Cardiac Physiology Yr1FA23 Flashcards
(229 cards)
1
Q
Each cycle of cardiac contraction and relaxation is initiated by
A
depolarization of the sinus node.
2
Q
True/false: The cycle of cardiac contraction and relaxation being initiated by the sinus node is seen on the EKG?
A
FALSE
3
Q
The P wave records
A
atrial depolarization and contraction.
4
Q
The first part of the P wave reflects
A
right atrial activity; the second part reflects left atrial activity.
5
Q
(the PR segment)
A
There is a brief pause when the electrical current reaches the AV node and the EKG falls silent
6
Q
ventricular conducting system
A
(bundle of His, bundle branches, and Purkinje fibers)
7
Q
The first part of the ventricles to be depolarized
A
the interventricular septum.
8
Q
Ventricular depolarization generates what on the EKG
A
the QRS complex.
9
Q
The wave of depolarization then spreads along the ventricular conducting system (bundle of His, bundle branches, and Purkinje fibers) and out into the
A
Ventricular Myocardium
10
Q
The T wave records
A
repolarization of the ventricular myocardium
11
Q
Is Atrial Repolarization seen on the EKG?
A
NO
12
Q
the time from the start of atrial depolarization to the start of ventricular depolarization.
A
The PR interval
13
Q
the time from the end of atrial depolarization to
the start of ventricular depolarization.
A
The PR segment
14
Q
the time from the end of ventricular
depolarization to the start of ventricular repolarization.
A
The ST segment
15
Q
the time from the start of ventricular
depolarization to the end of ventricular repolarization.
A
The QT interval
16
Q
measures the time of ventricular depolarization.
A
The QRS interval
17
Q
Alpha 1 Receptor Site
A
Vascular Smooth Muscle
Heart
18
Q
Alpha 1 Receptor Action
A
Arterial Vasoconstriction
19
Q
Alpha 2 Receptor Site
A
Vascular Smith Muscle
Presynaptic Nerve terminal
20
Q
Alpha 2 Receptor Action
A
Vasoconstriction of venous capacitance vessels
Local feedback, inhibition of norepi release
21
Q
Beta 1 Receptor Site
A
Heart
22
Q
Beta 1 Receptor Action
A
Increased inotropic and chronotropic activity
Increased Av node conduction velocity
23
Q
Beta 2 Receptor Site
A
Vascular smooth muscle
Bronchial smooth muscle
24
Q
Beta 2 Receptor Action
A
Vasodilation of peripheral vasculature
Bronchodilation
25
D1 Receptor Site
post-synaptic
Vascular smooth muscle
(renal, Splanchnic, cerebral)
Renal Tubules
26
D2 Receptor Action
Decreased norepi release
27
D2 Receptor Site
Presynaptic sympathetic nerve terminals
28
D2 Receptor Action
Decreased norepi release
29
V1 Receptor Site
Vascular smooth muscle
platelets
Hepatocytes
myometrium
30
V1 Receptor Action
Vasoconstriction
Platelet aggregation
Glycogenolysis
Myometrial contraction
31
V2 Receptor Site
Basolateral membrane of collecting duct
Vascular endothelium
Vascular smooth muscle
32
V2 Receptor Action
INsertion of AQP-2 H2O channels in the apical membrane
induce AQP-2 synthesis
release of vwf and factor VII
vasodilation
33
V3/V1B Receptor Site
Anterior Pituitary gland
34
V3/ V1B Receptor Action
Release of ACTH
Prolactin
Endorphins
35
Norepinephrine Dose
0.02-.2 mg/kg/min
36
Norepinephrine Receptors
