTOIN (Diphenyldantoin)
5. PROPRANOLOL
112
An anti-arrhythmic drug dangerous to use in heart congested heart failure
A. Quindine sulfate
B. Phenytoin
C. Procainamide
D. Propranolol
D. Propranolol
113
an anti-arrhythmic drug not effective for controlling supraventricular arrhythmias
A. Lidocaine
B. Phenytoin
C. Procainamide
D. Propranolol
A. Lidocaine
114
Subclass 1A members
* Quinidine
* Procainamide
* Disopyramide
115
Subclass 1B members
* Lidocaine
* Phenytoin
* Tocainide
* Mexiletin
* Aprindin
116
3 Supraventricular (atrial, AV nodal) arrhythmias
* Paroxysmal atrial tachycardia
* Atrial flutter
* Atrial fibrillation
117
3 ventricular arrhythmias
* Premature ventricular contraction
* Ventricular tachycardia
* Ventricular fibrillation
118
Adverse reactions to enalapril include
* GI distress (anorexia, vomiting, and diarrhea)
* Lethargy
* Hypotension
* Anemia
* Angioedema, and
* Vasculitis
119
mechanism of the indirect vagal action of digitalis
1. Direct stimulation of the centers in the brain
2. Sensitization of the carotid sinus baroreceptors to changes in blood pressure
3. Enhancement at the myocardial level of the response to acetylcholine
120
Which ion is primarily responsible for repolarization of myocardial cells?
Potassium ions (K⁺)
121
What can cause a shift from fast-response to slow-response behavior in myocardial fibers?
A) Increased oxygen supply
B) Hyperkalemia
C) Hypocalcemia
D) Hypoxia
Hypoxia
122
What is the primary mechanism by which sodium ions enter myocardial cells during depolarization?
A) Diffusion through leak channels
B) Active transport by sodium-potassium pump
C) Opening of voltage-gated sodium channels
D) Binding to potassium ions
Opening of voltage-gated sodium channels
123
How do fast-response fibers differ from slow-response fibers in myocardial cells?
A) Fast-response fibers have higher resting membrane potentials
B) Slow-response fibers have faster action potential durations
C) Fast-response fibers respond more quickly to depolarization
D) Slow-response fibers have greater sodium permeability
Fast-response fibers respond more quickly to depolarization
124
Which condition is associated with an increased risk of altered resting membrane potential in cardiac cells?
A) Hypocalcemia
B) Hypernatremia
C) Hyperkalemia
D) Hypomagnesemia
Hyperkalemia
125
What is the significance of the threshold potential in cardiac cells?
A) Initiates sodium influx
B) Triggers potassium outflow
C) Leads to depolarization
D) Maintains the resting membrane potential
Leads to depolarization
126
How does the sodium-potassium pump contribute to maintaining the electrochemical gradient in cardiac cells?
A) By pumping in sodium and potassium ions simultaneously
B) By pumping out more sodium ions than potassium ions
C) By exchanging sodium ions for chloride ions
D) By modulating calcium influx
By pumping out more sodium ions than potassium ions
127
128
What role does calcium play in myocardial cell function?
A) Initiates depolarization
B) Triggers potassium outflow
C) Stimulates contraction
D) Inhibits sodium influx
Stimulates contraction
129
How does hypoxia affect myocardial fibers?
A) Converts fast-response fibers to slow-response fibers
B) Converts slow-response fibers to fast-response fibers
C) Has no effect on myocardial fibers
D) Increases sodium influx
Converts fast-response fibers to slow-response fibers
130
What is the main function of the sodium-potassium pump in myocardial cells?
A) Maintain calcium homeostasis
B) Generate action potentials
C) Control the resting membrane potential
D) Regulate pH balance
Control the resting membrane potential
131
Which ion primarily contributes to depolarization in myocardial cells?
Sodium ions (Na⁺)
132
What are the usual intracellular and extracellular concentrations of potassium ions (K⁺) in myocardial cells?
A) [K⁺]ᵢ = 4 mM, [K⁺]ₒ = 150 mM
B) [K⁺]ᵢ = 150 mM, [K⁺]ₒ = 4 mM
C) [K⁺]ᵢ = 40 mM, [K⁺]ₒ = 100 mM
D) [K⁺]ᵢ = 100 mM, [K⁺]ₒ = 40 mM
[K⁺]ᵢ = 150 mM, [K⁺]ₒ = 4 mM
133
What is the role of potassium (K⁺) leak channels in myocardial cells?
A) Allow K⁺ to flow inward
B) Prevent K⁺ from leaving the cell
C) Facilitate K⁺ outflow
D) Maintain K⁺ concentration gradient
Facilitate K⁺ outflow
134
How does the membrane become partially depolarized in myocardial cells?
A) Decreased potassium outflow
B) Increased potassium outflow
C) Influx of sodium ions
D) Activation of calcium channels
Influx of sodium ions
135
What triggers the opening of sodium channels in myocardial cells?
A) Decrease in potassium outflow
B) Increase in potassium outflow
C) Depolarization to threshold potential
D) Hyperpolarization
Depolarization to threshold potential
136
137
What is the function of the sodium-potassium pump in myocardial cells?
A) Pump out 3 sodium ions in exchange for 2 potassium ions
B) Pump in 3 sodium ions for every 2 potassium ions
C) Pump out potassium ions only
D) Pump in sodium ions only
Pump out 3 sodium ions in exchange for 2 potassium ions
138
time course for inactivation for the fast channels during phase 0
0.5 milliseconds
139
time course for inactivation of calcium channels during phase 3
50 milliseconds
140
voltage – dependent activated at -40 mV
calcium channels