A1>B1& B2
37
Norepinephrine Inotropy
+
38
Norepinephrine Chronotropy
+
39
Norepinephrine SVR effects
+
40
Norepinephrine PVR Effects
+
41
Phenylephrine Dose
0.02-0.3 mcg/kg/min
42
Phenylephrine Receptors
Alpha1
43
Phenylephrine Inotropy Effects
<->
44
Phenylephrine Chronotropy effects
-
45
Phenylephrine SVR Effects
+
46
Phenylephrine PVR Effects
+
47
Vasopressin Dose
0.02-0.5 units/kg/hr
48
Vasopressin Receptors
V1 V2
49
Vasopressin Inotropy
<->
50
Vasopressin Chronotropy effects
<->
51
Vasopressin SVR Effects
+
52
Vasopressin PVR Effects
+
53
Nitroprusside Dose
0.2-5 mcg/kg/min
54
Nitroprusside Receptors
Increase cGMP in vascular myocytes
55
Nitroprusside Inotropy
<->
56
Nitroprusside Chronotropy
<->
+
57
Nitroprusside SVR
-
58
Nitroprusside PVR
-
59
Nicardipine Dose
0.5-5 mcg/kg/mni
60
Nicardipine Receptors
Calcium Channel Blocker
61
Nicardipine Inotropy
<->
62
Nicardipine Chronotropy
<->
63
Nicardipine SVR
-
64
Nicardipine PVR
-
65
Nitroglycerin Dose
0.2-10 mcg/kg/min
66
Nitroglycerin Receptors
67
Nitroglycerin Inotropy
68
Nitroglycerin Chronotropy
69
Nitroglycerin SVR
70
Nitroglycerin PVR
71
Epinephrine Dose
0.02-0.2 mcg/kg/min
72
Epinephrine Receptors
A1A2B1B2
73
Epinephrine Inotropy
+
74
Epinephrine Chronotropy
+
75
Epinephrine SVR
+
76
Epinephrine PVR
+
77
Epinephrine high-dose Inotropy
+
78
Epinephrine high-dose Chronotropy
+
79
Epinephrine high-dose SVR
<->
80
Epinephrine High-dose PVR
<->
81
Dopamine low dose
2-5 mcg/kg/min
82
Dopamine mid dose
5-10 mcg/kg/min
83
Dopamine high dose
>10 mcg/kg/min
84
Dopamine low dose Receptors
D1, D2
85
Dopamine mid dose receptors
B1, B2> A1
86
Dopamine high dose receptors
A1>B1, B2
87
Dopamine low dose inotropy
same
88
Dopamine low dose chronotropy
same
89
Dopamine low dose SVR
same
Reduces
90
Dopamine low dose PVR
Same,
Reduces
91
Dopamine mid dose Inotropy
+
92
Dopamine mid dose chronotropy
+
93
Dopamine mid dose SVR
<->
-
94
Dopamine Mid dose PVR
<->
95
Dopamine high dose Inotropy
+
96
Dopamine high dose chronotropy
+
97
Dopamine high dose SVR
+
98
Dopamine high dose PVR
+
99
Milrinone Loading Dose
25-75 mcg/kg
100
Milrinone Receptors
PDE3 Inhibitor
Increased cAMP
101
Milrinone infusion dose
0.25-0.75 mcg/kg/min
102
Milrinone Inotropy
+
103
Milrinone Chronotropy
+
104
Milrinone PVR
-
105
Milrinone SVR
-
106
Dobutamine Dose
2-20 mcg/kg/min
107
Dobutamine Receptors
108
Dobutamine Inotropy
+
109
Dobutamine Chronotropy
+
110
Dobutamine SVR
-
111
Dobutamine PVR
-
112
Function of Systemic circulation
Delivers oxygen to all body cells and carries away wastes
113
OXygenated blood is pumped to all body tissues via
The Aorta
114
Deoxygenated blood is pumped to the lungs via
Pulmonary arteries
115
Function of Pulmonary arteries
Eliminates CO2 via the lungs and oxygenates the blood
116
Deoxygenated blood returns to the heart via
Vena Cava
117
Oxygenated blood returns to the heart via
Pulmonary Veins
118
General function of the CV system
Transporting nutrients to the body tissues
Transporting waste products away
Transporting hormones from one part of the body to another
Temperature regulation
119
When valves are open, what is the skeletal muscle doing?
Contracted skeletal muscle
120
When valves are closed, what is the skeletal muscle doing?
Relaxed skeletal muscle
121
In cardiac Action potential, Phase 0
fast, voltage-gated Na+ channels open. K+ channels close
122
In phase 0 of Cardiac AP, is it fast or slow
Fast
123
In phase 0 of Cardiac AP, what are the Na+ and K+ Channels doing?
Voltage- GatedNa+ channels open
K+ channels close
124
Describe Phase 1 of Cardiac AP
transient outward rectifier potassium channels (Ito) open briefly
125
Describe Phase 2 of Cardiac AP
slow L-type Ca2+ channels
open (plateau).
126
Phase 3 of Cardiac AP
Ca2+ channels close. K+ channels re-open
127
Phase 4 of Cardiac AP
Resting Membrane Potential is re-established (K+ channels stay open)
128
RMP of Cardiac AP
-90
129
Phase 0 Membrane potential (mV)
-90-+20
130
Phase 1 membrane potential (mV)
+20
131
Phase 2 Membrane Potential (mV)
+10
132
Phase 3 Membrane Potential (mV)
-20
133
Plateau phase
actin / myosin molecules remain activated for 300ms.
Ca2+ enters here
134
Ca2+ entering during plateau phase helps
activate the muscle for sustained, forceful contraction.
135
Absolute Refractory Period (Definition)
all inactivation gates are closed no electrical stimulus will elicit another action potential.
136
Absolute Refractory period runs from
Runs from phase 0 through most of phase 3.
137
True or False: Heart Muscle can be tetanized
FALSE
Because of the long refractory period, heart muscle cannot be tetanized
138
Relative Refractory Period
Some inactivation gates are open
An action potential can be elicited but a higher stimulus voltage is required and not all channels participate.
139
In the SA Node, timing of depolarization to depolarization is
Intrinsic HR
140
In the SA Node, Pacemaker potential is due to
gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
141
Electrical Properties of the SA Node
gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
142
The heartbeat originates in
The SA Node
143
After the SA node, where does the electicity conduct through?
and spreads over the heart by cell to cell conduction through a complex pathway
144
Why is the SA Node the pacemaker?
because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.
145
Order of conductance of electricity through the heart
SA Node
AV Node
AV Bundle
Left and Right Bundle Branches
Purkinje Fibers
Ventricular Myocardium
146
Atrial Conduction Velocity
1-1.2 m/S
147
AV Node conduction Velocity
0.02-0.05 m/s
148
AV Bundle Conduction Velocity
1.2-2.0 m/s
149
Bundle Branches and Purkinje Fibers' Conduction Velocity
2.0-4.0 m/s
150
Ventricular Myocardium Conduction Velocity
0.3-1.0 m/s
151
SA Node Rate of discharge (B/min)s
60-100 B/min
152
AV Node Rate of Discharge
40-55 B/min
153
Bundle Branches/ Purkinje Fibres Rate of Discharge
25-40 B/min
154
Which tissue has the slowest conduction Velocity?
AV Node
155
Why is the AV node the slowest in conduction?
It has small diameter cells, few gap junctions and slow phase zero
156
Which structure conducts the fastest in Cardiac AP?
Purkinje FIbers
157
Why are the Purkinje Fibers the fastest for conduction?
It has small diameter cells, few gap junctions and FASTphase zero
158
Atrial , ventricular, and Bundle of His tissue conduct at what velocity
1m/sec
159
What is the only pathway to the Ventricles in Conduction?
The AV Node
160
The paucity of gap junctions in the AV node also causes a safety factor
(the amount of current passed to the next cell/the amount of current needed to reach threshold).
161
AV node is vulnerable to Injury from
disease which can cause loss of conduction to the ventricles.
(Heart block)
162
Ablation of the fast-conducting tissue below the AV bundle is very serious. Why?
the spontaneous rate for Purkinje fibers is dangerously low
163
Ablation of the AV node slows the heart rate down to that of
the next highest pacemaker (below the node)
164
Baroreceptors in_______detect changes in blood
Carotid Sinus and Carotid arch
165
Rising pressure stretches receptors
Leads to
Parasympathetic Activation
166
Decreasing pressure leads to
less stretch on receptors ->sympathetic activation
167
Why can heart muscle not be tetanized?
Because of the long refractory period
168
In SA Node conduction, is the sharp spike present?
Sharp spike is absent (no fast Na+ channels). Phase 0 from slow Ca++ channels
169
In SA Node conduction, how does pacemaker potential occur?
Pacemaker potential is due to gradual drop in K+ conductance and and an increase in Na+ conductance “the funny current” (If).
170
In the SA Node conduction, how is depolarization timed?
Timing of depolarization to depolarization is intrinsic HR
171
Why is the SA Node the pacemaker of the heart?
Because it has the fastest rhythm.
It is the first structure to show electrical activity with each beat.
172
How is the rate of Cardiac Pacemakers slowed?
-The Vagus nerve secretes Ach (Parasympathetic activation
-Ach increases K+ conductance at KAch channels, which hyperpolarizes the SA Node cells and opposes the Funny Current (Lf)
-CAMP is also decreased
173
How is the rate of Cardiac Pacemakers increased?
- Sympathetic nerves secrete norepinephrine which acts at beta receptors on SA node leading to increased cAMP
- cAMP opens the hyperpolarization-activated cyclic nucleotide-gated (HCN) sodium channels which increases If (funny current) during phase 4, thus increasing speed of depolarization.
174
Describe Sympathetic Neural Regulation of the heart:
Sympathetic stimulation :
Increases HR
Decreases AV Node ERP
Decreased PR
Increased Contractility (SV)
175
How are the Supraventricular and Purkinje Fibers innervated?
Vagal Innervation
176
How is everywhere bu the supraventricular and Purkinje fibers innervated?
Sympathetic Innervation
177
Receptors on Sympathetic Ganglia
AcH- NIcotinic
178
Receptors on Sympathetic nerves
Norepinephrine
179
Describe Vagal Neural Regulation of the heart:
Decreased HR
Increased AV Node ERP
Increased PR
180
What is the largest current in the heart?
Sodium Current
181
What is the status of Sodium channels at RMP?
Na+ Channels are closed at RMP
181
Has Alpha/Beta Subunits that are sensitive to cAMP-Dependent protein Kinase
Sodium Current
182
Regenerated spread of the action potential depends largely on what?
The magnitude of the Na+ Current
183
The depolarization caused by Na+ also activates what?
Lca
Ik
184
What inactivates the Na+ Channels in the heart
Sodium-Channel Blockers
185
L-Type Calcium channels are inactivated by
Dihydropyridines
Phenylalkylamines
Benzothiazepines
186
This current is activated by voltage, Deactivated by time
L-Type Calcium Channels
186
At RMP, what is the status of L-Type Calcium channels?
Closed at RMP
187
Why are Cardiac Action Potentials twice as long as skeletal muscle APs?
Because the K+ channels open so slowly
188
How is the K+ Repolarization current divided?
IKA- Rapid
IK- Slow
189
Early outward / A-type current
Found in atrial and ventricular muscle. Activated by depolarization and deactivated quickly. Contributes to phase 1
190
G-protein activated current
Ach to receptor to GIRK K channels resulting in outward K current. Prominent in SA and AV nodal cells
191
KATP channels in the sinoatrial node contribute to
HR Control
192
When fully activated, KATP channels can cause cardiac electrical activity to
STOP;
Contractile Failure
193
KATP channels play a role in
heart rate control, adaptation to hypoxia, and cardiac excitability
194
Where is the Funny Current found?
SA, AV and Purkinje fibers
195
How is the Funny Current Mediated?
by a nonspecific anion channel called HCN… Hyperpolarization activated Cyclic Nucleotide Gated channel
196
Funny Current conducts which currents?
Both Na and K
197
Does the Funny Current conduct at positive potentials?
No
Does not conduct at positive potentials
198
The funny current is activated by hyperpolarization during what phase of the Cardiac Action Potential?
phase 4 of the cardiac action potential, which is also known as diastolic depolarization
199
Where is the SA Node located?
Sits in RA near the junction of SVC
200
SA Node size in comparison to other atrial muscle fibers:
Smaller than the other atrial muscle fibers
201
Cardiac muscle differs from skeletal muscle in that
It has Slow L-Type Calcium Channels
202
Phase 0 in the SA Nodal cells is due to
Slow Calcium channels
203
The slowest conduction velocity occurs in the :
AV Node
204
What is true about aortic Arch baroreceptors?
Stretching of the receptors occurs when arterial pressure suddenly rises
205
All are true about the sympathetic nervous system EXCEPT:
A- Norepi acts on Beta receptors to increase cAMP
B. Activation of the sympathetic nervous system leads to increased heart rate.
C. Increased cAMP leads to Activation of K+ channels that hyperpolarize the cell membrane and increase the activity of the "Funny Current" during phase 4
D. Increased cAMP and increased opening of hyperpolarization-actiated cyclic nucleotide-gated (HCN) Sodium channels that increase activity of the "Funny Current" during Phase 4
C.
Increased cAMP leads to activation of K+ Channels that hyperpolarize the cell membrane and increase the activity of the "Funny Current" during Phase 4
206
All is true about the sympathetic ns Except:
A- Norepi acts on Beta Receptors to increase cAMP
B. Activation of the SNS leads to increased HR
C. Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the "Funny Current" during phase 4
D. Increased cAMP and increased opening of hyperpolarization-activated cyclic necleotide-gated (HCN) sodium channels that increase activity of the "Funny Current" During Phase 4
C.
Increased cAMP leads to activation of K+channels that hyperpolarize the cell membrane and increase the activity of the "Funny Current" during phase 4
207
Select the true statement about L-Type Calcium Channels:
A: Present in the heart and vasculature
B. They are activated by voltage and deactivated by time
C. They are open at very negative membrane potential
D. They are inhibited by Beta Blockers
B.
They are activated by voltage and deactivated by time
208
True or False: Fast Sodium channels open during Phase 0 of the AP in the SA Node
FALSE
209
The AV Node:
A: Is located near the Mitral Valve
B. Conducts very quickly
C. Gives RIse to Purkinje Fibers
D. Has an intrinsic pacemaker rate of 300 bpm
C. Gives rise to Purkinje fibers
210
Which leads would you see changes in for a bundle branch block?
Anterior
Anterior leads are leads V1, V2, V3, and V4. For a left bundle branch block you will see a “beach chair” formation in these leads and in a right bundle branch block you will see “bunny ears” in these leads.
211
Which of the following is an EKG change seen with hyperkalemia?
A. Sine wave
B. U wave
C. Peaked T waves
D. QRS widening
E. P wave flattening
F. A, C, D, E
G. All of the above
F. A, C, D, E
U waves are seen in hypokalemia not hyperkalemia. Changes seen with hyperkalemia are often progressive, starting with peaked t waves. This progresses to QRS widening and p wave flattening with the sine wave (and eventually torsades) following.
212
what arrhythmia reflects U waves on the EKG?
Hypokalemia
213
In which of the following scenarios is a pacemaker NOT indicated?
A. Second degree heart block type I
B. Second degree heart block type II
C. Third degree heart block
D. Third degree heart block caused by lyme disease
E. A and B
F. A and D
F. A and D
Third degree heart block caused by lyme disease IS reversible when treated with corticosteroids and antibiotics and may not indicate need for a pacemaker. Second degree heart block type I (wenckebach) rarely progresses to third degree heart block and is usually transient and benign. It also does not indicate need for a pacemaker. Type II second degree heart block on the other hand often progresses to third degree heart block and needs a pacemaker.
214
What is the fastest conduction system of the heart? What is the slowest?
A: SA node; AV node
B: purkinje fibers; AV node
C: AV node; SA node
D: SA node; purkinje fibers
B: purkinje fibers; AV node
This question is looking at conduction velocity NOT the rate of pacemaker discharge (BPM)
215
When discussing neural regulation of the heart, the right vagus nerve innervates what structure?
A: purkinje fibers
B: AV node
C: SA node
D: myocardium
C: SA node
The right vagus nerve innervates the SA node and the left vagus nerve innervates the AV node and purkinje fibers. There is sympathetic innervation everywhere in the heart.
216
What leads do you look at to determine axis?
A: aVR, I
B: aVL, III
C: aVF, I
D:aVF, II
C: aVF, I
217
If lead I is positive and lead aVF is negative, what is the axis?
A: Left axis deviation
B: Normal axis
C: Right axis deviation
D: Extreme right axis deviation
A: Left axis deviation
218
3. Which of the following is represented by the Q wave?
A. Atrial depolarization
B. Atrial repolarization
C. Ventricular depolarization
D. Septal depolarization
D. Septal depolarization
219
1. Which of the following will carotid massage/vagal maneuver terminate?
A. A flutter
B. A fib
C. PAT
D. AVNRT
D. AVNRT
Carotid massage should not regularly be done, but is theoretically only helpful in terminating SVTs such as AVNRT. It can be useful in determining if a rhythm is atrial flutter as the ratio to atrial/ventricular depolarizations will become longer (i.e. 1:2 to 1:3 or 1:4).
220
2. In which of the following arrhythmias would your patient most likely be on anticoagulation?
A. SVT
B. A flutter
C. A fib
D. V tach
C. A fib
Pretty much all a fib patients will be on anticoagulants as the quivering atria can allow blood to move slowly and form clots.
221
3. Which of the following arrhythmias is defibrillation (NOT synchronized cardioversion) used for?
A. A fib
B. A flutter
C. V tach
D. F fib
E. Asystole
F. Pulseless electrical activity (PEA)
G. A and B
H. C and D
I. A, B, E, F
J. C, D, E, F
K. All of the above
H. C and D
A fib and A flutter require synchronized cardioversion or else this can lead to R on T phenomenon and cause torsades. Asystole and PEA are non-shockable rhythms and you cannot use defibrillation or synchronized cardioversion on these patients.
222
Non-Shockable Rhythms
PEA
Asystole
223
Your patient in the ICU is found to have metabolic acidosis (pH< 7.35). Which way is their oxyhemoglobin curve shifted: left or right?
Right
With metabolic acidosis there is an increase in H+ ions which shifts the curve to the right. Anything that “increases” will shift the curve to the right (increased offloading of O2/decreased affinity) and anything that “decreases” will shift the curve to the left (decreased offloading of O2/increased affinity)
224
The Frank Starling curve relates:
a. Stroke volume and preload
b. Preload and afterload
c. Afterload and force of contraction
a. Stroke volume and preload
The greater the heart muscle is stretch during filling (PRELOAD/ left ventricular end diastolic pressure), the greater the force of contraction and the greater the quantity of blood pumped into the aorta (SV). The greater the preload (up until a certain point), the more the myosin and actin before aligned and the greater the contraction.
225
At low doses, dopamine acts of what receptors?
a. Alpha 1 receptors
b. Beta 1 receptors
c. Beta 2 receptors
d. Dopamine receptors
d. Dopamine receptors
2-5 mcg/kg/min D1, D1
5-10 mcg/kg/min B1>B2>A1
>10mcg/kg/min A1>B1, B2
226
2. Which of the following drugs would be the most useful in treating ventricular tachycardia?
a. Procainamide
b. Labetalol
c. Verapamil
d. Phenytoin
A- Procainamide
Class I antiarrhythmics are particularly useful in treating ventricular arrhythmias (wide QRS). Amiodarone and sotalol would be appropriate alternatives.
227
